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



  1. Mike,

    There is a highly ironic spelling mistake in the sentence where you say: “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 THEIR is a metabolic advantage that becomes manifest during low-carb dieting.” Intentional? Just thought I’d give you that heads up. OK back to reading the post.

  2. OK so I have read AC’s website and agree with most of what he says regarding saturated fat, low carb etc, so I was wondering what your retort would be. There surely HAS to be more than calories in/calories out as he is saying. Insulin plays such a large part in all of this with cells holding on to fat etc. I am a novice in this area and am reading and researching all I can. It is hard to know what to believe and what to do but thank you for clarifying that you have never stated that the metabolic advantage is never more than 100-300 calories.

    I am a victim of over 10 memberships to Weight Watchers with no success, only weight gain. I love that when I eat low carb I don’t crave food, I don’t count calories and I do lose weight. I totally do believe there is a metabolic advantage as shown by Tom Naughton in Fat Head the movie. I just can’t, for the life of me, understand why low fat/high carb is still promoted. Thank you for helping to change this perception.

  3. Fantastic article, Dr. Eades. Your propensity for dissecting these studies is mind boggling. Thanks so much for doing it for all of us readers, I know that I personally really benefit from all of your hard work. It all seems so clear once you explain the facts.

  4. ‘Mornin’ Dr. Mike, Good to see you in fightin’ form.

    I do not know where you get the intellectual stamina for such detailed analysis. But it is cool to see a forensic presentation of the difference between “ward” and “in-patient”, and of statistical significance. (It reminds me of the interesting fact that when “n=1”, one has mere “anecdotal” evidence, but the statistical significance for the population size – 1 – is truly gargantuan!)

    P S I was wondering if you were in two minds between gigantic and gargantuan when you chose gargantic – I, myself prefer gargantuan, as it connects a fat giant and Rabelais!

    1. Gargantic is a neologism that I made up and often use. It is a hybrid of the two words gargantuan and gigantic. I figured people would get it from the context. I just like the sound of it. Another one I like us hunormous. Both play hell with your spell checker, though.

  5. Well done, Dr. Eades,
    hope you can finally close that chapter. Some people aren´t worth any attention. My personally experiences with calories: if I want to lose I need to stay lower than 1500 with very low carb. In SAD times it used to bee strongly lower than 1000. With very low carb I have my set point by 3000! Former SAD times 2000. If that is not a metabolic advantage than I don´t know what. Greetings.

    1. Dude, think this through. Read what this guy is saying man. IT is complete bs. There is no metabolic advantage. Not even 100-300 calories or whatever the amount is this month. The satiating effect of protein and the even level of blood sugar keeps you from getting too hungry so you eat less calories over all. There is nothing magic about it. The metabolic advantage is completely made up.

      Don’t get me wrong I do use a non ketogenic low carbohydrate diet just for the reason that it keeps me from getting hungry and my blood sugar is stable. But don’t bs yourself by believing that there is a metabolic advantage to it.

  6. Hi,

    Just now saw the post. Will read it in a while. Hope that you have blasted that brat. (He is rude and incorrect). I very well remember reading in PPLP ages ago (2000?) your beautiful explanation about effect of calories on weight loss.

    Have a great day!


  7. I agree with some of your point, disagree with others.

    It is true that because the studies are all small, the fact that differences were nonsignificant doesn’t tell the whole story. If we find a constantly small increase in weight loss in the low carb groups, it is some evidence in favor for the metabolic advantage.

    However, I do not think it is reasonable to say the reason most studies didn’t show a significant difference is because the subjects can cheat. That would mean the low carb group constantly cheated by 100-300 calories more than the low fat group, to make up for the metabolic advantage. I don’t find it plausible, because everyone knows the effects a low carb diet has on appetite compared to a low fat diet. It is a stretch to imagine the low carb group just cheated more all the time in all the studies, that’s why they don’t show an advantage.

    Also, you say the subjects might not be educated enough, might not understand how important it is to follow the diet provided exactly etc. But, when you tell someone to go on a low fat or low carb diet, you just say go home, cut the fat out and eat like this, the results will be even more off base. They are not educated enough to follow the diet that is provided to them, they might cheat, but, when you tell them to cook themselves low fat meals for a couple of months, the results will be much much worse. Doubly labeled water studies have shown that humans can be way, way off in estimating the amount of calories they are eating. I mean seriously way off.

    Also, I agree some studies had very few calories and the metabolic advantage might not show effect at starvation times, but some studies had 1500 calories and more. Some were badly designed, but I doubt all were that bad.

    I would conclude the data is inconclusive.

    1. I think you missed my point about the cheating. Perhaps because I didn’t make it as well as I should have. There are many free-living studies showing people on low-carb diets lose more weight than people following low-fat diets of the same number of calories. AC doesn’t believe the data from those studies because he suspects all the subjects cheat. He will accept data only from ‘metabolic ward’ studies because in those studies (at least in the way he imagines them done) subjects can’t cheat. I was simply pointing out that people can, and, indeed, do cheat in metabolic ward studies.

      There are a number of different vectors all pointing toward the existence of a metabolic advantage:

      1. The second law of thermodynamics virtually demands the existence of a metabolic advantage
      2. Animal studies that can be carefully controlled do show the existence of a metabolic advantage.
      3. Probably half the studies (both free living and ‘metabolic ward’) show a weight-loss differential between low-carb and low-fat, i.e., a metabolic advantage.

      The deal is that the metabolic advantage isn’t all that big a deal. It’s probably a couple of hundred calories, three hundred at most, so why all the Sturm and Drang on the part of AC and sycophants?

      1. I’m curious about how the second law of thermodynamics is applicable here. I understand how you might make an argument with the first law (but that would say that a calorie is a calorie – not where you are heading, I think). Are you saying that there is a measure of the entropy of protein/fat vs. carbohydrates? Even if that were the case, I don’t see how the argument progresses. What do you define as the boundaries of your closed system? What does it mean for entropy to increase in this context and how does that impact a “metabolic advantage”? Maybe this was covered earlier and I just haven’t been reading your blog long enough?


      2. Dr. Mike – Great post!! Thank you so much for answering AC’s claims. It seems to me his whole beef with you was that he believed that you were making the metabolic advantage out to be much bigger than the few hundred calories you were already clear about. I never shared his belief, but I’m glad that you were able to show the dents in the “armor” of metabolic ward studies. Thanks again!

  8. There are a million, perhaps a jillion ways to lose weight. What I’d be more interested in seeing is which calorie-restricted diet caused the greatest fat increase above starting levels when the diet was discontinued – as nearly all diets eventually are.

    For example, Ancel Key’s starvation study at the University of Minnesota caused the subjects to decrease body fat levels by nearly 70% in the 24-week starvation study. By week 33 of refeeding their body fat levels were 40% higher than they were at the start of the experiment.

    When you look at that phenomenon as a whole, the only logical conclusion is that calorie restriction causes weight gain – specifically fat gain, and a poorer overall body composition.

    That’s what Colpo recommends doing, and the results of his recommendations, and I suspect a calorie-restricted low-carb diet often leads to the same Nike Swoosh-looking graph long-term.

    His book should be called the Fat Gain Bible.

    Crap, I can’t make any friends.

  9. Case closed!

    0f course, nothing anyone says will ever convince that dude. We call can all expect another unreadable Jerry Springer-ish ad hominem filled rant any minute now from the guy… to be echoed by his chorus of followers…

    AC has held forth via the internet on four subjects, that I know of:

    Lipid Hypothesis
    Training Methods (HIT versus Explosive, Cardio, etc.)
    Metabolic Advantage
    911 Conspiracies

    As much as he claims to be objective, only drawing conclusions based on the evidence, it appears to me at least, the guy has a heavy, heavy confirmation bias. He loves his style of training, therefore HIT is worthless. He’s convinced there is no metabolic advantage, therefore… well, you know the story.

    In my opinion, his stance on the 911 thing is the most revealing. I’ve looked over the so called evidence, and with a large stretch of credulity, I can see how someone might conclude, well, maybe this is possible. And that is a large stretch, and a very hesitant maybe. However AC has vociferously argrued that there was absolutely a conspiracy, that some sort of secret shadowy uber gov’t group was behind it all, that they somehow have managed to stay hidden.. I find this position laughably absurd. One could only logically go that far if you go into the evidence as a believer.

    So, he did get the Lipid Hypothesis right. Let’s give him credit for that! Cheers to Anthony Colpo!

    1. Cheers indeed. He’s gotten a lot right. I don’t know where his violent opposition to the notion of a metabolic advantage comes from.

  10. To add to Todd’s comment, again there is a misspelling in the software title you picture. So fun, they won’t even know THEY’RE learning. Who produces that?

  11. That 1992 paper looks like the “definitive” Rockefeller University studies cited in Gina Kolata’s review of _Good Calories, Bad Calories_ in the NYTimes:

    “Taubes ignores what diabetes researchers say is a body of published papers documenting a complex system of metabolic controls that, in the end, assure that a calorie is a calorie is a calorie. He also ignores definitive studies done in the 1950s and ’60s by Jules Hirsch of Rockefeller University and Rudolph Leibel of Columbia, which tested whether calories from different sources have different effects. The investigators hospitalized their subjects and gave them controlled diets in which the carbohydrate content varied from zero to 85 percent, and the fat content varied inversely from 85 percent to zero. Protein was held steady at 15 percent. They asked how many calories of what kind were needed to maintain the subjects’ weight. As it turned out, the composition of the diet made no difference.”

    Leibel didn’t finish his residency until 1972.

  12. “Do you think there might be just a little bias in this author and his co-workers?” – That’s a tremendously weak argument. It’s clear you have a bias so everything you should say should clearly be discounted as well. Next you use words like “doubt it” and “I suspect.” Then you imply the people who would sign up for such study are of such low class their must be genetic mutants such that their data doesn’t apply to the hoi palloi. Your bias shows clearly again. You are about as Scientific as Oprah. Really shoddy work.

    1. Even God is biased. I appreciate the ginormous effort of Dr. Eades or ME to read papers and give incite. AC quotes aposteriori knowledge w/c he considers as being built on rock and ME shows, rationally me thinks, that perhaps sand would be a better metaphor.

    2. I think it’s one thing when you’re reading a refutation by a person with a well-known, obvious bias, and quite another when it’s a “scientific” paper where the bias is hidden in the full text most people never see and rarely have access to. Abstracts fail to mention such bias, as do most people who write about the studies. I don’t see bias as too much of a problem as long as it’s clearly presented, and the raw data is available.

      Dr. Eades has (graciously) provided us access to the full texts, so we are free to draw our own conclusions from the papers. For me, that’s sufficient.

    1. A tiny bit, maybe, but overall The Great Cholesterol Con is a very good book. He was carefully arguing a thesis there, not rampaging about something.

  13. Another excellent post, Dr. Eades. I read AC’s diatribe against you the other day, and was surprised at the amount of invective he used. It diminished his argument in my mind, as facts don’t need insults as a “carrier”. I didn’t do the work of looking at his arguments because of that, but I’m glad you did.

    For other lay people wondering how to decide between all the different voices out there, one measure I use is to look at the person’s experience. I’ll take someone who has actually had patients, solved their individual medical mysteries, and has seen success in a clinical setting with real people over the ivory tower researchers (or even a barnyard mud-slinger).

    I don’t know how many people AC has helped lower triglycerides, raise HDL, lose weight and get blood sugar under control, but Dr. Eades can count me as one of many he and MD have helped. And all that for a measly $15 at the local bookstore.

  14. Firstly, you did claim that there was a slight Metabolic Advantage to the tune of “a few hundred (at most) calories per day” ref: Count, Dr.A_cula!! – Comments.

    Secondly, neither you nor anyone else has disproved my hypothesis that adipocytes can get as much glucose (and thus glycerol-3-phosphate) as they need even if serum insulin level is not raised. James Krieger pointed out that Glu-T1 (insulin-independent) transporters also transport glucose into adipocytes.

    Low-carb diets do have an appetite advantage for many people and many people do get significant thermogenesis from dietary fats, so I’m definitely not dissing low-carb diets.

