The number one winner going away was Lierre Kieth’s brilliant The Vegetarian Myth.  If you haven’t read it, grab a copy ASAP.  For those of you who don’t know, Lierre was recently the victim of an assault at a San Francisco reading.  Masked thugs came out from behind the stage and smashed her in the head and face with pies laced with cayenne pepper.  After the assault took place, while Lierre was trying to get the burning pepper out of her eyes, the audience (of mainly vegetarians) cheered.  It was truly disgusting.  Richard Nikoley and Tom Naughton reported on the assault here and here.  Jimmy Moore has a  interview with Lierre about the attack here. Tom Naughton proposes a rationale for such behavior here.

It appears that militant vegans have secured  Lierre’s name and other versions of her name on Twitter and are mounting a vicious smear  campaign against her.  Purchase her book to fight back.  Success is her best revenge.

Here are the books in descending order.

#1 The Vegetarian Myth by Lierre Kieth.  My review here.

#2 Mistakes Were Made (But Not by Me) by Carol Tavris and Elliot Aronson.  My review here.

#3 Good Calories, Bad Calories by Gary Taubes.  My review here.

#4 Lucy: The Beginnings of Humankind by Donald Johanson. My review here.

#5 Control Theory by William Glasser My review here.

#6 The Brain Trust by Larry McCleary, M.D. My review here.

#7 500 Low-Carb Recipes: 500 Recipes from Snacks to Dessert, That the Whole Family Will Love by Dana Carpender

#8 Natural Hormone Balance for Women by Uzzi Reiss.  A mention here.

#9 How to Cook Everything by Mark Bittman.  MD’s review here along with her entire list of essential cookbooks.

#10 Crucial Conversations: Tools for Talking When Stakes are High by Kerry Patterson et al.  My review here.

#10 Primal Body-Primal Mind by Nora Gedgaudas

#10 The Great Cholesterol Con by Malcolm Kendrick.  My review here.

#10 The Happiness Hypothesis by Jonathan Haidt My review here.

The last four books on the list sold exactly the same number of copies, so they all tied for 10th on the list.  I listed them alphabetically.

Although not a book, sales of the DVD of Tom Naughton’s brilliant film Fat Head would have put it at #2 on the list.  If you haven’t seen this film, order it today.  Here’s my review.

I want to thank all of you who have ordered not just books but all kinds of things through this site.  And I want to encourage you to continue.  The small commission I make on each order helps underwrite the maintenance on this site, which is much higher than I would have thought it would be.  Plus, I’m still paying off the recent redesign.

For those of you who don’t know what I’m talking about, any time you order a book or a DVD or a CD or anything (groceries, supplements, tee-shirts, whatever) through Amazon.com, I get a small commission on your order.  But I get this only if you go through one of the Amazon portals on this blog or MD’s blog or anywhere on the website.  What is an Amazon portal?  If you click the picture of The Six-Week Cure for the Middle-Aged Middle at the upper right of this post, you will be taken to the Six-Week Cure page on Amazon.  If you’re looking for something else, just type it in the search window, click the ‘Go’ button to the right, and you will be taken to wherever you want to go, and anything you purchase once you get there will earn me a tiny commission.

This whine for help with Amazon is my own version of those awful PBS fundraising telethons.  The difference is that here it doesn’t cost you anything; you simply have to purchase whatever you were going to purchase through Amazon anyway by going through one of the portals on this blog.  And your free programming will continue.

As some of you may have noticed, I finally removed the tacky Google ads that were at the bottom of each post.  I didn’t even realize they were there until I was having lunch with Mark Sisson one day, and he asked me what my relationship with Atkins Nutritionals was.  I told him I had no relationship with them.  He told me he figured I did because a fairly prominent banner ad for Atkins Nutritionals appeared at the bottom of each of my posts.  I checked myself, and, sure enough, there were the ads.  I looked into it and found out that I was making about $45 per month for these ads (not all were Atkins, but most were) so I ditched them altogether.  Had I been making $1500 per month on these ads, I may have had second thoughts, but as it was, I had no problem giving them the ax.

So, at this point, no ads are cluttering the pages of my blog or MD’s blog.  Other, of course, than those for our own books, which are the previously mentioned Amazon portals.  Order early and order often.

What gives is that I’m stuck in the airport in Seattle – my flight to Chicago is delayed for almost four hours because of bad weather in the Windy City.  I figured I would use this time to stick up a quick post about thermodynamics and provide a long quote from Robert McLeod, who writes Entropy Production, a physics (sort of) blog.  As you can see below, he pretty much trashes Bray and other nutritional researchers who blithely use the 1st Law of Thermodynamics to prove the old a-calorie-is-a-calorie notion.  To show the way the average nutritional writer looks at this law, I needed to find a quote.  As it works out, the only thing I have with me is Anthony’s book The Fat Loss Bible, which just happens to have the perfect quote.  So, sorry AC, I’m not really trying to pick on you.  And you certainly aren’t the only nutritional writer who thinks this way – you’re just the only one who has a quote handy I can use.

