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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The day after Labor Day (six days from today) our new book comes out, and our publisher finally gave us permission to excerpt it.  I’m going to post the entire introduction so you’ll know why we came to write this particular book.

The story you will read will be true and the names won’t be changed to protect the ‘innocent.’  Until the events transpired that you will soon be reading about, I was not especially a proponent of fast weight loss.  I mean a low-carb diet will make people lose weight quickly, but that’s not what I’m talking about.  I’m talking about the people who used to come into my office saying, “I’ve got my high school reunion in a month.  How much weight can I lose by then?’  I always considered these as fairly ludicrous requests because the requesters clearly weren’t concerned about health issues, but simply about how they would look in the short run, without an eye to maintaining their lifestyle.

As a consequence of dealing with so many of these patients, I really developed an aversion to the notion of quick weight loss to meet some sort of deadline where appearance counted.  But, as with so many things in life, it’s easy to pontificate until you find yourself in the same position as the people to whom you’re pontificating.

Go ahead and read this excerpt so you can see what I’m talking about, and we’ll pick up this conversation after.  This excerpt is from the manuscript version and not from the actual book so there may be slight differences, if you’re comparing the two.  I used the manuscript version because I could paste it in – had I used the actual book version I would have had to type it in.

Bob Hope famously quipped that middle age is when your age starts to show around your middle, and the audience always obliged him with a hearty laugh.  But for millions of adults the sad irony of the middle-aged middle is anything but funny.  Except for a select few metabolically-gifted individuals, crossing the threshold into middle age heralds the beginning of a battle of the bulge that seemingly never ends.  Granted some reach that threshold sooner than others; some acquiesce to the larger belt and the broader silhouette with some degree of aplomb, while others rail against time and fate. They take up and discard first one diet and exercise program and then the next in a frustrating quest to recapture the slender waist they can still recall, but no longer see in the mirror.

We’ve spent the majority of our medical careers helping people of every description with just this battle, combating overweight and weight-related health issues.  Although some were in their teens and twenties and some were in their seventies and eighties, the vast bulk of the many thousands of patients we guided to better health and lower weights were in middle age.  What we learned from these many years in the diet trenches is that middle-aged weight is stubborn; it’s different to deal with; it doesn’t respond readily to modest dietary changes or the incremental increases in exercise usually recommended by the purveyors of received medical and nutritional wisdom.  The factors driving middle-aged weight gain—which really does go straight to the middle—are like a perfect storm, metabolically speaking.  A confluence of changes in hormones, stress, lack of sleep, alcohol intake, medications, fat and cholesterol phobias, and a mountain of other nutritional misinformation combines to create a mid-life tsunami that seems to swamp the metabolism and fill every nook and cranny of the middle of the body with fat.

For more than twenty years we have researched this area of science, refining the tools to deal with it effectively, writing about it, lecturing on it, so you’d think that our expertise would make protect us from the tsunami, if it came our way.  But it didn’t.  Like everyone else, when the middle-age wave hit, we found ourselves floundering in the tide, paddling as fast as we could, and still not making much headway.  At least not until we dug back into the medical bag of tricks we had used with success in our middle-aged patients and applied them to ourselves.  Here’s how it all began.

Mike’s Story

Our wake up call came the morning we walked onto the set to film the pilot for our TV cooking show. Years before, I had gained a tremendous amount of weight while pursuing my career as a busy, practicing physician, then lost it on a diet I cobbled together from information I got rereading my old medical school texts and delving into the medical literature.  My weight loss did not go unnoticed by my patients, and soon many were clamoring for me to put them on the same diet I had developed for myself.  I did so with great success.  In short order my practice changed.  My wife, Mary Dan, left her busy family practice and joined me in what became a huge bariatric (the treatment of obesity) practice.  We refined the original diet and wrote about our methods in Protein Power, a book that sold nearly 4 million copies.  During the never-ending promotion of the book, we met a producer who proposed that we star in a TV cooking show designed around the precepts of our diet and a cookbook we had written.   We said “Let’s do it.”  He put the deal together and set the shooting schedule for the pilot.

We walked onto the set in sunny Southern California one morning filled with both enthusiasm and apprehension.   As we wandered through the semi-organized chaos that is a film studio, stepping over giant cables, ducking under the scaffolding for the overhead cameras, and dodging production assistants darting here and there, we began to wonder what we had gotten ourselves into.  The whirlwind of activity and the 30 or so people on the set were intimidating to say the least.  We had done countless live and taped television and radio interviews in the previous years, but never a project in which we were the sole actors on the stage, the ones who had to carry the entire show on our own shoulders.  A young man recognized us and directed us to the Green Room, telling us the director would be in to talk with us shortly.

The director, a total stickler for every aspect of the production, didn’t mince words when he joined us in the Green Room.  “We’re going to have to do something,” he said, “you guys are too fat to be starring in this kind of a cooking show.”

We were stunned.  I was a much lesser version of my former fat self and thought of myself as pretty slender.  Mary Dan had gained a little weight in the ten years since the publication of Protein Power, but certainly wouldn’t have been considered fat by anyone’s estimation.  People we met at lectures, book signings, and other appearances uniformly commented on how thin and healthy we looked and always added that we were good advertisements for our diet.

“Yeah, well, it doesn’t work that way on TV,” said the producer.  “If you’re the stars of a show on healthy eating, you’ve got to be thin.  Granted, you look better than the average Joes and Janes out there, but they don’t have their own health show.  TV is a youth-driven medium.  You’ve got to look young to make it on TV and young means thin, especially around the middle.  It’s like the golfer, Lee Trevino, says, the young guys are the ‘flat bellies.’  You’ve got to have a flat belly if you want to make it in this biz.  The camera is going to put 10 pounds on you and you’ve both got bellies starting out.  Imagine 10 pounds added to that.”

Bellies…?

“When you do lectures you’re dressed up, right?  You wear suits, don’t you?”

We nodded.

“At book signings you sit behind a desk, shake a few hands and sign books.  It doesn’t work that way on TV.  You’re going to be moving around, bending over, putting stuff in the oven; you’re going to be seen from all angles.  If we try to hide the fact that you’ve got a little extra weight around the middle, which will be hard since the camera will magnify it, the viewers will know.  Putting you in baggy sweaters or loose clothing will just make them think you’re fat and trying to disguise it, and the show will lose all credibility.”

In a flash, Mary Dan and I had both gone from being confident in our own 50-plus-year-old bodies to being aware of the small paunches that had suddenly seemed to materialize out of nowhere.  What before had seemed nothing more than a little tightening of the waistband now suddenly assumed Falstaffian proportions.

“What can we do?” we asked. “If we try to hide it, they’ll think were fat; if we don’t, they’ll know for sure.  It’s a Catch-22.  We can’t win.”

Our director said, “I haven’t worked in this biz for over 40 years and not learned a trick or two.  Here’s how we’re going to make this work.  Since you, Mary Dan, are going to be the main cook, we’ll keep you standing behind the counter.  You’re short enough that with the height of the counter and a little work with wardrobe we can keep you covered without appearing to do so.  Mike, we’ll have you do all the moving and bending, so you’re going to have to take the bullet.”

“Take the bullet?  What do you mean?”

He reached into his large canvas bag and pulled out what appeared to be a giant piece of black foam rubber.  “Before you go to wardrobe, let me help you put this on under your t-shirt.”The giant piece of foam rubber turned out to be a device called an abdominal censure; in other words, a giant girdle.

“I can’t wear that…” I said.

“Hey, don’t think you’re the Lone Ranger,” he replied, “why do you think I have this?  I didn’t buy it just for you.  A surprising number of the people you see on TV daily are wearing one of these.  Lift up your shirt.”

“Who?” I asked.

“I’m not going to tell anyone about you and I’m not going to tell you about anyone else.  Lift your shirt.”

I lifted my t-shirt; he wrapped the thing around my abdomen and put his knee in the middle of my back to cinch me in.  Feeling a little like the male equivalent of Scarlett O’Hara in the corset scene, I dropped my t-shirt down and looked in the mirror.  I had to admit, I looked better.

I wore the girdle and Mary Dan stayed behind the counter for the two days it took to film the pilot.  (Now we shoot two shows per day, but then we were raw beginners.)  Our show got picked up by PBS and we scheduled to start shooting about three months later.  Fortunately, the pilot was only shown to others in the industry, and now the show with me squeezed into neoprene and Mary Dan cloistered behind the counter has been relegated to the never-to-be-shown file.  What we took away from that day was the certainty that something had to be done and quickly…but what?

Not long after returning home from this experience we attended a large charity event at which we were seated at a table with several middle-aged women.  One was significantly overweight, but the others would be considered within or close to their normal weight range.  The discussion turned to weight loss.  The constant thread through the conversation was how much easier it was to lose weight overall, compared to the difficulty of losing it in the waist.  All the women bemoaned their stubborn middles.

