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

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

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

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

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

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

So, with that preamble, here it is.

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

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

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

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

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

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

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

To solve this problem, AC turns to what he calls

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Second subject:

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

Third subject:

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

Forth subject:

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

Fifth subject:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Wow!  Where do we start?

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

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

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

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

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

After going through all the data, Rabast et al conclude

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kinsell et al

Grey Kipnes

Rabast et al 1979

Rabast et al 1981

Yang et al

Bogardus et al

Hoffer et al

Leibel et al

Vazquez 1992

Vazquez 1994

Vazquez 1995

Piatti et al

Golay et al

Myashita

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

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

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

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

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

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

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

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

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

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

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

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

Give me strength.

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

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

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

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

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

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

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

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

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

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

Here’s what the authors wrote:

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

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

…compliance was assessed with objective biomarkers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Three weeks later:

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

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

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

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

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

Her labs told another story.

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

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

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

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

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

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

I am eternally grateful to them.

How does Dr. Oz recommend we detoxify our livers?  Let’s read and see.

I like a simple cleansing fast as an easy, inexpensive means of flushing out toxins and rebooting the system (a juice detox, say, which involves a short-term diet of raw vegetables, fruit juices and water). But it is important to remember that detoxifying the liver, the organ responsible for detoxing our bodies, would take a month of healthy living.

Brilliant!

Let me see if I get this straight.  You detoxify your liver by a fruit-juice fast, right?  Which means throwing back at least three or four glasses of fruit juice a day.  Okay, got it.

Sounds great.  But bit of critical thinking.

What happens to the liver to cause it to need detoxifying?  How about fat accumulation?  A fatty liver is one that needs detoxifying.  Fatty livers are way more common than you might expect.  Studies have shown that about a third of Americans are walking around with fatty livers, a disorder called non-alcoholic fatty liver disorder (NAFLD).  No one really knows what the long-term effects of this problem are going to be, but it is known that fatty accumulation in the liver can lead to an inflamed liver, which can then go on to develop cirrhosis and possibly even liver cancer.  Since this epidemic of NAFLD has arisen fairly recently, it’s unknown how it will play out over the long haul, but I doubt that it will be a good result.

So where does all this fat in the liver come from?  Most researchers think it comes from excess fructose consumption.  The pathways of the metabolism of fructose lead to fatty accumulation in the liver, and giving laboratory animals a lot of fructose gives them fatty livers.  If you couple this information with the fact that fructose consumption has skyrocketed over the last three decades, it makes sense that at least part of the NAFLD we’re seeing comes from too much fructose.

With these facts in mind, let’s take a closer look at Dr. Oz’s recommendation to undertake a juice fast to cleanse or detox the liver.

If you go on a juice fast, how much juice do you drink.  Three or four glasses a day, I would imagine.  And I would also guess that these would be decent sized glasses.  Most people don’t drink an eight ounce glass of anything.  Eight ounces is only a cup, which really isn’t all that much.  Even those little weenie juice boxes that parents put in their kid’s lunches are 8.45 ounces, and most glasses of juice that people drink are larger than that.  A regular-sized soft drink can contains 12 ounces, which is probably much closer to the size of a glass of juice most of us would drink, especially if we were on a juice fast.  Four glasses of juice – a not unreasonable amount to drink in a day if that’s all you’re drinking – would end up being 48 ounces of juice.

I went through the USDA database of foods looking for all the juices I could find that had fructose broken out from the total carbohydrate figure and tabulated them.  Take a look at the chart below which is total carbs and fructose in grams.  And remember that 100 grams equals a half a cup.  So when you see something listed at 111.6 grams of fructose, that means more than a half cup.

It should be clear from this chart that a fruit juice fast provides a whole lot of fructose and a whole lot of carbs.  The fructose is particularly problematic in that it encourages fat accumulation in the liver.  The amounts in 48 ounces of any of these fruit juices would be more than enough to stimulate the synthesis and storage of fat in the liver.

How Dr. Oz thinks this would detox the liver is beyond me.

