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.

It seems as though we possess a positive genius for having our timing screwed up.  Our past is littered with missed opportunities to promote our various books, all occasioned by situations beyond our control.  Let me give you a few examples.

We were scheduled to be the guests for the biggest part of one of Soledad O’Brien’s shows when word came down that Hillary Clinton was going to declare her candidacy for the U.S. Senate.  We were in NY (brought by our publisher, thank God) prepared to go on the show the next day when we got bumped to another time.  Another time that never materialized.

I was scheduled to be on O’Reilly live and, in fact, was in the limo sent by Fox to take me to the studio when I got a call on my cell telling me that the Texas fugitives had been captured in Colorado.  Since I was on the way, O’Reilly went ahead and did the interview, but it was taped and played a couple of months later when John Kasich (who is now apparently running for governor of Ohio) was the guest host and viewership was probably lower than had it been O’Reilly live.

MD and I were on our way to Miami (sent by our publisher once again) to appear on a couple of big live TV shows there when we got word that Elian Gonzales had been snatched by the Feds and was being sent back to Cuba.  Bumped again never to return.

We were to appear one afternoon on national TV rebutting the PCRM’s Neal Barnard, who had been all over the airwaves that morning with his ridiculous ‘study’ about low-carb diets.  We were in Santa Barbara at the time, and the network (I can’t remember which on now) had arranged for us to go to a local studio to be interviewed via satellite.  Just as we were about to leave for the studio, we got a call telling us our gig had been canceled because Michael Jackson’s plane was en route to the Santa Barbara airport where he was to turn himself in conjunction with the sexual molestation charges.  After that the news was all Michael Jackson.

I could go on, but you get the picture.  MD and I seem to be snake bit when it comes to book- and/or self-promotional timing.

Now we’ve finished a book, about to be released tomorrow, that is filled with all the latest science, much of it never before published other than in scientific papers, and we may be scooped again.  But in a different way.

Our new book includes info on saturated fat, fatty accumulation in the liver, diacylglycerol, D-ribose, L-leucine, visceral and subcutaneous fat, sagittal abdominal diameter, evolutionary psychology, and on and on, showing how all these things relate to the accumulation and loss of middle-aged fat.  But did we come out with it too late?

Maybe so according to a recent New York Times article titled “It’s Hip to Be Round” with the distressing picture below of various potbellies emblazoned across the top of it.

If this piece is to be believed, men at least have given up the flat-belly look in favor of the more portly Ralph Kramden body habitus.  If you’re of an age, you’ll remember Ralph Kramdem.  He was the character Jackie Gleason played on the television show The Honeymooners.  Taking a look at the photo at left.  That’s Jackie playing Ralph.  Remember Jackie Gleason’s nickname?  The Fat Man.  He was remarkable for his obesity because there was so little of it back then.  Notice, too, how Jackie, aka Ralph, wouldn’t have merited a second look today.  Half the people you see on TV today are more overweight.  And you think we don’t have an obesity epidemic?

According to the Times:

This summer the unvarying male uniform in the precincts of Brooklyn cool has been a pair of shorts cut at knickers length, a V-neck Hanes T-shirt, a pair of generic slip-on sneakers and a straw fedora. Add a leather cuff bracelet if the coolster is gay.

In truth this get-up was pretty much the unvarying male uniform last summer also, but this year an unexpected element has been added to the look, and that is a burgeoning potbelly one might term the Ralph Kramden.

Too pronounced to be blamed on the slouchy cut of a T-shirt, too modest in size to be termed a proper beer gut, developed too young to come under the heading of a paunch, the Ralph Kramden is everywhere to be seen lately…

The article goes on to lay out what I believe is an idiotic rationale (but obviously tongue in cheek) for all this (they blame it on Obama),  then adds

“I sort of think the six-pack abs obsession got so prissy it stopped being masculine,” is how Aaron Hicklin, the editor of Out, explains the emergence of the Ralph Kramden. What once seemed young and hot, for gay and straight men alike, now seems passé. Like manscaping, spray-on tans and other metrosexual affectations, having a belly one can bounce quarters off suggests that you may have too much time on your hands.