Meanwhile, still stinging from our recent brush with abdominal truth, we had begun looking at the mid-sections of non-obese middle aged men and it quickly became clear that they all had paunches of various sizes.  It appeared that there were no (or damned few) middle-aged flat bellies out there of either gender.  Young people who were a little overweight didn’t seem to have protuberant guts; they carried their excess weight all over.  But in middle age, it went straight to the middle.  Even young people with guts don’t look the same as middle-aged people with big bellies; there is a difference, easily recognized.  We realized that our director had been right; it’s not just normal body weight, but a flat belly that is the real sign of youth, so we set out to get one, too. .  Drawing on two decades of experience in clinical practice, helping thousands of patients of all ages, we dusted off and examined every weight loss trick in our armamentarium. We did the same thing we had done years before when we did our research for Protein Power, combing the worldwide medical literature for insight and scientific substance, but instead of concentrating on weight-loss in general, we focused our search on abdominal weight loss, more specifically abdominal fat loss.  We discovered that, although spot reducing is impossible, the diameter of the mid-section can be reduced quickly with the right nutritional tools.  Fortunately, many of those tools dovetailed perfectly with those we’d used successfully over the years with patients in our clinical practice.  After a couple of weeks of intense effort, we put together a flat-belly program for ourselves that combined a reworking of our old Thin So Fast and Protein Power diets that we had used in many thousands of patients, a number of nutritional supplements we had learned about from our wide-ranging medical research in the intervening years, and a unique, but simple, abdominal exercise plan, based on the laws of physics.

We had exactly 6 weeks before our next shoot, so we launched into the program with full vigor, with the goals of avoiding the dreaded cinch and the safety of the counter.  The regimen vastly exceeded our expectations.  The greatest changes occurred in the first two weeks with smaller, but still significant, changes taking place over the course of the next 4.  We appeared for the shoot with flat bellies, much to the delight of our director.  and were able to move from refrigerator to sink to counter, showing full physique and with nary a trace of neoprene.   We no longer had to suck it in every time we changed positions for fear that the camera might catch our mid-sections at an unfavorable angle. The regimen had been a slam dunk.

It’s been a little over two years (and 26 episodes of our show) since we developed and took The 6-Week Cure ourselves, but our success has inspired countless readers, viewers, relatives, patients, friends, and friends of friends to want to know exactly how we did it.  This book provides those answers.  In it, you will discover not only what happens in middle age that drives fat into your middle body, but more importantly, what you can do, physically and nutritionally, to harness the metabolic forces at work and turn the tide.  With a little hard work over a very short stretch, you, too, can regain a more youthful silhouette. When you do, we’re sure you’ll agree with what we discovered: there’s nothing that restores youth like curing your middle-aged middle.

MD and I have been on a low-carb diet (sometimes stringently; sometimes not so stringently) for about the last 25 years, so some may take this story to be a repudiation of such diets, but it isn’t.  Our diet wasn’t really at fault; it was the inexorable creep of time that caused the problem.

As we age, things change.  What worked 25 years ago, doesn’t work exactly as well now.  Especially when we get a little sloppy with it.  One of the problems with carb restriction is that people who do it for a while, get good at it.  They become experts at both abiding by the carb restriction yet consuming a lot of calories and tending to overlook small carb indiscretions—a small piece of bread at dinner, just a bite or two of dessert, an extra glass or two of wine or beer—that they would have scrupulously avoided during the first heady days of low-carbing.  We were certainly experts on low-carb diets and we fell into those traps.   And time marched on making us even more susceptible to little indiscretions and to carb creep.

Now, we never came close to Orson Welles or Mamma Cass proportions – in fact most people would have described us a slim – but we had picked up little middle-aged middles.  So we set out to lose them.  Fast.  To do so, we relied upon our 25 years in clinical practice, pulling out every tool we had learned to help solve stubborn cases of middle- aged overweight.

As we describe in the book, the kind of fat people pack on around their middles in middle age is different than fat packed on earlier in life, which is both good news and bad.  Middle-aged fat is, by and large, visceral fat, the kind that accumulates within the abdominal wall and around the organs.  The bad news is that it is a dangerous kind of fat – the good news is that it’s relatively easy to lose.  Especially if you do it the right way.  Which is why you can make enormous strides in only six weeks even if you have a lot to lose.

Although it does contain plenty of information you’re not likely to have read before, this book isn’t intended as a giant treatise on everything known about health and weight loss.  It’s, quite simply, a primer on how to get rid of middle-aged abdominal fat fast and safely.  We solved our own problem.  I hope those of you who grab a copy and give it a try achieve the success that we did.  And I hope you give us your feedback so that we can improve future editions.

A paper appeared recently in the prestigious Proceedings of the National Academy of Sciences (PNAS) that seems to have a whole lot of people on edge.  If you read the press accounts of this study, you might think anyone stupid enough to follow a low-carb diet would be doomed to certain death from heart attack.  But is that the case?  Or is it simply another instance of the media either failing to understand how science works or, worse, misreporting to get a better story?

I suspect the latter, but before we get into it, I need to go over a few blog housekeeping issues.

As I’m sure everyone has noticed, the look of this blog has changed – as has the look of the entire website.  Our designer and tech guys have been struggling to get everything working right, but, finally, my incessant whining got to them, and they went ahead and put the thing up in its not-completed state.  Please bear with us – it will ultimately work as it’s supposed to.  If you are having a problem, send me a description in the comments section.  Make sure you tell me what kind of computer you’re using (Mac (Intel or pre-Intel)  or PC) and which browser (Firefox, Internet Explorer, Safari, etc.) so that the gurus will know what to do to fix it.

I know the comments are screwed up right now, but don’t worry, they’ll be fixed.  Go ahead and comment away.  They’ll ultimately be up in a form you can recognize.

Once we get the blogs and website how they’re supposed to be, I’ll write a post describing all the features.

Also, our world-changing project has been slightly delayed through no fault of our own.  The new date for revelation has been pushed back from Sept 1 to Sept 15.  Sorry.  It’s been a real PITA for us, too.

Now, back to the PNAS paper.

As we all know, media reports can be totally misleading or even downright false.  Reporters have their own biases that creep into their work, and even when reporters think they are presenting the facts, they often report just one side of a story and ignore the other.  And, as we’ve seen from the previous post on the vitamin D-bate, reporters may just report a story in a way that makes for better reading without any regard for the substance of the issues.

The PNAS paper reported a study on genetically modified rodents, engineered to be more susceptible to heart disease.  As I’ve written many times in these pages, mice and rats aren’t just furry little humans – they are a different species altogether.  And although they are often used for medical experiments, the conclusions from the experiments cannot be applied to humans.  Like observational studies, rodent data can be used to establish hypotheses about human health and disease, hypotheses that can then be tested for validity.

In this case, the data on these genetically-engineered mice can’t even be extrapolated to normal mice much less humans.  Knowing just this much about the study tells us that whatever it shows has little relevance to us.  But that’s not what the media took away from the story.

The BBC came out with the following headlines that were picked up by a number of other media sources:

Low-carb diets ‘damage arteries’

And followed up with:

Low-carb slimming diets may clog arteries and increase the risk of heart attacks and strokes, a study suggests.

Diets based on eating lots of meat, fish and cheese, while restricting carbohydrates have grown in popularity in recent years.

But the Beth Israel Deaconess Medical Center in the US found such habits caused artery damage in tests on mice.

The researchers and independent experts both agreed a balanced diet was the best option.

Hmmm.  Sounds pretty brutal doesn’t it.  No hesitance there.  No equivocation.  Just a head on reporting of the facts.  I don’t think so.

Why not?  A number of reasons.  First, these researchers basically had a bias going in that low-carb diets cause heart disease even though they lower cholesterol and bring about other positive changes in lipid values, most notably reducing triglycerides, increasing HDL levels, and changing LDL particles from the small type B to the larger type A variety.  All of which changes, by the way, supposedly reduce the risk for heart disease.

The lead author of the study, Shi Yin Foo, MD, PhD, a clinical cardiologist,

first embarked on this investigation after seeing heart-attack patients who were on these diets – and after observing Rosenzweig [the researcher in whose lab she worked] himself following a low-carbohydrate regimen.

“Over lunch, I’d ask Tony [the aforementioned Rosenzweig] how he could eat that food and would tell him about the last low-carb patient I’d admitted to the hospital,” says Foo. “Tony would counter by noting that there were no controls for my observations.”

“Finally,” adds Rosenzweig, “I asked Shi Yin to do the mouse experiment – so that we could know what happens in the blood vessels and so that I could eat in peace.”

Do you think Dr. Foo has a little skin in this game?  Think she might have a motive for stacking the deck a little in setting this experiment up in a way that encourages a certain outcome?  This was not what you would call an unbiased quest for the truth.

I want to comment on something here as an aside.  I don’t know how old Dr. Foo is, but since she’s working in someone else’s lab, I would think she’s probably fairly new to the medical game.  She may have admitted a patient or two to the hospital with heart attacks, who, under questioning, may have admitted to following a low-carb diet at some point.  But I’m willing to put my experience with low-carb diets up against hers any day.  MD and I have followed over 10,000 patients on low-carb diets and have never had a single one have a heart attack.  So, I really doubt that Dr. Foo has admitted many – if any – patients who are actively following a low-carb diet.  But it does make for a good story.

