I’m going to tell you about the best low-carb book I’ve ever read. In fact, it’s exactly the book I wish I had written myself.  And I’ll tell you why I didn’t in a bit, but first I want to clear up a few misconceptions I may have spread in my last post.

I get feedback on the posts I write from three sources.  First, MD looks at them and tones them down if I’ve gone off on some sort of political tangent or if I’ve scattered in a bit of too colorful language.  After she gives me the go, I put the posts up and wait to see what the commenters have to say.  The third source for feedback is my friends, some MDs and/or PhDs and some not, who pick up the phone and call me.

MD okayed what I wrote. The readers who commented seemed to realize what I was trying to say.  But the phone calls were a different story.

One friend called to say she had been low-carbing since Jan 1, and when she read my post she became so depressed she almost quit.  “How can you tell people it’s hard,” she said.  “It’s the easiest thing I’ve ever done. I can eat till I’m full.  I’m losing weight; I’m losing the water I’ve been retaining; I feel great.  What a downer that post was.”

I heard different versions of that rant from three other people.  They all wanted to know why I would be idiotic enough to put up such a post right at the time everyone was trying to commit or recommit to losing weight.  Depressing was a word everyone used.

I guess I got off easy with the written comments on the blog.

I didn’t really mean for the post to be a downer.  Really.  I wanted to tell people who might be struggling to lose that MD and I fall prey to all the same problems.  We gained weight over the holidays.  We are back on the straight and narrow.  I was trying to say that we were right in there with everyone else working away to reestablish our own thinner selves.  (In fact, we’ve made great progress in the week or so we’ve been on the plan.)  I just wanted people to be aware that long-term weight loss requires effort and constant vigilance.  And to view the process as a life change and not a quick one-time fix. My goal was to get people to recommit seriously, not to depress them.

Obesity is a medical problem caused by a damaged metabolism, which is why one person, without the damage, can eat the same foods without gaining weight that pack the pounds on someone else.  Once you realize you have the underlying problem that leads to obesity, you simply have to recognize that you have to deal with it for the long term.

Let’s look at it in terms of another medical problem: high blood pressure.  For argument’s sake, let’s ignore the fact that about 80 percent of cases of high blood pressure can be reversed with a low-carb diet, and let’s just assume that the case we’re talking about is responsive only to high blood pressure medication.  If you were the patient with the high blood pressure, and I gave you a pill that brought your blood pressure down to normal, you would consider the medication effective.  Would you then say, Hey, my blood pressure is normal, yippee! now I can quit taking the medicine?   I doubt it.  You would say, Great, the medicine is working.  Furthermore, if you quit taking the medicine and your blood pressure went back up to what it was before you started taking the medicine, would you say the medicine didn’t work?

Of course not.  Your high blood pressure was kept in check with the medicine, and your BP, not surprisingly, went back up when you quit taking the medicine.  The medicine itself was effective.

Same thing with dieting.  If you have an obesity problem that responds to a low-carb diet and you lose to your target weight, then go back to your old way of eating and gain your weight back, it isn’t the low-carb diet’s fault.  You have a problem that responds to a low-carb diet, and you pretty much have to stick with a low-carb diet (although not in nearly as extreme a structure as when you are trying to lose) for the long haul.

Having said all that, I can tell you that in my experience there is nothing that helps people lose weight more quickly and with less deprivation than a good quality, whole food low-carbohydrate diet.  You don’t have to be hungry.  You can eat rich, delicious foods, you’ll get rid of heartburn, drop your blood pressure, ditch excess fluid, and feel remarkably better.  You’ve just got to hang in there until you lose what you need to lose (which process you can speed along if desired with a little Metabosol), then you can loosen up and start adding some of the foods you’ve been foregoing.  And continue to eat them in moderation on maintenance.

Virtually all the studies in the medical literature show that at worst the low-carbohydrate diet equals the low-fat diet in all parameters and at best completely leaves it in the dust.  As far as I’m concerned, there is no faster, safer, more delicious way to lose weight. Hell, a study was just presented recently showing that women who did low-carb just two days a week lost almost twice as much weight as women following a calorically-restricted Mediterranean diet daily.  So, to be clear: Is weight loss tough?  Sure.  Is it easier when you cut the carbs? Absolutely! Low carb rocks!

Which brings me to the book that started this post.  In my opinion, The Art and Science of Low Carbohydrate Living is simply the best how-to book on low-carb dieting ever written.  As I wrote above, it is the book I wish MD and I had written.

The reason we didn’t write it is because a) some of this information wasn’t available when we last wrote a book (much of it is now available thanks to the work of Drs. Volek and Phinney), and b) no mainstream publisher would pay an author for this book.  If a mainstream publisher would buy it, the editor would force the authors to change it.  What do I mean by that?

All books fall into different genres, as they’re called in publishing.  One genre is diet/nutrition books.  So if you come to a publisher offering a diet/nutrition book, it gets pigeonholed into that genre and has to conform structurally to that genre’s standardized format.  Editors of mainstream publishing houses believe that the great mass of readers of nutritional books are not very bright and so have to be served real scientific information in small, small bites and not very many of them at that.  So the genre formula for a diet book is to have the actual diet regimen way up front because these editors don’t believe the readers of these books are smart enough or patient enough to wade through the explanations of why a particular diet works in order to get to the plan.  They want the plan up front within the first couple of chapters so people can get started without really having to read the book.  They also want a ton of recipes and meal plans to fill up the last half of the book.  Squeezed in between the plan and the recipe section is where they want to meat of book cubbyholed, and, in their view, with as little science as possible.

MD and I fought this structure tooth and toenail with Protein Power and ended up beating our editor down by agreeing to write a summary of each chapter called The Bottom Line that explained what each chapter said in non-scientific terms.  (Fortunately, we’ve been able to use this strategy in most of our books.) We worked well with our first editor, but we ended up in the hands of another editor when the paperback came out.  Editor Number Two hated all the stuff on the Paleolithic diet and the data from the ancient Egyptians.  This info was the first time in the popular press that the pre- verses post-agricultural diet was used as an argument for low-carb dieting.  And she wanted to ditch it from the book.  We went postal on her, so she ended up agreeing to leave it but only if we buried it in the very back of the book as an Epilogue.  That was one of the chapters of the book I wrote, and I thought it was pretty exciting information.  So, apparently did many others. But not this editor.  Sadly, she is not unusual.  Most want to conform to the genre.

Drs. Volek and Phinney self-published their book, and, as a consequence, could write it however the flip they wanted.  It is extremely well written and suffers none of the usual flaws of a self published book.  And it lays out the rationale for a low-carb diet as the treatment of obesity and other related disorders in a linear fashion instead of adhering to the typical diet book format.

As I finished writing the above paragraph, I clicked over and checked for comments on my latest post and found one with the following line:

This low-carb world can be a lonely place if one needs a navigator…

I can think of no better navigators than the authors of this book. Both of them have done a large part of the hardcore research on low-carb dieting that is in the medical literature today.  Go to PubMed and enter Volek JS or Phinney SD in the search window, hit ‘Search,’ and you will be rewarded with more peer-reviewed scientific papers on low-carb dieting than you will have time to read.  Many of the experiments described in these papers are explained in easy to understand language in their book.

Disclosure: Both Dr. Volek and Dr. Phinney are friends and colleagues of mine.  But they did not send me a copy of their book for review.  I purchased it from Amazon and paid the full price of $29.95 (it is now $19.95).  I bought it months ago and carried it with me all over Europe and on a half dozen other trips since but didn’t have time to even crack it until I was on the last leg back from our holiday trek.  It sounds cliché, but I couldn’t put it down.  I read and annotated the entire book over the course of two long flights.  Virtually anything anyone could want to know about the science behind low-carbohydrate dieting can be found in this book.

I’ll give you just one example.  It is common knowledge among many nutritionist, doctors and journalists that saturated fats are bad for us.  Most believe eating saturated fats leads to higher levels of saturated fats in the blood, which they inevitably describe as ‘artery-clogging saturated fat’.  Drs. Volek and Phinney, who certainly don’t believe this nonsense, understand adaptation to a low-carbohydrate diet changes the way the human body metabolizes different fats.  Eating more fat on a low-carbohydrate diet speeds up the burning of fat in general and saturated fat in particular.

There are only three things the body can do with saturated fat from the diet (or saturated fat made from dietary carbohydrate — and, yes, the body can and does make saturated fat from dietary carbohydrate).  It can burn them, store them, or convert them to a mono-unsaturated fat.  When people go on low-carbohydrate diets, they reduce their insulin levels, which in turn allows fat to escape from the fat cells to become the body’s primary fuel.

But what happens when a person increases saturated fat intake as part of a low-carbohydrate diet?  Drs. V & P knew that saturated fat burning would increase, but would enough burn to offset the extra amount of saturated fat coming in as part of a high-fat, low-carbohydrate diet?

To find out, they put 20 subjects on a low-carbohydrate diet for 12 weeks and another 20 subjects on a low-fat, high-carbohydrate weight loss diet for the same length of time.  The subjects in the low-carb group consumed three times the saturated fat per day (36 g vs 12 g) as did those in the low-fat group.  The blood from the subjects in both groups was then tested to determine total triglyceride level and specific fatty acid composition.

What did the good docs find?

In the serum samples done at baseline and again after 12 weeks, serum triglycerides  in the low fat group went from 187 to 151 mg per 100 ml, a tidy 19% reduction.  But in the low carb group, the before and after values were 211 and 104, a whopping 51% fall.  Both visually (just looking at the numbers) and statistically, the low carbohydrate group had a much greater (better) reduction in serum triglycerides.

The above should come as no surprise, because everyone knows that a low-carb diet reduces triglyceride levels.  But what about the amount of saturated fat in the blood?

As a proportion of the total, the low carb group had 33% saturates [saturated fatty acids] at baseline and 29% after 12 weeks, whereas the low fat group started at 30 and ended at 29%.  So after 12 weeks of dieting, the proportion of saturated fats in the blood triglycerides was the same for both groups despite the fact that the low carb group was eating three times as many grams per day of saturated fat in their diet.

But there’s more.  Because the low carb group ended up with blood triglycerides of 104 mg per 100 ml compared to the low fat group’s 151, they actually had about 30% less total triglycerides circulating in their serum.  So although the two groups had similar relative proportions of saturates, this means that the absolute serum content of saturates in the low-carb group was 30% lower than the low fat diet group.  So what we found, in a nutshell, is that despite a higher intake of saturated fat, the proportionate blood level of saturated fats did not increase, and their absolute levels fell dramatically with the low carbohydrate diet.

The bottom line on this point is that when our metabolism adapts to a low carbohydrate diet, saturated fats become a preferred fuel for the body, and their levels in blood and tissue triglyceride pools actually drops.

To summarize, a three times higher intake of saturated fats leads to a 30% drop in saturated fats in the blood of those following a low-carb diet as compared to those following a low-fat, high-carb diet.

Which means, of course, that if you want to decrease the artery-clogging saturated fats (should that be what you want to call them) in your blood, a low-fat, high-carb diet, the very diet almost every health care professional recommends for the job, isn’t the way to do it.  All you have to do is simply follow a low-carb diet.

The description of what happens to saturated fats in the blood during a low carb diet took two pages out of a 300 page book, so you can imagine how much content the entire book contains.

There is so much invaluable information in this book that I’m having to fight back the impulse to quote the whole thing.  You’ll learn

why you need more sodium on a low-carb diet and why the sodium prevents lean tissue loss,
why you need to increase fat intake during maintenance,
why a low-carb diet decreases inflammation,
why the low-carb, high-fat diet improves gall bladder function,
why excess carbohydrate converts to saturated fat and how,
what all the lipid parameters mean and how they’re affected by a low-carb diet,
and what the Paleolithic evidence tells us about diet.

And this list is just scratching the surface.  As I read this book, I kept marking parts that I needed to use for this blog.  In going back through, I would have to practically reprint the whole thing to give you just the important parts because the entire book is a gem.

Unlike most traditional diet books, The Art and Science of Low Carbohydrate Living doesn’t contain a lengthy section on how to execute a low carb diet.  There are plenty of books out there – some written by MD and me – that do that.  The book does have about 10 pages of the authors’ favorite recipes for low-carb foods and a seven day meal plan incorporating many of these recipes. (Another disclosure:  The authors recommend Protein Power as a good book on low-carb dieting, but I would have written this review the same had they never mentioned our book.)

The strength of this book isn’t in its meal plans and recipes, although those are delicious, it is in the wealth of information about all aspects of low-carb dieting.  If you have a question, almost any question, about any facet of low-carbohdyrate dieting, this book will have the answer.  And the answer will grounded in science, and in many cases from work done by these two scientists on the front lines of low-carbohydrate research.

As far as I am concerned, if you are planning on going on a low-carb diet and can afford only one book, make The Art and Science of Low Carbohydrate Living that one book.  If you are a long time low-carber, this is the one essential reference book you should have on your shelf.