The First Law of Thermodynamics states that energy can neither be created nor destroyed. It can only be converted from one form to another. In other words, energy just doesn’t just magically disappear; it must be converted to something else. In the case of any excess calories you ingest, they will be stored as fat, used to accommodate an increase in lean tissue mass, or dissipated as heat through thermogenesis. Manipulating the proportion of protein, fat and carbohydrate you eat each day will not excuse you from the Law of Thermodynamics.

This is the way just about all nutritional scientists and writers look at the First Law.  Let’s take a look at how a physicist sees it.  Robert McLeod wrote a long post a while back reviewing Gary Taubes’ Good Calories, Bad Calories.  Near the end of the post, he discusses the energy balance equation and one of our old friends, Dr. George Bray, who gave Gary’s book a bad review in an obesity journal.  (I posted on this same review a couple of times here and here.)

Here’s what he says:

I was somewhat confused to see this [a nutritional description of the energy balance equation] Surely the nutritional scientists did not not really believe this, right? I mean, any idiot undergraduate students knows that the 1st Law is only useful in a closed system, and humans live on the planet Earth, not in an insulated box. Right?

Enter a rebuttal by G. Bray in the journal Obesity Reviews. Bray is a to be a major obesity researcher and one of the 2nd tier villains in the book. Taubes relates a story of Bray excising a section of a British report on obesity, where Bray removed the material pertaining to the relationship between insulin and obesity. He clearly has editorial support to make his case. Bray is one of the second-tier villains in Taubes’ book. Taubes has a footnote (p. 421), which suggests that Bray actively suppressed the carbohydrate-insulin hypothesis.

“According to Novin, when he wrote up his presentation for the conference proceedings Bray removed the last four pages, all of which were on the link between carbohydrates, insulin, hunger, and weight gain. “I couldn’t believe he would make that kind of arbitrary decision,” Novin said.”

Unfortunately, to a physicist this energy balance hypothesis looks like a silly hand-waving exercise, not a serious argument. Frankly I was flabbergasted when I first read this article. This conservation of energy argument is on the same scientific level as the ridiculous “drink cold water to lose weight” idiocy. A human organism is:

1. Not in thermal equilibrium with their environment. Last time I checked I have a body temperature around 38 °C and spend most of my time in 21 °C rooms.
2. Capable of significant mass flows (e.g. respiration).
3. Capable of sequestering entropy (e.g. protein synthesis).

Is wearing a sweater fattening (by insulating you from your environment)? Here’s a quote from the rebuttal,

“Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result. An energy deficit produces weight loss and tips the balance in the opposite direction from overeating.”

According Bray’s thermodynamics argument, wearing sweaters makes you fat. This illustrates the greatest fallacy of trying to apply the 1st Law to a human: it makes the implication that living organisms consume kilocalories for the purpose of generating heat rather than perform useful work (i.e. breathing, contracting cardio and skeletal muscle, generating nervous action pulses, etc.). In reality heat is the waste product of basal metabolism. The first law does not distinguish between different types of energy. Heat, work are all equal under the First Law of Thermodynamics.

Applying the 1st Law to living organisms is Proof by Tautology. Yes, 1 + 1 = 2, but this tells us absolutely nothing about the underlying mechanics. The 1st Law does not (I repeat N-O-T) tell us whether you store excess energy in the form of fat, or bleed it off into the atmosphere by dilating blood vessels next to the skin, sweating, etc. To do so would require an accounting of entropy.

What would a semi-rigorous description of the thermodynamics of a human organism look like? Look at the title strip on the top of the page. See that equation in the background?

[The above is the background of the header of Robert McLeod's blog]

This type of equation would be a bare starting point for energy balance in a complex system like a living organism. Good luck actually accounting for all the terms. Those Σs are sums.

We all fall victim to the confirmation bias and have to fight it constantly.  Gary Taubes thinks I may even have succumbed a little in the earlier post on AC and the metabolic advantage.  He emailed me saying he had read the post and thought it was great up to the point right at the end where I wrote that the data on the whole showed that, if anything, there was a metabolic advantage.  Gary thought the data presented in all the studies in AC’s chart was ambiguous and that I was going out on a limb a little in making the statement that I thought, if anything, that the papers argued for a metabolic advantage.

I disagree.

I decided to base this critique not on the scientific literature at large, but instead on only the papers that AC mustered for his argument.  I intended to make the critique much like a court case in which one side presents the information and the other attempts to counter it.  I didn’t want to go out myself and gather a bunch of papers that confirmed my viewpoint, because then we would have had nothing but a bunch of dueling Ph.Ds, a  bunch of he saids, she saids, that wouldn’t prove anything.  I stuck with the papers AC used and presented my arguments as to why I didn’t think his papers proved his case.  After going back and rereading the post, I still feel that if this ‘evidence’ were presented to a jury, the verdict would come back in favor of my arguments.  If anything, AC’s own ‘evidence’ argues for the existence of a metabolic advantage, and, at worst, certainly doesn’t ‘prove’ that one doesn’t exist.

Since I posted the first part of my critique, AC has responded using his customary restraint and understated gentility designed to appeal to his sort of reader.  His response – as I figured it would be – is merely a listing of even more papers he believes substantiate his claims.  Instead of undertaking a serious scientific inquiry, he is looking for more white swans.  Let me explain.