    1. As I understand your hypothesis, you’re saying in the presence of low insulin levels, the glycerol molecules stripped from dietary fat can be used to form the glucose required to make the glycerol that forms the “backbone” of fat (triglycerides) in the fat cells. Have I got this right? If so, I don’t think it will work. It’s like saying you can get better gas mileage on your car if you don’t stop at the petrol station, but instead siphon gas from your gas tank and then pour it back in.

      1. mreades said…
        “As I understand your hypothesis, you’re saying in the presence of low insulin levels, the glycerol molecules stripped from dietary fat can be used to form the glucose required to make the glycerol that forms the “backbone” of fat (triglycerides) in the fat cells. Have I got this right?”

        Not exactly. What I’m saying is that adipocytes can take in glucose from the blood to produce as much glycerol-3-phosphate as they need even when serum insulin isn’t raised as (and this is where I differ slightly from James Krieger) either Glu-T4 transporters are up-regulated due to lack of substrate downstream (me), or Glu-T1 transporters are up-regulated (him), or both.

        The liver (& also kidneys) maintain Blood Glucose by converting the glycerol stripped from serum TriacylGlycerols by LipoProtein Lipase into blood glucose. They also use Lactate, Pyruvate & glucogenic Amino Acids as required.


        1. I understand that the liver can produce as much glucose as it needs from lactate, pyruvate, amino acids and by recycling the glycerol stripped from triglycerides, what I’m wondering about is whether it would due to an increased intake of fat. If I had to bet, I would doubt that the gluconeogenic machine would be upregulated simply because one ate excess fat calories in the absence of carbohydrates. I’m not saying it might not happen, I’m just saying that I wouldn’t bet on it. I haven’t seen any papers in the literature saying it does, but I haven’t read every paper ever written. If you have one confirming your theory, I would love to see it.

          You can take a look at this paper from the AJCN (you can access full text from the link) to see what German researchers found when they increased fat intake by a few extra thousand calories under metabolic ward conditions, whatever that means.

          1. That’s an interesting study. From The Full Study, I noticed:-

            “At daily intakes of 300 to 400 g fat and higher, the test subjects reported a marked sensation of heat extending over the entire body and a marked tendency toward sweating, irrespective of the type of fat administered.”

            This indicates that dietary fats can be much more thermogenic than the 2% figure usually quoted. Where did the 2% figure come from, anyway?

            I’m a little worried about high-dose corn oil. Didn’t the US Veterans Study in 1971 show that a large corn oil intake greatly reduced CHD deaths but replaced them with cancer deaths? I can’t access the full study but Eddie Vos has a graph on his site HERE

            There’s definitely something weird going on with high corn oil intakes causing weight loss, but I wouldn’t want to try losing weight by swallowing shed-loads of corn oil.

            As for up-regulation of gluconeogenesis by liver & kidneys, that would occur naturally due to the excess of glycerol produced from post-prandial serum TGs split by LPL into FFAs & glycerol. The glycerol has to go somewhere. I don’t have any studies to support this, just a Metabolic Pathways textbook.

    2. You wrote:

      As for up-regulation of gluconeogenesis by liver & kidneys, that would occur naturally due to the excess of glycerol produced from post-prandial serum TGs split by LPL into FFAs & glycerol. The glycerol has to go somewhere. I don’t have any studies to support this, just a Metabolic Pathways textbook.

      This brings us back to siphoning the petrol out of the tank then putting it back in. The glycerol stripped from the triglycerides can indeed reform into glucose, but I would maintain that this would decrease the amount of glucose the liver needed to make from lactate, pyruvate and amino acids in order to keep the blood sugar stable. That’s if the FFA part of the triglyceride were oxidized for energy. Or, the most likely outcome, the glycerol would be used to reassemble the triglycerides inside the fat cell. It would take the glcycerol from two triglyceride molecules to make on molecule of glucose. This molecule of glucose, once inside the fat cell, could be used to reassemble two triglyceride molecules. But in a milieu of low insulin, hormone sensitive lipase (LPL’s counter hormone) would be doing just the opposite. So you would be taking glucose out and putting it back in again. And each turn of the crank uses a little energy.

      1. I’ll have to get back to you on this one. I have an important meeting with Social Services today re: my mum (who has dementia) so I’m a little tied-up right now.

      2. The liver uses whatever substrates are available to generate glucose under the control of insulin(inhibitor), glucagon, adrenaline/epinephrine & GH (also cortisol, for lowish BG).
        Rate of FFA oxidation depends on aerobic activity level.
        HSL is activated by adrenaline/epinephrine during exercise and by noradrenaline/norepinephrine from noradrenergic nerves.
        In the complete absence of insulin (untreated type 1 diabetics), there’s an excess of cyclic AMP due to a lack of active protein kinase B and this over-activates HSL.
        In the presence of some insulin, this doesn’t happen. So in healthy people & treated type 1 diabetics, there’s no useless cycling of FFA + g3p -> TG -> FFA + glycerol.

        1. You wrote:

          In the presence of some insulin, this doesn’t happen. So in healthy people & treated type 1 diabetics, there’s no useless cycling of FFA + g3p -> TG -> FFA + glycerol.

          Somehow I think there is a breakdown in communication here. Either we’re both saying the same thing or I don’t understand what you’re saying or you don’t understand me.

          I can’t see how the glycerol from excess fat can be used to recycle more fat. One unit of fat would be converting into another unit of fat. There would be no net gain. I’m not sure off the top of my head if I buy your explanation of the only way HSL is activated. But it doesn’t matter because a low insulin level allows fat to easily move from the fat cells to the circulation. I think in the vast majority of cases – as demonstrated in the paper I sent you – the body cranks up the metabolism to dispose of the excess fat when consumed in a milieu of low insulin levels.

          1. You wrote:
            “But in a milieu of low insulin, hormone sensitive lipase (LPL’s counter hormone) would be doing just the opposite. So you would be taking glucose out and putting it back in again. And each turn of the crank uses a little energy.”

            I pointed out that HSL doesn’t do that unless either serum insulin is zero or you’re exercising or certain nerves secrete noradrenaline. I got the explanation from my Metabolic Pathways book.

            The study you linked to above was very small, the initial weight loss was glycogen+water and there was a very high drop-out rate in the corn oil group. PUFAs may well crank up metabolic rate but high-dose corn oil is rather impractical (causes nausea) and the results have never been replicated.

          2. You wrote:
            “I can’t see how the glycerol from excess fat can be used to recycle more fat.”
            I didn’t say that. The glycerol from excess fat can be used to replace blood glucose that was taken in by adipocytes to store the excess fatty acids.

        2. I’m not persuaded that your metabolic pathways book has it exactly correct. It’s certainly different from the way I learned about glucagon and how I’ve read about it since. I’ll have to do a little looking on my own to make confirm all this before I change my thinking on it.

          The group that did the study I posted did more studies in hospital working with greater numbers of subjects with basically the same result. Here is one they refer to in a letter to the editor. You can do a PubMed search on Rabast U and/or Kasper H to see the body of their work.

          1. According to the metabolic pathways book, glucagon stimulates lipolysis in vitro, but has no effect on HSL in vivo. I don’t know what year you learned about glucagon, but this book is bang up to date with the latest research. I have the 2nd edition and am seriously considering upgrading to the 3rd edition. You really need to read the book!
            The conclusion in the above link is:- “the explanation for this phenomenon is probably to be found in a rise in thermogenesis.” An increase in kcals out on the RHS of the Energy Balance Equation is the most probable explanation. A reduction in drowsiness (something that I used to suffer from badly on a high-carb diet) also increases kcals out due to Spontaneous Physical Activity/Non-Exercise Activity Thermogenesis. I’d call that an apparent Metabolic Advantage as it’s not breaking any Laws of Thermodynamics.
            It’s definitely an advantage that a lot of people can feel great, get much improved bloodwork and not feel deprived eating a “meats, leaves & berries” type of diet.

          2. As far as I know, one can’t break the laws of thermodynamics. A metabolic advantage – as used in these discussions – means more weight loss on a one diet as compared to another with the same number of calories. If one group of subjects loses 4 pounds following Diet A than a similar group of subjects loses over the same period following Diet B (a diet providing the same number of calories as Diet A) then Diet A can be said to confer a metabolic advantage. Having said that, one has to be careful using the laws of thermodynamics to describe human activity because the laws of thermodynamics are applicable to closed systems. The human body is an open system. If not, we could all gain weight by sitting around in the house with jackets on or could lose weight by sitting around the house naked. It just doesn’t work that way.

          3. “The human body is an open system. If not, we could all gain weight by sitting around in the house with jackets on or could lose weight by sitting around the house naked. It just doesn’t work that way.”

            Great! Now you tell me! Hey, where are my clothes?

          4. After reading the lively banter between you and Nigel, I feel like I could easily qualify for one of those in-house metabolic ward studies.

      3. I’m not sure I’m about to hurt or help this discussion because I’m not 100% clear about the issue Nigel is trying to make, but I feel like he’s generally saying that because glucose can always be made/delivered, even in the presence of low insulin, [and here comes my interpretation of his point], that low carb diets that manage insulin are not really going to effectively curb glucose and the resulting problems that come with its elevation [apologies Nigel if I bungled your point]. It’s quite true that glucose can be made and delivered in the presence of low insulin; exercise is a perfect example, and this creation and transport of glucose into the cell occurs even independently of glucagon’s effects per a muscle contraction mediated effect.

        Where I’m getting spun around in this discussion…..is, well, let me just say, that the body only makes product when it’s needed. So it’s really demand based [demand for ATP, and how best to deliver on that demand]. So, you can have all the intermediate substrate [glycerol, lactate, pyruvate, aa’s]in the world hanging around to make glucose, but if you don’t need it [glucose levels are stable, or the ATP/ADP/AMP charge of the cell is reasonable], it won’t be made. Metabolic pathways are product limited. So if you need ATP in a hurry, say for high intensity exercise, or in diabetes or metabolic syndrome where ffa’s are not easily utilized, the liver will take whatever is hanging around and make glucose. But if you have all that intermediate substrate hanging around and you don’t need glucose, those metabolic pathways aren’t going to be cranking, and any excess intermediate will be disposed of in another way. For me, this is why the liver defect in diabetes is such a kicker. For the liver to crank gluconeogenesis in the presence of dietary substrate is a stunning derangement to me.

        Sorry if I completely misunderstood what you guys were trying to say.

        1. Hi LC. I’m an infrequent visitor here (and I don’t use e-mail notification) so I’ve only just seen your post.

          What I was trying to explain was that the body stores any dietary fat that doesn’t get burned as body-fat irrespective of serum insulin level (provided that there is some). Where insulin does make a difference is that high serum insulin inhibits lipolysis (fat-burning). People who are on low-carb diets still have serum glucose, though it is slightly lower and far more stable than in people on high-carb diets. People on low-carb diets are burning mainly fat for energy (except for anaerobic activity where carbs are still burned).

          Kurt Harris explains it well in his post Insulin is a doorman at the fat cell nightclub, not a lock on the door.

    3. I’m not as well-versed as I should be, but I think the question is, where is the glucose coming from? If ingested carbohydrate is sufficiently low, would it not come from gluconeogenesis (with perhaps a tiny amount from certain fatty acid metabolism byproducts)? If that’s the case, it would make an interesting argument for why excessive protein intake can disrupt some people’s weight loss, although not by too much. I can’t see it being too significant.

  15. Very interesting, entertaining and in general a fabulous post — thanks for your significant time input. Here’s to intellectual stamina! Your readers are better for yours.

    I agree with Ted only in that we are all biased and prejudiced – we couldn’t function without those attributes; we’d never make a decision on anything. In the face of that, however, there are those who are willing and able to follow the rules of scientific inquiry, set aside their bias and prove a point. I think you’re the type who would be propelled to do that work out of curious-ness (with a splash of cantankerous-ness now and then). I’m just grateful that you write it down and that I have access. Thx!

  16. We have not been receiving email notification of your last two posts either. (since your replies started appearing in color) I will try resubscribing, as suggested in reply to a previous comment.