If you are getting going on a low-carb diet the first part of this year, grab this book before you do another thing.  Once you see the world of benefits that will accrue to you from following such a diet, you will probably be able to overcome any depression that may have been inflicted on you from my last post.  So don’t hold off, grab a copy of this book today.  You will be very glad you did.

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.

In the last post we discussed ramping up the fat intake as the single best way to hurry the low-carb or keto adaptation along.  I didn’t mention it in the previous post, but another little secret is to keep an eye on the protein intake. Too much protein will prevent the shift into ketoses because the liver will convert some of the protein into glucose – this glucose will then be used first and slow down the ketogenic process.  Which, if course, prompts the question, how much protein is too much?  As long as you’re getting your protein from meat, especially fatty cuts of meat, you’re probably okay.  If you go for the extremely lean cuts of meat, say, skinless chicken breasts, or if you are supplementing your diet with low-fat protein shakes, you could have a little more trouble low-carb adapting.  If you’re going the shake route, I would recommend you add some coconut oil to the shakes for a couple of reasons.  First, you’ll hasten the keto-adaptation, and, second, the fat it coconut oil will help remove the fat from your liver (which I’ll discuss more later in this post).

A glass of Tinto de Verano pictured at left. A great way to hydrate. (See note at bottom of post.)

As I said, you need to really crank up the fat intake to push yourself over the adaptation divide as quickly as possible.  If you don’t like fatty cuts of meat, you can add a little medium-chain triglycerides (MCT) to your diet.  MCT are absorbed more like carbohydrates and are used quickly by the body.  They are almost never incorporated into the fat cells, so they burn quickly, and any extra that might be hanging around are converted to ketones.  So, MCT will drive the ketone production process.  And so will coconut oil if you prefer that.

You can find MCT oil at most health food or natural grocery stores.  It has never bothered me, but some people can get a little nauseated if they take too much of it, so if you decide to give it a try, start out slowly.  Or go with the coconut oil.

Aside from the occasional carb cravings, which we’ll deal with later, the most common symptoms experienced by those getting started on low-carb diets are fatigue, headaches, light-headedness or dizziness, and cramping.  I would say these four symptoms probably comprise 98 percent of the complaints we get from our patients we put on low-carb diets.  Not everyone experiences these symptoms – especially those who do what we tell them – but of those who do have symptoms, these are almost always the ones they have.  Let’s look at what to do to avoid them or treat them should you already be experiencing on or more.

Electrolytes

The most common cause of virtually all the symptoms listed above is an imbalance in electrolytes.  Following a low-carb diet results in a rapid lowering of insulin levels, which – though a good thing – can create problems in the early days.  We’ll address the electrolytes in the order of importance.

Sodium

When you are overweight and insulin resistant, you have a lot of insulin circulating in your blood most of the time.  This excess insulin does a number of bad things to you.  Gary Taubes wrote an entire book about how excess insulin makes you store fat in your fat cells.  But the story doesn’t end there.  Excess insulin also drives the kidneys to retain fluid, which is why many obese people retain a lot of extraneous fluid and experience pitting edema in their lower legs.

What is pitting edema?

If you push your finger into the tissue in the front (or just to the side of) your shin bone and your finger leaves an indentation – almost a finger print – that takes a while to fill back in, you have pitting edema.  Most overweight people experience this phenomenon late in the afternoon and/or at night after being on their feet all day.  The excess fluid pools around the lower legs and seeps into the soft tissues. In the morning, after the body has been horizontal through the night, the fluid redistributes, and the pitting edema goes away but then reoccurs as the day goes on.  Even people who aren’t all that overweight but who do have elevated insulin levels will have some degree of excess fluid accumulation even if they don’t experience pitting edema as evidence of it.

One of the first things that happens when people go on low-carb diets is a rapid improvement in insulin sensitivity.  Because the low-carb diet starts to quickly banish the insulin resistance, insulin levels fall quickly.  And as insulin falls, the stimulus to the kidneys to retain fluids goes away, and the kidneys begin to rapidly release fluid.  One of the common experiences at the start of low-carb dieting is the incessant running back and forth to the bathroom to urinate this excess fluid away.  Which is both good news and bad news.

The good news is that it’s great to get rid of the excess fluid but it comes at a cost, which is the bad news.  As the excess fluid goes, it takes with it sodium an extremely important electrolyte.  When sodium levels fall below a critical threshold (which can happen within a short time), symptoms often occur, the most common being fatigue, headache, cramps and postural hypotension.

Postural hypotension happens when you stand up too quickly and feel faint.  Or even pass out briefly.  It’s a sign of dehydration.  So if you’ve started your low-carb diet, made your multiple runs to the bathroom, and jump up off the couch to answer the phone and feel like your going to faint (or actually do pass out momentarily) and have to sit back down quickly, you’ve got postural hypotension.  It’s really easy to fix – you simply need to take more sodium and drink more water.  Salt your food more.  Increasing sodium is just another one of the many counter-intuitive things about low-carb dieting.  Just like eating more fat to lower your cholesterol.  You’ve got to start thinking differently.  The low-carb diet is one that absolutely requires more sodium.  A lot more sodium.

If you’ve got the brutal headaches that some people get when starting on a low-carb diet, add sodium.  And drink extra water.

Even if you don’t have pitting edema, postural hypotension or headaches, you still need more sodium if you are starting out on or following a low-carb diet. It’s critically important that you get extra sodium.  I can’t make this case too strongly.

An easy way to get extra sodium along with magnesium and potassium (a couple of other electrolytes we’ll discuss in a bit) is by consuming bone broth.  Unfortunately, you typically have to make the good stuff yourself because it’s difficult to find commercially.  You can get chicken broth and beef broth at most grocery stores, but it’s not nearly as good as the broth you can make yourself.  At the end of this post I‘ll give you a spectacular recipe that we have for a great bone broth we made at our now-defunct restaurant.  It is beyond good.  It requires a little time, but you can make a bunch and freeze it in small containers and keep it forever.

Short of making your own bone broth, you can use commercially available bouillon, which contains plenty of sodium and makes a nice hot drink.  Plop a cube in a cup of hot water and throw it back. Many patients have reported that drinking a cup of hot bouillon helps them get through carb cravings.  It’s easy and convenient, but can’t compare in taste to the real bone broth you make yourself.

In addition to broth, get some Celtic Sea Salt, Himalayan Salt or one of the other grayish, pinkish kind of grungy looking salts and replace your normal salt with these.  And don’t use them sparingly.  These salts have been harvested either from ancient sea beds or obtained by evaporation of sea water with high mineral content and contain about 70 percent of the sodium of regular salt (which has been refined, bleached and processed until it is pretty much pure sodium chloride, often with anti-caking agents added).  The other 30 percent of the volume is other minerals and micronutrients (including iodine) found in mineral-rich seas.  Consuming these salts is not just following a Paleolithic diet using modern food, but, depending upon the origin of the salt, it is consuming the same food your Paleolithic ancestors ate.  I much prefer these salts taste-wise to regular salt, and I salt the heck out of all my food with it.

Magnesium

The low-carb diet doesn’t really cause a massive depletion of magnesium like it does with the sodium and potassium (the next electrolyte on the list), but most people who are overweight, insulin resistant and/or hypertensive or diabetic are deficient in magnesium.  Even people with lipid problems are often magnesium deficient.  In fact, even people who don’t seem to have health problems can often be magnesium deficient because most people don’t get enough.   The last I read on the subject, about 70 percent of people don’t even get the minimum recommended daily intake of magnesium (which isn’t all that high).  So, in my opinion, it’s important to supplement this vital mineral.  Good magnesium levels help regulate potassium as well, so keeping your magnesium adequate helps with your potassium as well.

Nature has designed us so that approximately 300 plus of our enzymes require magnesium as a co-factor to make them work properly.  Which tells us that we evolved in a time when magnesium was readily available, otherwise the forces of natural selection wouldn’t have made such wide use of it.

Where did it come from?  I would bet most of it came from the water.  Most natural sources of water have a high magnesium content, so when you drink bottled water and softened and treated water, you get short changed.  Magnesium salts in water are one of the substances that tends to make deposits on your water pipes and makes it difficult to get a good lather with soap.  This problem is solved with water softeners, but the process gets rid of the magnesium.  In the old days when we all drank well water or stream water, we got a lot more magnesium.

Since magnesium is used in 300+ different chemical reactions in the body, a shortage of magnesium can cause problems.  One of the most common ones is an increase in cravings.  Often simply replenishing magnesium gets rid of many of the food cravings people have.

The best way to get magnesium is from supplements.  Get a good chelated magnesium supplement and take 300-400 mg per day.  We’ve found it best to take these supplements in the evening because magnesium is relaxing and taking it in the evening helps you sleep.  About the only problem people ever have with magnesium is loose stools, i.e., the milk of magnesium effect.  If that happens – and it is unwelcome – simply reduce your dosage until your stools normalize.

Purchasing magnesium supplements can be a little tricky because of the way they’re labeled.  First, a chelated magnesium supplement is one that ends with an ‘-ate,’ as in magnesium aspartate or magnesium citrate or magnesium citrimate.  The -‘ate’ ending tells you the magnesium is chelated, which means it’s attached to another molecule (the chelating agent..aspartate, citrate, or whatever) that helps with absorption.  Second, with magnesium supplements, the manufacturers sometimes list the dosage of both the magnesium and the chelating agent combined.  Since the chelating agents are a lot heavier than the magnesium, this labeling often ends up saying the dosage of each pill is, say, 1000 mg of magnesium aspartate.  This isn’t the amount of magnesium you’re going to end up getting because the magnesium is only about 15 percent of the weight of the total pill.

About the only way you can really tell how much actual magnesium your getting is to look on the label on the back and see how much of the RDI (Recommended Daily Intake) the dose is.  The RDI for magnesium is 400 mg per day so if you find the dose of the supplement you are considering contains 50 percent of the RDI, then you know each dose contains 200 mg of magnesium irrespective of what the dosage is on the front of the bottle.  As I say, I recommend 300 to 400 mg of magnesium per day.  The only downside of magnesium is loose stools.  Doesn’t happen to everyone, but does to a few.  For many people the magnesium seems to offset the constipation that some experience when starting a low-carb diet.  If you do experience loose stools, simply back off your dose of magnesium until things unloosen.

Magnesium is natures relaxant.  It makes many people sleepy, so we always recommend taking it at bedtime.

Potassium

Potassium is linked to sodium.  If you lose a lot of sodium through the diuretic effect of the low-carb diet, you’ll ultimately lose a lot of potassium as well.  Keeping your sodium intake up as mentioned above will help preserve your potassium as well.  And keeping your potassium levels up helps to ensure that you don’t lose a lot of lean muscle mass during your weight loss.  Plus, just as with sodium, adequate potassium prevents cramping and fatigue.

You can replace your potassium by taking potassium supplements.  In our clinical practice, we gave all patients starting the low-carb diet a prescription for potassium.  You can get the same dosage by taking four to five of the over-the-counter 99 mg potassium supplements you can purchase at any health food or natural grocery store.

There are a couple of prescription medicines that you’ve got to be aware of if you markedly increase your potassium intake, so if you’re on blood pressure medicines, ask your doctor if it’s okay for you to take potassium.

Before we move on to other supplements we can use to help with low-carb dieting, I want to address the subject of dehydration.

Hydration

A few years ago, I learned the lessons of adequate hydration the hard way, so take this as a cautionary tale and benefit from my painful experience.  I had always pooh-poohed the notion of drinking a lot of water in addition to coffee, tea and other non-caloric beverages because I always figured (and probably have even written in the pages of this blog somewhere) that coffee, tea, etc. are nothing but water with a little flavoring in them.  I mean, if you start out with a glass of water and put tea bag in it, the water doesn’t go away.  It’s still there; it just becomes tea-flavored water.  Well, turns out that’s not actually the case.

My daily ritual was as follows: Get up, stagger to the refrigerator and take a big gulp or two of sparkling water.  Then make my way to the espresso maker and crank out a cup of Americano.  Followed by four or five more Americanos over the course of the morning and early afternoon, interspersed with a gulp here and there of sparkling water.  A snort of Jameson in the early evening, maybe a glass of red wine with dinner and a decaf Americano after dinner.  If I watch a movie or read a book, I usually nurse another glass of Jameson.  I typically take my supplements at bedtime, so I throw back another half glass or so of sparkling water then.  Plenty of liquids, right?

Well, not exactly, as it turned out.

I began developing severe cramps in my hands and feet that I had a hell of a time massaging out.  That was just the beginning.  I started being awakened at night with brutal leg cramps, requiring my springing from the bed and walking them out.  My potassium is too low, thought I, so I started taking potassium.  No change in the cramping situation.  In fact, if anything, it got worse.  I was complaining to a friend who told me calcium had helped his cramps.  So I downed calcium at bedtime.  No improvement.