“It’s not cool to be seen spending so much time fussing around about your body,” Mr. Hicklin said.

And so guys can happily and guiltlessly go to seed.

So, there goes half our audience.  Always a day late and a dollar short.  I suppose we should have written a book describing how to develop the middle-aged middle before middle age.

On another note, if you still don’t think there is an obesity epidemic right now, take a look at this old video of Manhattan, NY filmed in the early 1920s.

Check at 1:50 and 9:16 to see the crowd scenes.  The people look like stick people.  They wouldn’t look that way if the film were made today.

And, if you want to read a little more about our new book, Tim Ferriss has excerpted part of one of the chapters here.

Last but not least, we’ve gotten some photos back of the first testimonials for our news book.  The photo on the right is the before, the one on the left, after six weeks on the plan.

Just kidding, of course.

Photo credits:

Troisdorf man

Large belly

Thin waist

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.

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.

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.

MD and I just spent a couple of days with the grandkids at Disneyland.  They’re here visiting for a couple of weeks, so we decided to bite the bullet and take them on the front end and get it over with instead of waiting until the end, as we usually do, and dreading it the entire time.  It was brutal but it is now over.

I loathe Disneyland and refer to it as the biggest people trap ever built by a mouse.  Which isn’t an original, but I’ve been saying it for so long that I’ve forgotten where I heard it years ago.

This year I at least was able to avoid the Small World ride.  Our 7-year-old grandson informed us that it was ‘lame.’  I couldn’t have agreed more.  I wasn’t so lucky a couple of years ago, however.  We took the kids then and did end up going on the Small World ride, which experience the grandkid remembered when he referred to the ride as being lame.

For those of you lucky enough to have escaped the Disneyland experience, the Small World ride is easily the most inane amusement park ride ever conceived by the mind of man.  You get in these little fiberglass flat-bottomed boats and cruise through this serpentine canal that wends its way around  tableaus of little dolls of various nationalities (as in photo above) doing their mechanical dances to what is easily the most nauseating piece of music ever written. Unlike most Disneyland rides that you wait an hour to get on and are then over in about 45 seconds, the Small World ride is interminable.  It goes on and on and on.  Which is, I suppose, its only virtue because at least it is dark and air conditioned, a welcome change from the heat radiating up from the vast concrete underpinnings of the park. (The downside is that you’ve been exposed to the nauseating song for so long that it has wedged itself into your brain and you can’t get it out for the rest of the day.)

When I last rode the ride,  it had just reopened after having been closed for almost a year for renovations.  I asked one of the attendants what had changed, hoping for an de-inane-ation of the ride.  The guy told me it hadn’t changed at all; they had just made the boats a little bigger and deepened the channel.  Then he told me it was because the guests of the park had become so much larger than when the ride went in in the 60s and were causing the boats to bottom out.

The park was so crowded and hot when we went two years ago that I kind of went brain dead.  All I wanted to do was slog through and get it behind me.  This time the weather was better and, thanks to the recession, the park wasn’t as crowded.  And I wasn’t so miserable, so I had a chance to look around a little more.

If Disneyland is any indication, there is no question we’re in the midst of an obesity epidemic.  I tried to make some kind of semi-accurate estimate by doing little statistical analyses when  was waiting around for rides.  It looked to me that about 40 percent of adults were out and out obese, some morbidly so.  And I would estimate that of the folks who weren’t actually obese, at least 85 percent of them were overweight. A normal weight adult at Disneyland was a rarity.

What really surprised me was the state of obesity of the Disneyland staff.  When I was in college I got a job at Disneyland (which in part accounts for my loathing of the place).  I was a conductor on the train that circumnavigates the park.  It was one of the worst jobs I ever had.  But it did have its perks.  At that time, all the employees were college students or college dropouts who were the full time workers.  In keeping with the Disney image at the time, just about all the young employees selected were clean cut and nice looking.  As a consequence, the place was kind of a meat market.  Employee parties were legendary.  That part I enjoyed, but my enjoyment was somewhat tempered by the fact that I had a steady girlfriend at the time who also worked at Disneyland.