One other note on his cleansing fast.  It’s not just fruit juices; it includes raw vegetables, too.  I assume Dr. Oz recommends the raw vegetables for all of the flavonoids, carotenoids, lycopenes and other phytonutrients.  I guess he never learned that most – if not all – of these nutrients are fat soluble.  Consuming raw vegetables and fruit juices without some fat along with them means you don’t absorb any of the nutrients.  Dr. Oz must have missed that day at medical school.

So, the actual result of his cleansing detox that is supposed to “flush out toxins [while] rebooting the system” is that more fat accumulates in the liver, insulin goes up thanks to all the carbs and you don’t even absorb the phytonutrients.  Sounds like just a hell of a deal to me.

Let’s spend just another moment looking at yet a different piece of idiocy in this small, small piece of writing.

Says Dr. Oz:

Caffeine throws off all the systems, so drink green tea, which has only a quarter of the caffeine of dark tea or coffee but packs a powerful energy punch.

Oh dear.  Where do we start?  Green tea has almost as much caffeine as coffee, not a quarter of the caffeine.  And, please tell me Dr. Oz, where do we get the “powerful energy punch” from green tea if it’s not from the caffeine?
No sooner had I finished reading the Financial Times Oz recommendations, which, by the way, struck me much more as a prescription from a witch doctor than from a trained physician, than MD pointed out that the same Dr. Oz was on the cover of the Sunday magazine that comes with our local paper.  Yep, USA Weekend features our friend expanding on his recommendations.

I’m not going to go through them all (you can read them here), but one did catch my attention:

Ditch extreme diets. People almost always fail to lose weight because they try diets that are too radical to stick with. For a lifestyle change to succeed, it must be sustainable. So instead of eliminating all foods that fit into a certain category or counting every calorie, try making changes that are less noticeable but no less significant. If you can eliminate just 100 calories from your daily intake, for example, you will lose about a pound per month. How hard is that?

This is a blatant attack on the low-carb diet without saying it in so many words.  And the notion that “if you can eliminate just 100 calories from you daily intake’” you will lose weight over time is the ultimate recommendation of someone who is clueless about the operation of the energy balance equation.

Pitiful.

I’m going to leave you with a poem that I believe is prophetic for Dr. Oz and his nutritionally-unsophisticated compadres.  Sooner or later science will out and these folks will be shown for the idiots they are, and they will be left as part of the detritus of the desert of faulty nutritional thinking.  Too bad they will leave a lot of corpses in their wake.

The poem by Shelley is titled, appropriately enough, Ozymandias

OZYMANDIAS

by Percy Bysshe Shelley

I met a traveller from an antique land
Who said: Two vast and trunkless legs of stone
Stand in the desert. Near them, on the sand,
Half sunk, a shattered visage lies, whose frown
And wrinkled lip, and sneer of cold command
Tell that its sculptor well those passions read
Which yet survive, stamped on these lifeless things,
The hand that mocked them and the heart that fed.
And on the pedestal these words appear:
“My name is Ozymandias, king of kings:
Look on my works, ye Mighty, and despair!”
Nothing beside remains. Round the decay
Of that colossal wreck, boundless and bare
The lone and level sands stretch far away.

*Said by Great and Powerful Oz
in The Wizard of Oz

We’ve had a great time with family and friends over the holidays, but now it’s time to get back into the swing of things.  We ended the year last night with a great dinner for friends.  MD went all out on one of her mega dinners, which, of course, included foie gras, her all-time favorite food.  (That’s my serving of foie gras pictured on the left.  The little jelly-like stuff is a pomegranate pepper jelly that was out of this world and well worth the four or five carbs.)  We had a terrific time ringing out the old year and ringing in the new. I, myself, could have done with a few fewer glasses of wine and the champagne we drank to toast in the new year.

MD’s menu for our New Year’s Eve feast:

• Roasted red pepper soup
• Foie gras (cooked sous vide)
• Duck breast (cooked sous vide) with cabernet cherry reduction
• Golden beets
• Fresh herb salad with vinaigrette
• Epoisses (a soft French cheese)
• Poached pears (cooked sous vide) with pomegranate reduction and heavy cream

Various wines for the different courses and champagne at midnight.

I’ve just now barely recovered.