Another friend told me that tonic water had helped her with cramps, but I only half believed it, so didn’t really try.  Then MD and I had family visit us in Tahoe for skiing.  I upped my booze intake, kept the coffee intake about the same, and probably decreased my consumption of sparkling water (or water of any kind, for that matter).  The cramps increased dramatically.  And what was worse, they stopped limiting themselves to the night.  When MD and I were driving over to Napa one day, the cramps were so severe I could hardly drive.  I had to keep the seat back as far as I could get it so I could straighten my leg when one hit me.  Then my hands started cramping just holding them on the steering wheel.  I pulled off the freeway and made a beeline for a convenience store and grabbed a one liter bottle of diet tonic water and proceeded to chug the entire thing as I drove down the road.  Miraculously, my cramps subsided.  So, I figured tonic water (quinine) was the solution.

One night – after being out of tonic water for a few days and being failed by my bride in resupplying – I had another brutal night of cramps.  The next day I was scheduled for blood donation.  After going through the long list of questions that must be answered verbally (and fighting down the impulse to tell my interrogator that I had recently paid for sex while imprisoned in Africa – those who have given blood lately will know what I mean), I was sent to actually have the blood taken.  The phlebotomist couldn’t find my vein, which had never happened before because I usually have rope-like veins in my forearms.  She asked if I was dehydrated.  I told her I didn’t think so since I had had my normal four of five cups of coffee that morning along with my gulp of water.  She brought me a couple of 16 ounce bottles of water that I drank, and, bingo, there were my veins.  Big and robust as usual.

It finally occurred to me that my cramping problem might be due to dehydration and that the diet tonic that solved the problem did so not because of the quinine but because I was drinking all the water the quinine was dissolved in.  And it occurred to me that the cramping was worse in the middle of the night because a lot of water is lost through the breath at night. (See my second post on the Anthony Colpo Smackdown to read more about this.)  You can lose a couple of pounds during sleep simply by breathing water vapor away, which was, I’m sure, what was happening to me.  I was barely hydrated enough to prevent cramping while awake, but when I slept and my fluid level fell due to my breathing water away, I hit some critical threshold of fluid that kicked off the cramps.

I started rehydrating first thing in the morning and throughout the day.  Now I get up, drink anywhere from 16 to 32 ounces of remineralized water (more about which later) first thing.  Then I head to the espresso maker and start my daily Americano regimen.  But I consume at least 8 ounces of sparkling water after each cup of coffee.  And I drink water after each shot of Jameson and/or glass of wine (or any other alcoholic libation),* and I’m proud to report that I have been cramp free since upping the water.

My brush with cramping misery inspired me to hit the medical literature to read about hydration.  And I learned many wonderful things. For example, I learned coffee is a diuretic (which I already knew but had chosen to forget), but that some acclimation occurs over time.  Still, due to the diuretic effect, you don’t get the full fluid from a cup of coffee that you would from an equal amount of water.  Same with alcohol.  Once I started calculating how much fluid of that I drank throughout the day I was actually retaining, I was amazed that cramping was the worst that happened to me.

I learned that water has a lipolytic effect (fat burning).  I read this in a number of papers that had studied it, and the data clearly showed that those who took in a lot of water had increased lipolysis.  I didn’t deny the data, but I couldn’t figure out the mechanism (and apparently neither could any of the authors because none described it).  I thought on it a while and finally came up with what I think is a plausible scenario.

When you drink water, especially cold water, you require some increase in caloric burning to bring the water to body temperature, but that increase doesn’t amount to all that much (the authors did describe this phenomenon), but you also dilute your blood for a bit until the water equilibrates with the fluid in all the tissues, and effect that takes some time.  During this time, while the blood is more dilute, the concentration of the various substances carried in the blood decreases.  Which would mean that insulin levels would fall.  The typical blood volume is about 5 liters, so drinking a liter of water would increase the blood volume temporarily by about 20 percent, which would mean the concentration of insulin and other molecules in the blood would fall by about 20 percent.  A 20 percent drop in insulin levels would allow fat to escape the fat cells and would facilitate its transfer into the mitochondria for burning.  At least that’s my explanation for the lipolytic effect seen in numerous studies of subjects increasing water intake.

Those starting a low-carb diet are prone to dehydration because excess ketones are gotten rid of via the kidneys along with a lot of fluid.  So, when you start your diet, consciously increase your fluid intake.  Do like I do now and come up with some sort of regimen that ensures you consume plenty of water throughout the day.  You’ll feel better; you’ll avoid cramping; and you’ll actually burn a little more fat.  And don’t make the mistake I did and assume that drinking a lot of coffee, tea, booze or other diuretic fluid is a replacement for water intake.

Since I drink either bottled water or water that comes through our RO filter, both of which are depleted of minerals, I always remineralize my water by adding a pinch of Celtic Sea Salt or one of the other such salts to each bottle.  I add enough so that the water just barely hints of a salty taste.

Supplements

Every patient whom we started on a low-carb diet left our clinic with six supplements:  lipoic acid, CoQ10, Vitamin E, magnesium, a good multi-vitamin and a prescription for potassium. (Now I would add a substantial dose of vitamin D3 to the list, a dose based on vitamin d levels and sun exposure.) We’ve already dealt with the potassium and magnesium, so let’s consider the others.

First, the good multi.  I’m a believer in getting most of what’s needed vitamin- and mineral-wise from food.  And I’m also a believer that I’m an excellent driver.  Yet I always purchase car insurance.  I see a good multi-vitamin as the same thing – cheap insurance against any kind of deficiency.  I would rather have my patients urinating away fifty cents worth of vitamins a day than risk that they have a deficiency in one.  And I feel the same way about myself.  So, find a good multi-vitamin without iron and take it.  Based on the experiences of my own patients, I can almost guarantee you’ll feel better. Why without iron?  Because most people on low-carb diets get plenty of iron in a very absorbable form.  And too much iron isn’t a good thing, so don’t take it in your multi.

Alpha lipoic acid (ALA)

ALA is, next to magnesium, just about my favorite supplement.  It acts as both a fat-soluble and water-soluble anti-oxidant so it can pretty much weasel its way in anywhere in the body and stamp out inflammation.  It protects fatty membranes and even acts as a cellular nutrient.  It also helps the body deal with blood sugar, which helps the whole low-carb adaptation process along.  Many studies have shown an improvement in blood glucose levels and insulin sensitivity with ALA supplementation.  ALA can rejuvenate other anti-oxidants, and has so many virtues that entire books have been written about it.  My standard dose is 300 mg per day for patients starting low-carb diets.  There is a newer, more potent version of ALA available now called r-alpha lipoic acid.  The standard stuff is a combination of the r and l varieties, and since the r isomer is the active one, a supplement made entirely of the r variety is going to be more potent.  And more expensive.  If you use the r-ALA you can take 100 mg a day.

CoQ10

Another superstar supplement, especially for those who have been on or are on statins.  Statin drugs interfere with the body’s synthesis of this important nutrient, and those who have been or are taking statins are usually depleted to some degree.  If you’ve been taking a statin, I would take 300 mg per day of CoQ10.  If you haven’t, 100 mg per day should do.

Vitamin D3

I would also add at least 1000 IU per day of this nutrient.  You need to have your levels checked at some point to make sure you don’t overdo it, but at 1000 IU per day, this is unlikely.  If you do test and find you’re deficient, I would take 5,000-10,000 IU per day until 25 (OH) vit D serum levels are up to at least 50 ng/ml.  Along with all the other benefits vitamin D3 provides (which I have written about elsewhere on this blog), there is some evidence that it even boosts weight loss a bit.

5-hydroxytryptophan

The last supplement I’ll mention is one I’ve had much success with in treating people who tend to have carb cravings late in the day.  5-hydroxytryptophan (5-HTP) is the precursor to serotonin.  Most people who have carb cravings have them because their serotonin levels fall.  Taking 5-HTP will bring them back up.  It also helps with sleep.  Best time to take it seems to be about 4 or 5 PM for those who go to bed at the standard 10-12 PM.  You can move the dose around to find a time that helps the most with your carb cravings yet doesn’t make you sleepy other than when you want to be.  I usually recommend 50-100 mg.  It’s available at most health food stores and natural food grocers.

Fatty liver

The last bit of advice I’ll give is that you need to work to defat your liver as quickly as possible.  The good news is that you can do it quickly on a low-carb diet.  Studies have shown major improvement in just 10 days or so.   It’s important to defat your liver to help you lose weight more quickly because the liver breaks down insulin.  If your blood sugar goes up, the pancreas makes and secretes insulin to drive it down. It does so by driving the glucose into the cells.  At the same time, insulin drives fat into the fat cells and keeps it there.  As long as the insulin is in the circulation, it’s going to be preventing fat from leaving the fat cells.  The liver is the organ that breaks down and gets rid of the insulin.  And a healthy liver does it a lot better than a liver full of fat.

One of the liver’s most important jobs is detoxification of harmful substances.  We all (at least I) consume medications, food and drink that is toxic.  We (I) drink coffee, tea and alcoholic beverages.  The caffeine and alcohol are toxins.  They don’t really hurt us in the quantities that most of us ingest, but they are toxic nevertheless.  The liver detoxifies them.  Same with many drugs – both prescription and over-the-counter.  Tylenol puts a major detoxification burden on the liver.  When you drink coffee, tea, and/or alcohol and take OTC meds, you occupy much of your liver’s detoxification capacity.  Which means it can’t get rid of insulin as well and can’t regulate metabolism in general as well as it does when it isn’t busily detoxing toxins.

So, if you really want to hit it hard in the early phases of your low-carb diet and reach low-carb adaptation at warp speed, I would recommend avoiding – or at least limiting – coffee, tea, alcohol and OTC meds.

I am a huge lover of coffee and alcohol (coffee more so than alcohol despite my constant talk of Jameson) so I know this is a sacrifice.  One way to have it both ways is to switch from caffeinated coffee to decaf espresso.  Decaf coffee to me sucks taste-wise.  But decaf espresso ain’t so bad.  If you don’t want to go completely cold turkey, you can switch from coffee to espresso since espresso has double (or triple) the taste of coffee yet only about half the caffeine.  My favorite way to drink espresso is as Cafe Americano.  I love it so much that I even made a video of how to make it to send to people.  Take a look if you haven’t seen it yet.  It’s the best cup of coffee you’ll ever have. (I have one on the table next to me as I write these words on the patio in Cuenca, Spain.)

That’s about a wrap on my tips and tricks for kicking off a low-carb diet.  I’m sure many of you have tips and tricks of your own.  Please feel free to share them in the comments section.

The bone broth recipe at the very bottom of this post is from our defunct restaurant that I wrote about here.  We had this going on the stove all the time and used it as a base for about half the dishes we served.  It is absolutely spectacular.  I would eat is as a soup (we didn’t serve it that way) and take home bags of it and freeze it.  You can do the same.  I’ll provide the restaurant-sized version so you can either make a large amount in a big stock pot and freeze a bunch of it in individual packages.  Or you can cut it down to a smaller recipe.  If you do, just make sure to cut all the ingredient amounts proportionally.

A note of interest: I wrote the first part of this post flying between San Francisco and Dallas.  The middle part during a flight from Dallas to Atlanta.  And the last part (along with the words I’m typing now) over the Atlantic on a flight from Atlanta to Madrid.  I’ll transfer it to WordPress, put in all the links and photos when I get to the hotel in Madrid.  So you’ll end up with a post that was written about halfway around the world.

Another note of interest: I’m finishing this post in Cuenca, Spain (including some of the edits I made above) because the internet connection in our hotel in Madrid sucked.  The hotel was great, the food was pretty good, but the internet was abysmal.  I kept getting kicked off, so I abandoned all but the most necessary internet functions (email, mainly) until I got to more reliable service.  Here we are in Cuenca where the hotel sucks, the food really sucks but the internet connection is great.

One housekeeping note: Since the internet has been so unreliable, I have been unable to deal with the 100 or so comments that have accumulated.  I’ll get to them as soon as this post is up.  I did perform one of my most-hated tasks last night and went through the spam filter to fish out legit comments that had gotten snared before deleting the zillions of spam comments.  So if you’ve been waiting a long time for a comment to appear, it was probably one of the handful that I rescued from the sea of spam.  I’ll get it up as soon as I can. Just bear in mind that I’m headed for my next stop, Zaragoza, as soon as I hit the ‘Publish’ button on this post and will be on a forced march for a bit. So, be patient with me on the comments.

This is the restaurant recipe for massive quantities, so you can reduce accordingly.  Just make sure you reduce all ingredients proportionally.

2 oz roasted garlic (weight)
10 oz roasted red onions (weight)
4.5 gallons water (volume)
22 oz tomato paste (weight)
4 oz cilantro with stems
2 pounds chicken back bones (weight)
16 oz tomato pulp (weight)*
6 oz salt (weight) I would use Celtic Sea Salt or other such salt here
1 oz black pepper (weight)
1 oz olive oil (volume)

Roast onions and garlic in olive oil for approximately 15 to 20 minutes.