Now, the young employees are a reflection of the population in general.  At least half of them are obese, some almost morbidly so.  I don’t know if this represents the student body of the local college or what, but it certainly has changed over the past few decades.

Despite my kind of flippant tone in this post, I don’t find the large numbers of obese guests (as the Disneyland staff refers to the people paying to go there) and staff amusing in the slightest.  I think it is tragic.  As I’ve said many times before, we have all been the unwitting subjects of a long experiment, the hypothesis of which is that since fat is bad and carbs are good, we should all eat low-fat, high-carb diets.  If so, says this hypothesis, obesity will go away.  Well, it hasn’t.  It has gotten much, much worse.  And the sad, sad thing is that this hypothesis was never validated scientifically before we were all enrolled in the experiment.  When I see dozens and dozens of young people looking like the one pictured above, it makes my blood boil.  Most of the people who inflicted this nonsense on us are still around and still pushing the carbs and still blaming the fat in the diet. Tar and feathers spring to mind.

When I thought I was going to have to subject myself to the Small World again before my grandson got me out of it by not wanting to go himself, I remembered what the attendant had told me previously about the ride being renovated because of the increase in obesity.  I wondered if it were an urban legend or if it were really true.  When I got back to a computer, I checked it out.

There are a number of investigative reports on the idea, and the consensus seems to be that the renovation was due to the boats bottoming out due to the increased weight of the passengers.  Based on what I saw, I suspect that’s the case because just taking the average weight gain over the last 40 years means the boats are carrying 200 extra pounds more than they were designed for..  Disney officials are staying mum, however.

During my own investigation on the issue, I ran across an interesting article on Snopes.com.  A new twist has been added to many of the rides at Disneyland, especially the ones that hurtle you along in the dark.  Cameras are placed in strategic locations and take photos as the ride comes through.  After you get off, you can go see a photo of yourself and your entire boat or log or train car or whatever conveyance dropping over a precipice projected on a screen near the exit.  Most people are pictured screaming and holding on for dear life.

One of the rides – Splash Mountain – has achieved some notoriety because it has become common for female riders to pull up (or down) their tops as they approach the cameras.  This flashing has become so common that the ride has become known as Flash Mountain.  All of the photos are looked at by park officials before being put up on the screens for all to see.  Here is the Snopes link to the article – a little (very little, actually) navigating will get those with a prurient bent to a page of these photos.  I, of course, had to look as part of my investigation for this blog post.

The Disney officials are good at weeding out these bawdy photos and they are very good at feeding the hordes of overweight people exactly what they want.  Disneyland is carb heaven.  That’s just about all you can find.  There are sweetened cold drinks, a variety of ice cream products, cotton candy, gummy sweets, funnel cakes and other high-carb junk of every stripe.  It is almost impossible to avoid carbs there.  It can be done, but it is difficult and requires a lot of effort.  The vast majority of the people I saw weren’t making the effort.

If I’m lucky, I’ll be able to avoid the Magic Kingdom for at least another couple of years. When I do get dragged there again, I’ll stumble along as I normally do, putting one tired foot in front of the other counting the hours until it’s over. But, admittedly, I will approach Splash Mountain with a little more exuberance than I have in the past.

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.

Echinacea for colds. Ginkgo biloba for memory. Glucosamine and chondroitin for arthritis. Black cohosh for menopausal hot flashes. Saw palmetto for prostate problems. Shark cartilage for cancer. All proved no better than dummy pills in big studies funded by the National Center for Complementary and Alternative Medicine. The lone exception: ginger capsules may help chemotherapy nausea.

Acupuncture and some of the hands-on manipulative therapies fared a little better.

As for therapies, acupuncture has been shown to help certain conditions, and yoga, massage, meditation and other relaxation methods may relieve symptoms like pain, anxiety and fatigue.