I wrote a long post a couple of years ago on Sir Karl Popper and the metabolic advantage.  Popper set the standards by which hypotheses should be structured.  A well-stated hypothesis should be able to be falsified.  That doesn’t mean it will be falsified, but it should be structured in a way that it can be.  And real scientists – of which, sadly, there are all too few in the field of nutrition – don’t try to confirm their hypotheses: they try to refute them.

One of the examples Popper used in explaining how a hypothesis should be established involved swans – white and black.  He used the following as an example of a good hypothesis:  All swans are white.  He made the case that this hypothesis cannot be confirmed by simply pointing out more and more white swans.  The hypothesis can be strengthened by doing so, but it can’t be proven.  It can, however, be disproved by the discovery of even a single black swan.  Popper argued that scientists should be working to find black swans instead of simply adding more and more white swan sightings to their data.  The more effort scientists expend to find a black swan without finding one, the more their hypothesis is strengthened.  Diligently searching for black swans is a much more valid scientific endeavor than simply looking for more white swans.

Many scientists don’t want to hunt for black swans, however, because they don’t want to blow up their hypotheses.  The easy way to bolster their hypotheses is to continue to tally up all the white swans they find and forget about looking for black ones.

Which, of course, is what our young friend AC has done and written about in his latest missive.  He tallies up a bunch more white swans and ignores the black ones, even the black ones in hiding in plain sight in his own list of papers.  This failure of his to try to puncture his own hypothesis leads me to believe there exists a large chasm of incomprehensibility between the way AC thinks and the scientific method.

To give but one example of this, AC argues in his book that the studies by Rabast that clearly show a metabolic advantage aren’t valid because, as AC puts it,

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.

(In other words, AC is saying: that black swan over there isn’t really a black swan, because all the other swans I’ve pointed out are white.  And since all the others are I’ve pointed out are white, that one can’t be black.  It’s impossible.)

In point of fact, Rabast’s group in Germany has performed a number of studies showing a significant metabolic advantage in subjects in metabolic wards who follow low-carb, high-fat diets as compared to those taking in the same number of calories as high-carb, low-fat diets.  This group pursued this line of inquiry and published a number of studies showing this metabolic advantage.  Suddenly, however, they quit publishing on this subject and turned their attention elsewhere.

While in the research phase for Good Calories, Bad Calories, Gary Taubes interviewed Dr. Rabast about his group’s work, and here is what he said.  They were inspired by an old scientific paper (more about which later) that offered up some data they found interesting and wanted to test themselves.  They did the studies using formula diets, so they could more easily control intake and confirmed the data from the old study.  They continued to perform these studies, all with similar outcomes, until Dean Ornish published his paper on dietary fat and heart disease.  Dr. Rabast and his group decided that Ornish might be correct.  They felt that although their own data showed that high-fat diets brought about substantially better weight loss than low-fat diets of equal calories, their work might encourage people to consume more fat, which, thanks to Ornish and the low-fat movement, they had come to believe may cause heart disease.  So, they abandoned their research on high-fat diets and moved on to other interests.

The study that inspired them to study high-fat diets?  An study from the 1950s done by a couple of British researchers, Dr. Alan Kekwick and Dr. G.L.S. Pawan.  Their famous paper showed a definite metabolic advantage, a black swan writ large, as it were.  And their famous paper is well known to AC, who has a few things to say about it.  As you might suspect, given the results of this study, he declares it not worthy of consideration. Here is what he says in his book after he’s gone through his list of white swan studies, which, of course, are all worthy of mention.

Not-so-worthy mention

There is one metabolic ward trial that due to its short duration did not qualify for inclusion in Table 1a, but still warrants a mention. Incessantly cited by supporters of low-carb diets, this is the famous metabolic ward study conducted in the 1950s by Kekwick and Pawan. The London researchers conducted two experiments. In one of these, they claimed that patients maintained or gained weight on a typical mixed diet of 2,000 calories, yet consistently lost weight when placed on a 2,600 calorie low-carbohydrate diet for periods ranging from 4 to 14 days. In the second of their experiments, they had 14 patients alternate between four different 1,000 calorie diets, spending a grand total of 5-9 days on each diet: 1) 90 % protein; 2) 90% fat; 3) 90% carbohydrate, and; 4) a mixed diet. According to Kekwik and Pawan, all of the subjects in the protein, fat, and mixed diet groups lost weight, with the high-fat group experiencing the greatest weight loss of all. However, despite the very low calorie intake, many of the patients reportedly gained weight during the high-carbohydrate diet! Not surprisingly, the Kekwik and Pawan study is frequently cited by supporters of low-carbohydrate nutrition. That they ignore the studies in Table 1a, yet eagerly embrace a short-term study conducted over 50 years ago, speaks volumes about their complete disregard for rational scientific inquiry. [Italics in the original]

Here’s why: Firstly, it has long been known that in the first week or two of low-carbohydrate dieting, there is often a far greater reduction in water weight due to excretion of sodium and/or glycogen, both of which bind water in the body. Therefore, studies of such short duration are next to useless as indicators of the comparative longer-term weight loss effects of these diets.