Add all ingredients to water, chicken and tomato paste.

Let simmer over medium fire until cooked.

Approximate yield is 640 ounces or 5 gallons.

*We used a ton of diced Roma tomatoes in the restaurant for just about everything.  We removed the pulp from these tomatoes before dicing them.  We saved the pulp and used it in the stock.

*Here in Spain I have discovered a wonderful way to drink wine and stay hydrated.  They have a drink called Tinto de Verano (see photo at top), which is half fruity Spanish wine and half sparkling water poured over ice with a slice of orange and slice of lemon thrown in.  It’s kind of sangria lite.  Each time you drink a glass of it, you get half wine and half water, so you rehydrate the water lost from the little alcohol in the half glass of wine.  It’s tremendously refreshing, and I’ve drunk my weight of it since arriving.

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

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

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

Mark Twain, Advice to Youth

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

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

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

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

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

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

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

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

Say what?

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

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

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

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

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

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

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

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

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

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

A study appeared this week sure to drive members of the low-fat and vegan tribes sprinting for their Protexid.

Ron Krauss and his group published a paper in the Articles in Press section of the American Journal of Clinical Nutrition (AJCN) stating there is no evidence that saturated fat intake increases the risk for heart disease.  The paper, titled Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, is not a study per se, but is a meta-analysis, a compilation of numerous studies looking at the relationship between saturated fat intake and the risk for developing heart disease.

As I’ve discussed before on these pages, meta-analyses are not my favorite types of studies.  I’ve attacked them when they’ve been used to ‘prove’ the low-fat diets are better, so I can’t very well embrace meta-analyses when they present a conclusion I agree with.  And I really can’t embrace meta-analyses when they are compilations of observational studies, which are themselves next to worthless.

For those who don’t know, meta-analyses are compilation studies in which researchers comb the medical literature for papers on a particular subject and then combine all the data  from the individual studies together into one large study.  This combining is often done to bring together a collection of studies, none of which contain data that has reached statistical significance, to see if the aggregate of all the data in the studies reaches statistical significance.  I think these types of meta-analyses are highly suspect, because they can lead to conclusions not warranted by the actual data.

To give you an example of what I mean, let’s assume that we have a study looking at a flipped coin.  If a researcher flips a coin 10 times and comes up with 6 heads and 4 tails, runs this through a program checking for statistical significance, he/she will discover that the 6-4 ratio isn’t a statistically-significant difference because of the low number of overall flips (10).  Now, let’s say that 50 researchers did the same kinds of study and some found that their coins came up heads 6 times out of 10 or 4 times out of 10, etc.  If a researcher then wants to ‘prove’ that heads comes up more times than tails on a coin flip, he/she can gather all the studies showing heads come up more times than tails, add them together in a meta-analysis and come up with 25 studies, each with 10 flips, showing that heads came up 63 percent of the time.  Now we’re talking 250 flips and we would probably reach statistical significance.  We know that over the long run a flipped coin is going to come up heads about 50 percent of the time and that the more the times it is flipped the more likely the number of heads will close in on the 50 percent figure.  But, the meta-analysis that selected the studies showing the 63 percent heads is statistically significant because the studies were cherry picked.

Researchers using meta-analyses set up selection criteria to pick which studies will be included in their final product, which leaves the door open for all kinds of mischief.  For example, let’s say a researcher wants to make the case that low-fat diets reduce cancer. He/she would create a set of criteria, do a literature search for all the studies that meet those criteria, then do a statistical analysis of all the data.  If the data demonstrate that low-fat diets are linked to lower rates of cancer to a statistically significant degree, the researchers submit their paper for publication.  But let’s say that when the data is crunched, it doesn’t show any such relationship?  It’s easy to go through all the studies and find which ones strongly show the opposite of what the researchers want to show and then figure out how to change the study-selection criteria in such a way as to keep those studies from being selected, run the whole process again, and repeat until enough studies are found to make the meta-analysis show the link between low-fat diets and lower rates of cancer.

Sad to say, this is often how it is done.  Which is why I don’t give a lot of credence to meta-analyses.

But having said all this, I’m still happy to see a researcher with the academic credentials of Ron Krauss coming out with a meta-analysis showing no correlation between saturated fat intake and cardiovascular disease risk.  And getting it published in the AJCN, probably the world’s most prestigious nutritional journal, no less.  It’s called putting your money where your mouth is.  Many academics whom I’ve spoken with admit that there is no correlation, but wouldn’t risk their academic reputations doing a meta-analysis to ‘prove’ it.

I’ve had many people tell me that it’s really nice to finally see some studies coming out vindicating saturated fats.  Or at least not attacking them.

I have to tell them that pro-saturated fat studies have been around for years.  Not just observational studies or meta-analyses, but real controlled studies looking at death rates from heart disease as a function of fat intake.

Let’s look at a couple.

Over 40 years ago, way back in 1965, there were two studies published showing that heart patients – the kind of people who today assiduously avoid saturated fat – who ate saturated fat were more likely to survive than those who didn’t.

One paper titled Low-Fat Diet in Myocardial Infarction, published in The Lancet, looked at the survival of subjects who had suffered heart attacks who went on either low-fat diets or their regular high-saturated-fat diets.

Here’s what they did:

264 men under the age of sixty-five, who had recently recovered from a first myocardial infarction and who had been in the Central Middlesex, Edgeware General, or West Middlesex hospitals took part in the trial.  On leaving hospital they were allocated at random to one of two groups at each hospital.  One group was placed on a low-fat diet, which the other group continued with their normal diet.

The trial, which ran from 1957 to 1963, was managed by four research medical registrars working at the three different hospitals.
What was the low-fat diet?

Patients in the diet group were allowed to take 40 g fat daily [under 20 % fat].  The daily allowance included 14 g (1/2 oz) butter, 84 g (3 oz) of meat, 1 egg, 56 g (2 oz) cottage cheese, and skimmed milk.  The nature of the fat consumed was not altered, nor were any additional unsaturated fats given.  The diet was often unpleasant, [my italics] and where possible, it was modified to suit individual tastes.

The body of the article states that the control subjects on their regular diet consumed about 2.5 times the fat eaten by those on the low-fat diet. (106-125 g for the former; 44-45 g for the latter.)  I ran the saturated fat calculations on the low-fat study diet and found that it contained about 30 g saturated fat, which is about 13.5 percent of total calories.  Most ‘experts’ today recommend keeping saturated fat under 10 percent of total calories.  Given how the data was presented in this paper, there was no way to tell how much saturated fat the control group got, but we can estimate their total fat intake to be about 46 percent, which was the average fat content of the typical American diet when I first got into this biz way back in the early 1980s just as the low-fat jihad was kicking off.  I would guess that the control diet contained 60-70 g of sat fat or about 25 percent of calories.  You can see the difference in fat intake in the graph above on the left.

The patients on the low-fat diet had pretty close counseling during the course of the multi-year study, and, consequently, they hewed fairly closely to their diet.  The researchers knew this because the study group consumed about 400 fewer calories per day as compared to those subjects on their regular diet and lost weight.  The researchers also used serum cholesterol levels as a measure of compliance to the diet.  In 1965 it was well known that reducing fat in the diet, especially saturated fat, made cholesterol levels go down.  As you can see from the chart on the right, cholesterol levels went down on the low-fat diet and stayed there.

What did the researchers find after observing these subjects for years?  They found that putting people on unpleasant low-fat diets didn’t help them live any longer nor avoid another heart attack.  Over the course of the study, the same number of subjects died in both groups.

What were the recommendations of the authors of the study?

It is concluded that in men under the age of sixty-five who have survived a first myocardial infarction, a low-fat diet does not improve their prognosis.

Summary

A controlled diet of a 40 g low-fat diet was carried out on 264 men who had survived a first infarction.  Despite a lowering of the blood-cholesterol and a greater fall in body-weight in the treated group, the relapse rate was not significantly different in the two groups.

A low-fat diet has no place in the treatment of myocardial infarction.

Ah, how things have changed since 1965.  And not for the better.

Here is another.

A paper published in the British Medical Journal (BMJ) in 1965 titled Corn Oil in Treatment of Ischemic Heart Disease looks at the differences in the rates of death or a second heart attack in patients following one of three diets: Their regular diet (control diet), a high-olive-oil diet, or a high-corn-oil diet.  After determining the caloric intake of the control group, the researchers had subjects in the other two groups restrict their intake of fat from foods as much as possible and replace it with supplements of either olive or corn oil in amounts calculated to match the calories they reduced by getting rid of animal fat.  The subjects getting one of the two oils ended up getting about 80 g per day.

The aims of the study were as follows:

Our purpose was to study the effects of prescribing a vegetable oil and a restricted fat diet to patients with ischaemic heart disease.  The primary interest was in an unsaturated oil with a cholesterol-lowering effect.  But large doses of any oil may have secondary effects on diet and nutrition, so that differences between an unsaturated-oil group and a control group might be due to these secondary effects rather than to unsaturated fatty acids as such.  It could, for example, be relevant that mortality from heart disease is low in Italy and Greece, whose inhabitants consume much olive oil; this oil has no major effect on serum cholesterol level, its main fatty acid (oleic acid) being only mono-unsaturated.  The trial was therefore designed to study the effects not only of a more highly unsaturated oil (corn oil) but also of olive oil.  It seemed likely that if any differences emerged between the olive-oil and corn-oil groups these would reflect the specific effects of polyunsaturated fatty acids.

After starting the diets to which they were randomized, the subjects were followed closely for two years.  As with the last paper, the researchers used serum cholesterol levels to monitor compliance with the diet.  You can see the differences in serum cholesterol in the three groups in the chart below.  Note that the cholesterol levels in the control group did not change a significant amount, which would be expected.  The same held true for the olive oil group: no significant change.  But those subjects in the corn-oil group dropped their cholesterol levels significantly.

Over the course of the study a number of patients died or had a second heart attack.  The researchers knew which subjects were on the control diets but were blinded (as were the subjects) and so didn’t know which were consuming the olive oil or the corn oil.

When the codes were broken and the data analyzed, it turned out that 75 percent of subjects following their standard high-fat, high-saturated-fat diets were remaining alive and free from a second heart attack whereas only 57 percent of subjects on the olive oil had done so.  The group with the worst outcome was the corn-oil group.  Only 52 percent of those subjects remained alive and heart-attack free.

The authors’ summary:

Eighty patients with ischaemic heart disease were allocated randomly to three treatment groups.  The first was a control group.  The second received a supplement of olive oil with restriction of animal fat.  The third received corn oil with restriction of animal fat.  The serum-cholesterol levels fell in the corn-oil group, but by the end of two years the proportions of patients remaining alive and free of reinfarction (fatal or non-fatal) were 75%, 57%, and 52% in the three groups respectively.

It was concluded that under the circumstances of this trial, corn oil cannot be recommended in the treatment of ischaemic heart disease.

In this same issue of the BMJ appeared an editorial about this study.  The author of this editorial points out that

the patients treated with corn oil had the worst experience, though initially their outlook was apparently similar to that of the other groups.  There is a 1-in10 to 1-in-20 chance that corn oil had a deleterious effect; the probability of its having any beneficial effect is remote.

This came at a time when corn oil was being touted on advertisements everywhere as the best oil to prevent heart disease because it is polyunsaturated.

The editorial goes on to grumble about the outcome and discusses a few other studies with conflicting outcomes.  The writer finally declares that maybe the problem is that this and other studies have been done on subjects who already have heart disease.  Maybe that’s too late in the game to make a difference.  (The outcome of this study wouldn’t indicate that, but the writer didn’t let that fact get in the way of his opining.)

Maybe it doesn’t help to lower cholesterol or increase polyunsaturated fats in those already afflicted; maybe what really needs to be done is to increase polyunsaturated fats and lower cholesterol levels in healthy people with no sign of heart disease.

A different approach, and a formidable one, is the prevention of ischaemic heart disease by altering the diet of healthy people.  A study of the organization of such a scheme in the U.S.A showed that it was practicable, and an anti-coronary club for men has been in existence in New York since 1957.  Its 814 members take a “prudent diet” in which fat is moderately reduced and equal proportions of saturated, monounsaturated, and polyunsaturated fats are eaten.  Already there is evidence  that the development of “coronary events” is being prevented.  Again, we await confirmatory evidence.

What the editorialist is waiting for is evidence to confirm his bias that reducing fat generally and saturated fat specifically (while increasing polyunsaturated fat) and the lowered cholesterol levels arising from such changes will prevent the development of heart disease.  Unfortunately, for him, this confirmatory evidence was not forthcoming.

From Gary Taubes’ Good Calories, Bad Calories (pg 36 hardcover):

Overweight Anti-Coronary Club members were prescribed a sixteen-hundred-calorie diet that consisted of less than 20 percent fat.