Everyone is busily making resolutions for the new year, and I suspect that in many cases the list includes weight loss.  In cruising through the web today while regaining my sobriety, I came across a number of posts offering to help by giving weight loss recommendations.  As a weight-loss method, it seems this year that caloric restriction is all the vogue.  Most of the articles I read had a sort of smarmy condescending nature to them, as in, hey, guys, it’s really, really simple to lost weight.  All you have to do is just cut your calories and you’ll lose.  It’s not difficult.  Just do it.

One particular article on losing weight that was representative of most was in Wired Wiki How-To.  By his tone, it’s pretty obvious that the author of this article figures he’s found the holy grail of weight loss.  It’s easy and fast and foolproof.

What does he recommend?

First, you decide how much you want to lose and how long you want to diet. You then multiply the amount (in pounds) you want to lose times 3,500 (the number of calories in a pound of fat).  Take this number and divide it by the number of days you plan on dieting, and you’ve got the number of calories you’ve got to cut back by to lose the weight you want to lose.

The article even gives an example to show how it works.  Let’s say you need to lose 10 pounds and you’re willing to spend two months dieting to lose the weight.  You multiply 10 times 3,500, which gives you 35,000 calories you need to get rid of.  Divide this 35,000 by 60, and you find you need to reduce your intake by 583 calories per day, and, Voila!, your ten extra pounds will be gone at the end of the month.  What could be easier?  Why didn’t I think of that?

The author even presents a version of the energy balance equation to show what he’s talking about.  It’s just a system, says he, and all you’ve got to do to be thin is operate the system.

If it were only that easy, no one would be overweight.

Here is the energy balance equation:

Change in weight = Calories in – Calories out

Below is another way of stating the same thing:

Change in weight = Calories from food consumed – Calories from BMR and exercise

It all sounds so easy.  If your calories coming in from food are balanced by the calories you get rid of during daily living, then your weight remains constant.  If you decrease your intake of calories and keep the calories going out the same, then you’ll decrease your weight.

Problem is, these two terms ‘calories in’ and ‘calories out’ aren’t independent of one another.  If you reduce the number of calories coming in, you’ll also reduce the number of calories you burn.  Your metabolic rate will drop, you will decrease your activity more, and your weight won’t change as much as you would expect.  If you ratchet up your exercise, then you’ll compensate by unconsciously increasing the food you eat by a bit.  The fact that these two components of the energy balance equation aren’t independent is what makes losing weight by counting calories so difficult.

In my opinion, it’s much easier to lose excess body fat by following a diet that both restricts calories without your having to think about it and that does it in a way that doesn’t really cause you to drop your metabolic rate.  Plus, a good diet followed correctly actually gives you a little boost in that it provides a small metabolic advantage.  In other words, you lose a few extra calories (maybe up to 200-300 per day) without having to do anything to lose them other than following the diet.

Take a look at this post on Is a calorie always a calorie? I wrote a couple of years ago to see what I mean.

But beware.  This post comes with a caveat.  If you are in the least bit psychologically unhinged, you might not want to read the post.  It was this very post that pushed Anthony Colpo over the edge.  It inspired him to launch a jihad against me and against anyone else who might possibly believe that a slight metabolic advantage exists.  He wrote an entire book that he made available free to anyone who wanted it showing how Gary Taubes, Richard Feinman, and MD and I were idiots.  Of course, my redneck genes, such as they are, compelled me to answer.  For those of you who weren’t readers in those days, the end result of the whole affair was that after receiving a number of pretty severe canings on this blog, our friend Anthony just sort of drifted away, never to be heard from again.

All this aside, read the post and come to your own conclusions as to what the best diet is for simple, quick weight loss and act accordingly should one of your New Year’s resolutions be to lose weight.

If you need some motivation to jump in with both feet and do it, then read this post, this one and this one.

Best of luck with all your resolutions.  I look forward to continuing our journey together in 2010.

Click here to view the embedded video.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Mike’s Story

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

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

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

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

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

Bellies…?

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

We nodded.

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

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

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

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

“Take the bullet?  What do you mean?”

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

“I can’t wear that…” I said.

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

“Who?” I asked.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Now, back to the PNAS paper.

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

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

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

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

Low-carb diets ‘damage arteries’

And followed up with:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Says the NY Times:

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

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

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

Pretty sleazy, if you ask me.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Click here to view the embedded video.