The article didn’t give a rundown of every alternative or non-mainstream therapy tested, so I don’t know what they all are, but I can add one to the list if it wasn’t tested in this $2.5B testorama.  I would add the use of HCG for weight loss.

Many practitioners are using injections of human chorionic gonadotropin (HCG) injections coupled with an extremely low-calorie diet to help their patients lose weight.  Many practitioners and many patients swear by this regimen.  But, a number of randomized, double-blind, placebo-controlled studies have shown that the HCG regimen is no better than placebo.

But if this is so, how come so many patients and practitioners believe so strongly in this HCG/diet combo?  Simple answer.  Because it works.

But if it works, why is it a worthless regimen?  Because it doesn’t work any better than placebo.

If you go to a doctor who tells you that he/she is going to start you on an extremely powerful weight-loss program that involves multiple injections along with a stringent diet composed of specific foods to be eaten on a rigid time schedule (especially if these foods add up to only 500 calories per day), you will come away convinced that you are going to do well.  Especially after you’ve paid the bill, which is considerable in these HCG centers.

If you go in for all the injections and scrupulously follow the diet, you will lose a fair amount of weight pretty quickly.  And you will develop and unshakable believe that this regimen did the trick for you.  You will tell your friends, all of whom have witnessed your rapid weight loss, and they, too, (at least those who can afford it) will go to the same practitioner and fork over for the treatment.

Problem is this treatment works the same if the patients are given a salt-water shot or an HCG shot.  There is no difference in outcome.  The HCG doesn’t do diddly.  It’s the fact that you get a shot that makes the difference.  If you simply went on the 500 calorie per day diet you would lose the same.  But it’s the magic of receiving the shot, especially after being told (as most are) at the practitioner’s office that the shot will help overcome the hunger of being on a drastically calorically-reduced diet.  And it does.  But it doesn’t matter if it’s a saline shot or a dose of HCG.  It’s the magic of having something done.

Which is why in the $2.5 billion tests, the manipulative therapies worked and the others didn’t.  There is something about having a procedure done that makes you feel like your getting a more powerful treatment.

I can’t tell you how many people came in to see me when I had a regular medical practice who demanded a shot because they were convinced that shots worked better than oral medications.  For some things they do, but for most, they don’t.  But you couldn’t convince most of my patients of that.

There are a few of what many would consider alternative medicines that do work.  I posted on one that does here.  But, as the large conglomeration of studies reported on by the AP showed, most don’t.

As you might imagine, the report of the failure of most alternative therapies was like catnip to mainstream physicians, researchers and writers.  They were absolutely giddy with joy.  Here are just a few representative comments:

Well, since I’ve been bagging on the alt-med nonsense lately, I simply couldn’t pass up this headline.  And folks… the headline says it all… “No Alternative Cures Found”… Zilch… Nada… Zip… Zero!  Despite their inability to understand the most basic aspects of science and the associated math, I think that zero is a number that even alt-med woo-meisters can grasp

(Woo is the derogatory term these mainstreamers have come up with for any treatment or therapy not taught in traditional medical schools or developed by Big Pharma.)

I never thought I’d see it, but I have. After an a decent article on the infiltration of quackademic medicine into American medical centers and a very good article on cancer quackery, Marilyn Marchione of the AP has done it again:

AP IMPACT: $2.5B spent, no alternative med cures…

I’ve documented the woo funded by NCCAM on multiple occasions. I mean, NCCAM is funding studies of that woo of woos, homeopathy, fer cryin’ out loud! I”m [sic] glad that the mainstream media is finally noticing.

One more.

Here’s a shocker for you: after a decade and 2.5 billion (with a b, folks) dollars spent, a government study shows that almost no alternative medicines worked.

So, they used actual scientific testing processes instead of anecdotes, and found that most of these simply don’t work. Like I said: shocker.

… the studies have shown that most of these remedies don’t work. And will this change the minds of their advocates?

HAHAHAHAHAHAhahahahahahaha! Oh man, sometimes I crack myself up.