    1. I’ll see if I can get my web guy to spring into action on this. I don’t really know what has happened. I subscribe to my own RSS feed just to make sure my posts go out, and I haven’t gotten the last two either.

          1. For some reason, a blank line is being put at the top of the XML file for the feed before the XML declaration, causing parsing to fail. Get your web guy to remove the empty line above the XML declaration and you should be good to go.

  17. Hi Dr.

    Thanks a lot for this review. I think even if there’s a metabolic advatange, it’s still important to educate people on the importance of calorie, because, as you stated, if there’s ever one, it’s in the neighborhood of 100-300 calorie. It is important because many person get away with the idea that they can eat as many calorie as they want as long as they are low-carb. Not so long ago on another blog, Fred Hahn was saying that on a 3500 calorie diet of pure fat/protein, it would be impossible to gain weight. I’m not sure, but I don’t think this is the message that you are trying to send. I think low-carb works very well mainly because it spontanueously reduces caloric content, and usually retain LBM better (but this is probably due to the higher protein content of the diet rather than the lowering of carbs). If there’s ever a metabolic advantage, that’s good, but I wouldn’t base my weight-loss strategy on this.

    Thanks again!

  18. This might be simplistic but wouldn’t there be a metabolic advantage if one is in ketosis and peeing out ketones (energy). This is my first post to your blog but I’ve been an avid reader. I’m a physician and now am basically studying on my own to learn what I should have learned in medical school. Thank you.

    1. At one time it was thought that the loss of ketones contributed to the metabolic advantage, but upon measurement of the energy contained in the amount of ketones released in a typical ketogenic diet, it doesn’t add up to a lot.

  19. You mention that the metabolic advantage is between 100 to 300 calories. Do you think it’s more accurate to say that it’s a percentage of calories consumed rather than some fixed number?

    From what I can see the metabolic advantage with LC is that energy is more freely available to feed the cells and be burned. Fatty acids are free to go in and out of the fats cells to be used for energy and are not trapped by binding with the glucose molecules that enter the cell.

    On a HC/LF diet the energy eaten is stored as fat and cellular starvation occurs. You feel more tired and expend less energy as less energy is available for your cells.

    That is my understanding anyway. There are many other benefits to LC that I can see such as reduced blood pressure, improved blood lipid profiles…etc…etc…


    1. I’m not sure I would call it a function of calories because it doesn’t really exist until one gets out of the starvation range.

  20. I note with great relief that Michelle Obama has pitched in to end childhood obesity in the next generation. Too bad her husband won’t even consider throwing the sugar and grain lobbyists out on their ears. Now that’s change I could believe in!

    “Let’s move,” indeed. Michelle, I know a neighborhood in Chicago you and your family would enjoy. Move. Please.

  21. Thanks for this awesome post, Dr. Eades! I just bought your book (Protein Power) and am looking forward to the read!!

  22. Ken said:
    “The definition of an Australian ” A person with a chip on both shoulders””

    Unwarranted. Don’t write stupid things like that and yes I’m Australian.

    1. Nice piece in the Independent. Thanks for sending. Strangely, our book is doing much better in the UK than it is here.

      1. That’s too bad your book is doing better in the UK than in the U.S. I’ve lost 19.5 pounds since Jan. 4th on the 6 week cure. My wife also lost quite a bit of weight but had to drop the really low carb portions of the diet (not because of the diet itself, but she became pregnant; apparently, a protein shake isn’t appetizing under those conditions ;-).

        1. Glad to hear you’re doing so well. And I’m glad to learn your wife is pregnant (assuming you feel the same way.) 🙂

          Don’t know why the book isn’t doing better here. It gets a ton of clicks on the Amazon page, but not a lot of purchases. Probably because the comment that continues to remain at the top isn’t very favorable.

          1. Mike – maybe (also) because people like me, who already own the book, use the one on your products page as a portal to Amazon. I thought that helped you out too? Please let me know if I’ve got it wrong . . .


          2. Yes, clicking through to Amazon through any of the book icons on the site will allow us to get a small commission on anything you might purchase. Thanks very much for your support.

  23. Thank you so much for doing all this work for our benefit. I am giving a low-carb presentation to a group of my friends tomorrow, and of course your information (including that presented in your books) is forming the backbone of my talk. I’m hoping to make a convert or two, and most of all to dispel ignorance.

  24. Great post, Dr. Mike. I’ve been eagerly awaiting the forensic exam of AC’s book for over two years — thanks for delivering!

    The “definition of an Australian” comment is hate speech. Please consider deleting it and perhaps also any comments referring to it (including mine — this portion of it, at least), as you would any inappropriate remarks. To bring my point into focus, try substituting some other ethnic (or other category of) groups for “Australian.” And no, I’m not Australian.

    1. I assume you’re referring to the ‘chip on both shoulders’ bit. If so, your threshold for hate speech is much, much lower than mine. This is an old, old joke that I’ve heard told by a dozen people. I don’t find it offensive at all. If it were in reference to an ethnic group, maybe, but not in reference to the citizens of an entire country. Aussies refer to us Yanks as Seppos, which, if you understand the origin of the word (septic tank), is not very flattering, but it doesn’t bother me at all. In fact, I find it kind of funny and ofter refer to myself as a Seppo when dealing with an Aussie.

      In the long history of this blog – five years, I think; maybe longer – I’ve deleted only three comments that I can recall. One used vile, homophobic language in reference to a person appearing on a video I put up. One was filled with so many expletives that it almost couldn’t be read. And one attacked another commenter in a spiteful and grossly hateful way.

      1. What I find offensive is that the original poster didn’t get the joke right!
        It’s: Q: What is an Australian with a balanced attitude? Ans: One with a chip on BOTH shoulders!
        As I’ve said before, we’re rather relaxed about insulting names. Love the annecdote of Joan Sutherland yelling over the street to colleague Luciano Pavarotti, “Hello, you Old Bastard!” Of course they were the best of friends, as Joan’s husband had hired LP when he was a completely unknown tenor for the opening season of the Australian Opera (C. 1966). The moment he stepped on stage for his first performance the audience and the critics realised here was something very special and he rocketed to world fame. BUT, he always remained an active member of the Australian Opera, performing here in season after season for years thereafter.

      2. I second your reaction to the “hate speech” claim. We have all gotten waaaaay too sensitive to any little jibe. I would be stunned if the Australian joke wasn’t told far more often by Aussies than by anyone else. The world is not going to be a better place if we’re all rendered into a bunch of humorless scolds.

      3. Hmm I’m Australian, but I can’t say I have ever heard of the term Seppos. It’s usually yanks or sometimes arrogant yanks and now mostly jokes about Bush 🙂

    2. hehe…. if that’s the worst thing you can say about an aussie.. i’m sweet with that..
      It was just a joke.. being an aussie, we call each other much worse..

      about the Septic Tank thing.. I think you will find it’s more about the rhyming slang than comparing americans with toilets.. think tank= yank
      have a good one!
      PS.. I used to be a fan of AC before i learned more about Low Carb.. I really don’t know what he is on about these days..

    3. Breathe. It’s just a silly comment on the Internet. It’s not harming anyone. If someone posts something you find distasteful, you can always fire back and tell them what you think. I think censoring someone for a stupid comment is in itself idiocy, and prefer to let everyone point and laugh. There is a line, but I think it has to be pretty far out in order to be worth censoring.

      I don’t like the idea of “hate speech”, though. Like I said, I think it’s better to let people speak freely so it’s clear who’s worth responding to and who’s just an ass to be shunned.

  25. Speaking of nutballs with bad advice…

    I read this press lease yesterday. “A common cholesterol drug fights cataracts, too”, in which you can find statements like “But before long we may be taking a daily statin pill along with our daily vitamin tablet, Dr. Chodick believes.”, and “But now we have even more good reasons to keep taking statins ― like an apple a day.” Methinks Dr. Chodick has his hands in the pocket of a pharmaceutical company.


    The drinking water is next. Maybe not the dams, but certainly the fortified bottled water market.


  26. Dr Eades,

    I applaud you for your blog, as it contains the best nutritional information anyone could hope to find. In large part, in my opinion, this is a result of your use of published medical studies to support your conclusions, as opposed to anecdotal reports that so many others rely on.

    However, when one has published as many written words as you have, sometimes you can appear to be inconsistent.

    To wit: above, you caution against relying too much on metabolic ward studies, stating “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.”

    Yet, on p. 46 of “The Protein Power LifePlan”, you cite a metabolic ward study conducted at Geneva University Hospital and conclude, “Inpatient studies of this sort are worth their weight in gold because the data is reliable.”

    Dr Eades, has your opinion of the value of such metabolic ward studies changed over the years?

    1. Yes, it has. I used to think of metabolic ward studies as the gold standard of studies, and I still do to a certain extent if one can be sure they are well run. I have Anthony Colpo to thank for my realization that metabolic ward studies can be of all different kinds and are not immune to the effects of cheating. Had he not written his book, and had he not attacked me, I probably wouldn’t have looked into these studies to the degree that I ultimately did. Had I read that a study had been conducted in a metabolic ward, I would have thought that it meant what Anthony thought it meant. When I started looking carefully, though, I realized that it could mean a number of different things: people who are under constant observation 24 hours per day, people who spend the night in the hospital and are let loose during the days and on weekends, and people who check into the hospital to get their initial testing and spend a day or two acclimating to the diet, then are sent home for the rest of the study only coming back to the hospital to obtain their packaged meals for the day or even for the week. All these situations have been referred to as metabolic ward studies. So I’ve learned to be much more careful as to what I read into the term ‘metabolic ward studies.’

      The study to which you refer, the one I wrote about in the PPLP, was an inpatient study. Patients were hospitalized for the entire six weeks of the study, but, I’m sure, had the opportunity to cheat if they really wanted. In the next and final post I write about the AC book, I’m going to give an example of what researchers doing these kinds of studies have to contend with in terms of cheating.

    1. I’m not holding my breath. Actually, AC set it up in such a way as to make it impossible to collect on the challenge.

  27. Dr Mike wrote:
    “Don’t know why the book isn’t doing better here. It gets a ton of clicks on the Amazon page, but not a lot of purchases. Probably because the comment that continues to remain at the top isn’t very favorable.”

    He’s too darned self-effacing to ask y’all to do it — but you folks who are describing how well you’re doing on the 6-Week Cure might consider dropping by Amazon and writing your results there too! I read your results here with a wistful sadness because I’m NOT having much luck (despite treating my thyroid for the past couple years; sex hormone treatment is next: maybe THAT will finally help!) — but reading all-y’alls results keeps me from giving up in total despair.

    Pay a little forward and help him sell his book!

  28. Dr. Eades,

    There are very many words in that post, but most of them are a waste of server space. Could you have possibly fit more weasel words into one article without rendering it meaningless? Would it be possible to use more inflammatory, suggestive, and misleading language in one article without outright calling Colpo a liar and a fraud?

    The comments by your cult followers, I mean supporters, are indicative of the kind of people who are persuaded by this nonsense. Please Dr. Mike, tell me how to think, so I won’t have to do it on my own! Please?!?!?

    Try posting an objective criticism of Colpo’s book without all of the hyperbole and demagoguery and then maybe I’ll start listening to what you have to say.


    Michael Miller

    1. Uh oh. You’d better be prepared. There is a whole bunch more weasel words, hyperbole and demagoguery coming up in my next and final post on l’affaire Colpo.

    2. Actually, this Eades guy has surprisingly nice things to say about Mr. Colpo’s book. Perhaps a bit of “[insults,] hyperbole and demagoguery” on the MA wars, but the nastiness-weighted IH&D(Eades) / IH&D(Colpo) ratio is something like 1/100, and I don’t think that I’m exaggerating. Colpo’s writing is really, really extreme.

  29. Nice job, Dr. Eades.

    More polite than your subject deserves and very convincing.

    False objectivity or pseudorigor ( a phenomenon we see in the application of mathematics to economics, for instance) is rife in medical research, and I am seeing a lot of it used by internet nutrition gurus.

    If we just read papers and toss out references without very critically evaluating them, we end up stuck with the lipid hypothesis (x number of papers and y number of experts say…) or justifying weird new theories we dream up that are implausible on the face of it.