Second, we’ve already mentioned that the mice were genetically engineered to be more susceptible to heart disease, so data generated from these rodents can’t be extrapolated even to other mice let alone to humans.

Third, the diet used wasn’t even a typical low-carb diet.  The researchers

had a diet specially made that would mimic a typical low-carb diet,” explains Foo. “In order to keep the calorie count the same in all three diets, we had to substitute a nutrient to replace the carbohydrates. We decided to substitute protein because that is what people typically do when they are on these diets.”

Oh, really?  This one statement shows Dr. Foo’s ignorance of low-carbohydrate dieting.  People don’t typically “substitute protein” when they go on a low-carb diet.  As anyone knows who has been on one, people substitute fat, the macronutrient that provides most of the calories on any low-carb diet.  The mice in this study were getting 45 percent of their calories from protein, which can be done, but isn’t what one finds in most typical low-carb diets.

MD and I have been traveling extensively lately, so I hadn’t really had the time yet to delve deeply into this study, but, fortunately, as it turns out, I didn’t have to.  Others have done it for me.

The Metabolism Society issued a press release on the paper to all its members.  You can read it in full below:

Researchers use mutant mice genetically engineered to be susceptible to heart disease to ‘prove’ carbohydrate restricted diets may harm arteries.

Defects in ApoE -/- result in defects in processing blood cholesterol.

As human studies continue to show the benefits of low carbohydrate diets and the general failure of low-fat diets, it is necessary for the nutritional establishment to find more and more obscure methods of attacking dietary carbohydrate restriction.

One method is to prepare mutant animal models, to use odd diets that humans would never consume, call them low carbohydrate diets and then show some deficit.  Because mice are not generally susceptible to atherosclerosis, it was necessary for Foo and coworkers to use an ApoE-/- mutant and a ridiculously high protein diet to vilify low carbohydrate diets which have been a useful alternative for many people suffering from obesity, diabetes and metabolic syndrome.

In keeping with the traditions in scientific research, the authors do not cite the numerous studies showing benefit of low carbohydrate diets compared to the low fat diet that has been in place during the obesity and diabetes epidemic.  That the NIH and other government agencies continue to fund this kind of biased research is probably a minor political problem in health care but should still be of concern to people who are confused about what their diet should be.

According to Dr. Richard D. Feinman, Biochemistry Professor at Downstate Medical Center in NY,  “It is a mistake to consider one experiment in a mouse mutant over riding the scientific literature where similar research trials on actual human beings clearly show benefit of carbohydrate restriction for all markers of metabolic syndrome. For some reason these studies are not the ones picked up by the media. I suppose actual advances in science aren’t hot topics for headline news stories when it concerns the proven benefits of carbohydrate restriction.

Volek JS, Ballard KD, Silvestre R, Judelson DA, Quann EE, Forsythe CE, Fernandez ML, Kraemer WJ: Effects of dietary carbohydrate restriction vs low-fat diet on flow-mediated dilation. Metabolism 2009.

Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD: Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids 2009, 44(4):297-309.

Of course, as you might expect, the press release wasn’t picked up by any of the major media outlets.

Jimmy Moore weighed in on the issue in an article in the Examiner.com in which he quotes numerous experts who have their say on this study.

And, Peter at Hyperlipid wrote two great posts taking the researchers to task and exploring  the kind of protein used and various other aspects of this study. (Here and here.)

So, I was left with nothing more to add other than to say what I’ve said countless times before:  Don’t rely on media reports to tell you anything.

(With apologies to Philip K. Dick for the title of this post.)

Don’t panic.  I don’t have a paid ad for the RealAge Test stretching across the top of my blog post today.  This one is for illustration purposes only.  If you are like me, however, you’ve run across this banner countless times in your online surfing.  It seems to pop up everywhere.  Or at least it used to.  It hasn’t too much lately since the big New York Times exposé, more about which later.

But first let’s take a look at something else brought to the public by the team of Roizen and Oz.  I came across this page on their RealAge website while I was googling something else.

According to these two (or their team of ‘world-renowned scientists and doctors’) we should all avoid fructose and load up on glucose, the ’sugar that staves off hunger.’

Sugar is sugar, right? Maybe not. Turns out that there is one type of sweetener that helps fill you up, while another leaves you craving more.

The two sugars in question: glucose and fructose. Glucose appears to quell hunger, and fructose seems to ramp it up.

The sugars may affect your appetite differently because of the unique ways in which they affect malonyl-CoA, an important appetite-suppressing molecule in the brain. Glucose causes malonyl-CoA to rise, resulting in less food intake. Fructose, on the other hand, lowers malonyl-CoA, resulting in more food intake.

The implication of their message is that if you eat glucose you won’t be hungry, but if you eat fructose you will.  They go on to discuss how important it is to cut fructose from the diet since fructose makes you eat more.  And, by implication, to add glucose.

I agree that we should all cut most of the fructose from our diets, but not for the reasons these guys (and their team of purported experts) give.

I would assume that both of these docs went to medical school and had many years of post-medical school training.  I would also assume the same about their ‘world renown’ staff of experts.  What I don’t understand, then, is how they can make such stupid statements that have no grounding in actual biochemistry.

The ‘important appetite-suppressing molecule’ under discussion is malonyl-coenzyme A (malonyl-CoA), which is one of the major signaling molecules in the body.  Malonyl CoA sits at the crossroad of fat storage and fat burning and drives the reaction one way or another.

If we’ve eaten a lot, especially a lot of carbohydrate, malonyl-CoA levels increase.  Increased levels of this substance then shift the flow of fat away from burning and toward storing.  Among its activities, Malonyl-CoA stimulates fatty-acid synthase (FAS), the enzyme that converts carbohydrate to fat.  And it inhibits the enzyme (CPT-1) that carries fat into the mitochondria where it is burned for energy.

If we haven’t eaten, or if we have been eating a low-carb diet, the opposite happens.  Malonyl-CoA levels are low, which removes the inhibition of CPT-1.  Fat is shunted away from storage in the fat cells and instead is transported into the mitochondria where it is burned.

Since malonyl-CoA is one of the main substances in the body that determine what happens to fat, it would make sense that this molecule would somehow be involved in the regulation of hunger.  Elevated malonyl-CoA levels indicate that we’ve got plenty of fuel aboard and that the body is in the process of getting it stored away, so it would stand to reason that these elevated levels may affect the hunger centers in the brain, sending the message not to eat any more.

Researchers have looked into this notion, and it indeed appears – in rodents, at least – that elevated levels of malonyl-CoA do suppress the hunger centers in the hypothalamus.

If you do a quick thumb through any decent medical biochemistry textbook looking for what makes malonyl-CoA go up, you’ll find that it is driven up by insulin and glucose, the surrogates for being well fed.  But here is where Roizen/Oz and the team of experts go off the rails.  The glucose in question isn’t dietary glucose – it’s blood glucose.  As I’ve written about before, the entire amount of glucose we have circulating through us if we have a normal blood sugar level is around 4 grams, a little less than one teaspoon.  If we eat a medium-sized baked potato, we ingest about 50 grams of glucose (potato starch is made of pure glucose), which is more than ten times the amount regularly circulating in our blood.  Our bodies quickly deal with this excess by increasing insulin and driving the glucose into the cells.  As a practical matter, dietary glucose never really impacts malonyl-CoA.  What does impact it is the level of blood sugar.  So if blood sugar is higher than normal, then more malonyl-CoA is made, and more fat is stored.  Which is one of the reasons type II diabetics are usually obese to some extent.  These people have the double whammy of too much sugar and, since they’re almost always insulin resistant, too much insulin.

Any readers who have type II diabetes will have increased levels of malonyl-CoA.  I will ask those of you who have this condition: are you less hungry?  I didn’t think so.  Despite the fact that in rodents (and probably in people who are normal weight) malonyl-CoA may suppress hunger, it doesn’t seem to do so in those who are overweight and insulin resistant.  It may a little, but there are other forces driving hunger more than the malonyl-CoA suppresses it.  And in any case, it doesn’t have anything to do with dietary glucose – a fact our illustrious crew of ‘world renowned’ experts should have known.  Their implying that adding glucose to one’s diet will decrease hunger is just plain stupid.

But let’s look at something a little more sinister than just plain ol’ stupid.

These same guys are behind the RealAge test that (until fairly recently) was popping up every time you turned on your computer.  I saw the ads for this test over and over and over again, and I wondered what they were selling to justify the huge expense such unremitting advertising requires.  Then I read a New York Times article that explained it all.

As it turns out, the RealAge test is a means for Roizen/Oz et al to gather health information from those who take the test.  I’ve taken the test, which requires many pages of questions, and discovered that I am about 8 years younger than my chronological age.  I also discovered that I would be younger yet if I didn’t eat so much red meat.  You can guess how to perform well on the test: tell them you eat no red meat and a lot of soy.  (My choices on the red meat were: no red meat; red meat once per week; or red meat more than once per week.)