This is just one more arrow in our quiver, but the alternative medicine believers will continue to move the targets around. Stay vigilant, and remember: people waste money, people get sick, and people die because of this antiscientific thinking. That’s why testing this, publicizing it, and fighting the misinformation is so important.

Believe me, this is just a small sampling of what I came across on the internet when I searched for links to the AP article.

Hostile and condescending as the tone of these remarks is, the people who made them are pretty much on the money.  These treatments need to be evaluated in the harsh glare of double-blind, placebo-controlled studies.   Now they have been, and, just as with the HCG regimen for weight loss, they’ve been found lacking.

But that’s not necessarily the end of the story.  We don’t know the details about these studies.  Was there just one study for each alternative therapy?  Or were there multiple studies, each of which demonstrated no effectiveness?  If just one, then the above criticisms may not be valid.

Absence of evidence is not necessarily evidence of absence.  Just because we can’t get a positive result in one study doesn’t mean there isn’t a positive result to be had.  Science is the continual testing of hypotheses until the evidence is overwhelming that the hypothesis is valid or it isn’t.  But even overwhelming evidence doesn’t always prove out in the long run.  Newton’s laws were held to be valid after centuries of testing, then Einstein came along.

What interests me so much about the glee with which these mainstreamers greet the failure of alternative medicine (at least the failure shown by $2.5B worth of research) is that the vast majority of these same folks believe in the notion that people are overweight because they eat too much and exercise too little, an idea that scientifically holds little water.  A myth, really.  But they all believe it because on the surface it seems to make sense to them.  All the scientifically valid arguments that, say, Gary Taubes makes fall on deaf ears.  (Here is a video of a recent lecture Gary gave to doctors at Dartmouth.  Do you think any of them were moved to give up their antiquated views by the science presented?  It’s highly doubtful.)

And while most of the people pooh poohing woo are doing so, they are out pushing statins for all their worth.  And statins – other than for a small group of people – have the same efficacy as the alternative medicines they are so quick to disparage.  Let’s see, how did that one writer put it?  “…Zilch… Nada… Zip… Zero!”

That’s right.  The category of drugs that are the top selling drugs worldwide have no efficacy in terms of reducing overall mortality, at least as shown by randomized, double-blind, placebo-controlled studies, in any group except men under the age of 65 who have been diagnosed with heart disease.  This doesn’t mean men under 65 who have elevated cholesterol, but men under 65 who have actually been diagnosed with heart disease or who have had a heart attack.  And even in that group, the efficacy is questionable.

The mainstreamers such as those quoted above don’t question the effectiveness of statins even though at least $2.5 billion has been spent to test them and found them lacking, but readily discount alternative medicines simply because they don’t fit with their belief system.  Based on the evidence at hand, I wouldn’t give people Echinacea, shark cartilage and all the rest because the studies show they don’t work better than placebo, but for all the same reasons, I wouldn’t give a patient a statin either.  In fact, I would probably give the Echinacea before I gave the statin because, as far as I know, no one has died taking Echinacea, of which the same can’t be said of statins.

If alternative medicines are going to be held to scientific standards, so should be pharmaceuticals.  Snake oil is snake oil no matter what its bottle it looks like.

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

In the last post I wrote that I would explain why George Bray and his brethren in the academic obesity research world are in great measure responsible for the toxic world they all blame for the obesity epidemic.  We live in a world, they say, filled with impossible to resist foods that throw us into hedonic overdrive.  As long as we live in such a world, there is no hope – other than drugs, of course – for the obesity epidemic to be reversed.  They may be correct.  But, as I said, they are in part responsible.  Let’s see why.

You can’t just go around gibbering as they do about a toxic environment without defining what it is that is toxic about it.  If pressed, these folks almost always default to the position that it is the elevated levels of fat in the diet that are toxic.  They will often say – as Bray did in his rebuttal to Taubes – that the ready availability of high-fat, high-sugar foods is what makes the environment toxic, but that is just a kind of code for high fat, which is what they really believe causes obesity.

The statistics show a different story however.  Most food consumption data indicates that fat consumption has actually been falling or, at worst, has remained about the same.  Caloric intake has been on the rise, however.