Secondly, the Kekwik and Pawan study was a poorly controlled mess. The researchers were even driven to denigrate their study participants, writing: “The first and main hazard was that many of the patients had inadequate personalities. At worst they would cheat and lie, obtaining food from visitors, from trolleys touring the wards, and from neighbouring patients. (Some required almost complete isolation.)” [Italics in the original]

Given that protein and fat have been shown numerous times to exert satiating effects, while low-fat, high-carbohydrate diets (especially the liquid, low-fiber variety!) typically result in ravenous hunger, it’s not hard to guess during which diet the participants may have ‘cheated’ the most!

The researchers also wrote: “The results we report are selected, a considerable number of known failures in discipline being discarded”. Note how the researchers included the words “known failures”; how many failures did they not know about? How many of the patients were crafty enough to sneak extra food without being caught? Why should we trust Kekwik and Pawan’s unlikely results, given their study’s numerous flaws? The answer is simple: Unless you are a famous low- carb diet ‘guru’ who has made millions promising people they will lose extra weight at the same calorie intake by cutting carbs, we shouldn’t! At least not if we believe good science mandates a tightly controlled process of investigation. [Italics in the original]

As we shall see shortly, this commentary is all so much piffle.

(Here is the full-text version of the Kekwick and Pawan study so that you can pull it down and follow along with the rest of the discussion if you like.)

Let us begin.

It is apparent from his critique that AC read the first part of this study, found a black swan, used a bunch of incorrect gibberish and swagger to try to say it wasn’t really a black swan and moved on without ever getting to the important part of the paper. Or, an alternative explanation is that, as with the Leibel study mentioned in my first critique, he either didn’t really read the paper thoroughly or he seriously misunderstood what he read.

Drs. Kekwick and Pawan start off by explaining why they undertook this study in terms that any of us who have struggled with excess weight and found different results with different diets can understand.

Many different types of diet have been successfully used to reduce weight in those considered obese.  The principle on which most of them are constructed is to effect a reduction of calorie intake below the theoretical calorie needs of the body.  Experience with these patients has suggested, however, that this conception may be too rigid.  Many of them state that a very slight departure from the strict diet which can hardly affect calorie intake results in them failing to lose for a time.  Though it is realized that evidence from such patients is notoriously inaccurate owing to their approach to this particular condition, it is too constant a belief among them to be entirely discarded.

Drs. K & P did a number of experiments.  First they kept hospitalized subjects on diets of similar macronutrient composition but differing calories and found that reducing calories made the subjects lose weight.  And, unsurprisingly, the more the calories were cut, the more weight the subjects lost.  Next, the good doctors decided to see if changing the macronutrient composition of the diets made a difference.  They started the subjects on 1000 calorie per day diets of one of the following three structures: 90 percent of calories as carbohydrate; 90 percent of calories as protein; or 90 percent of calories as fat.  The structure of the diets made an enormous difference in how much weight the subjects lose.  As Drs. K & P wrote:

So different were the fates of weight-loss on these isocaloric diets that the composition of the diet appeared to outweigh in importance the intake of calories.

In an effort to confirm their findings, Drs. Kekwick and Pawan went on to a third series of experiments as described here:

…patients…were put on to 2000-calorie diets of normal proportions to show that their weight could be maintained while in hospital at this level and then placed on high-fat, high-protein diets providing 2600 calories per day.  It was demonstrated that these patients on the whole could maintain or gain weight on 2000-calories but, except in one instance, lost weight consistently on a 2600 daily calorie intake.

It’s easy to see why AC doesn’t like this paper.  And we haven’t even gotten to the good stuff yet, which AC doesn’t make mention of in his book.  We’ll get to that in a bit, but before we do, let’s take a look at AC’s critique of this much of the study (which is, apparently,  all he bothered to read). You can read along from the above quote in his book.

His first complaint is that the study is over 50 years old.  I find this a strange complaint, since the first study he lists in his chart of studies ‘proving’ his point was published a mere eight years after this Kekwick and Pawan study.  The Kinsell paper was published in 1964, 46 years ago.  Is there some magic cutoff date at 50 years that makes scientific papers unreliable?

Second, he claims that on low-carb diets all the weight loss from the first two weeks is water, and since these studies lasted less than two weeks, the difference was all water.

Kekwick and Pawan were a little smarter than Anthony gives them credit for being.  They understood well the notion of water loss.  (As we will see shortly, they understood it vastly better than our young friend.)  They pointed out the following:

During these periods [the different diet studies] the patients were weighed daily and in some of them balance studies were carried out in respect of water, nitrogen, fat, sodium, chloride, and potassium.  Total body-water and the basal metabolic rate were estimated weekly or at the end of each period on the diet.

If you look at the full-text version of the study I linked to above, you can see graphically how this all plays out.  In these studies the weight loss was definitely not all water.

In an effort to be meticulously accurate, not only did K & P monitor all the above carefully, they even went further.  Since these patients were not on formula diets but were on real foods instead, making it more difficult to accurately determine caloric intake, the staff would take representative samples of the foods eaten, blend them into a soup, then analyze samples to make sure the protein, carbohydrate and fat content were as estimated in the food tables.  It was hardly a “poorly controlled mess” of a study.