During the course of the test, after a long list of medical problems that are to be checked if the test-taker suffers from them, this question pops up:

If the answer is yes, you may be bombarded with information from various pharmaceutical companies that make drugs to treat the checked diseases. Or if, according to the Times, you decide to become a RealAge member.

Yep, that’s right.  These guys who seem so compassionate and are giving away their RealAge test (after capturing your email address) and providing all kinds of lifestyle change recommendations are really capturing your info and peddling it to Big Pharma.  Which, of course, is how they can afford the many ads for their ‘free’ RealAge test.

Says the NY Times:

But while RealAge promotes better living through nonmedical solutions, the site makes its money by selling better living through drugs.

Pharmaceutical companies pay RealAge to compile test results of RealAge members and send them marketing messages by e-mail. The drug companies can even use RealAge answers to find people who show symptoms of a disease — and begin sending them messages about it even before the people have received a diagnosis from their doctors.

While few people would fill out a detailed questionnaire about their health and hand it over to a drug company looking for suggestions for new medications, that is essentially what RealAge is doing.

Pretty sleazy, if you ask me.

They still provide their RealAge test, but as far as I can tell, only if you go to their website.  They are probably waiting for the fallout to be over from the Times piece.  Until then, they are dragging people to their website with idiotic pieces such as the one I discuss above.  If you are googling a health problem, nutrient, diet, etc., you may come upon their website and be presented with the RealAge test.

But, if the article I read is any indication of the value of their advice, I would be real leery.  The advice may be stupid, but the strategy behind the RealAge test is definitely sleazy.

Second, I’m not particularly pro-feminist.  And I certainly don’t hang around with any self-proclaimed radical feminists.  I have a wife who is smarter than I am, who is more talented than I am, and who, pound for pound, is probably a better athlete than I am, and I’m not bad. (In my defense, I can read much, much faster than she, but, she has better comprehension.) I long ago gave up the idea (if I ever really considered it seriously) that men are superior to women in any ways other than brute strength.  Having said that, however, I do believe that men are better suited to certain endeavors than woman and vice verse, but that doesn’t mean either men or women should be denied the opportunity to give whatever it is they want to do a whirl just because of their sex.  I guess I consider myself an egalitarian.  But from what I’ve seen of radical feminists, I’m not sure that I would count myself a big fan.

Given the above, you wouldn’t think I would enjoy and recommend a book written by a self-proclaimed radical feminist who is obviously a believer in global warming and the impending end of the earth as we know it.  I wouldn’t think so, either. Not my cup of tea even when it is sort of preaching to the choir.

But I can tell you that Lierre Keith’s book is beyond fantastic.  It is easily the best book I’ve read since Mistakes Were Made, maybe even better.  Everyone should read this book, vegetarian and non-vegetarian alike.  If you’re a radical feminist, you should read this book; if you’re a male chauvinist, you should read this book; if you have children, especially female children, you should read this book; if you are a young woman (or man) you should read this book; if you love animals, you should read this book; if you hate vegetarians, you should read this book; if you are contemplating the vegetarian way of life, you should definitely read this book; if you have a vegetarian friend or family member, you should this book and so should your friend.  As MD said after she read it, “everyone who eats should read this book.”

Anyone who has ever read a book on writing has come across the hackneyed piece of advice to cut open a vein and bleed on the page.  Lierre Keith, the author of this book, has come closer to literally doing that than almost any writer I’ve ever read.  Not only does her passion for her subject bleed through in almost every sentence, she is a superb lyrical prose stylist.  My book is dog eared, underlined and annotated from front to back – I can’t remember anything I’ve read that has contained so many terrific lines.

In fact The Vegetarian Myth is filled with so many good quotes (most by the author but some from other authors) that I was reminded of the old joke about the redneck who went to see a performance of Hamlet.  When the show let out, someone asked him what he thought of it.  Replied he:  It wasn’t nothin’ but a whole bunch of quotes all strung together.  As you’ll see when I ‘quote’ them below, The Vegetarian Myth contains quotable lines and paragraphs at about the same rate Hamlet does.

Ms. Keith was a practicing vegetarian (vegan) for twenty years, driven by her passion for kindness and justice for all creatures.  She couldn’t bear the thought of even killing a garden slug, or, for that matter, even removing a garden slug from her garden to a place where something or someone else might kill it.  Her years of compassionate avoidance of any foods of animal origin cost her her health.  Her story of coming to grips with the realization that whatever she ate came as a consequence of some living being’s having to die form the matrix onto which her narrative hangs.

You can read the first 14 manuscript pages of the book on the author’s website.  I have quoted from these 14 pages liberally below.

The introduction to The Vegetarian Myth explores Ms. Keith’s rationale for writing such a book, a book that, given her years of walking the vegetarian walk, must have been incredibly difficult to write.  She says as much with her first sentence.

She ponders the idea of factory farming, which she loathes, and the misbegotten idea that most people hold (not most readers of this blog, but most of the people in the world) that grains are good, not only for people, but for many animals as well.  And the common misconception that agriculture, the growing of annual grains and plants, is a wonderful, kind, sustainable activity.

This misunderstanding is born of ignorance, an ignorance that runs the length and breadth of the vegetarian myth, through the nature of agriculture and ending in the nature of life. We are urban industrialists, and we don’t know the origins of our food. This includes vegetarians, despite their claims to the truth. It included me, too, for twenty years. Anyone who ate meat was in denial; only I had faced the facts. Certainly, most people who consume factory-farmed meat have never asked what died and how it died. But frankly, neither have most vegetarians.

The truth is that agriculture is the most destructive thing humans have done to the planet, and more of the same won’t save us. The truth is that agriculture requires the wholesale destruction of entire ecosystems. The truth is also that life isn’t possible without death, that no matter what you eat, someone has to die to feed you.

I want a full accounting, an accounting that goes way beyond what’s dead on your plate. I’m asking about everything that died in the process, everything that was killed to get that food onto your plate. That’s the more radical question, and it’s the only question that will produce the truth. How many rivers were dammed and drained, how many prairies plowed and forests pulled down, how much topsoil turned to dust and blown into ghosts? I want to know about all the species—not just the individuals, but the entire species—the chinook, the bison, the grasshopper sparrows, the grey wolves. And I want more than just the number of dead and gone. I want them back.

After she had seen the error of her ways as a vegan and had been eating meat for two years, for reasons unknown to her, the author continued to surf the same vegan websites and message boards she had for years.  Until she read one post that was so bizarre that she finally realized the large intellectual gap that had widened between her rationale thinking and the cult like thinking of, well, a cult.  It would be funny if it weren’t so pathetic.

But one post marked a turning point. A vegan flushed out his idea to keep animals from being killed—not by humans, but by other animals. Someone should build a fence down the middle of the Serengeti, and divide the predators from the prey. Killing is wrong and no animals should ever have to die, so the big cats and wild canines would go on one side, while the wildebeests and zebras would live on the other. He knew the carnivores would be okay because they didn’t need to be carnivores. That was a lie the meat industry told. He’d seen his dog eat grass: therefore, dogs could live on grass.

No one objected. In fact, others chimed in. My cat eats grass, too, one woman added, all enthusiasm. So does mine! someone else posted. Everyone agreed that fencing was the solution to animal death.

Note well that the site for this liberatory project was Africa. No one mentioned the North American prairie, where carnivores and ruminants alike have been extirpated for the  annual grains that vegetarians embrace. But I’ll return to that in Chapter 3.

I knew enough to know that this was insane. But no one else on the message board could see anything wrong with the scheme. So, on the theory that many readers lack the knowledge to judge this plan, I’m going to walk you through this.

Carnivores cannot survive on cellulose. They may on occasion eat grass, but they use it medicinally, usually as a purgative to clear their digestive tracts of parasites. Ruminants, on the other hand, have evolved to eat grass. They have a rumen (hence, ruminant), the first in a series of multiple stomachs that acts as a fermentative vat. What’s actually happening inside a cow or a zebra is that bacteria eat the grass, and the animals eat the bacteria.

Lions and hyenas and humans don’t have a ruminant’s digestive system. Literally from our teeth to our rectums we are designed for meat. We have no mechanism to digest cellulose.

So on the carnivore side of the fence, starvation will take every animal. Some will last longer than others, and those some will end their days as cannibals. The scavengers will have a Fat Tuesday party, but when the bones are picked clean, they’ll starve as well. The graveyard won’t end there. Without grazers to eat the grass, the land will eventually turn to desert.

Why? Because without grazers to literally level the playing field, the perennial plants mature, and shade out the basal growth point at the plant’s base. In a brittle environment like the Serengeti, decay is mostly physical (weathering) and chemical (oxidative), not bacterial and biological as in a moist environment. In fact, the ruminants take over most of the biological functions of soil by digesting the cellulose and returning the nutrients, once again available, in the form of urine and feces.

But without ruminants, the plant matter will pile up, reducing growth, and begin killing the plants. The bare earth is now exposed to wind, sun, and rain, the minerals leech away, and the soil structure is destroyed. In our attempt to save animals, we’ve killed everything.