The latest NHANES data show that the average American consumes about 250 calories more per day.  If fat is falling or remaining the same, and calories are increasing, those calories can come from only two sources: protein or carbohydrate.  Since protein intake pretty much mirrors fat intake, it’s most likely that the increase in calories has come from an increase in carbohydrate intake.  Which is what the data actually show. NHANES data confirm that this 250 calorie increase comes from carbohydrates.

So, if anything has changed in the diet over the past 40 years, it is that carbohydrate intake has increased, which is a pretty good argument to say that if the food environment has become toxic, it is the increased carbohydrate intake that has made it so.

If you look at the scientific literature and try to find a study that shows that consuming more fat causes health problems, you’re going to come away empty handed.  Sure, there are a lot of studies out there showing that bad things happen when fat intake goes up, but subjects in those studies are eating a ton of carbs along with the fat.  I religiously read the medical literature, and I haven’t found any studies showing a decline in health with an increase in fat without an increase in carbs or calories going along with it.

It ain’t the same with carbohydrates.  The scientific literature is crawling with papers showing detrimental effects from overconsumption of carbohydrates.

It’s pretty obvious to anyone who cares to look that if there is indeed a toxic environment out there luring us all to overeat and become obese, that toxic environment is made of carbohydrate.

If this is true – and I think it is – then why are Dr. Bray and his henchmen responsible?

Easy.  They encourage carb consumption by focusing the public’s attention on fat and away from carbohydrates.  Bray and friends are the go-to experts driving the recommendations of various governmental agencies that ultimately drive large food manufacturers to produce products adding to the toxicity of the environment.

General Mills, Nestle, General Foods, Kellogg, and other giant food companies aren’t managed by intrinsically evil people who set out to make us all fat.  These companies – just like Microsoft, IBM, Exxon and others – are in business to make an honest buck for their shareholders.  Shareholders want to see growth in value and a steady income for their investments, and management wants to deliver.  But these companies are constrained by what they sell.

Basically they sell calories.  If you take the number of people in the United States (we’re just talking domestic production here) and multiply that number by the average caloric intake per person, you can arrive at the total number of calories consumed by the population.  That’s the market for these companies.

If you are running a food company selling calories, you can grow your company in just a few ways.  You can do nothing and just grow as the population grows, but all food companies can do that so you don’t achieve any advantage over the competition.  You can improve your branding and merchandising and/or develop new products to try to gain a bigger market share of the calories consumed.  You can buy one of your competitors.

And you can work to simply increase the average number of calories consumed by each person and therefore make the overall caloric intake of the country rise.  How do you make people eat more?  Simple.  You make products that are convenient, tasty, inexpensive and widely available.  And you make them addictive.  What makes them addictive?  Carbohydrates, of course.  What gets the blame?  Fat, of course.

These processed foods are typically a mixture of fat and sugar, which provides a taste sensation that most people seem not to be able to resist.  They want more and more of it.  And food companies are happy to provide it.  The USDA’s School Nutrition Dietary Assessment from 2007 showed that the three products groups consumed the most in schools were candy; cookies, cakes and brownies; and soft drinks.  All fat and sugar and, in the case of soft drinks, sugar alone.

All of these foods are thought of as sweets.  People who crave them are often said to have a sweet tooth.  Yet most academic obesity experts criticize these products because they are high in fat.  In their minds, it’s the fat that’s the problem, not the sugar.

Since these academicians fill the seats of all the government panels that convene to come up with solutions to the obesity problem, the usual message is to cut the fat.  So the food companies cut the fat or change the type of fat…and leave the sugar.  The addictive part of the equation doesn’t change.

Lest you think this is a problem only for children in schools, I would encourage you to go to just about any office in America and take a look in the break room.  You’ll find cakes and cookies and brownies and chips and all the rest of the stuff you find in schools.  The problem is endemic.

And it is going to be extremely difficult to change.
I just finished one of the better books I’ve read in a long time.  It’s a book that opened my eyes as to why it will be difficult to change and why Bray et al are going to make it even more difficult.