[It was reported] in February 1966 that the diet protected against heart disease.  Anti-Coronary Club members who remained on the prudent diet had only one-third the heart disease of controls.  The longer you stayed on the diet, the more you benefited, it was said.  But in November 1966, just nine months later, the Anti-Coronary Club investigators published a second article, revealing that twenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent.  Eight members of the club died from heart attacks, but none of the controls.

Like the maze shown at the top of this post, the people who have a bias against fat are trying to make things more complex than they are.  The simple solution is to look at the mortality, which no one wants to look at because it doesn’t confirm their bias.  They all want to look at more complex issues that have little bearing on the most important issue – whether one lives or dies.

Even the authors of the study showing the members of the Anti-Coronary Club members dying at enormously higher rates than non-members and dying with heart attacks want to look at other more complex information.

Gary Taubes continues

This [the deaths by heart attack of the club members] appeared “somewhat unusual,” Christake [the author of the paper] and his colleagues acknowledged.  They discussed the improvements in heart-disease risk factors (cholesterol, weight, and blood pressure decreased) and the significant reduction in debilitating illness “from new coronary heart disease,” but omitted further discussion of mortality.

Classic behavior from someone whose mind is made up.  Ignore the evidence denying your hypothesis and focus on that confirming it.  Instead of focusing on which people actually die of heart disease, let’s spend our time running through the maze looking at how our beloved low-fat diet reduces supposed risk factors. Which brings to mind a wonderful Winston Churchill quote:

However beautiful the strategy, you should occasionally look at the results.

How many people have died or been incapacitated with heart disease since 1965 when the evidence above was presented?  How many fathers, mothers, aunts, uncles, grandfathers and grandmothers could have had more years of productive lives if only the people who do these studies had looked at just the two mentioned above and taken the tack that maybe they had been going down the wrong path?  Had they done that instead of ignoring these results and continuing to try to prove an hypothesis that can’t be proven, how many lives might have been saved?  I’m glad it’s not on my conscience.

For maze at top
hat tip to FAILblog.org

Applebee's Quesadilla Burger

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

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

Click here to view the embedded video.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

I have been dilatory in posting over the past few days and embarrassingly dilatory about approving comments.  I’m way, way behind, but I’ll get caught up ultimately.  So, if you have a comment doing time in comment Purgatory, don’t despair.  I will get to it.  Ultimately.

My excuse for not devoting my normal amount of attention to this blog is that I’ve been extremely busy as of late.  MD and I made a quick trip to Seattle to work on our world-changing project, then came back and spent a couple of days at the zoo that is Expo West (more about which momentarily), then the Seattle team came to us and we continued to work.  During all this, MD had a concert in which she had to perform Mozart’s Requiem and Lauridsen’s Lux Aeterna (my favorite piece of choral music) along with a couple of lesser pieces.  And tomorrow we drive back to Tahoe.  So, we’ve been busy little beavers and this blog has suffered.

Expo West has got to be the world’s largest natural foods expo.  It takes place every year at about this time in Anaheim.  And every year at about this time we drag ourselves to it.  The photo at the top of this blog represents one tiny little portion of this gathering.  To see how huge it is, take a look at the photo below of the map of the thing.

Find the red You-are-here arrow on the top middle left.  The picture at the top of this post is looking to the left from that spot on this map. And you can see only a short space down, kind of to where the aisle turns.  Imagine that view in each direction, then add a couple of floors made of several large multiple gymnasium-sized rooms, and you can kind of get the picture.  There are thousands of exhibitors and thousands of attendees.  It is one monster extravaganza of foods, supplements, beauty supplies, and anything else you might imagine having anything to do with diet, health, food and natural clothing.

I hate to go to the thing because I hate throngs of milling people and I hate the exhibitors always trying to sell you something.  But I also really enjoy it because I find new stuff and I learn a lot.  And there are the booth babes, to boot.  Although not so many this year.  Times are tough and booth babes are costly.

Each time I go to Expo West, I notice trends.  And this year was no different.  So, for what it’s worth, here are the trends I noticed after God only knows how many hours spent and miles walked traipsing through the giant Anaheim Convention Center.

Tea

There were a multitude of tea purveyors.  There was black tea, green tea, white tea, herbal teas of every description, and a dozen kinds of maté.  Way, way more tea than I’ve ever seen.  I guess the spate of recent studies that have appeared showing the purported health benefits of drinking some kind of tea has not been lost on tea vendors.  They were there in droves.  And all were babbling about studies demonstrating how tea cures this or that disease.  I didn’t have the heart to tell them that all of the studies they were using were observational studies and not worth a flip for proving that tea helps anything.

Agave

Agave was the big new product this year.  Last year there were a few vendors; this year they were everywhere.  They were selling agave syrup, agave nectar, agave crystals, agave this and agave that.  An entire other group of vendors was promoting various products sweetened with agave.  For those of you who don’t know, agave is the latest entry into the caloric-sweetener sweepstakes.  It comes in a variety of forms – syrup, nectar, crystals -  from the agave plant, a succulent plant found mainly in Mexico.  The claim to fame of this sweetener, which was emblazoned on banners, literature, labels and just about everywhere, is that it is a low-glycemic sweetener.  And it is was being touted as a great food for diabetics and any others with glucose-intolerance problems.  And it is indeed low-glycemic because it is composed of about 90 percent fructose.  If you think high-fructose corn syrup is bad at 55 percent fructose, just imagine what Agave syrup can do for you.  Yet all these ignorant people are ga ga over it as if it were the second coming.  My advice is to avoid it like death.  But be prepared to be seeing it everywhere.

Xylitol

There were a lot of products made with xylitol on display.  Products that are probably pretty good, but that I would never have imagined.  Nose spray, for example.  Xylitol is a sugar alcohol that is antibacterial, which is why it is in gums that dentists recommend.  It actually prevents tooth decay because of its antibacterial properties.  It does the same thing if sprayed into the nose, a place where a lot of bacteria live.  I saw a product made of xylitol that was to be dissovled in water and used in a Neti pot to irrigate sinuses, which, like the nose spray, makes sense.  There have been randomized control trials showing the benefit of xylitol for prevention of tooth decay and prevention of ear infections in kids.  I didn’t see any papers showing studies on the nose sprays or other products, but it’s a reasonable assumption that they probably work.  I certainly wouldn’t hesitate using them.  Based on the number of vendors I saw, expect to see a lot of xylitol-containing products in the days to come.

Sweeteners

There were a fair number of non-caloric sweeteners on display.  Most were made of combinations of RebA, the active ingredient in stevia, and other non-caloric sweeteners.  I saw a lot of erythritol and erythritol combinations as well.  If numbers of vendors are any indication, expect to see a bunch of non-caloric sweeteners hitting the shelves.

Coconut milk and oil

In what I view as an extremely positive trend, there were a zillion purveyors of coconut milk and products made from coconut milk.  In the past, there weren’t many, but this year they were everywhere.  There were a bunch of companies making ice creams and gelato made of coconut milk.  These aren’t low-carb by any stretch, but they are still more healthful (in my opinion) than regular ice cream because of all the great fats in coconut milk and oil.  I took one for the team and tried several of these, and I can tell you that they were delicious.  There were also outfits selling coconut milk that was like regular cow’s milk.  It didn’t taste quite the same, but it wasn’t far off the mark.  I thought it tasted better, but others might disagree.  The milk comes in cartons just like regular milk.  There were chocolates and any other product you could think of that would normally be made of milk or dairy made of coconut milk or oil.

Soy

In what I would consider another positive trend, there were way, way fewer companies selling soy products than ever before.  Since I’ve been attending Expo West soy has been everywhere and in everything.  All of a sudden, this year it’s kind of taken a powder.  There were a handful of people there selling soy-based products, but not anywhere near what has been there in past years.

Nuts

Every year there are people there selling nuts.  This year they wre all over the place.  I’ve never seen so many nuts on display.

Low-fat

Surprisingly there wasn’t a lot of emphasis on the low-fat nature of products.  Previously it was much more visible with banners and stickers on anything that could make the claim, but not so much this year.  Many more products were advertised as having no added sugar or sugar-free than were advertised as being low-fat.  I think the times they are a changing.

Low cholesterol

Strangely, there was more emphasis on low-cholesterol than I’ve noticed in the past few years.  More emphasis, in fact, than there was on low-fat. There were many products on display that proudly proclaimed their cholesterol-lowering properties.  The one that took the cake is pictured below.  The company makes tortilla chips that allegedly lower cholesterol.  Now you know what to do if your cholesterol is a little high: go face down in these chips.  Not!  Actually, they would probably do you less harm than taking a statin.

Meat and eggs

Yet another positive trend was the large increase in the number of vendors selling both fresh and processed meats.  Way more vendors than in the past.  And a large number selling eggs.  I saw many booths that had packets containing two hard boiled eggs and a little salt and pepper.  A good kind of fast food, if you ask me.

Resveratrol

I was expecting there to be a zillion people selling resveratrol, but there weren’t many.  In fact, I couldn’t find anyone selling just the raw stuff.  The only vendors I found selling it were selling their own proprietary versions in which resveratrol was mixed with other compounds.  Given all the press lately about resveratrol I was really surprised at how little there was.

Krill oil

All the krill oil sellers were there, and I spent a good amount of time with them.  They all had large booths, so it was apparent that krill oil has been very, very good to them all.  I finally learned all the distinctions between all the oils available and will be doing a post on them as soon as I have a little time to go over all the papers I’ve pulled to make sure I am accurate.

Vegetarian products

It’s hard to say, but if I had to bet, I would bet that there were slightly fewer this year than last.  They were still there, and they were still obnoxious, but just not in the numbers as before.  At least it appeared that way.

One of the things that constantly amazes me about Expo West and all the other natural food and health food shows I go to is how typically American all the people look who are selling this stuff.  They truly are a mirror of American.  The vast majority are overweight and they don’t look like the picture of health, yet there they are pimping products that are supposed to make the purchasers of them healthy.  If I looked like most of these people, I would hire someone who at least look lean, trim and healthy to man my booth, but these people don’t.  Most are definately not walking advertisements for their products.

Here are a couple of photos to show you what I mean. These pictures give you an idea of what a typical booth at Expo West looks like and typical people working these booths.  I didn’t pick these just because they were hawking vegetarian products, I picked them because I happened to have my camera at hand and they were right across the aisles from one another.  They were not out of the ordinary.  They look like most of the vendors.

I plan to dragoon MD into doing most of the driving tomorrow so that I can catch up on my medical reading (as much as I can anyway while keeping a close eye on the road).  When we get home, I’ll get back on my normal schedule of posting.  Hang in there ’til then.

Paleolithic paintings from Lascaux cave in southern France

I imagine most readers of this blog would expect a group of subjects to do better on a Paleolithic diet as compared to a standard American diet, but there are few studies actually making the comparison. One was posted yesterday in the Advance-0nline-Publication section of the European Journal of Clinical Nutrition that shows subjects following a Paleolithic diet made major metabolic changes, and made them rapidly.

Before we get into the study, let’s make sure we’re all on the same page when we discuss the Paleolithic diet. We we say Paleolithic diet, what are we really talking about?

The Paleolithic era refers to that period of history of the genus Homo, which began more than 2 million years ago and ran until the Neolithic period started circa 10,000 years ago. The Neolithic era dates to the time when early man set down roots both literally and figuratively when he started to cultivate plants for food and domesticate animals. The Paleolithic era ends and the Neolithic era begins with the advent of agriculture.

So what did Paleolithic man eat? We don’t know precisely because Paleolithic man didn’t leave any written records, menus, cookbooks, etc. The only records Paleolithic man left are the cave paintings, of which Lascaux in France is the most famous. Virtually all of these paintings feature animals prominently, which would lead one to believe that animals figured greatly in the lives of Paleolithic people. Since they didn’t domesticate these animals, and since it seems unlikely that they kept zoos, the most obvious reason these early people focused so much artistic effort on these animals is that they ate them. Carbon-13 isotope studies bear out that idea as the same carbon isotopes found in grass are also found heavily concentrated in the bones of Paleolithic man and other known carnivores, which leads to one of two conclusions: either Paleolithic man spent his days grazing or he ate animals that grazed. I would opt for the latter interpretation.

Keep this idea of Paleolithic man as a meat eater along with the idea of the cave pictures in your mind. We’ll return to them later, but first, let’s look at this study.

Nine healthy, sedentary, non-obese subjects (6 men; 3 women) over the age of 18 recruited from the San Francisco Bay area completed the study. These subjects had their starting diets analyzed – all were on their own version of the standard American diet – and a battery of tests done on them to evaluate multiple metabolic parameters.

Once the beginning data was in hand, the researchers started the subjects on a ramp up to the full Paleolithic diet by giving them daily increases of fiber and potassium.

For the intervention phase, beginning day 1, for adaptation purposes, a series of 1-day cycle diets with gradually increasing levels of potassium and fiber were developed by the research dietitians. This was to allow the subjects’ intestinal tract and potassium handling systems to adjust to the markedly higher dietary content of fiber and potassium. ‘Ramp 1′ diet was given for 1 day, ‘Ramp 2′ diet for 3 days, ‘Ramp 3′ diet for 3 days and finally the ‘Paleo diet’ for the remainder of the study.

