AC anti-metabolic advantage dismemberment

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

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

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

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

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

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

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

So, with that preamble, here it is.

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

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

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

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

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

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

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

To solve this problem, AC turns to what he calls

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Second subject:

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

Third subject:

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

Forth subject:

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

Fifth subject:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Wow!  Where do we start?

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

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

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

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

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

After going through all the data, Rabast et al conclude

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kinsell et al

Grey Kipnes

Rabast et al 1979

Rabast et al 1981

Yang et al

Bogardus et al

Hoffer et al

Leibel et al

Vazquez 1992

Vazquez 1994

Vazquez 1995

Piatti et al

Golay et al


Are all diets the same?

Synchronicity strikes again.  The seeds of this post were sown when Gary Taubes emailed me about a study published in early 2009 in the New England Journal of Medicine (NEJM) that I had seen at the time, briefly skimmed and tossed aside as worthless.  Gary agreed that the study was of little value, but notice that it contained a peculiar statement by the authors, an interesting admission about HDL, the lipophobe’s favorite lipoprotein.  And not only had the authors made this strange admission, but so had another prominent lipophobe who wrote the accompanying editorial.

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

Four patients who changed my life

In the early 1980s MD and I were laboring away in anonymity in our clinics in Little Rock, Arkansas.  By that time I had gone through my thin-to fat-to thin again metamorphosis, and I was starting to treat patients for obesity.  My own transformation had been fairly striking, a fact not lost on many of my overweight patients, a number of whom were seeking my professional advice on treating their own weight problems.  I was still doing a fair amount of general primary care medicine, but more and more of my time was being diverted to helping people lose weight.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Three weeks later:

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

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

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

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

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

Her labs told another story.

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

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

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

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

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

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

I am eternally grateful to them.

Pay no attention to that man behind the curtain*

As I was thumbing through the weekend edition of the Financial Times (my favorite newspaper) on a lazy Sunday morning, my eye fell on a little boxed off squib titled Dr Mehmet Oz on the January Detox (scroll to bottom to see the piece).  If I ran across something like this in a local daily newspaper, I wouldn’t think much about it, but in the venerable Financial Times?  Since we all know how much good the wonderful Dr. Oz has done Oprah (as evidenced by the photo to the left – were I she, I certainly wouldn’t be toasting him), I decided to read it to see what he had to recommend on detoxing.  I wasn’t disappointed.  He lives up to his billing.

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.


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.


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


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

Happy New Year 2010!

MD and I wish all of you a most prosperous and healthful New Year!

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.

Low-carb gaining a foothold…with the mainstream

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

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 Vegetarian Myth

Before I get into a discussion of the absolutely phenomenal book you see pictured at the right, I’ve got a few disclosures to make.  First, I’m not much of a believer in the notion of man-made global warming or climate change (as they now call it since temperatures have been constantly falling instead of rising).  I’m a denier, in the pejorative term used by those who are believers.

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.

Hard at work in Seattle

Mt St Helens blog

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

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

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

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

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

Seattle skyline blog

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

Boat in winter blog

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

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

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

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

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

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

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

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

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

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

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

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

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

Request for help promoting our new book

I’m almost afraid to say it, but it looks like after being delayed two times our new book is actually coming out on September 8.  As we have done with all our books, we will be expected to be available for all kinds of media appearances and interviews.  It is a giant pain, but it has to be done.  It’s part of the book-writing gig.  If you don’t sign up to do the PR, they don’t sign up to publish your book. (If you want to see a little of what a book tour is like, read this piece by Joe Queenan to see what we’re up against. Sometime I’ll write a piece on the nightmare of my first three-week-long book tour and my dealings with the escorts that are a part of the book tour experience.)

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

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

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

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

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

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

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

Send to:

6weekcure at gmail dot com

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

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

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

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

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

Low-carbohydrate diets increase LDL: debunking the myth

Instructor teaches Friedewald equation and bad cholesterol

Instructor teaches Friedewald equation and bad cholesterol

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

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

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

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

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

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

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

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

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

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

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

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

And how did they fare?

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


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

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

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

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

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

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

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

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

The abstract of the study echoes this warning.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

LDL = Total cholesterol – HLD – VLDL

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

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

LDL = Total cholesterol – HDL – TGL/5

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

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

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

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

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

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

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

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

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

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

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

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

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