The book, titled Stuffed: An Insider’s Look at Who’s (Really) Making America Fat, was written by Hank Cardello, a former executive in the food industry who spent his career at General Mills, Coca Cola and other food giants.  Mr. Cardello got sick and, after experiencing an epiphany about his own diet and health, realized that the companies he had worked for (along with many others) were in great measure responsible for his illness.

If you are interested in finding out how the food industry drives us to overeat, you need to read this book.  I can’t recommend it highly enough.

I had no idea how the various arms of the food industry – food manufacturers, grocery stores and restaurants – all work hand in hand to make us fat.  The government is in there, too, always making the wrong moves and usually making the situation worse.  I was always naïve enough to think that if only McDonalds or one of the other fast food giants would make some minor changes, the world would be a better place.  But after reading this book, I can see why those changes are almost impossible to effect because of the structure of the industry.  Who would have thought that purchasing agents are responsible for much of the problem?  Yet they are trapped in the system and can’t change without creating huge problems for themselves (read: their own unemployment).

The first four fifths of the book are a brilliant expose of the food industry.  It’s actually not so much of an expose as it is an accurate description of why the industry is locked into the way it is and why change is damn near impossible.  The book shows why food manufacturers makes foods that make us fat, why the grocery stores are set up to beguile us into buying things we shouldn’t, and why restaurants trick us into ordering not what’s best for us, but what’s best for the restaurant’s bottom line.

The first four fifths more than justify the price of the book, which is a good thing because the last couple of chapters are pretty weak.  Pretty weak, but not without their highlight moments, one of which we will soon see.

The last chapters are weak because, sadly, Mr. Cardello has bought into the idea that what really makes us fat is that we eat too many calories.  In his mind, it doesn’t matter what those calories are made of, they’re all the same.  Except for saturated fat, or course.  He’s convinced that saturated fat will do us in.  He has pretty much bought into the notion that fat and calories make us fat, and the last couple of chapters of the book are a compilation of his ideas as to how to change the food industry.  He thinks that people love nasty processed food and they’re going to eat it no matter what, so why not make it lower in calories and lower in fat.  Most of his ideas revolve around making smaller portion sizes and products with lower fat and calorie counts.

Why does he buy into all this?  Because of Dr. Bray, among others.

Writes Mr. Cardello about a conference in which nutritional scientists sit down with food industry people to discuss how to solve the obesity problem:

It also was refreshing for me to listen to and learn from Dr. George Bray, the esteemed biomedical researcher and professor of medicine at Louisiana State Medical Center in Baton Rouge.  To many insiders, he’s known as the founding father of the obesity issue.  Bray is a doctor and scientist who has been practicing his craft for fifty-one years, and he still has the energy and curiosity of colleagues who are half his age.  When he first began studying obesity, he was a doctor gently sounding a warning bell, but nobody was listening.  The American population was about 14 percent overweight at the time.  Now 30 percent of us are fat, so he said the problem has doubled since he began his work.

Now there is a backhanded compliment if I’ve ever seen one.   I don’t think the author was being ironic, but it sure came out that way.  And it corroborates my suspicions.

Bray truly has been a founding father of the obesity issue in ways that he probably doesn’t like.  When he started working on the problem, the rate of obesity was 14 percent.  After 51 years of effort on his part, the rate of obesity has more than doubled.  That should tell anyone with sense enough to listen that Bray is a part of the problem, not a part of the solution.

Let’s imagine a world in which nutritional scientists actually pay attention to the growing mountain of studies showing that high-carbohydrate diets are bad and that low-carbohydrate diets do all the good things the readers of this blog know they do.  Let’s imagine that these nutritional scientists make recommendations to the government to limit the advertising of carbohydrates in an effort to improve the health of the nation.  Let’s imagine that people stores and restaurants started stocking and serving low-carb foods and that overweight people who were face down in the carbs were looked at with disdain.  And let’s imagine that when someone suffers a heart attack or is obese, everyone says, well, he/she deserves it because he/she was a carbaholic.