    Your theory may or may not be true, but may only not have been proved wrong yet because some of us have not done the work to do so. I think the thing missing in your analysis is dynamic equilibrium – are TGs being assembled in adipocytes faster than lipolysis occurs – it is not an on-off switch here. FWIW I agree there are holes and oversimplifications in the GCBC description but it is much more right that wrong.

    1. Kurt G Harris MD said:
      “Your theory may or may not be true, but may only not have been proved wrong yet because some of us have not done the work to do so.”
      Please do. The more people that examine my theory, the better.
      However, according to the Carbohydrate Hypothesis, it’s impossible to gain significant weight/body fat on a virtually zero carbohydrate diet. It only takes n=1 to disprove a hypothesis. Dr. A and Jenny Ruhl have reported weight gain/failure to lose weight on a low-carb diet. Also note that Jazwaza is currently maintaining at ~200lbs on a very low carbohydrate diet.
      As the impossible has happened, the Carbohydrate Hypothesis is hereby disproved.

      1. This is the study Gary is trying to raise the funds to test. I agree that it takes only n=1 to disprove an hypothesis, and I’ve never claimed that any medical therapy or dietary therapy works the same for every single individual on the planet. There is simply too much biological variability. But, then again, we can’t let anecdotal evidence take the place of a controlled study, which I agree needs to be done. When you are a doctor treating patients, you try to design an therapy that you feel is going to have the greatest probability of helping the patient you’re working with. Over the years, I’ve learned that it’s the reduced carb diet that gives me the greatest chance of creating a good outcome.

      2. @Nige

        That’s not the way Taubes defined “the carbohydrate hypothesis” or at least that is certainly not the central point of Taubes’ long and detailed book.

        The carbohydrate hypothesis is simply the idea that there is some relationship between the diseases of civilization and “refined carbohydrates – sugar and white flour” to use the phrase Taubes uses over and over. The carbohydrate hypothesis is just the contrapositive to Ancel Key’s assertion that saturated fat is the cause of the diseases of civilization.

        Could you give me a page number where Taubes says that his “carbohydrate hypothesis” is that it is impossible to gain weight on a zero or low carb diet? I’m not saying there is no such quote, but if it is there it is hardly the main point of the book ( nor is the metabolic advantage) and I don’t recall where he said that. He does emphasize that net fat storage ceteris paribus is less with lower insulin levels but that hardly constitutes a claim there are no black swans does it?

        No offense, Nige, but this is biology, not engineering or physics. “Such and such never happens” is just not a claim that gets made a lot in biology and medicine

        Those of us with any clinical experience in this area see the results all the time. The question of whether LC is better than low fat or calorie restriction is better is interesting to some of us.

        The question of whether someone with an irretrievably damaged metabolism or Kluver-Bucy syndrome or a hypothalamic tumor can gain weight by overeating with low insulin levels may be interesting to you, but hardly would put a dent in the main point of Taubes’ narrative.

        Yes, I’ve encountered folks who have difficulty losing on nothing but meat and fat. Not a single one of them would have less difficulty or lose more weight if they ate 50 % of calories as carbs, though.


        1. @Dr. Harris

          I agree that the main focus of Taube’s book is to define the “carbohydrate hypothesis” as a relationship between refined carbohydrates and disease. However, he unfortunately titled his book “Good Calories Bad Calories”. Did he market it with the intent that many would perceive the book to be about weight control and boost his bottom line? Perhaps not, but I’m sure he understood the connotation. I wonder if your quote “the question of whether LC is better than low fat or calorie restriction is better is interesting to some of us”, means better how – in the realm of disease resistance or weight loss? My point is that all of the low carb [and paleo] books out there (many written by MDs) are marketed as books to control weight. Will yours? Because if you and others market a book to people with weight issues, the damaged metabolism should be of great interest to you; that is where the biggest questions lie and those are the people who really need your help. Lets put all you brilliant minds to solving that issue. Otherwise we can all agree — be mindful of calories, eat protein, stay away from bad fats and refined carbohydrates… and call it a day.

          1. @kb

            re: your post to Dr. Harris:

            The weight issue *is* the metabolic issue. There are very few individuals in my experience who’s overweight doesn’t also come with metabolic issues [maybe if they train, but exercise doesn’t bullet proof people]. Gaining weight is the sign that metabolic problems are at play, and losing weight pretty much fixes them. So there aren’t two targets: overweight people and damaged metabolisms; they are the same. However, the remedy is not often as simple as you suggest, which is the reason for all the work on dietary composition and the books which result from that work.

            Questioning whether Taubes named his book in a way to pad his bottom line by making it sound like a diet book frankly made me laugh out loud. I have colleagues who resist reading that book because it’s such a dense tome, and requires even professionals like me to read sections a couple of times to really get what he’s saying. I give that book to diabetic, metabolic syndrome and weight loss clients to read who look at me like why didn’t they hear about my lobotomy. I just implore them to read the first 50 pages, read the first 50 pages, and then they’ll be pissed off enough to keep reading. Even that doesn’t tend to work much. There are those of us in the field, and those with enough interest to hit the blogosphere and so maybe it looks like huge numbers are reading this work. But I’ve been working in weight loss for 20 years, and if it don’t have recipes……..

          2. About the title of the book, it was decided by his publisher – he complained about it in a podcast. His preferred title was “The alternate hypothesis”, but the published deemed it too stuffy.

            Plus, I am ready to vouch for there being “bad calories”, no matter if there is a metabolic advantage or not. I have just suppressed my cravings for Ben and Jerry´s with meat, salad and fat.

            After all, appetite is the key regulator of weight. Overeating on meat, vegetables and fat is hard. That is the major issue where good vs. bad calories come into play.

          3. If I remember correctly, US publishers chose the title. It was published in the UK as “The Diet Delusion”, which I think is a much more fitting title. “Good Calories, Bad Calories” make it seem like a diet book, likely a deliberate choice with the idea of selling more copies.

        2. My best friend is one of those people who gains (or fails to lose) weight on very low carb. She’s also gluten and (A1) casein intolerant, and avoids them. She pretty much sticks to rice for grains, and potatoes otherwise. The diet she does best on not too terribly high carb. Probably closer to Kwasniewski than other plans, and certainly not 50% carbohydrate.

          My stomach HATES (HATEHATEHATEHATES) most plants, so I’m a meatitarian/dairivore myself. We can still eat meals together.

        3. On page 217/390 in my electronic copy, Taubes wrote:-

          “Just a few more details are necessary to understand why we get fat. The first is that the amount of glycerol phosphate available to the fat cells to accumulate fat—to bind the fatty acids together into triglycerides and lock them into the adipose tissue—also depends directly on the carbohydrates in the diet. Dietary glucose is the primary source of glycerol phosphate. The more carbohydrates consumed, the more glycerol phosphate available, and so the more fat can accumulate. For this reason alone, it may be impossible to store excess body fat without at least some carbohydrates in the diet and without the ongoing metabolism of these dietary carbohydrates to provide glucose and the necessary glycerol phosphate.”

          O.K. He wrote may be, not is. I’m not disagreeing with the other 99% of his book.

  30. I’ve never heard of the word seppos used by anyone here in Australia. I probably over-reacted on the comment chip on both shoulders.

    Anyway, GLUT-1 are distributed within the following tissue – erythrocytes, fetal tissue, placenta, brain blood vessels.
    GLUT 4 – muscle, adipose tissue.
    Just about to start nutritional biochemistry unit.

  31. I laughed as I read your description of what typical subjects of such studies must be like. You see, I participated in a hospital guided fast/study, and every week after our meeting and weigh-in, I drove to Modern Pizza in New Haven and ate a whole grated cheese pie, by myself. After all, I was starving, consuming only 500-800 calories a day in the form of a low fat protein shake, for weeks — indulging in that thin, crispy, cheesy, greasy pizza was a sensory experience like no other; madone! Why would I have been so stupid, you ask, as to interfere with the efforts of all involved, especially my own? I like to think that it’s the dumb ones that always do as their told. ☺

    1. After finally having had my first taste of a real Frank Pepe tomato pie this week (I spent my 30th birthday way off my meat-only diet, on a burgers and pizza tour of Connecticut), I can easily see why.

      Actually, between b-day celebrations and Mardi Gras, I’ve been eating bread, pasta, and sweets for about five straight days now, and I really can’t wait to get back on the straight and narrow. My allergies have been really acting up lately, and I doubt that it’s just a coincidence.

  32. Thanks for finally posting this!!! As usual, you did an excellent job of putting it all in easy to understand language!!

    Notice you’re commenting a lot though!!! LOL

    As to the poster who noticed the typo in the ad! I love it!! One of my pet peeves, and I missed it!

  33. I hate to admit I’ve lost interest in this whole thing with AC. I’ve learned that there are some people that simply have to have attention focused on themselves at any cost, and there is no point fighting their fight. In any case, I always read your posts because I value your clear discussions of complex biochemistry and also your insight as a practitioner.

    I wanted to point out a section that might need clarification. You wrote, “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.” At the beginning of this post, you pointed out that metabolic ward studies didn’t necessarily have the subjects 24 hours a day, only metabolic chamber studies. As long as you’re taking all this time to refute AC’s position, let’s not give him any footholds to respond.

    1. I, too, had lost all interest in the AC debacle, which is why I hadn’t gone to the trouble to do an exegesis of his book. But he reared his head recently, and several readers wrote me asking about the promised refutation. So I put in the time and did it so I can put it behind me.

      As to your other point, some studies conducted in metabolic wards do keep subjects in for 24 hours, but not all. That’s why it’s important to try to figure out what the author’s of any paper mean when they refer to metabolic ward studies. Some are 24 hour inpatient, some are check in at night only and some are come in for a few days at the start of the study then finish it at home. You just need to know what you’re dealing with because there is no firm definition of a ‘metabolic ward’ study.

  34. Dr Eades,
    I am a personal trainer and I have recently found your blog thanks to a few sources. I am reading Good Calories, Bad Calories and doing a lot of research on carnivorous diets in humans. I usually prescribe high-fat, high-protein, Paleo-style diets to my clients and friends, but I have encountered two cases recently in which doctors have restricted protein intake due to nephritis (one has lupus nephritis and the other is an 80 year-old client who suffers from chronic heartburn and kidney problems). Have you encountered troubled with nephritis in your practice? It seems as if high protein diets are not the cause of the nephritis, but is it safe for people with nephritis to eat a high-protein, high-fat diet?

    1. It is safe for them to eat a high-fat diet. I always put patients with compromised kidney function on adequate, but not high, protein diets along with plenty of fat while keeping carbs low.

  35. I have taken a course in thermodynamics. I teach a section about it in biochemistry. Gary Taubes has a Bachelor’s in Physics (you have to have had thermo to earn that degree in that subject). Thermo is actually a pretty neat topic if you ask me. If humans were furnases and only turned what we eat into heat (and not every last bit of it either, there is always waste), then indeed a calorie would be a calorie would be a calorie. But we are not heaters and we are not ‘bomb calorimeters’ from a thermo lab. We do not defy any of the 3 laws of thermo- EVER. The animal fat we consume supplies the body and brain with hormones, neurotransmitters, membrane material (100 trillion cells with 100 trillion membranes) and the structure and substance for the maintenance of our big constantly changing, working, adapting, ‘growing’ brains. The neurotransmitters turnover and need replacing constantly, second by second, day after day, year after year, our entire lives. The brain needs fatty fuel……, AND structural fat fat fat fatty substance.
    Please, Good Dr. Eades, you have to read “The Other Brain” by Douglas Fields, PhD. It’s about the 85% of our brains that are glia and not the more attention grabbing (and of course important) neurons. We are indeed FATHEADS.

  36. Dr Eades,
    I was around for the origional debate and this is terrific! I, for one, am happy that you have addressed this guys work and it’s flaws. He is such a snotty whiner! It’s irritating and not very professional so it makes taking him serious very difficult. Thank you, for the detailed critique and for the full text links!