AC next attacks the study because the researchers admitted as to how difficult it is – even in hospitalized studies – to prevent cheating.

In such a study the difficulties are formidable.  The first and main hazard was that many of these patients had inadequate personalities.  At worst they would cheat and lie, obtaining food from visitors, from trolleys touring the wards, and from neighbouring patients. (Some required almost complete isolation.)  At best they cooperated fully but a few found the diet so trying that they could not eat the whole of their meals.  When this happened the rejected part was weighed, and the equivalent calories and foodstuffs were added to a meal later in the day.  The results we report are selected, a considerable number of known failures in discipline being discarded.

Kekwick and Pawan simply wrote of the difficulties in preventing cheating.  They were on the lookout for it, threw out data they knew was compromised, and compensated for episodes of cheating of which they were aware.  I believe the fact that they recognized cheating as going on and were keeping an eagle eye out for the cheaters makes their data more accurate, not less.

I also find it strange that AC is more than willing to toss data because of cheating in this study and is more than willing to accept data from other studies in which there was probably just as much – if not more – cheating that the authors neglected to mention either by design or because they didn’t realize it was happening.

One other thing that points to the degree into which K & P watched over this study is one that all female readers who have had trouble losing will be familiar with.

Another factor of importance which could not be eliminated was that many patients were women, in whom the retention and the losses of water associated with the menstrual cycle affected the daily weight and the estimation of total body-water.  We were surprised to find how great such factors could be, amounting in one woman to the retention of more than 3 litres of water.

Only a fool or a seeker of white swans only would think the good doctors didn’t monitor this study closely.

Now to the fun part, the part AC probably didn’t read.  And the part that really demonstrates the metabolic advantage.

The first part of this paper, the part AC has critiqued, is only a minor part of the paper.  The majority of the paper is devoted to the efforts the Drs. K & P made to determine what happened to the excess weight lost in dieters on the higher-fat diet.  They checked fat loss in the stool, they checked (as mentioned previously) water loss, they checked about everything they could think of.  You can read in the full version how careful they were.

After sifting through all the data and finding no reason that their results should have been invalid, the docs checked yet one more item.  They looked at insensible water loss.

Insensible water loss is the loss of water we all experience minute by minute that we not aware of.  We know we lose water when we urinate and/or defecate, and we know we lose some water when we visibly sweat, but we are not aware of the large amount of water we are getting rid of through our breath and via sweating that we don’t notice.  And this amount of water we lose is fairly large.

Do this experiment.  Get an accurate scale and weigh yourself immediately before going to bed.  Go ahead and urinate (and do anything else you might need to do) before weighing.  Don’t drink or eat anything, hop in the sack and sleep through the night, then get up and weigh before you urinate in the morning.  I absolutely guarantee that you’ll weigh less than before you went to bed.

If you breathe on a mirror, you will fog it from the water vapor in your breathe.  This vapor is water that you lose every single time you take a breathe.  You breath approximately 12 times per minute (while resting), which means you breathe 720 times per hour and 17,280 times per day.  And that’s if you’re at rest.  If you are active, you take a lot more breaths than that.  Probably something in the neighborhood of 20,000-23,000 breaths per day, depending upon activity level.  Each one of these breaths contains water vapor that you are losing from your body, which is why you drink liquids throughout the day.  If you didn’t replace this water, you would become dehydrated.

If you have a fever or if you exercise, you breathe a lot more rapidly and lose a lot more fluid.  Thus, one of the things doctors have to be concerned about in very sick patients with high fevers is dehydration.

You also lose insensible water through constant perspiration.  When you awaken in the morning, if you’ve slept tightly covered up, you’ll notice you’re a little damp.  Not a lot, unless you’ve had a fever, but a little.  This is insensible water that you lost.

I remember how amazed I was the first time I ever looked at my own hand under a dissecting microscope.  Looking at my hand with my naked eye, it appeared normal and dry.  When I stuck it under the scope and looked, I could see little volcanoes of perspiration bubbling up from unseen pores.  It’s part of the way we regulate our temperature, and unless we work up a visible sweat, we never notice.

This loss of insensible water is why we lose weight overnight.  In eight hours of sleep, we breathe out about 5,760 breaths filled with water vapor and we sweat all night.  This water weight usually ends up being between 1 to 2 pounds or even a little more.

If I were to take a bunch of thyroid hormone or take an amphetamine, I can assure you that my metabolic rate would rise and that my insensible water loss would increase.  In fact, insensible water loss is a surrogate for metabolic rate.  If your metabolic rate rises, your insensible water loss rises.  And since insensible water loss can be easily measured, the metabolic rate can be easily estimated without having to do metabolic chamber studies.

Which is exactly what Drs. Kekwick and Pawan did with several subjects on the various diets.

They kept the subjects isolated and under supervision and weighed them on extremely accurate scales throughout the day.

Measurements were made by weighing the patient at intervals of one hour on scales specially constructed for this purpose by Messrs. W. & T. Avery Ltd. which are sensitive to 2 g. over the range of weights concerned.  During these hours no food was taken and neither urine nor faeces voided, and errors due to temperature, activity, and air draughts were avoided as far as possible.