If all this came to pass, public opinion would turn against high-carb consumption and my guess is that the obesity epidemic would end.

But is this all a pipe dream?  Could it really happen?  Not while Bray and friends are around ignoring the scientific evidence and continuing to push carbs on us all.  But if these guys ever shuffle on off, there is a chance.  It’s happened before.

Fifty years ago everyone and his brother smoked.  It was the thing to do.  When I was a kid my parents smoked and all my friends’ parents smoked.  Every time I ate dinner, my mother had a cigarette going at one end of the table while my father had one going at the other.  A haze of smoke always hung in our house. But I didn’t think anything of it because a haze of smoke hung in the houses of all my friends.  Whenever I went someplace in the car with my parents or with the parents of my friends, the car was full of smoke.  It was a way of life.  As my mother – who is now a nonsmoker – never tires of telling me, back then if you didn’t smoke, you were considered some kind of freak.

If you watched TV at that time, it seemed that every show was sponsored by a cigarette company.  It’s difficult to believe now how pervasive smoking and cigarette commercials were at that time.  I’ve posted videos of a few of these commercials here and here.  Everyone got into the act.  Even the Beverly Hillbillies.

And actors.

And professional athletes.

There were no nonsmoking sections in restaurants.  People smoked on planes and even in theaters.  If you want to get some notion of what is was like, look at a few episodes of Prime Suspect, the terrific Brit detective series starring Helen Mirren.  You can almost get nicotine toxic just watching.  Granted, this series was filmed in the UK, but it presents smoking the way it was so widely done in the US a generation or two ago.

Now substantially fewer people smoke, and those who do are, for the most part, apologetic about it.  Now there aren’t just nonsmoking sections in restaurants, the entire restaurant is nonsmoking.  People can’t smoke in office buildings, public buildings, or much of anywhere else.  There are no ads for cigarettes on TV or in magazines or newspapers and there are no billboards encouraging smoking.  As far as smoking is concerned, it’s a different world.

What happened?

The scientific community figured out that smoking was a huge health problem.  Scientists worked through the government to launch an enormous public health campaign to get people to quit smoking.  It started with warnings on cigarette packages and went from there to a prohibition against advertising, first on television, then ultimately to just about everywhere else.  And it has worked.  Rates of smoking have plummeted, which is amazing considering how addictive nicotine is.

If this kind of scientific driven public health campaign can work to get people to give up a tremendously addictive and enjoyable habit, why wouldn’t it work to change the way people eat?  I’m sure it would if it were ever initiated.  But the problem is that as long as you have Bray and others telling the powers that be that the only thing causing the problem is calories and that carbs are wonderful, it never will happen.

When the public health campaign against smoking started, the only scientists who spoke out against it were those hired by the tobacco companies.  And, of course, people realized that these spokesmen had a dog in the fight and pretty much ignored them.

Now we would have scientists who are not in the employ of the food industry who are telling us that carbs are good, fat is bad, and the reason we are all obese is simply that we eat too many calories and don’t exercise enough.  As long as these people are spouting off, there will be no change.

Just like there were nonsmokers back then who bucked the trend (and were thought of as freaks by my mother and other smokers), there are those of us who buck the high-carb trend now (and are probably thought of as freaks by the rest of the population).  We all have to rely on our own internal public health campaigns to keep us going.

I don’t know that there will ever be a public health campaign against the high-carb diet, but I know that if there is, it will work.  If people can be broken from the chains of tobacco, they can certainly be weaned from carbs.

There has been a nutritional public health campaign of sorts, but unfortunately it has been misguided.  Bray and others have gotten the government on board for a jihad against fat, particularly saturated fat.  And, as anyone can see, the campaign has been successful.  Sadly, they picked the wrong macronutrient to campaign against, as is evidenced by both the generalized fear of fat along with a doubling of the rate of obesity.

Public health campaigns do work.  We’ve just got to work to get the right one.

Hat tip to Whole Health Source blog for the nutrient intake graphs