On the ruminant side of the fence, the wildebeests and friends will reproduce as effectively as ever. But without the check of predators, there will quickly be more grazers than grass. The animals will outstrip their food source, eat the plants down to the ground, and then starve to death, leaving behind a seriously degraded landscape.

The lesson here is obvious, though it is profound enough to inspire a religion: we need to be eaten as much as we need to eat. The grazers need their daily cellulose, but the grass also needs the animals. It needs the manure, with its nitrogen, minerals, and bacteria; it needs the mechanical check of grazing activity; and it needs the resources stored in animal bodies and freed up by degraders when animals die.

The grass and the grazers need each other as much as predators and prey. These are not one-way relationships, not arrangements of dominance and subordination. We aren’t exploiting each other by eating. We are only taking turns.

That was my last visit to the vegan message boards. I realized then that people so deeply ignorant of the nature of life, with its mineral cycle and carbon trade, its balance points around an ancient circle of producers, consumers, and degraders, weren’t going to be able to guide me or, indeed, make any useful decisions about sustainable human culture. By turning from adult knowledge, the knowledge that death is embedded in every creature’s sustenance, from bacteria to grizzly bears, they would never be able to feed the emotional and spiritual hunger that ached in me from accepting that knowledge. Maybe in the end this book is an attempt to soothe that ache myself.

How anyone who can read these 14 pages and not purchase and read this book is beyond me.

After the introduction which deals with why the author wrote the book, The Vegetarian Myth is divided into four sections: Moral Vegetarians, Political Vegetarians, Nutritional Vegetarians, and To Save the World.

The first three of these sections are the author’s in-depth refutations of the moral, political and nutritional arguments that vegetarians are constantly putting forth.  She does a masterful job.

In the Moral Vegetarians chapter, the author addresses the moral issue of killing animals for our own food.  She beautifully makes her case by cutting to the heart of the matter:

What separates me from vegetarians isn’t ethics or commitment.  It’s information.

And while she was in her 20-year trek in the vegetarian wilderness, she shielded herself from information as most cultists do:

I was on the side of righteousness, and like any fundamentalist, I could only stay there by avoiding information.

She finally realized the truth about agriculture; she figured out that the amber waves of grain are as death dealing as any slaughterhouse.

And agriculture isn’t quite a war because the forests and wetlands and prairies, the rain, the soil, the air, can’t fight back.  Agriculture is really more like ethnic cleansing, wiping out the indigenous dwellers so the invaders can take the land.  It’s biotic cleansing, biocide. … It is not non-violent.  It is not sustainable.  And every bite of food is laden with death.

There is no place left for the buffalo to roam.  There’s only corn, wheat, and soy.  About the only animals that escaped the biotic cleansing of the agriculturalists are small animals like mice and rabbits, and billions of them are killed by the harvesting equipment every year.  Unless you’re out there with a scythe, don’t forget to add them to the death toll of your vegetarian meal.  They count, and they died for your dinner…

Soil, species, rivers.  That’s the death in your food.  Agriculture is carnivorous: what it eats is ecosystems, and it swallows them whole.

In Political Vegetarians she refutes the politics (predominantly liberal) of the vegetarian movement and describes the dark side of political meddling in our ecosystem approved of in the main by PETA and other vegetarian groups.  She follows the money.

Rice, wheat, corn – the annual grains that vegetarians want the world to eat – are thirsty enough to drink whole rivers.

The result has been an unending river of corn, drowning our arteries and our insulin receptors, our rural communities, and poor subsistence economies the world over.  The corn comes at a huge environmental toll: there’s a half gallon of oil in every bushel.  And it’s essentially a massive transfer of money from the US taxpayer to the giant grain cartels, who are able to command the price of grain to be lower than the cost of production, with all of us making up the difference – five billion dollars in subsidies for corn alone, straight into the pockets of Cargill and Monsanto.

Nutritional Vegetarians is about the nutritional inadequacies of a vegetarian and especially a vegan diet.  And she does an absolute bang up job of laying out the rationale for following a no-grain, low-carb diet.

I have a disclosure to make here.  Much of the information in this chapter is based on Protein Power and The Protein Power LifePlan.  MD and I are listed in the acknowledgments, but I swear I didn’t know this until I bought the book.  We aren’t the only ones, but there are plenty of quotes from us in this chapter.  Gary Taubes, Malcolm Kendrick and (dare I say it) Anthony Colpo are quoted liberally as well.  I would have loved this book just as much if we had never been quoted.

Ms Keith has made a few minor innocuous errors in this chapter, but, all in all, she has done a tremendous job of synthesizing the scientific information into an easy to read, informative format.

The Nutritional Vegetarians section isn’t just about the science of why vegetarianism is bad and meat eating is good, it gets into the nutritional politics (as opposed to the vegetarian politics in the previous section) as well.  Ms Keith shows how we got to where we are by the nutritional strong arming by the McGovern committee back in the late 1970s.  George McGovern (a senator from a grain-producing state) and his cronies basically set the nutritional standards under which we are still oppressed.  They have been a disaster, as some scientists at the time predicted they would be.

And some scientists knew ahead of time that they would be.  Phil Handler, the president of hte National Academy of Scientists asked Congress, “What right has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?”  Dr. Pete Ahrens, an expert on cholesterol metabolism, told the McGovern committee that the effects of a low-fat diet weren’t a scientific matter but “a betting matter.”

It’s twenty-five years later and we aren’t winning this bet.  Each US American now eats sixty pounds more grain per annum and thirty pounds more cheap sugars, mostly from corn.  [Is it any wonder we're all fat?]

The result, Dietary Goals for Americans, set in motion a cast sea change in the public’s beliefs and behaviors. … Dietary Goals was a predictable victory in a war that started ten thousand years ago.  What really won were those annual grasses that had long since turned humans into mercenaries against the rest of the planet.  We would now enshrine them like demi-gods, those whole grains and their sweet, opiate seductions, believing in their power to bestow health and long life, even while they slowly ate us alive.

I don’t think I’ve ever read a book review that was positive from beginning to end, and this one is no exception.  Based on the many comments I’ve gotten on this blog and my response to them, I’m sure many of you will find my main objection surprising.  There is too much politics in the book.  Not nutritional politics, but feminist politics.

I know, I know, I let my libertarian leanings come through in all kinds of blog posts and comment answers, but there is a difference.  My blog is just that – a weblog of things I find interesting or informative.  And it’s free.  I don’t particularly like to pay for a book (and I paid full price for this one plus shipping) on a given subject then be beaten over the head with a political viewpoint.  I guarantee you that our new book has zero politics in it.  And if people bought our book expecting to learn about getting rid of their middle-aged middles and were fed a generous dose of my politics mixed in with the information, I would expect them to be flamed.

To give the author her due in this matter, the vegetarian ideology that had her in its grasp for 20 years was intertwined with her feminist politics, so a bit of said politics are necessary to describe how she was so taken in for so long.  But I think she went a little overboard with it.

And, I think the last section of the book – To Save the World – is the weakest part of the book.  The author makes several recommendations, all of which (save one) are, in my opinion totally unrealistic.  But I’ll leave it to you to draw your own conclusions after you’ve read the book.

I’ve read that when people are asked to recall what they remember of something they read, they tend to remember the first thing in the piece and the last thing.  Most of the middle melds into a vague memory of what the article was about.  I certainly don’t want people to remember this last negative part I wrote and let it dissuade them from reading this book.  The good parts of the book so far outweigh the not-so-good parts that there is really no contest.

At a time when PETA and other vegetarian groups are mobilizing and ramping up their activity levels, a book such as this one bringing sanity to the debate is more important than ever.  And don’t think these groups aren’t becoming more active.  In the past, PETA and PETAphiles pretty much devoted their educational efforts toward the idea that eating animals was cruel.  Now they are starting to make the case that a vegetarian diet will solve the obesity epidemic.  Take a look at this billboard in Jacksonville, Florida.

If you find this sign annoying, buy The Vegetarian Myth and do your part to fight back. And if you have or know anyone with a daughter who is contemplating going vegetarian (young females are the most common victims), please make this book available.  It could be the most important thing you ever do for the long-term mental and physical health of a young woman.

If you’ve made it this far in this long review, take a couple of minutes and watch this YouTube of Lierre Keith at a book event; she’s as fascinating to listen to as she is to read.

Click here to view the embedded video.

I haven’t posted in a week because MD and I have been hard at work in Seattle and at Orcas Island, the largest of the San Juan Islands located in northwestern Washington.

We’re working on our project that we’ve been keeping under wrap.  No, it’s not the new book, and, no, it’s not Metabosol.  It is something pretty cool and even revolutionary in its own way.  Barring further bumps in the road (there have been a few), we should be able to reveal all on September 1. The reason for the secrecy is that this project is most press worthy, but, for reasons that will be obvious when we reveal what we’ve been working on, we don’t want the press to report it prematurely.