(Scales that are sensitive to 2 g are extremely sensitive.  Two grams weighs about seven one hundredths of an ounce.)

So, here is what the researchers did.  They first fed the subjects the standard diet available to the patients on the ward and discovered what the insensible water losses were throughout the day.  You can see how this came out in the graph below, Fig. 11.

When Drs. K & P put a single patient on the different diets – 90 percent fat, 90 percent protein or 90 percent carbohydrate – and measured the insensible water loss throughout the day, the table below, Fig. 12 shows what happened. There was an increase in insensible loss with the high-protein diet as compared to the high-carb diet, and a much greater increase in insensible water loss with the high-fat diet.

The area of the chart that I colored in is the difference between insensible water loss, which represents a change in metabolism, between the high-carb diet and the other two diets.  This colored part of the chart represents the metabolic advantage of the high-protein and high-fat diets compared to the high-carb diet of the same number of calories.  The peach colored part of the chart represents the metabolic advantage of the high-fat diet as compared to the high-protein diet while the grayish color represents the metabolic advantage, as measured by increased insensible water loss, between the high-protein and high-carb diets.

The researchers wanted to make sure this wasn’t an isolated phenomenon, so they analyzed three other patients and created the graph below, Fig. 13, which mirrors the results in Fig. 12 and demonstrates that this wasn’t an outcome isolated to just one subject.

The ever cautious Drs. Kekwick and Pawan interpreted their findings thus:

The rate of insensible loss appears to be much affected by the type of food, provided that the water and sodium intakes are kept constant throughout the period of observation; whether this increased rate of insensible loss is a measure of bodily metabolic activity must remain in question.  Even if metabolic activity cannot be measured directly, the difference in weight responses seen with these diets does not seem to be completely due either to an altered state of hydration or to a simple deficiency of calories.  We suggest that the rate of katabolism of body-fat may alter in response to changes in the composition of the diet.

And their summary:

As the rate of weight-loss varied so markedly with the composition of the diets on a constant calorie intake, it is suggested that obese patients just alter their metabolism in response to the contents of the diet.  The rate of insensible loss of water has been shown to rise with the high-fat and high-protein diets and to fall with high-carbohydrate diets.  This supports the suggestion that an alteration in metabolism takes place.

If you haven’t already, I would encourage you to read this entire study and make your own judgment.  I’m sure you won’t find it the “poorly controlled mess” that AC does.  In fact, I suspect you’ll find just the opposite.  Unlike most of the studies published today, this one is not loaded with incomprehensible jargon, is delightfully well written and is extremely accessible to those with little medical or scientific knowledge.  You can see for yourself how precise these researchers were and now meticulously they looked for anything that might confound their results.  It would be great if more studies were done this carefully today and written this clearly.

This is the end.  I am through with AC. I’ll leave it to the readers of this post and the previous one on this subject to make their own decisions as to whether or not a metabolic advantage exists for low-carb, higher-fat diets.  I won’t be provoked again into jumping into the mud and wrestling around.  So this is my black swan song on the subject.

I read a quote a few days ago by Nassim Taleb, the author, appropriately enough, of the book The Black Swan and, for my money, the infinitely better Fooled by Randomness that is apropos to this situation:

A good foe is far more loyal, far more predictable, and, to the clever, far more useful than any admirer.

So, to you, Anthony Colpo, I raise my hat. Had you not attacked me out of the blue, I would be less knowledgeable than I am today.  I wouldn’t have bothered to dig into all the ‘white swan’ papers you posted trying to figure out why these researchers got the results they got.  I, like you, would still be mired in the notion that metabolic ward studies are squeaky clean without any hint of sullied data as a consequence of cheating.  Like you, I would still probably be confusing metabolic ward studies with metabolic chamber studies, which are horses of a much different color.  Also, I thank you because I had kind of blown off the Kekwick and Pawan papers (there are others besides this one from The Lancet) as being too old to be worth studying.  You forced me to take another look, and I was delighted at what I found.  And, sad to say, like you, I, too, had read only the first part of the these studies, the parts about the diet comparisons.  It wasn’t until your attack that I actually read this paper all the way through and found the gold mine in the latter pages.

So, AC, I sincerely hope the best for you; I thank you for pushing me into this exercise and wish you godspeed on your journey through life.

I’ve had a family medical emergency that’s been occupying my time for the past week so I haven’t really had the consolidated time I’ve needed to finish off Part II of the AC book critique, but I haven’t forgotten about it.  I should have it up in a day or two.

Until then, I’ll give you a little thermodynamics to chew on so you, too, can see that it is far from simple.

A commenter wrote the following in response to Part I of the AC critique:

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.

This came in while I was in the throes of dealing with the family problems, so I didn’t take the time to go back, pull the paper, figure out what the commenter was talking about and put my two cents worth in.  I simply posted it as it was.

Thankfully, Dr. Feinman saw it and wrote a response on another website.  I asked for permission, which he gave, to put it up here.