  37. Perhaps AC will respond better to a theoretical approach:

    If we expand the energy balance equation slightly we get:
    Delta Fat Weight + Delta Protein Structures Weight = Calories in – Calories out (1)
    Equation (1) has four unknowns; we therefore need three more equations to obtain a solution. Most “authorities” add the following three (unstated) equations:
    Delta Protein Structures Weight = 0 (a)
    Calories in = Arbitrary Constant, C1 (b)
    Calories out = Arbitrary Constant, C2 (c)
    With these substitutions, Equation (1) becomes
    Delta Fat Weight = C1 – C2 (2)
    Equation (2) looks so simple, but it is wrong, because (a) is wrong (People on the Auschwitz Diet had severly depleted protein structues.) and (b) is wrong because it denies the effect of hunger.
    Equation (1) is the very small tip of a very large iceberg; I think it is the core of a very large (many hundreds) system of simultaneous equations, many of which will be non-linear and will contain parameters specific to a particular individual.
    Lots of luck in your attempts to talk sense to AC.

  38. Since the low-carb diet is protein sparing it would be truly remarkable even if the weight loss were identical for the low-fat diet. The low-carb dieters should end up with a much larger total energy loss than the low-fat dieters for identical weight loss. The energy content of fat is 2+ times that for protein and CHO. The nutritional and even the medical community want to ignore feedback mechanisms that promote homeostasis. The prior statement can be generalized beyond weight loss to cholesterol values to even control of high body temperatures. It is much more important for survival to reduce metabolism if one is losing one pound of protein as opposed to losing one pound of fat. Perhaps the nutritional community should focus more on losing body energy content instead of losing pounds.
    This subject also brings to mind about what kind of diet would be optimum for maximum survival times for a severe caloric restriction. It would seem that a high carbohydrate diet would depress the metabolism more and allow one to lose less energy content. Perhaps this might be one of the few scenarios where a high-carb diet would be superior. But what would I know. I am not a nutritionist, I am only a physicist.

    1. Your last paragraph is thought provoking. I’m sure that in Paleolithic times meat was the preferred food. It would be only when meat wasn’t available that early man would turn to carbs for energy, which would be during lean times foodwise. It would make sense then that carbs would depress metabolism, allowing the body to spend less energy to survive the lean time.

      1. Just the opposite, in fact. T3 levels are reduced as one cuts carbs from the diet. T3 is the primary hormonal regulator of metabolism.

        I can verify this from personal experience. Whenever I go low carb, I become more cold sensitive, and have to jack the furnace up 4-5 degrees to compensate in winter.

        The theory is that, since T3 is catabolic, it’s levels are reduced (and thus metabolism) during low carb periods in order to preserve the precious muscle protein which is going to be needed to fuel gluconeogenesis for those few tissues that absolutely must burn glucose in order to survive.

        1. Hmm… John, my experience is the opposite.
          Whenever I eat low carb, I become hot as an oven!
          My cold tolerance has gone up considerable ever since I started to eat low carb more or less regularly.
          My parents can’t even stay in my room because they think it’s freezing and I find the rest of the house almost too warm.
          I also used to have ice cold hands and feet, but no more.

          1. Same here, I am much more tolerant of cold now! Also, my joints seem to feel better. And here all I was trying to do was lose weight (that’s happened, too)!

          2. Ha! Exactly this. I not only feel too warm even when it’s cold, I start acting like a walking space heater. Nobody wants to sit anywhere near me because it gets too hot. I warm ice cold rooms enough that people comment. Walking outside in the summer results in overheating so severe I need to take an ice cold shower (or bath with ice) to cool off.

            It’s really funny.

        2. The implication that high-carb diets would increase T3, thereby ultimately increasing metabolism, would then imply that an isocaloric high-carb diet would cause more weight loss than a low-carb diet. There is an interesting article that would imply the opposite. The abstract is on PubMed:

          Isocaloric carbohydrate deprivation induces protein catabolism despite a low T3-syndrome in healthy men.
          Bisschop PH, Sauerwein HP, Endert E, Romijn JA.
          Department of Endocrinology and Metabolism (F5), Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. P.H.Bisschop@amc.uva.nl
          Clin Endocrinol (Oxf). 2001 Jan;54(1):75-80.

          1. I too, am interested in the relationship between T3 and macronutrient composition. I recently read this paper, which is a review of the lit focused on iodine deficiency disorders, but has relevance to this discussion:

            Koop, Wolfgang (2004). Medical Hypotheses 62, 871-875.

            From the abstract:

            “An increased iodine requirement as a result of significant changes in human nutrition rather than a decreased environmental iodine supply is suggested to represent the main cause of the iodine deficiency disorders (IDD). The pathomechanism proposed is based on the fact that serum concentrations of thyroid hormones, especially of trijodothyronine (T3), are dependent on the amount of dietary carbohydrate. High-carbohydrate diets are associated with significantly higher serum T3 concentrations, compared with very low-carbohydrate diets. While our Paleolithic ancestors subsisted on a very low carbohydrate/high protein diet, the agricultural revolution about 10,000 years ago brought about a significant increase in dietary carbohydrate. These nutritional changes have increased T3 levels significantly. Higher T3 levels are associated with an enhanced T3 production and an increased iodine requirement. The higher iodine requirement exceeds the availability of iodine from environmental sources in many regions of the world, resulting in the development of IDD.”

            They then go on to say: “The sharp decline in T3 levels as a result of very low carbohydrate diets is not associated with a reduction in the resting oxygen uptake, or symptoms of functional hypothyroidism (cold intolerance, dry skin, increased need for sleep). Despite decreased decreased T3 concentrations, basal TSH levels are normal or even mildly decreased. The lack of clinical symptoms, together with normal or mildly decreased TSH levels suggest that the organism does not suffer from a deprivation in thyroid hormone in association with carbohydrate restriction……..indicating that the metabolization of dietary carbohydrate is a thyroid hormone consuming process.”

            As a thyroid patient and an exercise physiologist who looks at a lot of folks’ labs, I also have questioned these findings regarding higher carb diets and the metabolic drive on T3. But all of my thyroid clients [and me] can only lose weight on carb-restricted regimens, and some don’t even get results until they push it quite low, either at or near ketosis [and carb-rich isocaloric diets do not work, so it’s not a question of calorie reduction]. I have a couple of folks doing Volek’s Phase 1 [ketogenic but food not shakes] who are due for bloodwork and we’ll see the T3 results. What I now wonder is whether T3 levels are so directly related to things like body temp or if this relationship might be more complex.

          2. I am very familiar with the above paper. (This same author has a series of papers in Med Hypoth that I’ve enjoyed.) When it came out I went through some old patient data that I still had, but wasn’t really able to tell if thyroid had changed much in those on low-carb diets. Problem is, I didn’t check serial thyroid levels. I checked on the first visit, then didn’t have a thyroid panel as part of my recheck labs. Only those with thyroid problems going in got rechecked.

            If I had rechecked, I probably wouldn’t have noticed anything since, according to this article, TSH doesn’t go up as the T3 goes down on a low-carb diet. The paper does make sense, which is why it prompted me to go back and recheck my data. I plan on posting on this paper as part of a longer post on low-carb and the thyroid.

            Keep me posted on the lab results you get as they come in.

          3. So if TSH doesn’t go up whilst T3 goes down on a low-carb diet then the hypothalamus and anterior pituitary don’t see it as a problem?

        3. I also am much more cold tolerant since I cut the carbs. My hands and feet also aren’t constantly cold like they used to be.

          1. There is research out there that shows the link between carbohydrate intake and T3 levels in very low calorie diets.

  39. Dr Richard Mackarness died in 1996 at the age of 81. Among other things he studied and warned against food additives which became prevalent during his life, and wrote a book on this, Chemical Victims, in 1980.

    But, he was also ahead of the curve in another area: the paleo diet. In 1958 he released a book, Eat Fat and Grow Slim, which presented his “stone age diet.” This book is online here: http://ourcivilisation.com/fat/ (A quick summary of the diet is here: http://ourcivilisation.com/fat/guide.htm)

    There’s little difference between it and the now recognized paleo diet. It avoids grains and high-starch foods. And, it promotes all animal meats and fats. In the book’s first chapter, we have this:

    —– Begin Quote —–
    “This book explains that there is. To-day a lot more is known about how fat people get fat and why. Many of the facts have been known for years, but because they have not fitted in with current theories on obesity, they have been ignored.

    “In the last ten years, however, atomic research has given the physiologist enormous help in unravelling the biochemical reactions which go on in the body.

    “Radio-active isotopes have been used to ‘tag’ chemical substances so that their progress through the body could be followed, in the same way as birds are tagged in order to establish the paths of their migration.

    “By this means, details of the metabolism of fats and carbohydrates, previously shrouded in mystery, have been clarified and with the new information so gained old experimental findings have been given new interpretations and the jigsaw of seemingly contradictory facts about obesity has clicked into a recognisable picture.

    “The first thing to realise is that it is carbohydrate (starch and sugar) and carbohydrate only which fattens fat people.”
    —– End Quote —–

    Dr Mackarness also explains something that most doctors even today STILL DO NOT GRASP:

    —– Begin Quote —–
    The beauty of this method of slimming is that once you have got the hang of the proportions of fat, protein and carbohydrate in the foods you choose to eat, you can afford to ignore calories altogether. The much publicised diets with emphasis solely on calories are fallacious. It is excess carbohydrates and not calories only that make a fat man fat.”
    —– End Quote —–

    BTW, this was all later explained with far great scientific evidence in the much more recent book, Good Calories Bad Calories.

    Dr Mackarness knew about the metabolic advantage 50 years ago, along with many other doctors of his day.

    (This comes from my original Immortality Institute forum post in Dec: http://is.gd/8aKEU )

  40. thank you so much for taking the time to put up so much great info and for all your research!!

    my problem has never been with weight loss, my problem has been with frequent urination. starting in my early 20’s. for the past 10 years i have been to multiple doctors and urologists. ive been tested for diabetes and for prostatitis, and many many other things. but nothing ever really helped my frequent urination. until i did some research about my diet.

    my previous daily diet was about 100g of sugar, 5000mg of sodium, and about 350g of carbs, about 15g fiber. reading all the research out there its amazing i’m not very very ill right now. but like i said i’ve never really had trouble with my weight (being 6’5 200) and i believe my frequent urination had to do with insanely high sugar levels. and i’m sure i was developing diabetes or hypoglycemia.

    my question is i’ve changed my levels of food and types of food dramatically cutting out sugar 0g, fiber 30g, sodium 1700mg and carbs about 115. my question is this healthy for someone who is fairly active 6’5 tall or should these levels be lower or higher? i’ve only been working on a diet set up like this for about two weeks but have already had a few nights of not having to get up to go to the bathroom (the first few nights in about 10 years!!)

    i thought i would ask because most of the roads i have been travelling on the net have lead to your info repeatedly so i thought it was worth a shot.

    big thanks in advance for any advice and big thanks also for the critical info you are putting out!!

    1. The diet as you’ve structured it sounds fine to me. If you were trying to lose weight I would recommend a little more carb restriction, but since you don’t need to lose weight and since your problem has – at least in this short term – been solved, the carb level is probably fine. You may be a person who has a low threshold for kidney retention of sugar. If your blood sugar goes up a bit, you may be spilling it into the urine, a situation that will make you urinate constantly. But, having said that, you really need to get a workup from a physician who truly understands diabetes and the nutritional management of the disorder. I have very little history to go on here, so I’m basically taking a shot in the dark.

  41. “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. ”

    Huh? Do you mean to imply that burning an average of 200 calories/day more has a different impact if caloric consumption is in the 1500-2000 cal range than if it is in the 2500-3000 cal range?

    1. Yep, that’s what I mean. But it takes too long to explain why in a comment. I should probably post on it at some point.

  42. Dr. Eades,

    Do you have any studies on hand that look at “fat” loss rather than merely “weight” loss. Weight loss isn’t all that interesting. I’d like to see some information on fat loss and retention of lean body mass while dieting. Do you have any studies on hand that compare low-carb diets to high or moderate carb diets, and take into account fat loss, lbm retention, and/or use devices like DEXA scans or hydrostatic weighing or at least calipers? I’m genuinely curious about this issue. Thanks a bunch.