We flew into Seattle Sunday afternoon after buzzing across the top of Mount St. Helens and looking into the crater left when the top 1300 feet of the mountain blew off on May 18, 1980.  After landing, we got picked up by our partner and taken to his boat for an afternoon on Lake Union.  A huge annual celebration was taking place, so we spent the afternoon on a lake made choppy by a thousand other boats while the Blue Angels zipped through the sky overhead.  Seattle has been experiencing brutally hot temperatures, which we got blasted by on Sunday afternoon.

When we were in Seattle in December, we got caught in the worst snow storm in 30 years.  All the while we were slogging through the snow, our hosts were telling us to come visit in the summer when the weather is always beautiful.  So, we come in the summer only to be confronted with the worst heat wave since temperatures have been recorded.  I hate to imagine what we may encounter on the next trip.

Here is the Seattle skyline on Sunday afternoon.  Notice the chop on the water.  We were one of God only knows how many boats in the lake.  After getting pounded by the chop and brutalized by the heat, we tied up to a nice restaurant and had a lovely dinner complete with (at least for me) copious amounts of Jameson to go along with the copious amounts of Jameson I had already swilled to combat the heat on the lake.

Our partner’s boat, which is his pride and joy, is a handmade Venetian water taxi.  He worked with a guy who makes such boats in Venice, Italy several years back, had it built to his specs and then transported to Seattle.  It is a gorgeous boat, and, one day, I hope to go out on it in clement weather.  Below is a photo of MD standing by the boat tied up to another restaurant the last time we went out in it.  The temperature was about 23 degrees (not counting the chill factor), and you can see by the lack of chop on the water surface that we were the only fools out there.  (In case you were wondering, it is heated inside…but not air conditioned, thought the back of the roof slides open to admit fresh air and sunshine.)  As I say, our partner loves to show off his boat.

After our Sunday respite (which it was, despite the heat and chop), we crashed and for the next two days worked from early morning until late at night.  We didn’t have time to answer emails, deal with blog comments, or do much of anything other than work.

We started each day with a quick breakfast at Louisa’s, a little restaurant close to the office where we spent our days.  One of the menu selections, fittingly enough, was called Mike’s Special, so how could I resist.  Especially when it was such a great low-carb option: two poached eggs on a bowl of sauteed spinach, red and green peppers and onions.  Good, good, good.  It came, of course, with a giant piece of toast that was at least an inch thick, which I ate a couple of bites of just to try.

As we were eating breakfast on the last morning, a man was eating alone while reading the paper at the table next to us.  He looked to be about 70 or so and was fairly thin with a pot belly.  He had on two pressure stockings on his lower legs and bruising in the crook of one of his arms from where, obviously, blood had recently been taken.

Watching him eat, I created an entire story about him that I’ll bet is not too far from the mark.  Even if it is not accurate in this man’s case, it is totally (and sadly) accurate in many thousands of others.

The man was eating a bowl of oatmeal.  He had a glass of skim milk so fat free it was almost blue that he poured little bits of into his cereal from time to time.  Along with his oatmeal, he was eating one of the giant pieces of toast the restaurant serves.  He took one pat of butter (I assume there was no margarine available) and cut it in half.  He carefully spread one half pat on one half of his toast then loaded it with an entire individual serving of jelly.  After eating the first half piece of toast, he prepared the second half the same way and ate it.  The only fat he got from his entire meal was that that came from that one pat of butter.  Based on the size of the bowl of oatmeal and the size of the toast (and the skim milk), I calculated that this guy consumed about 100 grams of carbohydrate. (Thirty grams in the oatmeal; at least 30 in the toast; 15 in each container of jelly; and about 10 in the skim milk.)

I imagine (here is where I’m speculating) that he has elevated cholesterol and has been told by his doctor to watch his fat.  And he is complying. He got a whopping 4 grams of fat in his one pat of butter (36 calories-worth) while getting 100 grams of carb in the rest of his meal (400 calories-worth). The tiny bit of fat he got contained short-chain fatty acids that are immune enhancing whereas the 100 grams of carb he got provided really no health benefit.  Since the 100 grams represents 20 times the amount of sugar circulating in his blood, his pancreas had to release a large amount of insulin to deal with it.  His pot belly indicates that he is already insulin resistant with an abdomen full of visceral fat, so he no doubt secreted a lot more insulin than a person without insulin resistance.  This excess insulin help him store fat in his liver, increase his level of visceral fat, ratchet up the inflammatory process, injure his blood vessels even more and increase his risk for heart disease, the very thing his doctor was trying to prevent by putting him on a low-fat diet.

How much better off this guy would have been had he joined me in the Mike’s Special.  But, his cardiologist, I’m sure, would have been apoplectic.  A sad state of affairs indeed.

MD and I were so busy this entire week that not only haven’t we been able to keep up with even our emails, we haven’t been able to go through the over 300 requests we got for a copy of our new book.  We will go through those and respond to everyone over the next couple of days.

Also, I have about 60 comments dating back for months that are stacked up in my awaiting-moderation queue. My plan is to deal with six of them per day and have them all cleared out within 10 days.  And this all while keeping current on new comments coming in.  So if you have had a comment languishing, it should be up within the next ten days.

Our newly designed site is supposed to be up this next week.  Keep your fingers crossed.  I’m certainly keeping mine crossed.

For those of you who still can’t get your minds around the idea that exercise doesn’t make you thin, read next week’s Time. The cover story, ‘Why Exercise Won’t Make You Thin,’ is a long article parroting what Gary Taubes wrote about a couple of years ago.  The notion has finally made it to the mainstream.

Finally, I’ll end with a book recommendation.  I finished The Girl with the Dragon Tattoo on the flight to Seattle.  If you haven’t read it, and if you like offbeat mystery/thrillers, give it a whirl.  A disgraced investigative journalist headed for prison teams up with Lisbeth Salander, the eponymous girl with the dragon tattoo, and one of the strangest and most interesting protagonists to ever find her way into fiction, to solve, at the request of an aging industrialist, a decades-long mysterious disappearance.  The novel, set in Sweden and written in Swedish but masterfully translated, has become a world-wide phenomenon.  The book is satisfying throughout, and I highly recommend it.  As soon as I catch up on all my work, I’ll start the second book in the series, The Girl Who Played with Fire.

Tomorrow I’ll post on working, crabbing and eating on Orcas Island.

MD and I have been in discussion with our publisher and have gotten permission to excerpt part of the book, which I will do on this blog soon.  The book is about the weight gain that seems an inevitable part of moving into and through middle age and how this weight is different from that gained in the younger years.  It’s a kind of bad news, good news story because middle-age weight comes from a more dangerous kind of fat (the bad news), but a kind of fat that is fairly easy to lose (the good news).  But despite its being easier to lose, it still requires some effort…and a little different approach.  And, surprisingly, most of this fat can be lost in a 6-week window.  That doesn’t mean that we promise that all weight will be lost in a 6-week window, but most of the middle-aged weight can be ditched or at least significantly shed in this time period – thus the title.

Since we don’t have an active practice right now, most of the subjects we’ve given the diet to are former patients, friends and relatives.  We have had almost unbelievable success with those who gave the program a fair try.  We had one middle-aged friend who had struggled with lipid problems for years.  Despite our telling her not to worry and not to go on a statin because those drugs have never been shown to be beneficial for women, she was worried.  Her doctor was hectoring her, telling her that she would have to go on a statin if her lipids didn’t come into line.  She had an appointment in two weeks, so she went on the first two weeks of the program, then went to her doctor.  Not only did she lose eight pounds in her first two weeks, her lipid numbers plummeted.  Her total cholesterol fell from 240 to 174; her triglycerides dropped to below 100; and her HDL ran up to 60.  Happily, this all happened during the editing phase of the book, so we were able to include her story.  Other subjects have done as well if not better.

Another story is that of a business associate of ours who has gradually gained weight over the past 15 years who tried the plan.  She has tried diets of one kind or another for about 10 years.  She loses a little, but it’s been a tough slog for her.  She went on the new program and also lost eight pounds the first two weeks, which was a much greater loss than she had ever experienced.  A 60-year-old friend of ours easily lost 20 pounds over the course of his 6-week effort and had remarkable improvement in his lipids.  His wife had been on an HCG program that we had tried to talk her out of.  When she saw her husband lose substantially faster than she did, and without going on a 500 calorie diet, she switched to our program and her weight loss picked up and her measurements improved dramatically.

We have had multiple successes like the ones above, but, as I said, all are friends, relatives or business associates.  And they are not people who are keen on giving their testimonials to various media sources.  The first lady, mentioned above, works in the entertainment business – she was the director of a popular sitcom that most readers of this blog would probably be familiar with.  She doesn’t mind telling her story, but she doesn’t want her picture shown.  We found this out when the PR department of our publisher contacted us about some major interest in our book by a major women’s magazine.  They had read an advance copy of our book and were interested in making it a cover story.  They asked if we had any success stories they could interview and build a story around complete with photos.  We said sure and started calling all our ‘patients.’  Each one declined to be interviewed or would be interviewed but didn’t want her actual name used.  All refused to have their photo appear in the article.  So, we were left holding the bag, so to speak.