Once ramped up, the subjects went on the full Paleo diet for 10 days.  An interesting twist to this study was that the subjects were monitored carefully for any signs of weight loss over the course of the study, and any subjects losing even small amounts of weight were encouraged to eat more of the Paleo foods in an effort to maintain their starting weights.  Since weight loss itself can bring about metabolic changes, the researchers wanted to make sure that any changes came about as a result of the diet composition and not as a side effect of weight loss.

What did they eat?

Meat, fish, poultry, eggs, fruits, vegetables, tree nuts, canola oil, mayonnaise and honey were included in the Ramp and Paleo phases of the diet. We excluded dairy products, legumes, cereals, grains, potatoes and products containing potassium chloride (some foods, such as mayonnaise, carrot juice and domestic meat were not consumed by hunter-gatherers, but contain the general nutritional characteristics of preagricultural foods).

Hmmm. More about which later. For now, here is a layout of the specific foods the subjects ate during the ramp and the full Paleo diet.

Table 2

The macronutrient composition of the regular diets of these subjects was 18% protein, 44 % carbohydrate and 38% fat.  The Paleo diet was 30% protein, 38% carbohydrate and 32% fat, mostly unsaturated, as the authors were quick to point out.
After the 7 day ramp period and the 10 days of Paleo dieting, subjects experienced large changes in most parameters measured.  Lipid changes are shown in the table below.

Derived from Table 3

As you can see, there were significant decreases in triglycerides, total and LDL-cholesterol with no change in HDL-cholesterol.

The body of the paper reports an insignificant decrease in blood sugar after the Paleo diet, but the units listed in the paper are incorrect, which is one of the hazards of dealing with a pre-publication paper.  All the kinks haven’t been worked out.

Fasting insulin levels plummeted by more than two thirds in (11.5 to 3.6 µU/ml) and the total area under the insulin curve was lowered by almost half.  What these figures tell us is that the diet made these subjects much, much more sensitive to their own insulin.  In other words, they required substantially less insulin to keep their blood sugars in the normal range.  Since they were producing less insulin, they had less circulating insulin, which meant less fat storage, less arterial stiffening and less of all the things that too much insulin causes.

Along with the improvements in lipids and insulin sensitivity, the subjects experienced a significant drop in diastolic blood pressure and a decrease in mean arterial pressure.  These improvements likely occurred in part because these subjects had substantially increased brachial artery diameter, a measure of arterial distensibility.  There arteries had become less stiff and more pliable over a mere 17 days of dietary change.

Urinary potassium loss increased, indicating an increased potassium intake by the subjects.  And urinary calcium excretion decreased.

Another interesting aspect of this study is that these findings were pretty much across the board.  Instead of a couple of hyper responders raising the average, either all nine or in a couple of cases, eight of the nine subjects demonstrated pretty much the same changes, indicating

consistently improved metabolic and physiological status with respect to circulatory, carbohydrate and lipid metabolism/physiology.

The authors of this paper found

in a small group of sedentary, slightly overweight, but not obese adult humans, that switching from their usual diet to a paleolithic-type diet, which contained no cereal grains, dairy [or] legumes, resulted, after only a short period of time [17 days] and without weight loss or increase in activity levels

significant positive changes in all the parameters discussed above.

I was fascinated by this study because the changes were so rapid, but I was a little put off because it could have been so much better.  I mean why didn’t they test a real Paleolithic diet?  Probably because of nutritional correctness, i.e., fear of saturated fat.

During Paleolithic times, man primarily subsisted by hunting.  The preferred food was large game animals, and Paleolithic man, a skilled hunter, wiped most of them out.   And not just the large grazing animals.  Paleolithic man completely decimated the Cave bear.  As you can see from the photo of my Cave bear skull below (from a slide I use in presentations), these were enormous animals that didn’t go down easily.  Cave bear, like all bears, had high levels of body fat, which must have been highly desired because these ferocious animals were hunted to extinction about 15,000 years ago by people wielding little more than pointed sticks.  I would have to value fat a whole lot more than I do to tackle one of these guys.  The largest bears that I could find the fatty acid composition for were polar bears, which should be appropriate since cave bear lived in northern latitudes.  Polar bears have on average 30 percent saturated fat, 50 percent monounsaturated fat and 15 percent polyunsaturated fat.  (I know these figures don’t add up to 100 percent, but they are the figures as presented in the article.)

The majority of the large animals that roamed the world are gone thanks to the depredations of Paleolithic man.  If you ever get the chance to go to the American Museum of Natural History in New York, take a stroll through the many large halls filled with the enormous skeletons of these animals that used to roam what is now the United States.  Experts estimate that it took Paleolithic man only about a thousand years to range from northern North America were he crossed the Bering strait to the southern tip of South America wiping out all the large game that existed at the time.

These large mammals that Paleolithic man decimated are now only present in skeletal form so we don’t know for sure what their fatty acid composition was.  But we do know that of those left, the larger the animals, the larger the percent body fat.  And the larger the percent body fat, the greater the percentage of saturated fat.  Given those two facts, one has to conclude that Paleolithic man consumed a large percentage of his energy as saturated fat.  We can’t look at the fat content of deer, for example, and use that to estimate the saturated-fat content of the Paleolithic diet.  Deer, as we know them today, were tiny animals as compared to those Paleo man typically dined on.

If you look at the fatty acid breakdown of the horse, a large animal (not grain fed) that we are all familiar with that is comparable in size to many of the animals Paleolithic man hunted to extinction, you find a large proportion of saturated fats.  Horse fat is about 36 percent saturated fat, 34 percent monounsaturated fat, and the rest polyunsaturated fat.  Even rabbits carry over 40 percent of their fat as saturated fat, but rabbits have much less fat per weight than the larger animals.

It seems pretty obvious that Paleolithic man would have eaten considerable saturated fat.  Which begs the question: Why always cut the saturated fat in experimental diets testing the hypothesis that the Paleolithic diet is more healthful?

I don’t know the answer for sure, but I expect that it’s due to the nutritional equivalent of political correctness, which I call nutritional correctness.

Researchers are simply afraid to imply that saturated fats might actually be harmless, so they go through all kinds of contortions to present their data in such a way that it couldn’t possibly present saturated fats in a positive light.  And much good research and reporting has suffered as a consequence.

A case in point is a otherwise wonderful book published 20+ years ago titled The Paleolithic Prescription.  This fascinating book goes into great detail describing the physical exploits of our ancient ancestors based in large part of reports by European explorers encountering ‘primitive’ peoples untouched by the forces of ‘civilization.’  The authors, based on the anthropological literature, describe the size of our Paleolithic forebears as being similar to our own, but their strength was significantly greater:

These people were strong – stronger by all estimates than most agricultural and industrial people (including ourselves) who lived after them.  Skeletal remains reflect strength and muscularity: the size of joints and the sites where muscles are inserted into bones indicate both the mass of the muscles and the magnitude of the force they were able to exert.  Average Cro-Magnons, for example, were apparently as strong as today’s superior male and female athletes.  Strange as it may seem, Cro-Magnons and other hunters and gatherers may have worked fewer hours per week than did the agriculturalists who followed, yet they were significantly more robust.

Think about this last sentence for a minute.  Strong, robust Cro-Magnons who settled into a life of agriculture circa 10,000 years ago, and who worked harder than their pastoral predecessors, showed a decline in strength and muscle mass.  Why?  What The Paleolithic Prescription says about energy expended is true.  The skeletal remains of agriculturalists show much more arthritic changes and incidence of joint wear implying much more regular physical activity than hunters.  So why did agriculturalists develop less muscle mass and strength?  Could it be because of a switch from diets high in fat and protein to diets low in fat and protein and high in carbohydrates?  Makes sense to me.  Same genetic material, greater exercise, different diet, yet weaker and less robust.

Getting back to my original point about this book, the authors presented a mass of data showing our Paleolithic ancestors to be more robust, healthier and able to routinely perform feats of strength that are almost unbelievable to us today.  And they dwelt on the massive amount of hunting that sustained these ancient peoples.  Then, when it came time to apply these dietary lessons to people of today, the authors tried to shoehorn their findings in a nutritionally correct regimen that followed the low-fat diet precepts that academicians are so attached to.  It’s really a shame because this could have been a wonderful book.  It’s still well worth reading, but simply ignore the dietary advice.

It would have been great had the authors of the paper above used a real Paleolithic diet for their study instead of an imaginary Paleolithic diet that conformed to the tenets of nutritional correctness.

Based on my own experience with thousands of patients, I can predict what the findings would have been.  Lipid parameters would have been improved, but with LDL staying about the same or maybe going up a little.  HDL would have gone up significantly.  Triglycerides would have fallen maybe more.  The all-important triglyceride/HDL ratio would have plummeted much more than with the faux Paleo diet.  Fasting insulin would have dropped like a rock and the area under the insulin curve would have fallen at least as much, if not further.  Blood pressure would have decreased and all the measures of vascular pliability would have improved.  All in all, my prediction is that the outcome of the study would have been better than the outcome of the study as it currently exists.

The Paleolithic diet data indicates that early man ate more saturated fat than he did carbohydrates.  And he was molded by the processes of natural selection to thrive on such a diet.  When he bolted from that meat-based diet, as he did when he settled in to life as an agriculturalist, he paid dearly for it with a devolution in health.  Since the evidence is so obvious that a diet higher in saturated fat worked wonders for Paleolithic man, it seems like some academicians somewhere would ranger up and test such a diet.  But it appears that the pox on saturated fat is so virulent that no one wants to risk it.

If such a study were done and the results tally with what I’m positive the results would be, the authors would find themselves in the untenable position of having to at least tacitly imply that saturated fats aren’t harmful.  And that could ruin an academic career.  No more invitations to present at meetings. Expulsion from the club.  People tsk tsking behind their hands.  It just couldn’t be done.

A couple of weeks ago I posted that Gary Taubes had agree to answer questions from readers of this blog.  Over a hundred readers sent in questions through the comment section.  Many of these questions were actually multiple questions, so Gary ended up with probably 200+ questions to deal with.

I’ve gone through and compiled a list of the most common questions and presented them to Gary.  Here are the questions followed by his responses.

The most commonly asked question was how do Asians and others living a seemingly high-carb existence manage to escape the consequences?

The Asian question first. I do address this in the book and I address it again in the afterward of the paperback. There are several variables we have to consider with any diet/health interaction. Not just the fat content and carb content, but the refinement of the carbs, the fructose content (in HFCS and sucrose primarily) and how long they’ve had to adapt to the refined carbs and sugars in the diet. In the case of Japan, for instance, the bulk of the population consumed brown rice rather than white until only recently, say the last 50 years. White rice is labor intensive and if you’re poor, you’re eating the unrefined rice, at least until machine refining became widely available. The more important issue, though, is the fructose. China, Japan, Korea, until very recently consumed exceedingly little sugar (sucrose). In the 1960s, when Keys was doing the Seven Countries Study and blaming the absence of heart disease in the Japanese on low-fat diets, their sugar consumption, on average, was around 40 pounds a year, or what the Americans and British were eating a century earlier. In the China Study, which is often evoked as refutation of the carb/insulin hypothesis, the Chinese ate virtually no sugar. In fact, sugar consumption wasn’t even measured in the study because it was so low. The full report of the study runs to 800 pages and there are only a couple of mentions of sugar. If I remember correctly (I don’t have my files with me at the moment) it was a few pounds per year. The point is that when researchers look at traditional populations eating their traditional diets — whether in rural China, Japan, the Kitava study in the South Pacific, Africa, etc — and find relatively low levels of heart disease, obesity and diabetes compared to urban/westernized societies, they’re inevitably looking at populations that eat relatively little or no refined carbs and sugar compared to populations that eat a lot. Some of these traditional populations ate high-fat diets (the Inuit, plains Indians, pastoralists like the Masai, the Tokelauans); some ate relatively low-fat diets (agriculturalists like the Hunza, the Japanese, etc.), but the common denominator was the relative absence of sugar and/or refined carbs. So the simplest possible hypothesis to explain the health of these populations is that they don’t eat these particularly poor quality carbohydrates, not that they did or did not eat high fat diets. Now the fact that some of these populations do have relatively high carb diets suggests that it’s the sugar that is the fundamental problem. Ultimately we can only guess at causes using this kind of observational evidence. To know anything with certainty we’d need the kind of randomized controlled trials I yearn for in the epilogue of GCBC.

What is your opinion on leptin in the grand scheme of obesity and fat storage?

I mostly ignore leptin in the book because I think leptin is primarily a signaling molecule and so a downstream effect. In other words, leptin is secreted from the fat cells; it doesn’t regulate directly the amount of fat that accumulates. Moreover, if the primary regulator of fat storage is insulin, which it is, and leptin is secreted in proportion to the amount of fat stored, which it is, then insulin has to regulate leptin.