    Michael Miller

    1. I don’t have a bunch of different studies at my fingertips right now, but most of the studies in Colpo’s list show exactly what you’re looking for. A number of them were done to explore this very issue. Even AC agrees – based on the literature – that low-carb diets result in less lean muscle loss and greater fat loss than low-fat, high-carb diets; he just doesn’t believe there is any weight loss differential.

  43. ‘Protein Power’, ‘The 6 Week Cure’, Eades, ‘Good Calories, Bad Calories’, Taubes ‘The Vegetarian Myth’, Keith, and ‘The Other Brain’, Fields, are all fantastic, paradigm changers for me. I’ve read much more since it all started for me with Taubes, June 16, 2008, but these books are the spectacular sparks.

    1. Colpo’s “The great cholesterol Con” should also be on that list. As Eades has mentioned, it’s worthwhile and is the reason, I suspect, that Eades spends anytime dealing with Colpo.

  44. Dr. Eades,

    I’ll take a look at the studies that Colpo posted, thanks.

    A few minutes ago I read the Feinman and Fine paper that you linked. I’m still confused as to how the info about TEF relates to the 2nd law and the metabolic advantage of low-carb diets. If the TEF for the macronutrients look like this protein > carbs > fat, and the TEF of protein is several times greater than the other macronutrients, then wouldn’t the protein content of the the diet be the most important feature with respect to metabolic advantage?

    Given what the Feinman and Fine paper say about the relative TEFs of the different macronutrient types, I guess I’m confused as to how a low-carb, moderate-protein, high-fat diet will show a metabolic advantage over a moderate-protein, low-fat, high-carb diet if both dietary treatments contain the same number of grams of complete protein and the same number of total calories.

    Thanks in advance for clearing this up for me.


    Michael Miller

    1. I think the TEF of food is a small, small part of it. It’s more of a different pathway thing. You can think of it in this way (it’s kind of a dumb example, but it is illustrative). (1) Let’s assume you need to pick up three things from the grocery store. You leave your kitchen with list in hand, drive to the closest store, grab the three items, drive home and end up back in your kitchen with the three items. (2) You leave your kitchen with list in hand, drive to the nearest store, but find only one of the items you need. You get back in your car, drive the next nearest store, find (unfortunately) only one of the other two items you need. You purchase it and drive to yet a third store to get the last item. Finally, you end up back in your kitchen with the three items you went out to get. Now, in comparing these two examples, you started at the same place (in your kitchen empty handed) and ended up at the same place (in your kitchen with the three items), but you expended a lot more energy to get there in the second example.

      Your body uses glucose. If you get it from food, you absorb it into the blood, it is transported into the cells where it is used. If you don’t get it from food, the liver has to make it from amino acids, from the glycerol stripped from triglycerides or from a few other substances. The gluconeogenic process consumes a much greater amount of energy to provide the same amount of glucose than does simply the absorption of glucose via the GI tract.

  45. Great post, thanks! There is a famous story about a student who goes to learn about Zen studies. I forgot how it goes but the basic idea is that a Zen teacher asks a student if he wants a cup of tea. A student said yes and a teacher kept poring without stopping untill all tea spilled over the table and the floor. To make a short story long the teacher told the student that before you are ready to accept new info that might totally shake up your old belief system your cup or brain cant be overfilled and should be somewhat empty metaphorically speaking. Even after seeing much improvement in my brother in law health markers his doc still thinks its dangerous in a long run. So he convinced my brother in law to go back to his old so called way of eating except cutting calories. So he is way to his old way of feeling hungry and miserable! Oi wey! And about the Australian joke, come on!

  46. Hey Cassandra (er, that is, Dr. Mike),
    You’re not alone crying truth to the world! Here’s someone else who actually looks at studies published in the lit. and reports on their flaws and … funding effects.

    (Jenny over at Blood Sugar 101 wrote:)

    “First off, ignore the article’s title. As is becoming more and more common, the titles of research studies are being slanted to appeal to whatever the fashionable belief of the year might be in diabetes research. And as is also common, that fashionable belief is heavily influenced by the mechanisms used by whatever new drugs are being peddled by Big Pharma. Since right now incretin drugs are the hottest (i.e. most expensive) new drugs, the researchers pitched this article as if it was a study documenting the effect of the defective TCF7L2 gene on incretin hormones. In fact, its results show something else entirely.

    What the researchers did here was take eight subjects with the specific variant of the TCF7L2 gene that has been linked to Type 2 diabetes and compare them to a group of 10 controls lacking this gene variant. The tool used was a fancy 5 hour glucose tolerance test. (Yes, I know this is a pitifully small sample which makes its result suspect, and thanks for noticing.)”

    Here’s the article/entry URL:

    She starts with this interesting info:

    High quality research suggests very strongly that most Type 2 Diabetes results from genetic damage. This damage may be inherited or it may be caused by environmental pollutants like arsenic, PCBs, pesticides and popular prescription drugs. The environment of the womb can also permanently alter the expression of certain genes in ways that promote the development of Type 2 Diabetes.

  47. Dr. Eades, I found this comment following an article Jimmy Moore wrote about the Colpo incident way back in Aug of 2008 on WellSphere.com. I thought the comment was right on the money…

    btw Dr. Mike I’m curious, why is Colpo on the TOTAL HEALTH BREAKTHROUGHS “board of experts”? And, do you think he “plays nice” with the opposition? LOL

  48. good god, the first thing i saw was a glaring “their” in place of “they’re”.

    i’m sure others had noticed it too, but mediocrity is depressing.

    1. I had a different reaction to the quote: it meant

      “This way of learning is so much “fun” they will not “know” the material at the end of it” OR “So much distraction that the child is amused but not educated”.

      Either way, I would never have bought the product!

    2. Shel, are you referring to this line?

      “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.”

      “Cheating” is clearly a noun here; “their” is completely correct.

      1. ‘Cheating’ is a gerund. Gerunds and gerund phrases (any phrase starting with a gerund) take the possessive. So ‘their cheating’ is absolutely correct.

  49. Totally off topic, but I didn’t know how to let you know otherwise…

    Your link to to LowCarbCookworx.com takes users to a parked domain page. The site is now gone. Did the domain name not get renewed on purpose?

  50. Hoards of females still awaiting clarification on 6 Week Cure’s hormonal/weight challenge. Well, one hoard, anyway.


  51. Just wondering if you thought that a paleo-type diet would be harmful to a gout sufferer? Seems like the high purine content of hunter-gatherer diet would spike uric acid levels.

    1. Could be a little problematic in the switching over, but not always. As far as I’m concerned, I feel the low-carb diet is the best treatment out there for gout. It’s what I used very successfully with all my gout patients.

    2. According to this article by Dr Georgia Ede https:undefinedundefinedwww.diagnosisdiet.comundefinedfull-articleundefineddoes-meat-cause-gout the dietary advice commonly given for the relief of gout actually exacerbates it & the foods that people are advised to avoid would actually be beneficial.

  52. Colpo and I have exchanged some verbal fisticuffs in the past.
    He still will not talk to me unless he wants to sell something.

    Because I question him on some topics he feels threatened
    and resorts to abuse.

    Abuse I do not mind, he is an Australian. I am a New Zealander.
    We know how to deal to loud-mouth Australians.

    This a pity because his book “Cholesterol Con” was very well researched. (That is a compliment AC)

    It is a shame that he did not apply the same critical analysis
    to the notion that “a calorie is a calorie” notion. Probably has something to do with his “body building” obsession.

    Mind you if building the perfect body is your goal the truth about metabolism is probably irrelevant.

    Gossip around the gym is more likely to be accurate.

  53. Good day, mr. Eades and greetings from Bulgaria.

    Can I ask you for a study that shows the 100-300 calories metabolic advantage of a low carb diet against a low fat diet?

    Petar Sturm Konstantinov
    Sofia, Bulgaria, Europe

    1. There are no specific studies that I know of that identify the metabolic advantage at 100-300 calories. That’s the number I’m estimating based on the many studies I’ve read over the years. Thanks for writing.

      1. We have a joke here in Bulgaria, stating that the facts ruin the arguments…
        The jokes aside, thank you for your answer and good luck!

        With respect
        Petar Sturm Konstantinov
        Sofia, Bulgaria, Europe

  54. Hello Dr. Eades,
    great post, as usual. Love your blog and appreciate the time and effort you are putting into it. It has benefited me a great deal.
    Two somewhat unrelated questions, though:
    – From the comments on your post “Metabolism and ketosis” it appeared that there was a lot of confusion as to how RDAs for protein relate to LC or even ZC diets. You kinda promised to follow up on that in a later post, but that never seems to have materialized (though I may have missed it). Anyway… Does the amount of protein additionally required for gluconeogenesis have to be counted on top of those (and your) recommendations or is it already part of that with enough left over for maintenance and building more muscle?
    – Secondly, I’ve read all your posts on intermittent fasting as well as some other material. I’ve been doing it for almost three years now, but that was mostly before I went LC. What I can’t figure out is whether or not IF has any beneficial effect that is not directly or indirectly attributable to a relatively low level of insulin for most of the time. In other words: If I’m not eating the bad stuff in the first place (LC), does it still matter when or how often I eat (IF)?

    1. I really do need to write a post on the protein issue. I’ve spent enough time answering it in the comments to have written five posts on it.

      It takes about a gram of protein to make from 0.7-0.8 g glucose. Most people require around 200 g of glucose per day to feed those cells that use glucose. Around 70-80 g of glucose can be replaced by ketones, so when one is in ketosis, the glucose requirement drops to 120 g per day. If one gets, say, 50 g of glucose per day from a low-carb diet, that leaves 70 g of glucose that must be provided via gluconeogenesis. If one is losing fat on the low-carb diet – which usually happens – 15 percent of the fat is glycerol, which can be made into glucose. So lets say that our theoretical dieter is losing one kg per week of fat – a reasonable assumption. That 1 kg of fat per week would provide about 40 g of glucose per day from the glycerol. If we subtract that from the 70, we end up with roughly 30 g of glucose that must come from protein. At 0.7 g glucose per g of protein, that equates to about 45 g protein just for substrate for gluconeogenesis. Protein required for repairing wear and tear is probably 50 g or so, which means that on a diet of 50 g carb per day it takes about 100 g of protein to prevent muscle loss.

      There are supposedly advantages with the IF, mainly the increased production of BDNF. But, I, myself, follow an LC diet and eat only when hungry. So I go long periods during the day without eating, which makes it sort of a combined LC IF diet.

  55. Sirs Hola..is Apheresis when removing platelets any better at getting rid of POPS than doing the fast and drinking caffeine etc..
    The local blood oiks are pushing to do this presently

  56. Thanks for the post, Mike.
    As you said in an earlier comment “Even AC agrees – based on the literature – that low-carb diets result in less lean muscle loss and greater fat loss than low-fat, high-carb diets; he just doesn’t believe there is any weight loss differential.”
    I am confused why AC thinks that greater fat loss and less muscle loss isn’t a metabolic advantage… it sure sounds like a major advantage to me!

    1. There is no doubt it a major advantage, but not in the classical sense of a metabolic advantage. As AC sees it, a metabolic advantage exists when two diets of the same caloric value result in a weight loss differential. The one providing more weight loss (not necessarily fat loss) is the one that is said to have a metabolic advantage. This is how AC defines it, but he doesn’t believe it exists. Mainly because of these studies listed in his book.

  57. Good post.

    Do you mind stating what you consider the carb range in grams to be for a

    VLC diet
    LC diet
    Moderate carb diet
    and where a high carb diet starts?

    1. As far as I know, there are no generally accepted standards for these classifications. I would say that a VLC diet would keep carbs at below 20 g per day. A LC diet would keep carbs below the 60-70 g per day range. I would call, say, 75-150 a moderate carb diet, and anything over 150 (especially over 200) g per day a high carb diet. But that’s just my classification.

      1. Thank you very much for providing me with your opinion of the range of VLC to HC. I understand there are no generally accepted standards. In light of that I think your opinion is probably the best guide I’m going to get.