1. The approach taken by many that the idea of metabolic advantage has to be consistent with thermodynamics is correct.  However, one has to understand and apply thermodynamics correctly, especially as it is used in bioenergetics.

2. People who get involved in this discussion have not followed the approach in biochemistry texts and traditional bioenergetics but have not explained why that approach is wrong.  In the traditional approach from bioenergetics, for example, one usually looks at the Gibbs Free Energy, G rather than the internal energy, E.  (G includes the effect of entropy from the second law).

3. What Figure 1 of the paper shows is that metabolic advantage must exist between systems that rely to different degrees on gluconeogenesis.  You learn this in biochemistry: it costs you 6 ATP to obtain glucose from GNG but, of course nothing if you start with glucose.  So, there is a built in metabolic advantage.  Not could be.  Not debatable.  It is there.  Period.  That is an absolute biochemical fact.  So just as people thought metabolic advantage was excluded by the “laws” of thermodynamics (by which they meant the first law), “a calorie is a calorie” is excluded by the combined first and second law.  (To try to use the first law in the absence of the second law is like, actually exactly like, using gravity without considering friction).

4. Now whether you measure it [the metabolic advantage] in any particular experiment, whether the effect is great, whether it is compensated for by other processes (in low fat diets you make fatty acids which costs many ATP although the net effect may be to increase fat storage) is a different question than whether it is there or whether you want to ignore it.

5. Most of the time, as in Leibel’s experiment with the hospital patient, there is calorie balance but Leibel’s group have also done experiments with catch-up fat where there is not energy balance.  But, again, application of the theory is different than what the theory says must be true.  We have made the point that thermodynamics predicts a difference between high and low carbohydrate diets.  It when it is not found that has to be explained.  (The explanation lies in the specific homeostatic mechanisms of biological systems, not in physical law).

6. I personally believe a) Volek’s studies show the effect because the level of experimental error necessary to account for differences would be too large and, more important b) given the potential benefit in palpable metabolic advantage it would be worthwhile to try to find the conditions in which it can be seen and that this would be time better spent than in trying to disprove it with incompletely understood thermodynamics.

7. The other reason for looking for how the theory could be seen in a real weight loss experiment, is that it occurs unambiguously in numerous other biological systems: hypo- or hyper-thyroid conditions, catch-up fat in humans and animal models, animal knock-out or over-expression experiments.

8. I generally don’t pull rank on anybody and I don’t know that there is special criteria for being a scientist but you do have to understand the difference between an effect that is absolutely dictated by physical science (e.g. general theory of relativity) and the difficulty in demonstrating it experimentally (waiting for a solar eclipse and winding up with unreadable photographic plates).

9. Along these lines, like most chemists (or maybe most everybody), I have always found thermodynamics difficult and I am willing to learn from anybody who has an insight.  However…

10. I grew up in Brooklyn so I am capable of a dialogue in the style favored by Colpo and Lyle McDonald but I mostly outgrew it and don’t want to debate at that level.

11.  Relevant ideas to ponder:  I once challenged Colpo to give me a definition of the nutritional calorie (because this makes clear what the issue is), that is, not the definition of the physical calorie (raises a gram of water 1 degree C ) but what we mean when we say carbohydrate has 4 kcal/g.  His answer suggested that he had undergone spontaneous combustion but anybody else can answer the question.  The other question is that in bioenergetics we talk about calories as the free energy, G, which is a potential, analogous to gravitational potential.  When you throw the boulder off the cliff its potential energy is converted to kinetic energy and then goes to zero when it hits the bottom.  Where does the energy go?  The delta G (energy of reaction) for hydrolysis of a peptide bond is about 2 kcal.  When it reaches equilibrium (amino acids) the energy is zero.  In other words, thermodynamics talks about dissipation of energy, not conservation.  How is that possible?  Where does the energy go? 

Hope this helps.

Richard David Feinman
Professor of Cell BiologyTher
SUNY Downstate Medical Center

As a bit of lagniappe, here is a short video Dr. Feinman created on thermodynamics and irreversibility:

Click here to view the embedded video.

Addendum:

Richard Nikoley over at Free the Animal posted his take on the latest Colpo meltdown. As a part of his post, Richard dug out and put up one of my responses to a commenter from a post I wrote a couple of years ago. I had completely forgotten about it, but since it applies to the situation discussed above, I’m reprinting the comment by Ryan and my response below.  A hat tip to Richard for ferreting this out:

I have a question that may be related to this.

On several low carb forums right now, there is a debate going on about what happens to the extra fat calories if carbs are kept extra low so that insulin is kept low. Some say it will be stored as fat anyway, others say it will be burned as heat and still others say it will be excreted. One member even did near-zero carbs and very high fat for a week (4500 calories instead of a normal 2500, with an average of about 80-90 g of protein). He lost a pound off of his already lean physique.

So, where does that extra fat go? Is it excreted? The detractors say that fat is completely digested before reaching the colon but I am not sure. If it is excreted, could you go ultra high fat, zero carb for a week or so and get the same detox results as the cosmic pizza grease?

Hi Ryan–

Your comment raises an interesting question. Where does all the excess energy go?