Where leptin may play a primary role is in the liver. A few years ago Jeff Friedman of Rockefeller University published an article in Science showing that leptin down-regulates SCD-1 in the liver (the only place they looked), which worked in turn to increase oxidation of fatty acids. This makes sense homeostatically: if leptin is released in proportion to the fat accumulated then it is a signal of how much fat we have in reserve. So long as the mitochondria in our lean tissue and organs know that we have fat in reserve, they can continue to burn it without fear of systems failure should they run out of fuel completely. Leptin resistance would then work, like insulin resistance, to make us burn less fat and store more, while the rest of the body would have to rely on carbohydrates (blood sugar) for fuel.

In general, though, I’m interested in the cause of obesity and I don’t think discussing leptin adds much. Here’s what I say about this issue in afterward of the paperback edition of GCBC:

“Another variation on the can’t-possibly-be-so-simple argument that I have heard frequently since Good Calories, Bad Calories was published is the molecular biology theme. The last fifteen years, since the discovery of the hormone leptin in 1994, has seen obesity research become a sub-discipline of molecular biology. As a result, a search of the keyword “obesity” in the National Library of Medicine database will now identify over 100,000 relevant articles in the professional journals (nearly 20,000 review articles alone), a large proportion of which focus on the fruits of molecular biology research and the science of genomics.: It’s a burgeoning field with a cast of thousands, including the role of obesity-related gene variations known technically as polymorphisms, of signaling molecules with names like adiponectin, leptin and grhelin, of the receptors for those signaling molecules and the inhibitors for those molecules and inhibitors of the inhibitors, and so on. The obvious question is how can this research be so extraordinarily fruitful, and yet mostly irrelevant to the cause of obesity? It’s hard to imagine it’s not, and so, as I’ve frequently been told, any discussion of the cause of obesity that doesn’t discuss these molecules, receptors, inhibitors, etc. must be considered amateurish and woefully inadequate. The truth must be complicated.

“Again the counter-argument seems itself simple and straightforward: if you’re hit over the head with a hammer, it will cause both pain and inflammation. The mechanisms of pain and inflammation have also yielded up a wealth of knowledge to the tools efforts of the molecular biologists. These physiological phenomena are understood to be mediated via signaling pathways and molecules (in this case, prostaglandins, tumor-necrosis factors, etc.) that emerge in response to the damage done. The more researchers learn about these responses and the molecules involved, the more complex the pathway from hammer to pain and inflammation to healing will appear. But the relevant fact to all those immediately involved is that both the pain and ensuing inflammation were caused by the hammer and perhaps the person who swung it. Everything else is downstream and may be relevant only to the question of which drugs will best deal with the pain and perhaps accelerate the healing process. “

A number of questioners asked why you think it is more difficult to lose weight the second or third time around on a low-carb diet?  And why it seems more difficult to lose on low-carb with increasing age?

I’m curious whether this is in fact true. Another possibility is that it’s more difficult to lose weight on low-carb as we get older; that the carbs effectively do chronic damage to our tissue and so the longer we’ve been overweight or obese, the harder it is to lose weight. I can imagine a scenario in which the fat tissue becomes hypersensitive to the insulin we secrete, or the pancreas becomes hypersensitive to the carbs and secretes even more insulin, or the insulin resistance in the lean tissue becomes less tractable, and so the longer we remain fat, the more our fat tissue compensates when we restrict carbs. It’s also possible that repeated low carb dieting somehow exacerbates this process, but I’d want to see definitive studies (and on all this speculation) before I believed it.

Several people asked for a comment on any important studies that you may have left out of GCBC.

The issue isn’t leaving out studies so much as not wanting to get into the he-said, she-said game of quoting particular studies that support my preconceptions. In this business, you can always find studies that support a particular hypothesis, or at least seem to if you selectively interpret the data. So when I had to make a point about the efficacy of a particular treatment — exercise, for instance, or semi-starvation diets — used meta-analyses or Cochrane Collaboration systematic reviews, which are designed to minimize author bias, to make the general points. When I discussed the saturated fat/cholesterol/heart disease hypothesis in the first few chapters, I did indeed mention virtually every study and certainly every meaningful clinical trial, because I knew if I left anything out I would be accused of cherry picking the data (which, of course, I was anyway). I did omit much of the observational epidemiology on the nature of a healthy diet because I find it meaningless and impossible to interpret correctly, in part for the reasons I discussed above about the Asian diet issue.

When I cut the book down from the initial 400,000 word unfinished draft, a lot of what was removed were indeed the counter- and counter-counter arguments. For instance, obesity researchers will argue that obesity causes hyperinsulinemia, not the other way around. That way they can still say that obesity is caused by over-eating and once we get fat, that causes insulin resistance and jacks up insulin levels. I spent, literally, months writing a lengthy section explaining how this view came about and what the evidence actually did and did not demonstrate. Then when I realized the book had to shrink dramatically, and with the benefit of sage advice from my editor, I decided that it was unnecessary to explain why the mainstream researchers would disagree with my take and then spend yet more space explaining why they were wrong to disagree. One thing I did cut from the book that I regret was a section linking gout to fructose and uric acid, and discussing the history of gout and how it’s frequency in populations and socioeconomic groups paralleled the spread of sugar. Nobody had ever made that point before and I wanted to make it, considering that people have been speculating on what aspect of diet or lifestyle causes gout back to Hippocrates. Still, my friends rightly argued that when your book is a few hundred thousand words long, you can’t afford to keep a section about gout, even if a lot of people get gout these days and, of course, they’re more likely to get it if they’re overweight or obese. Along these lines Dan Harrington asked why his gout goes away on the Atkins diet and that’s my answer: no sugar, primarily, means no fructose and so no fructose-induced hyperuricemia. In other words, fructose raises uric acid levels and gout is caused by the elevated uric acid in the blood stream.

It is true that you can find studies in the literature that seem to contradict the hypotheses in GCBC but are not mentioned in the book, When Gina Kolata reviewed my book in the NY Times, she evoked a study by Jules Hirsch and Rudy Leibel, then both at Rockefeller, suggesting that nutrient composition of the diet has no effect on weight. As I explained in a letter to the Times, the study failed to refute the carbohydrate/insulin hypothesis of weight regulation for a variety of reasons — the subjects, for instance, could have gained as much as 15 pounds a year on one particular diet composition but not another, and the study would not have detected it. And the subjects, almost exclusively, were lean middle-aged individuals. What we’re interested in here, though, is why why people predisposed to obesity get fat, and that may not be something you can study in people who have remained lean into their 40s and 50s. Would Leibel and Hirsch have obtained a different result if they had used, say, obese subjects who had first been slimmed down by some kind of diet (Atkins or a starvation diet)? These types of subjects are considered pre-obese, since they’re so highly likely to go back to being obese. And if Leibel and Hirsch had used them, they might have found that they stay relatively lean on a low carb diet and put on weight easily on a high carb diet. Anyway, rather than get into this kind of too-and-fro in the book, I made the decision not to mention these types of ambiguous studies. I would like to think that had there been a single compelling study refuting the hypothesis — or better yet, two, since you’d like to see things replicated in science — I wouldn’t have written a different book.

What you think of a Slow Burn type of exercise and low-carb dieting?  Do you still stand by your notion that exercise doesn’t help people lose weight?

I haven’t looked into the science behind slow burn exercise (although I know Mike has) but I now do it regularly (with Fred Hahn in Manhattan at Mike’s recommendation) and it seems to be helping my lower back pain immensely. I can let you know next spring whether it helps my softball game, where my ability to hit with power has been deteriorating sadly with the advancing years. What fascinates me about it is the weird confluence of the desire for self-improvement with what seems to be deep-set sadomasochistic tendencies. It’s torture when you do it, and then you look forward to going back.

As for exercise, I do not believe that it causes long-term fat loss. I think it might be helpful in a weight loss program only because it gives you a kind of positive feedback that dieting per se does not. You can feel good after a work-out, while it’s hard to feel too good after a meal that didn’t include either the calories or the carbohydrates you preferred. On the other hand, since it does make you hungry — work up an appetite — I worry whether for some or even most people the psychological benefits could be counterbalanced by the drive to consume even more calories than you might have expended during the work-out.

Are you familiar with the work of Dr. Jan Kwasniewski, and, if so, what do you think of it?

I am not.

What kind of response have you gotten from the medical/scientific community about GCBC?

In general, I think it’s safe to say that I’ve been ignored. If obesity researchers have read the book, they haven’t bothered to tell me. When GCBC was published we sent out 150 copies to obesity researchers, authors of obesity task force reports, foundations that fund obesity research, everyone at NIH who funds obesity research, etc. etc. I heard back from 3 or 4 thanking me for sending them the book. Two followed up to tell me they had read it. Some later told me outright that they didn’t have the time to read a 500 page book, and particularly so when they already know what I think because of the 2002 NYT Magazine article and don’t particularly agree. That said, I may be making some progress in getting people to pay attention.

Whenever I do hear from someone who is sympathetic, I ask them to try to set up a lecture at their institution. Often I ask them to contact other researchers they might know and get me lecturers at those institutions. Through this kind of networking, I’ve been invited to lecture at some of the more influential obesity research centers and at least some of those people have taken my arguments seriously. A few months ago, I heard from some contacts at the NIH, that I might be invited down to lecture to the nutrition coordinating committee at NIH, which would be a big step forward, but the fact that I haven’t heard anything since then (August) makes me pessimistic.

When I do give these lectures a common response that I get from nutritionists and obesity researchers, and one that I find profoundly disturbing, is that they find what I say interesting but don’t see it as anything they should think about further. In other words, they have their schtick (as my wife, an almost-academic calls it); whatever research they get their funding to pursue, and even though in theory we’re all in this to cure and prevent obesity and chronic diseases, their schtick may have nothing to do with my schtick. If they’re studying, say, genetic strains of obese rats or questionnaires to improve the accuracy of diet assessment in epidemiologic studies, what does that have to do with my argument that obesity is caused by carbohydrates? So they listen politely, ask a few intelligent questions (in an ideal world) and then go back to their research, because that’s how they make a living. They don’t say to themselves, I’m going to read Taubes’s book and, if I find it compelling, switch my research over to studying the efficacy of carbohydrate restriction. And even if they did, they wouldn’t get funding to do so because they’d have no track record in that field.

So, bottom line, at the moment is that I know of a handful, maybe as many as a dozen researchers, who find the arguments in the book compelling and are doing what they can, in their limited spare time, to help get the message out and maybe get us to the place where the hypotheses are taken seriously and are rigorously tested. The rest either don’t care or don’t know GCBC even exists or just think what I say is wrong and so not worth further discussion, either because they read the book or some of it and think its crap or because they think its crap based solely on what they know about me or heard about the book and so don’t have to read it.

What’s next?  Another book?

What am I doing next? As suggested by many readers, I am going to write a short, easy-to-read version of the weight section of GCBC. It won’t be a diet book — no recipes — but it will be far more of a self-help book than GCBC. I might also do a weightier (no pun intended) serious investigation into the sugar and corn syrup industries; their history, political influence, lobbying, etc — that would be interwoven with a more intensive look at the potential health effects of sugar and HFCS and fructose particularly. The first book will definitely be done; the second depends on getting the funding to do so. I’d also like to get back to straight science writing for a while, since I do enjoy writing about good science, which is how I started my career, and it would be a pleasant change from the mainstream nutrition and health nonsense.

How about a blog?

As for a blog, I just haven’t got the time at the moment, although I always hope that that will change in the future.

Many wrote that GCBC had changed their lives.  Can you think of a book that has changed your life?

Did any books change my life? Yes, All the President’s Men, by Woodward and Bernstein. I read it in my last year of college or my first year of graduate school and it made me decide that I wanted to be an investigative reporter rather than go to business or law school, which was the direction I seemed to be headed.

What do you know about Dr. Simeon’s HCG protocol?

Mostly nothing.

What led you to the idea that saturated fat doesn’t cause heart disease?

It was a progression of steps. Back in the late 90s, I was reporting a story for Science on the salt-hypertension controversy and one of the worst scientists I ever interviewed (and having written a book about cold fusion, Bad Science, I had interviewed quite a few terrible scientists) took credit not just for getting Americans to eat less salt, but getting them to eat less eggs, meat and butter, too. I literally got off the phone with this guy and called my editor at Science and said, “when I’m done writing about salt, I’m going to do a story on dietary fat. I don’t know what the story is, but if this guy was involved in any substantive way, I know there’s a story to be done.” So that’s what I did. I finished the salt story and then spent a year working on the fat story, which was published in Science.

The story made the point that there was virtually no evidence that a low-fat diet prevented heart disease, but let open a window for saturated fat having some deleterious effect. Then a couple of years later, I was reporting the New York Times Magazine story that would become “What If It’s All A Big Fat Lie?”, when I heard about these five clinical trials comparing low-fat, calorie-restricted diets to Atkins diets. Since the Atkins diet is a high-fat, high saturated fat diet and it improved cholesterol profiles in all these trials, that pretty much clinched it. I’ve been arguing since that these diet trials have to be perceived as tests of the hypothesis that saturated fat is a “bad” fat, although the medical establishment still prefers to ignore that fact.