  58. Re: http://bit.ly/bGny3f – The potato and butter study.

    I read it with interest and sent the following comment to the Journal of Nutrition.

    “This study had 32 subjects. It seems to me that a 3 way crossover design between the 3 “fats” would have given a much reduced variance on the result reported – by in effect, providing the possibility of testing whether the order in which the “fats” were ingested had any bearing.
    The extra cost of providing the subjects with 3 meals, and doing the “bloods” 3 times was surely not a consideration?”

    One of the most obvious ways of getting statistical significance is to reduce the variance of the “material” upon which “tests” are being made.

    When comparisons are being done, then the tests ought to be done in some order on subsets of all the subjects, not just one test on one subset.

  59. Thanks for such a great site. I will purchase my next book from you via the link here. I just got Protein Power.
    I would be so grateful for some quick feedback. Is it possible that the metabolic advantage (especially given that it is quite small) doesn’t really exist for those that are already slim and just want to lose a few pounds (and just stay slim in general)? I’ve tried the low carb diet so many times without luck. In fact, the one time I was really serious about it for a week, I actually gained weight despite eating around 500-800 cals. In fact it was until I finally gave up and had a high carb day that I lost some water weight and felt slimmer the next day. Admittedly, I’m still fat phobic so I was eating mostly low fat protein (chicken breast etc.) and greens. What gives? I’m totally convinced though after reading Taubes book at least twice and so much about your book and philosophies. I want to live this lifestyle but in practice it’s been disappointing. 🙁 THANKS!!

    1. I think the metabolic advantage is more a function of a sort of caloric sweet spot, which is itself a function of an individual’s weight. Without a whole lot more info, I couldn’t say why you would gain weight on a low-carb diet in the 500-800 calorie range. The only thing I might even speculate is that the increased protein went to build muscle, which would be the case had you been protein deficient for some time. But, that even seems doubtful at a starvation range of calories.

  60. Will you be commenting on Clinton’s needing stents after his bypass surgery? I remember reading here that he was a follower of Ornish. Seems to good to pass up.

    1. I don’t know if I will given all the other posts I’ve got on the schedule right now. It is almost too good to pass up, though. I did post on it – in a mini post – on Twitter.

  61. Dr. Mike, for whatever its worth, I [respectfully] have to tell you I am not crazy about the comment section of your post. I usually welcome change if it is for the better, but it seems a bit overkill right now. I like the concept of being able to comment on comments directly, but it is difficult to follow new comments without going through the whole thing looking for latest dates. It seems a bit cumbersome. Maybe simpler is better?

    1. I’m starting to feel the same way. It’s great for me because I can answer the comments so easily. But it’s a real pain when I have to go back and look for something myself. I’ll try it a little longer before I make another change. Maybe I (and you) will get used to it.

      Any others with strong feelings about it out there?

      1. The only way I can keep up is by just reading the comments via email as they come in. Otherwise just looking at the blog your website I’d never be able to see all the new responses.

        I wonder if there is a wordpress plugin that allows comments that haven’t been seen by you to be highlighted or surrounded by a colored box or something. It would be done either using cookies or by logging in or something.

        If not one should definitely be created.

      2. I think it is important to have the format easy for you to answer comments. We need to keep you engaged or you might become distracted and go off inventing some new contraption again. ☺

        I’ve resorted to reading comments via email also. Because of this, I actually read the comments more so than I would have previously – just have to remember to check the notify me box.

  62. My grandmother used to say, “It’s good to try and help people, but there’ll come a time where you might have to just step over them and keep on going.”

  63. Great post, but I am a bit confused. I’ve been doing pp for about the past 3wks, doing well but need 40g/protein/meal. However, after reading Barry Groves, Eat Fat Get Thin, he states that this might be too much protein and states a 70/20/10 regimen is better. I have 150lbs to lose and don’t want to mess up by converting the protein I eat into “carbs” by my liver. Am I reading this correctly or am I missing something. Thanks for the help.

  64. Dr. Eades,

    Correct me if I’m wrong but nearly everyone of those studies taken from AC’s book had the subjects on severe calorie restriction which would cause a massive slow-down in their overall metabolic activity. So, under those circumstances wouldn’t that inherently skew the results towards depressing the effects of the different diets? In other words, the effect of metabolic slowdown would dominate and the differences between diets be suppressed. This would exaggerate the natural variability of individuals and lead to the conclusion of ‘no statistical significance.’ Would you agree?

    Worse then that, the only study where people ate something close to a normal amount of calories he reinterpreted Rabast’s (1979) data to, in effect, throw it out and give it the big thumbs down on Metabolic Advantage, when the data clearly shows a greater amount of weight loss on the low-carb diets. Wow.

    I live by the motto that the two most prevalent things in the universe are not hydrogen and stupidity but rather hydrogen and the human capacity for self-delusion.

    Thanks for all the great work. I lost nearly 20 pounds on the 6-week cure and have a much better understanding of my body’s dietary limits. Best to MD. Be well.


    1. You are correct in that virtually all of the macronutrients go toward caloric burning in extreme calorically-restricted diets. I would expect an 800 cal diet of all carbs to be no different than an 800 cal diet of all fat. But, if you read these papers AC uses as the underpinnings of his thesis, even lower-carb diets at those levels of calories show some metabolic advantage in certain individuals.

      Glad to hear you’ve done so well on the 6WC.

  65. Some problem with the link to paper “Rabast et al 1981”. It’s the same link of “Rabast et al 1979”. Thanks.

  66. There is a metabolic advantage though, heres a study of rats fed either Crappy (High Fat/High Carb) diet, Ketogenic diet, or Calorie Restricted.

    “Animals fed ketogenic diet ate the same number of calories as animals that were fed either chow or a high-fat diet but nevertheless failed to gain weight. Remarkably, animals eating ketogenic diet lost a small amount of weight and achieved the same weight and body composition as animals that were calorie restricted to 66% of usual daily intake. ”

    It’s a pretty good article they test a lot of differences between the diets, insulin, testosterone, etc. But the more interesting thing is they also do genetic analysis to see what genes are active in the mice. One I found particularly interesting was gluconeogenesis:

    “Furthermore, fatty acid synthesis, cholesterol synthesis, and glucose-handling pathways were reduced in ketogenic diet-fed animals. Additionally, critical enzymes of gluconeogenesis, PEPCK, and G-6-Pase were suppressed, consistent with the reliance of these animals on ketones and fatty acids as energy substrates.”

    As much as there is the belief in some of the low carb community that if you eat too much protein it can be converted to sugar, when in a ketogenic diet, you aren’t really using the gluconeogenesis pathway.

  67. “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. ”

    This contention is just preposterous. Logically, this doesn’t make any sense and I don’t see you presenting any proof to back this up either.

    I’ve myself been a part of a metabolic ward study. I can tell you the chances of cheating are slim to none and you’d have to go far to cheat. We were never permitted to leave the compound unsupervised. ALL the food we had were given and prepared to us individually by the staff there. Patients and visitors were instructed that cheating was forbidden (under threat of not being paid). The only way of cheating would have been if the visitors brought food, but then this would mean that if you got caught you would receive no payment (which was quite a substantial amount of money). They even checked our damn bags for food when we arrived.

    This part of your post aside – this whole post just seems like a disingenuous attempt to discredit Colpo.

    1. As you can see from one of the comments above, not all people who enter metabolic ward studies stick to their program.

      Since the program you were a part of was so strict, it must have generated some very good data. Can you give me the citation for the paper(s) published. There must have been at least one because no one goes to this expense and doesn’t publish. I’m eager to hear.

      And you are right, the whole post was an attempt to discredit AC. It just wasn’t disingenuous. I was right up front about it.

    2. Are you sure you are not AC? 😉

      Were you part of a MW study or a MC study? Sounds like you were part of a MC study. However, your MW study might be one that was strictly controlled. The point is that not all are.

      You are not what you eat. You are what your body does with what you eat. AC lacking formal nutritional education can only argue from a layman’s perspective. He thinks he knows, but the fact is he doesn’t know much WRT nutritional science. And because he thinks he knows he’s rendered himself ineducable on this subject.

      Do you really think a 30+ year old personal trainer with an axe to grind with virtually everyone who disagrees with him is as qualified to discuss nutrition as Dr. Eades, Dr. Feinman, Dr. Fine, etc.?

      I don’t. Truth be told, AC can’t even evaluate simple exercise related research papers properly. He’s clever and can indeed turn a phrase, but that’s about it.

  68. Sorry to just stick this here, but I had to tell you…

    My mother, age 74, diabetic, and morbidly obese, has been watching the Dr. Oz Show recently and tells me about some of the stuff he proposes. Tonight she was visiting and we were discussing, once again, the low carb WOE. She said out of the blue, “I wish Dr. Eades had a television show… I’d listen to him.”

  69. @LC
    For whatever reason, I came to the rescue of a commenter I felt was being criticized for making an inaccurate interpretation of Taubes’ book. Since Taubes’ journalistic objectivity style of writing is sometimes so non-committal, I felt it was possible that some of the information presented could be open to interpretation. Believe me, I admire and appreciate all the interest and effort put in by scientists, journalists and brilliant doctors such as Eades and Harris. And I did think Taubes’ book was groundbreaking and loved reading it.

    Aren’t you simplifying a bit by saying the weight loss issue is the metabolic issue? I think you would agree that there are people who gain weight simply because they are over-indulgent and then there are people with metabolic syndrome who develop diseases as a result. As simplistic as it sounds, I think being overweight is pretty much due to eating too much and moving too little. What is complicated though is why people seem to have little or no control over this.

    My last comment was somewhat tongue and cheek. I think false advertising is offensive and irresponsible. If an author publishes a book titled, I’m ok, you’re a cave man, but implies on the cover that it will help you loose weight — when we all buy the book, don’t tell us we’ve missed the point when we try to find the weight loss connection.

    1. @kb,

      There may be exceptions to my statement that the weight issue is the metabolic issue, but I don’t think there are too many. The over feeding studies don’t leave too much doubt that the overweight are overweight basically because the calories out side of the equation is broken. In people without the metabolic defect, grossly overfeeding them just causes calorie wasting and the subjects without the metabolic problem either defend their weight homeostasis or quickly return to it at the end of overfeeding by cellularly wasting calories. Taubes goes so far to suggest that the overeating and sedentarianism in the overweight is the result of, not the cause of, the metabolic defect, and he vigorously argues against your point to the contrary in GCBC. His position is that the inability to utilize dietary calories because they are being stored as fat with a relative vice-like clamp on the storage, causes both the hunger and fatigue associated with excessive eating and lack of movement. The body can’t utilize its stored calories for its energy demands and so ceases activity and demands energy. It is my clinical experience that this is correct until the diet effectively manages insulin.

      Yeah, Doc, the comments section is a bit gnarly around finding and replying to comments.

      1. I agree on the comments issue. It really makes it much, much easier for me to deal with them because I simply reply. Problem is, I never know where that reply goes. I’m going to stick with it a little longer and re-evaluate. Thanks for your take on it.

      2. LC – I do remember that from GCBC. Thanks for the clarification, I appreciate it. Might be time to read the book again.

  70. “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.”

    Couldn’t a low-carb metabolic advantage also be described as a “magical property” in this sense? My hi-carb friends would pounce on that statement.

    1. Maybe I didn’t put it in the most felicitous way, but what I was trying to get across was that at the time many people (scientists included) thought that some property of dietary fat made it more likely to be deposited as body fat as compared to an equal number of calories of carbohydrate or protein. Thus the spate of books published during that time positing that all one had to do to lose weight was to cut the fat. Eat all you want, they promised, just limit the fat, and you will lose. Leibel et al were simply trying to show that fat didn’t cause any greater weight gain than an equal number of any other kind of calories.

      I don’t think a low-carb diet has any ‘magical’ properties that cause greater weight loss – there are sound thermodynamic underpinnings of why it happens. Thermodynamics, not magic.

  71. Dear Dr. Eades,
    I read the Feinman-Fine second-law article you cited above with interest, but found a mistake in the Figure 2 plot and the corresponding text. I didn’t notice any erratum either.