So, here is my request.  If any of you out there who are middle-aged and overweight would like to try the program, we will send you an advance copy of the book.  The deal is that you must be willing to have your real name and photo used by any media that approach you. This could be magazines, newspapers, online articles, and/or radio. You must also be willing to go on TV with us (or by yourself) – either national or local – and tell your story.  Should a TV appearance be required, generally all your expenses will be picked up by the television station, and if not, then you need not appear.  All you have to do is read the book, follow the program, keep us updated about your progress and tell anyone from the media who might contact you how you fared on the regimen.

Our publisher will let us recruit only 20 people for this project, so we can’t make it available to everyone who wants to do it.  We will select the 20 people from the applications we receive.  I have no idea how many that might be: it could be five or it could be 50.  I just don’t know.

I’ve set up a gmail account for anyone who is interested.  Please send an email giving your particulars, i.e., age, sex, weight, dietary history (what kind of diets you’ve been on, when and with what degree of success), medications, other disorders (diabetes, heart disease, kidney disease, etc.), contact info and a photo if you have one.

Send to:

6weekcure at gmail dot com

Put ‘6weekcure’ in the subject line of your message.

We’re also looking to recruit a few people in other categories for some more immediate media exposure.  So, if you have used the shakes for weight loss that I have given the recipe for multiple times in the comments section of this blog, send an email to the above gmail address and put ‘Shakes’ in the subject line.

If you have been on an all-meat diet and done well, drop us a note and put ‘All meat’ in the subject line.

MD and I thank you, in advance, for being willing to help.

Addendum:  We have received over 300 requests from people wishing to try the program in our book.  Since our publisher is providing us with only 20 copies, we have to terminate the offer at this point.  We will go through the 300 plus submissions and contact all those who wrote shortly.  Thanks for all your interest.

Instructor teaches Friedewald equation and bad cholesterol

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

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

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

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

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

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

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

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

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

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

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

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

And how did they fare?

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

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

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

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

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

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

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

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

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

The abstract of the study echoes this warning.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

LDL = Total cholesterol – HLD – VLDL

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

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

LDL = Total cholesterol – HDL – TGL/5

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

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

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

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

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

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

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

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

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

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

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

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

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

English breakfast at our hotel. A good low-carb diet.

It was bound to happen.  Forever the low-fat diet promoters, whenever asked about low-carb diets, would always say: Show me the studies.  Well, we showed them the studies, the vast majority of which demonstrated the superiority of low-carb diet, but they didn’t like what they saw.  So they demanded more.  The rallying cry became: Show me the long-term studies.  Now that those are in, the anti-meat folks are running out of options.  But one of their own great lipophobes (Lipid  = fat; phobic = fear of.  Lipophobe = fearer of fat.), David Jenkins, has come to the rescue.

Since the low-carb diet has proven so effective, opines he, why not make it even more so by making a vegetarian version?  Then dieters can have all the advantages of a low-carb diet along with all the advantages of a plant-based diet.  That is, assuming there are advantages to a plant-based diet, more about which later.

Although the low-carbohydrate diet has proven itself a cut above the low-fat diet in virtually all parameters measured, in one little measurement it has fallen short, at least in the minds of the lipophobes.  A number of studies of subjects following low-carb diets show that LDL-cholesterol levels don’t fall to the levels found in subjects following lower-fat, higher-carbohydrate diets.  And this troubles the lipophobes mightily.

To a lipophobe, LDL-cholesterol is all that matters.  These people have bought in to the premise that LDL-cholesterol is a major driving force behind the development of heart disease, and in their minds, anything that doesn’t lower LDL-cholesterol levels is a very bad thing, indeed.  It doesn’t matter to them if a particular nutritional regimen improves every other parameter relating to general health and even cardiovascular health, if that regimen doesn’t also lower LDL-cholesterol levels, it is suspect.

It matters not to them that there is no evidence showing that LDL-cholesterol levels cause or worsen heart disease; they believe with all their hearts that it does.  In their fat-deprived brains, the lipid hypothesis isn’t a hypothesis at all.  It is fact.

And so they set out to test the hypothesis that a low-carb diet without meat could achieve the Holy Grail of lipophobery: a lowered LDL-cholesterol.

The study published in this week’s Archives of Internal Medicine was picked up and reported on by multiple media outlets. It starts out with an opening statement laying out the problem of low-carb diets from the lipophobe’s perspective.  Remember as you read this that virtually none of the statements presented as facts have ever been proven to be so.

There is a dilemma relating to the proportion and source of fat, protein, and carbohydrate that constitutes the optimal weight loss and cholesterol-lowering diet. Newer dietary approaches for the prevention and treatment of chronic disease increase the consumption of fruit and vegetables but reduce meat consumption either directly as part of the dietary strategy or displace meat by advocating increased intakes of fish, poultry, and low-fat dairy foods. Running counter to this advice has been the promotion of low-carbohydrate diets with increased meat consumption for body weight reduction and also in the longer term for the prevention and treatment of diabetes and coronary heart disease (CHD). These diets not only challenge the concept that red meat intakes should be reduced but also reverse the dietary macronutrient profile with fat and protein as the major macronutrients and carbohydrates as the minor macronutrient. Such low-carbohydrate diets have been shown to be effective in inducing weight loss, reducing insulin resistance, lowering serum triglyceride (TG) concentrations, and raising high-density lipoprotein cholesterol (HDL-C) concentrations. However, the higher meat diets have not resulted in lower low-density lipoprotein cholesterol (LDL-C) concentrations, but have tended to increase LDL-C concentrations except when vegetarian sources of fat and protein were included. This lack of a benefit for LDL-C control is a major disadvantage in using this dietary strategy in those already at increased risk of CHD.

There it is, the sticking point for lipophobes and the low-carb diet.  It doesn’t matter what kind of good results those following low-carb diets achieve, in their minds all that matters is the LDL-cholesterol.  Read that last sentence again.  After all the description of the multiple benefits of low-carb dieting, it all boils down to LDL.

This lack of a benefit for LDL-C control is a major disadvantage in using this dietary strategy in those already at increased risk of CHD.

A major disadvantage they say.  Will someone show us, please, all the evidence that there is a disadvantage?  Gary Taubes wrote an entire book about the lack of evidence of any advantage to achieving a lower LDL and the lack of data showing saturated fat causing any increase in risk for heart disease, but that information is lost on these guys.

The authors of this paper are going to fix the low-carb diet problem.  Here’s what they did in their own words.

In view of the apparent success of low-carbohydrate diets for weight loss and the demonstration that relatively high-carbohydrate diets low in animal products lower CHD risk factors, we determined the effect of a low-carbohydrate weight-loss diet, without the use of animal products, on serum lipid concentrations compared with a higher carbohydrate diet.

Let’s take a look at what they did.

They recruited 50 subjects, 47 of whom actually started the study.  The researchers randomly assigned the subjects to either a low-carbohydrate or a high-carbohydrate, calorie-reduced diet of a one-month duration.  Couriers delivered the food, all of which was prepared in a metabolic kitchen, to the subjects, all of whom presented themselves to the clinic weekly for evaluation.

Here is a description of the diets:

Metabolically controlled diets in which all food was provided were consumed by the participants. The low-carbohydrate diet provided the minimum level of carbohydrates currently recommended (130 g/d) and eliminated common starch-containing foods, such as bread, baked goods, potatoes, and rice. The protein content was provided by gluten (54.8% of total protein), soy (23.0%), fruits and vegetables (8.7%), nuts (7.5%), and cereals (6.0%). Gluten was provided in the nut bread and wheat gluten (also called “seitan”) products and, together with soy, in burgers, veggie bacon, deli slices, and breakfast links. In addition, soy was provided as tofu and soy beverages. Nuts included almonds, cashews, hazelnuts, macadamia, pecans, and pistachios. The fat was provided by nuts (43.6% of total fat), vegetable oils (24.4%), soy products (18.5%), avocado (7.1%), cereals (2.7%), fruits and vegetables (2.3%), and seitan products (1.4%). The diet was designed to provide 26% of calories as carbohydrates, 31% as protein, and 43% as fat. The high-carbohydrate diet was a low-fat lacto-ovo vegetarian diet (58% carbohydrates, 16% protein, and 25% fat) using low-fat or skim milk dairy products and liquid egg whites or egg substitute to ensure a low–saturated fat and low-cholesterol intake. All diets were provided at 60% of estimated calorie requirements using the Harris-Benedict equation with allowance for exercise.

The low-carbohydrate diet featured viscous fiber-containing foods, including oats and barley, for the relatively limited amount of carbohydrates allowed, and the production of a “no starch” high-protein bread made entirely from ground almonds, hazel nuts, and wheat gluten. The carbohydrate foods and low-starch vegetables, emphasizing okra and eggplant, provided 6 to 7 g of viscous fiber per 2000-kcal diet. The bread was provided as part of the diet.

Whoa there!  Did we read that correctly?  Did it say that the low-carbohydrate diet contained 130 grams per day of carbohydrate?  It sure did.  Doesn’t sound much like a low-carbohydrate diet to me.  It takes a restriction of carbohydrates down to the 50 or so gram per day level to get the real benefit of low-carb dieting, the so-called low-carb magic.  Anything much above that is simply a low-calorie diet with a little less carb.