Is there anything new or updated in the paperback version of GCBC or is it the same as the hardback?

It’s the same as the hardback, but there is a 3000 word (or thereabouts) afterward that’s worth reading.

I tried to come up with a selection of questions that represented the majority of questions asked.  I know that some went unanswered, but when Gary agreed to do this I promised him that he wouldn’t have to answer an exhaustive list that would require days of time.  So, I’m sorry if any specific question went unanswered, and I hope you understand.  Thanks to everyone for the terrific response.

Dinner tonight at Casa Eades

Last Sunday the New York Times published a color spread on the US Department of Agriculture (USDA) data on the changes in food consumption in this country between 1970 and 2006, which got me to musing.

To the uninformed, which, sadly, probably means most people working in the nutrition industry and even those employed in a nutritional capacity at the USDA, these changes (all save two) seem to be in a positive direction. The intake of dairy products has decreased; the intake of vegetables has increased; the intake of red meat has fallen; the intake of fish, chicken and skyrocketed; the intake of fruit is up; the intake of grains has increased markedly; and the intake of vegetable fats has almost doubled. The only two negatives are that sugar and sweeteners have increased and overall food consumption has gone up by about 11 percent, or an addition 1.8 pounds per person per week.

At the same time all these positive changes have been taking place, changes that all the (misinformed) people in the mainstream nutritional biz have been advocating, there has been an enormous increase in the rate of obesity. According to the Centers for Disease Control (quoted in the Times article) the rate of obesity has more than doubled since 1970, which is interesting because up until 1970 the rates of obesity hummed along at about the rate of 15 percent for decades.

What has happened since 1970 to cause this enormous societal change?

If asked, people give many answers: too much saturated fat, too much refined carbohydrate, too much food, etc.

I have my own opinions, which I will elaborate. I believe that the obesity epidemic has probably been driven by several dietary changes that have occurred since 1970. These changes are an increase in fructose and vegetable oil consumption and a decrease in saturated fat consumption. I believe that another contributing factor is the increased overall consumption of carbohydrates, which leads to an increased food consumption in general.

I want to emphasize that these are my opinions based on a pretty good knowledge of nutrition, metabolism, biochemistry, and physiology.

First, a sort of no-brainer. Since the USDA came out with the idiotic Food Pyramid we all loathe, there has been a major strategy in the food industry to move away from fats and toward carbohydrates. We have all seen this in various food consumption statistics. And we can tease it out from this Times piece if we look at which foods have increased and which have decreased in the diet. There has been a large increase in carbohydrate consumption as evidenced by the large increase in grains, vegetables, fruits and sweeteners.

Forgetting about all the metabolic events that carb intake precipitates that we all know cause obesity (i.e., increased blood sugar, increased insulin, etc.), let’s focus on simply one of the brain processes that carbs affect. The satiety center, located in the hypothalamus, is the part of the brain that tells us when we’re full. Unfortunately, it runs about 20-30 minutes behind our actual eating pattern, so we can stuff food in for a good while before our brains tell us we’ve had enough. Fortunately, it works a little more quickly (thanks to the help of cholecystokinin and some other gut hormones) when we eat primarily fat. If you eat a big steak, you feel full more quickly than if you eat a lot of carbs. Carbs tend to override the satiety center, allowing you to eat more. Let me describe a situation we’ve all experienced, and you’ll see what I mean.

You’re at a restaurant. You’re just at the end of a big meal and you’re stuffed. One of your dinner partners asks you to try a bite of his wonderful swordfish. It’s the best he’s ever tasted, he tells you. You say, I just can’t eat another bite. If I do, I’ll be sick. Then appears the waiter with the dessert tray, loaded with wonderful gooey treats. You look them over and say: I’ll take the carrot cake (or the chocolate mousse or whatever). How can you eat this calorically-laden dessert when you’ve just refused a bite of meat because you were so full? Because your brain’s satiety center is overridden by the carbs. And you haven’t even eaten the carbs yet. But experience has taught you that no matter how full you seem to be, there is always room for carbs. And fat, since most desserts are pretty high in fat as well. But it’s the carbs that do the satiety-center-blunting trick. It’s the reason dessert is always at the end of the meal. If you ate the dessert first, you would never be able to eat all the steak. And this carb overriding of the satiety center is why people don’t binge on steak, eggs and bacon. They binge on cake, chips, cookies and other high carb treats because they can stuff them without their satiety center telling them they’re full.

Since we’ve (as a nation) significantly increased our carb intake, it only makes sense that we’ve also increased the overall amount of food we eat. Carbs let us do that without even trying.

We have definitely increased our intake of fructose since 1970. I used the figures in the Times article to make my own calculations. Considering that table sugar is one half fructose and high-fructose corn syrup is 55 percent fructose (the most commonly used variety; some go as high as 90 percent fructose), I calculated that we ate about 50 grams of fructose per capita per day in 1970. By 2006 that figure had increased to 75 grams, a 50 percent increase. And we’ve got to bear in mind that these are average figures. I eat maybe 3 grams of fructose per day, and MD eats the same. That means that two other people out there are eating their 75 grams plus our extra 72 to make the averages come out as they do. I would suspect that most of the people reading this blog eat very little fructose, leaving a lot of other people to consume their share to keep the averages up.

But even 75 grams of fructose is a helluva lot. A little fructose – the amount you might find in a piece of fruit, for example – actually helps with glucose metabolism. It more or less primes the pump so that less insulin is required to reduce blood glucose. Large amounts of fructose are a different story, however. Fructose bypasses the enzyme phosphofructokinase, which is the rate-limiting enzyme in the glucose metabolism pathway. Consequently, large amounts of fructose are shunted past the sugar-regulating pathways and into the fat-formation pathway instead. The liver converts this fructose to fat, much of which, unfortunately, remains in the liver. ( Here is a nice paper on fructose metabolism. Ignore the idiotic conclusion, which is just another ad hoc attempt to make the data fit a preconceived notion acceptable to all academics.)

With continued consumption of large amounts of fructose, fat tends to accumulate in the liver leading to a condition called non-alcoholic fatty liver disorder (NAFLD). At this point, not only are we in an obesity and a diabetes epidemic, we are in an epidemic of NAFLD. Studies on ‘normal’ adults have shown that a little more than a third have significant fat accumulations in their livers. Even worse, 15-20 percent of children show the same thing.

NAFLD is the same disease people get who chronically over consume alcohol. Under the microscope NAFLD looks exactly the same; pathologically it acts the same. The only way to differentiate is by history of alcohol consumption: if there is fat in the liver and no history of chronic alcohol abuse, then NAFLD it is.

NAFLD has the same progression as the alcoholic variety. First, an accumulation of fat that becomes inflamed leading to a condition called non-alcoholic steatohepatitis (NASH), which means a non-alcoholic inflammation of fat in the liver. This condition can then progress to liver fibrosis, then to cirrhosis, then, ultimately, to liver cancer. Not all NAFLD follows this complete progression just as not all alcoholics get cirrhosis, but enough follow it to not make you want to get NAFLD if you can help it.

And one of the big ways not to get it is to avoid fructose.

By increasing fat in the liver, fructose also increases circulating insulin levels, which can lead to hyperinsulinemia and insulin resistance. How? Because a liver full of fat doesn’t work as well as a non-fatty liver. One of the jobs of the liver is to metabolize hormones and clear them from the circulation when their work is done. When you consume carbs or protein you stimulate the release of insulin to deal with them. Once insulin has done its job, the liver breaks it down to its amino acid components and puts them back in the circulating amino-acid pool. If the liver is filled with fat, it can’t do this as well. Insulin stays elevated (and in a diabolical twist even stimulates more fat synthesis in the liver) and tends to downregulate the insulin receptors, making them less responsive. The entire process can lead to insulin resistance, hyperinsulinemia and ultimately to obesity.

Below is a nice chart showing how the increase in obesity has paralleled the rapid increase in sugar consumption. Remember that table sugar is half fructose. Also remember that correlation is not causation. But in this case we do have the biochemistry of why worked out.

From Johnson RJ et al, AJCN 2007; 86:899-906

What about saturated fat? How does a decrease in saturated fat cause obesity. First, the decrease in saturated fat has tracked with the increase in vegetable oils, which are typically rich in omega-6 fats. Omega-6 fats have been shown in numerous studies to be proinflammatory. They have also been shown to worsen alcoholic fatty liver disease, and, one would assume, NAFLD as well. I haven’t seen any studies showing a worsening of NAFLD with increased consumption of vegetable oil – it hasn’t been studied as far as I know. (Maybe one of you readers can dig up a paper.) But it has been shown repeatedly with alcoholic liver disease, and since NAFLD is basically the same disorder, it makes sense that vegetable oil would worsen NAFLD as well. And if vegetable oil indeed does worsen NAFLD, then it promotes obesity by the mechanism described above.

Saturated fat is a healthful food. Read this article by Mary Enig that describes in detail the health benefits that come from eating saturated fat. I’ll address a couple of different issues.

Saturated fat is, well, saturated. That means that every carbon in the fatty acid chain has a full complement of hydrogens attached to it. There are no double bonds. In the picture below you can see a saturated fatty acid on top and a monounsaturated (one double carbon-carbon bond) fatty acid on the bottom.

Double bonds make fats unstable. These double bonds are the places that free radicals strike to convert unsaturated fats into peroxides, or oxidized fats. The more carbon-carbon double bonds a fatty acid has, the more susceptible it is to oxidation. Oxidized fats don’t function as well as non-oxidized fats. They make faulty cell membranes and less than optimal membranes for all the organelles within the cell. Oxidized fats can themselves become free radicals attacking adjacent fats and damaging them, or worse, starting an entire free-radical-fat-damaging cascade. All these forces work even more effectively at higher temperatures, so unsaturated fats shouldn’t be used for cooking. Unless, of course, your goal is to eat oxidized fats.

Saturated fats have no double bonds. They are immune to free radical attack. They are immune to heat damage. You can cook with them, you can hit them with a hammer, you can throw them on the floor and jump up and down on them. And they stay the same. Saturated fats are stable fats.

Most people don’t realize this, but the body has the ability to convert saturated fats to unsaturated fats. But the body doesn’t have the ability to convert unsaturated fats to saturated ones. The body can make saturated fats (palmitic acid, a 16-carbon-chain fatty acid) from excess carb consumption, but it can’t make a saturated fat out of an unsaturated one. If nature hadn’t wanted us to have saturated fat, why did she make us so that we make our own if we eat too many carbs. Could it be that during our evolutionary past the only time we might over consume carbs would have been when there was no meat available…and we needed the saturated fat? Sounds reasonable to me.

We have enzymes called desaturases that desaturate, i.e., add carbon-carbon double bonds, fats. We can take unsaturated fats and make them more unsaturated. And we can take saturated fats and make them unsaturated. But we can’t go the other way. In order to have saturated fats that provide the necessary structural stability that only saturated fats can provide is to get them in the diet, which we can do by eating saturated fats or by eating a whole lot of carbs. Since over consuming carbs comes with its own set of problems that we would rather avoid, that leaves eating saturated fats.

So how does avoiding saturated fats lead to obesity. In my opinion in a couple of ways. First, indirectly, by having them replaced by vegetable oil, particularly hydrogentated vegetable oil, i.e., trans fat. Due to their stability, saturated fats have cooking properties that no other natural fats have. Food chemists have created trans fats to have the same cooking properties – and in some situations even better cooking properties – as saturated fats. But the addition of trans fats to the diet creates a host of other problems. The medical literature is crawling with studies showing that trans fats drive the development of obesity.

The other reason is that saturated fats compose the lion’s share of normal membranous fats and of the brain. When membranes don’t work as well, especially mitochondrial membranes, our energy storage and regulation system doesn’t work as well. Anything that impairs membrane functioning impairs signaling function. If signaling function falls off, then various hormones, neurotransmitters, etc. lose function. As insulin loses function, more insulin is required, more insulin leads to more downregulation of receptors, all of which ultimately leads to obesity.

Even overeating carbs doesn’t help even though saturated fats are produced as a result. Carbs stimulate the production of palmitic acid, a 16-carbon chain fat. For proper membrane function and signaling we need shorter-chain saturated fats as well. These we can’t make – we get them from diet only. We can make shorter fats longer with elongase enzymes, but we can’t make longer fats shorter. We’ve got to get them via mouth.

Since this is speculation on my part – educated speculation, but speculation nevertheless – we may ultimately find that there are other reasons for the obesity epidemic instead of these or in addition to these. In fact, I can think of a few other minor causes, which I’ll save for a later post.) But I’ll bet that when all the work is done – which may not be for a hundred years given the academic climate of today – I’ll bet these ideas will be close to the mark.