    The figures in section “Efficiency and thermogenesis” should add up to 1825.5 kcal effective yield and not to the 1848 kcal given.
    They seem to have interchanged the thermogenesis percentages of CHO (7%) and lipids (2.5%) in their calculation. The error source was perhaps the order in which they list the numbers: first percentages for F, C, and P from Jequier’s review, and then the diet C:F:P = 55:30:15. Go figure.

    Nevertheless, it doesn’t affect the main result about metabolic advantage, weakens it a bit, though.

    1. Hi Toni,

      I read the Feinman-Fine article also, and after playing with a spreadsheet for a bit, I agree about the flipped percentages.

      In fact, it seems that lipids are more efficient then carbohydrates. The thermogenesis percent of Carbs (7%) is higher than that of Fats(2.5%). The real metabolic advantage appears to come from shifting calories to Proteins(thermogenesis 27.5%).

      I wonder if I’ve misunderstood something?


      1. Hi Chris,
        Yes, those are the percentages, but I don’t know how they were derived, since I have seen the abstract of the source paper only. Jequier’s viewpoint seems to have been on the limit-fat-intake side for this metabolic and other satiety reasons.
        I find another quick-to-read article far more informative on the overall metabolism and efficiency issues: the Fine-Feinman 2004 review in Nutrition & Metabolism which you find from the cited-by list of the original link.

        What I would like to find is an article where the thermodynamic data and the physical chemistry of macronutrients was worked out in detail in terms of equations.

        Now it’s time for my protein snack.

    1. Meanwhile Colpos statements are no longer only annoying, but heavily insulting. The warning on his website “This article contains strong language. Please close this page immediately if you are a minor or easily offended” is no excuse at all for insulting others in a pathological way.

      Very probably he suffers from a serious mental disorder, but this doesn’t mean he lives outside the law. Either he has full legal capacity and is responsible for his actions or he is mentally ill and therefore a case to be placed unter disability and hindered from injuring others.

      It should honestly be considered to sue him, even across the legal and geographic borders.


      P.S.: An objective discussion about the mentioned nutritional aspects nevertheless is worth to be continued.

  72. “Dude, think this through. Read what this guy is saying man. IT is complete bs. There is no metabolic advantage. Not even 100-300 calories or whatever the amount is this month. The satiating effect of protein and the even level of blood sugar keeps you from getting too hungry so you eat less calories over all. There is nothing magic about it. The metabolic advantage is completely made up. Don’t get me wrong I do use a non ketogenic low carbohydrate diet just for the reason that it keeps me from getting hungry and my blood sugar is stable. But don’t bs yourself by believing that there is a metabolic advantage to it.”

    Dude –

    Try this thought on for size. When you eat less on a LC diet you ASSUME that this is due to the satiety of a LC diet and therefore, it is the lowered calories that cause the greater fat loss than LF diets. But what you, Colpo, McDonald, etc. fail to consider is WHY the subjects eat less. How can they be satisfied on fewer calories? This makes no sense if as you all say its all about calories.

    Subjects on LC diets eat less because more fat is being released from the fat cell to make up for the energy deficit. So even though less calories are being shoveled into the mouth, more calories in the form of stored body fat are being released in the LC subjects to make up the difference.

    That’s your MA.

  73. Author: Mike Howard
    I always get a kick out of you, Fred. Your arguments and your methods have become so completely predictable that it’s laughable.
    [Fred Hahn says:] Glad you are having fun.

    You act very tough when your ensconced into a low carb-zealot-friendly comfort zone, but anyone who isn’t off-the-charts low carb and/or super slow training-biased thinks you’re a complete joke.
    [Fred Hahn says:] Wow I didn’t know you knew so many people. Congratulations!

    James has been picking apart your sacred cows for years now. While I admire your dogged pursuit of your dietary and exercise ideals, you’ve been given every opportunity to provide evidence of your claims and you have failed. Miserably. You are clearly frustrated that James has science slapped you all over the internet and has repeatedly called you out on your dichotomous generalizations, mistruths, half truths and flat out lies.
    [Fred Hahn says:] Really? Hmn. I’ll have to clean up my act then huh?

    Your method of arguing is hilarious and anyone who disagrees with you is aware of your tactics and logical fallacies. Your bias is clear Fred and to claim that you, Eades or Taubes has the same objectivity as James is quite funny – especially since James has repeatedly stated he is in no way against low carb.
    [Fred Hahn says:] And your point is…..? Your trouble is two dimensional thinking.

    If you actually had any evidence against James’ assertions against Taubes’ conclusions, you would have had something substantive to say about it on his site. Instead, you whined about how “scientist don’t talk that way” and proceeded on your usual red herring diatribe about Bray’s critique – which had little to nothing to do with James’ critique.
    [Fred Hahn says:] Do you know what a ‘red herring’ is? I don’t think you do Mikey.

    Tangentially, I wonder why you are even engaging in a debate with James. According to your logic (from one of your posts on the Colpo thread), “those lacking formal nutritional education can only argue from a layman’s perspective”. Does that mean we should all take your opinion as simply a “layman’s perspective”? From that logic alone, why should anyone listen to you over James? Or is parroting spoon-fed information from Fein, Eades, Taubes etc considered ok?
    [Fred Hahn says:] I (like James) am a layman so take it as you wish. I think presenting what science and biochemistry have to say is worth repeating. Is that what you mean Mikey?

    I guess it would be easier just to buy into every aspect of GCBC without questioning anything – you know, ‘cause the first 200 pages are a “masterpiece” (therefore the entire book is infallible.)
    [Fred Hahn says:] Well when you actually read the book, come on back here and blather. Then you can present the faults of Gary’s hypothesis yourself – no need to rely on your God James. So, I give up. I admit it – I am totally incapable if thinking for myself. I surrender to your great wisdom. Let’s hear what you have to say. Oh wait – “A calorie is a calorie” right? “The first law of thermo is indisputable” correct?

    I understand your tendency to lash out here, Fred. You and others wish that people like James didn’t exist so you could go merrily along your way spewing whatever nonsense you want without accountability. The problem is that anyone with an ounce of intelligence, logic and objectivity will call you on your BS pretty quickly. This is evident from your own blog, the JP fitness site, Alan Aragon’s blog and Baye’s site. I’ll provide some links later.
    [Fred Hahn says:] Please do. Make sure and offer up your own ideas rather than your Gods James, Alan and Lyle’s ideas.

    The bottom line is that you’ve clung to your absolutist beliefs and nobody is going to change your mind about it. You will continue to argue in circles, moving goalposts, throwing out red herrings and relying on personal anecdote, other irrelevant examples (like your 13 yr. old 7 footer) and appeals to authority to prove your case.
    [Fred Hahn says:] You betcha! I’ve the mind of a Bonobo so what else can I do??

    Eades got called out for making a spurious and unsubstantiated claim and instead of retracting, he danced in circles and launched an ad hominem. This is the original contention which has been lost amongst the LCT who prefer to just whine about James’ presence and Geiger-count for any smidge of misstep on his part. James addressed his comment on Taubes’ background as a journalist. Perhaps Dr. Eades and Fred can retract on their follies, too?
    [Fred Hahn says:] Ad hominem attacks huh? You mean just like Colpo, McDonald, Krieger, Aragon, YOU, etc. Like that? You’ve yet to say anything intelligent Mikey. You sound like an angry 5 year old who knows he’s beaten but doesn’t have the wherewithal to deal with it.

    Here’s your argument in a nutshell:

    “You’re wrong Fred and you’re stupid. You think you’re smart but you’re not! My friends are smarter than your friends by like a lot! You’re so silly saying things that,well, you’re just stupid that’s all and you won’t admit it but you know you are!”

    Here’s my response:

    “I know you are but what am I?”

  74. Why do people get all fired up about this whole notion that low-carbers are just eating like pigs? First off, unless I’m taking food directly out of the hand of a starving person, what I eat is my business and no one else’s. ‘Scuse the hell out of me if you (general “you”, not specific) think I’m eating too much, but I don’t recall *asking* you what you thought.

    Second off, if I get my carbs low enough, my experience is that I don’t care so much about eating! I have to TRY to break 2000 calories a day. At least insofar as what goes into my mouth. I’ll get to that in a minute.

    Maybe people who have eaten low-fat for years, or whose carbs have been consistently too high, don’t understand that that gnawing pit in your stomach when you’ve gone an hour without a meal is NOT NORMAL. Well? It’s not. Taubes talks about this in his book: if your metabolism is doing normal things, your adipose tissue should be releasing fatty acids in between meals to give you energy until you can sit down and eat again. The difference between a healthy, normal person and a person with deranged metabolism, fat or not (and frequently, they’re not!), is that the latter finds themselves craving crap fifty times a day. And I don’t mean a sort of “wouldn’t it be nice if I could have a bag of chips right about now?” but more of a “ARGH I NEED STARCH OR I WILL DIIIIEEEEE!!!”

    Sorry for the caps, but you know that’s how it is. How many patients have you counseled by now with that problem? Hahaha.

    Hunger, rather than being a character issue, is usually your body’s way of saying it’s having an energy crisis and would you please strike food again before it’s too late? I think there’s another kind of hunger that comes with needing more nutrition in general, not just energy, but that one feels different. When I’m low-carbing, if I wait too long to eat in a given day, I get that kind of hunger eventually.

    But the other kind, the gnawing pit in the stomach thing? Not so much. And I think it’s like Taubes said, that because my insulin isn’t constantly elevated and my blood sugar is therefore not doing dips and whorls throughout the day, I’m able to release some of those stored fatty acids and get my energy from them. So my body doesn’t ever get to the point of energy crisis. Why would it? I’ve got something like fourteen years’ worth of extra energy stored up and all the time in the world to get rid of it.

    Speaking of which. People get all hung up about the calories thing–the truth is, nobody really knows how many calories a low-carber is burning. They can make some good ballpark guesses, but (as you know) here’s a hint: the count doesn’t stop at what goes in your mouth. If you’re burning your fat stores, that counts as calories burned too.

    So someone like me who has to struggle to *eat* 2000 calories a day, some days, when I’m low-carbing… I probably *am* getting 2000 calories a day, *minimum*, in between my food and my fat-burning.

    I have reason to believe from everything I’ve read that your average low-fatter isn’t actually doing all that much fat-burning. Muscle-wasting, sure; bone-degradation, probably (especially since it’s looking more and more like you need saturated fat to assimilate calcium and what fat are they avoiding? thank you)–but fat-burning, not so much.

    Maybe when they figure out that whole fat-burning thing, they can come tell us how stupid we are for not forcing ourselves to limit intake to 1500 calories or less a day, particularly those of us disgusting folks who got over 100 pounds overweight *raises hand*. So far, though, it’s looking like they need to do less talking and more listening. I could be wrong… but I don’t think so.

    1. Dana, I simply loved your post! I hope you will hand it to your physician [if it’s not Dr. Eades] or to any personal trainer you may engage to assist you when they start to give you the inevitable lecture.

      If I may, I’d like to request your permission to forward your post here to my clients, who have all felt as you do, and who would appreciate hearing your emancipation and fully righteous words as it speaks to their own experience. Thanks and good luck with your weight loss [I stopped by your site].

  75. Hi,

    I have just been diagnosed with Nonalcoholic fatty liver disease (NAFLD) & my doctor has recomended switching to a mediterranean diet. I was I am 39, 5’9, 221lbs. I was wonder if a low carb diet would help with my NAFLD or make it worse.

    Thank you,

  76. Hi Dr. Eades,

    I know that you haven’t checked in on this particular blog in a while, but I’m confused….I follow a high fat / low carb diet and eat only when hungry, but I am at most getting 1,200-1,300 calories per day. I’m 5’4″ and 155 lbs currently, but I’m not really hungry enough to eat past this amount of calories. Would you consider this caloric range to be in starvation mode? I’m slightly confused, but at higher caloric intakes on my high fat/low carb diet, I didn’t gain or lose. I had to decrease my caloric intake in order to start losing. Can you clarify on this issue please? Thank you! 🙂

    1. If you’re truly following a low-carb/high-fat diet and are eating until full, I wouldn’t worry about the calories. They should take care of themselves over time.

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