What were the results of this experiment after both groups were on their respective diets for a month?  Well, it’s hard to say for sure because of the way the data were looked at.  Fifty subjects were recruited, but only 47 actually started the program.  Of these 47, only 44 completed the study (22 in each group).  But the data were evaluated using an intention-to-treat analysis, which, at best, gives less than valid answers.

Here is the chart showing the study outcomes:

If we ignore the fact that these data were derived using an intention-to-treat analysis and take them as presented, we can see that the lower-carb veggie diet out performed the higher-carb, lower-fat diet in a number of parameters.  Let’s look at those that were statistically significant (a P value of less than 0.05).

Satiety was greater in the higher-fat diet.  As you can see, subjects on the low-calorie, high-carb diet got hungrier as the study progressed.  Those on the lower-carb diet got minimally less hungry as compared to the start of the study, which isn’t a surprise as fat is filling.

Total cholesterol and LDL-cholesterol both fell to a larger extent on the lower-carb diet.  Finally, a low-carb diet in which LDL-cholesterol dropped.  I’m sure the researchers were orgasmic.

As anyone with any experience with low-carb diets would predict, triglycerides fell markedly as compared to those on the control diet.

All the lipid ratios were improved more on the low-carb diet.

Apo B (a measure of LDL particle number) fell to a greater extent on the low-carb diet and the apo B to apo A1 ratio was lower on the low-carb diet, a fact the researchers made much of.

Both the apo B concentration and the apo B–apo A1 ratio fell significantly more for the low-carbohydrate vs the high-carbohydrate diet…

Most low-carbohydrate diets have not reported the effects on apolipoproteins. The reduction in apo B and the apo B–apo AI ratio observed in the present study is a further confirmation of the potential CHD benefit that might be expected from this dietary approach to body weight reduction. In some studies, the apolipoprotein concentrations have been claimed to have greater predictive value for CHD events than more conventional lipid variables.

This emphasis on the apo ratios is interesting.  Apo B is the protein associated with LDL-cholesterol and apo A1 is the protein associated with HDL-cholesterol.  One of the big bugaboos about low-fat, high-carbohydrate diets is the fact that although these diets generally bring about a fall in LDL-cholesterol, they also bring about a greater decrease (percentage-wise) in HDL-cholesterol.  This study is remarkable because HDL-cholesterol fell in the low-carb arm whereas in most low-carb diets HDL-cholesterol goes up.  HDL-cholesterol is fat dependent (probably saturated-fat dependent if you want my opinion), and since most low-carb diets are high-fat diets, HDL-cholesterol goes up in subjects following them.  I’m sure these researchers desperately wanted the same to happen here, but, alas, it didn’t.  HDL-cholesterol fell just as it did in the high-carb arm. They are trying to cover for this by focusing attention on the apo B to apo A1 ratio, which did fall, meaning, basically, that LDL-cholesterol levels fell more than did HDL-cholesterol levels.  On a good quality low-carb diet you would typically find that LDL-cholesterol levels stay about the same (or maybe fall a little or even rise a little) while HDL-cholesterol levels go up.

I find the last sentence in the above quote really intriguing.

In some studies, the apolipoprotein concentrations have been claimed to have greater predictive value for CHD events than more conventional lipid variables.

Since apolipoprotein levels are indicators of the various cholesterol particle sizes, I would say this is a great understatement.  Virtually all of the research on this subject has shown that low-fat, high-carbohydrate diets – even though they reduce LDL-cholesterol – end up resulting in LDL-cholesterol of the small, dense particle size, which is much more atherogenic than the larger, fluffier particles found in subjects after following low-carb, higher-fat diets.  To report that this is the case in just some studies is disingenuous to say the least.  But to report it otherwise would give the lie to the notion that LDL-cholesterol levels by themselves amount to much of anything.  And we wouldn’t expect a true lipophobe to do that, would we?

When we slice and dice all the data from this study, what do we find?  We find that a lower-carb diet (not a low-carb diet, but a lower-carb diet) so complicated it basically requires a metabolic kitchen to prepare provides the same benefit as a real meat-based low-carb diet with the only difference being that the plant-based lower-carb diet gives a little lower LDL-cholesterol reading.  When you consider that this lower LDL-cholesterol reading came at the expense of a reduction in HDL-cholesterol and a major effort required to prepare the diet, one has to ask if it is really worth it?

I would bet that if the plant-based lower-carb (130 g/day) diet were compared with a meat-based real low-carb diet (50 g/day or under), the real low-carb diet (such as the one pictured at the top of this post) would win across the board.  The LDL-cholesterol number may not go down as much, but who really cares?  LDL-particle size would be larger (I calculated particle size in this study, and there was no change) and all other parameters would probably be improved more.

Maybe someday someone will do such a study and prove me right.  Or wrong.  In any case, this study has some value in that now maybe all those docs who have shied away from prescribing low-carb diets to their patients because of ungrounded fear of a minimal increase in LDL-cholesterol will give this version a try.  For all its faults, it’s better than the low-fat, high-carb diet.

*Lipid  = fat; phobic = fear of.  Lipophobe = fearer of fat

After our meeting at the factory we’re working with, the president of said factory treated us all to a feast at our restaurant.  As Chinese tradition dictates, such feasts are accompanied with many, many toasts.  The toast works this way:  the person making the toast picks out a specific person to toast, walks over to that person, raises his/her glass and gives the toast.  The translator translates.  The person receiving the toast answers back.  The translator translates back.  Then both toaster and toastee down drinks in one swallow.  After this, the glasses are immediately refilled by one of the servers.

In our case, the liquor used for toasting purposes was either red wine or bai jiu, a Chinese white wine that is actually more of a distilled liquor.  The Chinese love bai jiu, which has a distinctive flavor.  It’s about 50 percent alcohol and has a front end taste that is kind of like the essence of an infusion of dirty socks in some sort of floral alcohol and a back end like lighter fluid.  It’s an acquired taste, and one that I had sort of acquired after a zillion toasts.

As the meal progressed, the toasting evolved into each toast requiring the downing of both a glass of red wine and a glass of bai jiu.  Thank God we ran out of red wine and baiu jiu before I ran out of consciousness.  The photo above shows me just before downing a glass of each after a toast from the head of operations at the factory.

The meal we had was spectacular. And pretty low-carb.  I kept a photo log of it, which I will lay out below. (We had another good meal earlier in the day that MD posted about moments ago.)

We started with shark fin soup, which I didn’t take a picture of because…I don’t have a good reason.  I just didn’t.  I guess I didn’t think about taking photos until after the shark fin soup.  From there we moved on to a giant prawn and an abalone.  Both were delicious, especially the abalone.  I don’t know what kind of sauce it was cooked in, but it was savory and out of this world.

Then came a weird dish that was served with plastic gloves.  It was a baby dove with head included.  You put the gloves on and tore the little bird to pieces and gnawed the bones.  And, yes, we ate the head.  We didn’t just throw it back and chomp it; we nibbled off the small amount of meat on it .  I watched the Chinese so I could follow suit, and that’s what they all did.  After picking the bones clean, we all removed our gloves and awaited the next course.

What came then was some sort of seafood salad.  And remember, all this food was interspersed by dozens of toasts.

After the seafood salad came the main course, which was a piece of succulent steak that was extremely tender.  It was served with a little pile of fried garlic chips and a stalk of broccoli.

Following the steak, we had a dish of some kind of green vegetable.  I never could figure out what exactly it was, but it was very tasty.  I asked the woman sitting next to me what it was, but she didn’t know the English word for it.  All she could tell me was that it was grown in the area where we were.

Then came a tiny bowl of fried rice.  You can see the size of the bowl by comparing it to the spoon next to it and the little glass the bai jiu is served in.

The we had some sweets, which I admit to eating.  Everyone of them.  By that time, after all the wine and bai jiu, I would have eaten anything.

And finally we were served a small plate of fruit for the end of the meal.

By that time all the wine and bai jiu were gone, thank God.  I thought we had made it through the worst of it, but the factory president, who was the founder of this feast, had brought two kegs of German beer, so nothing would do but that we all traipsed upstairs to a small room and drank glass after glass of mildly chilled beer and ate dried squid, squid jerky, I guess you could call it.  The beer and squid were served along with, believe it or not, french fries.  I ate no fries, but did eat a fair amount of the squid jerky, which was pretty tasteless but did give the jaws a good workout.

It was a memorable evening, and I can even remember all of it.  I even woke up the next morning feeling fine.

I’m rushing to get everything together to catch our flight to London.  I’ll post later on my thoughts on the China and Hong Kong experience. I do want to make one observation, though.  Earlier in the day that this feast took place, we toured the factory.  There were probably at least 400 people working there of all ages.  I didn’t see a single obese person – all were thin.  You may think that they weren’t obese because they were working hard.  You would be wrong.  Almost all of them had fairly sedentary jobs.  They were sitting doing very little strenuous labor.  Mainly just screwing one component on to another as they came down a line.