I’ve had a number of patients and countless letters from readers who have had the same experience. They consume a ton of fat, but don’t gain weight…or even, as with the guy you described, lose a little. Mostly the letters we get are from people who complain that they are following our diet to the letter, yet not losing weight. When we investigate, we find that in virtually every case these people are consuming huge numbers of calories as primarily fat. We always ask them if it doesn’t strike them as strange that they’re eating as much as they are, yet not gaining.

In order to lose weight, one must create a caloric deficit. This can be done in a number of ways. People can burn more calories by increasing exercise; they can eat fewer calories; or they can increase their metabolic rate. Or they can do any combination of the above.

Most people going on a low-carb diet decrease their caloric intake. A low-carb diet is satiating, so most people eat much less than they think they are eating even though the foods they’re consuming are pretty high in fat. Some people, however, can eat a whole lot on a low-carb diet, and, can in fact, eat so much that they don’t create the caloric deficit and don’t lose weight. But the interesting thing is that they don’t gain weight either. They pretty much stay the same. They are eating huge numbers of calories and not gaining, so where do the calories go?

First, I don’t think they go out in the bowel. If they did, people would have cosmic pizza grease stools whenever they ate a lot of fat over a period of time, and they don’t. And a number of studies have shown that increasing fat in the diet doesn’t increase fat in the stool.

Eating a very-low-carbohydrate diet ensures that insulin levels stay low. Unless insulin levels are up, it’s almost impossible to store fat in the fat cells. With high insulin levels fat travels into the fat cell; with low insulin levels fat travels out. So, it’s pretty safe to say that the fat isn’t stored. So what happens to it?

The body requires about 200 grams of glucose per day to function properly. About 70 grams of this glucose can be replaced by ketone bodies, leaving around 130 grams that the body has to come up with, which it does by converting protein to glucose and by using some of the glycerol backbone of the triglyceride molecule (the form in which fat is stored) for glucose. If one eats carbs, the carbs are absorbed as glucose and it doesn’t take much energy for the body to come up with its 200 gram requirement; if, however, one isn’t eating any carbohydrates, the body has to spend energy to convert the protein and trigylceride to glucose. That’s one reason that the caloric requirements go up on a low-carb diet.

The other reason is that the body increases futile cycling. What are futile cycles? Futile cycles are what give us our body temperature of 98.6 degrees. Futile cycles are just what the name implies: a cycle that requires energy yet accomplishes nothing. It operates much like you would if you took rocks from one pile and piled them in another, then took them from that pile and piled them back where they were to start with. A lot of work would have been expended with no net end result.

The body has many systems that can cycle this way, and all of them require energy. Look up the malate-aspartate shuttle; that’s one that often cycles futilely.

Another way the body dumps calories is through the inner mitochondrial membrane. This gets a little complicated, but I’ll try to simplify it as much as possible. The body doesn’t use fat or glucose directly as fuel. These substances can be thought of as crude oil. You can’t burn crude oil in your car, but you can burn gasoline. The crude oil is converted via the refining process into the gasoline you can burn. It’s the same with fat, protein and glucose–they must be converted into the ‘gasoline’ for the body, which is a substance called adenosine triphosphate (ATP). How does this conversion take place? That’s the complicated part.

ATP is made from adenosine diphosphate (ADP) in an enzymatic structure called ATP synthase, which is a sort of turbine-like structure that is driven by the electromotive force created by the osmotic and electrical difference between the two sides of the inner mitochondrial membrane. One one side of the membrane are many more protons than on the other side. The turbine-like ATP synthase spans the membrane, and as the protons rush through from the high proton side to the low proton side (much like water rushing through a turbine in a dam from the high-water side to the low-water side) the turbine converts ADP to ATP.

The energy required to get the protons heavily concentrated on one side so that they will rush through the turbine comes from the food we eat. Food is ultimately broken down to high-energy electrons. These electrons are released into a series of complex molecules along the inner mitochondrial membrane. Each complex passes the electrons to the next in line (much like a bucket brigade), and at each pass along the way, the electrons give off energy. This energy is used to pump protons across the membrane to create the membrane electromotive force that drives the turbines. The electrons are handed off from one complex to the other until at the end of the chain they are attached to oxygen to form water. (If one of these electrons being passed along the chain of complexes somehow escapes before it reaches the end, it becomes a free radical. This is where most free radicals come from.)

There are two parts to the whole process. The process of converting ADP to ATP is called phosphorylation and the process of the electrons ultimately attaching to oxygen is called oxidation. The combined process is called oxidative phosphorylation. It is referred to as ‘uncoupling’ when, for whatever reason, the oxidation process doesn’t lead to the phosphorylation process. Anything that causes this uncoupling is called an ‘uncoupling agent.’

You can see that the whole process requires some means of regulation. If not, then the electromotive force (called the protonmotive force, since it’s an unequal concentration of protons causing the force) can build up to too great a level. If one overconsumes food and doesn’t need the ATP, then the protonmotive force would build up and not be discharged through the turbines because the body doesn’t need the ATP. The body has accounted for this problem with pores through the inner mitochondrial membrane where protons can drift through as the concentration builds too high and by proteins called uncoupling proteins that actually pump the protons back across. So we expend food energy to pump protons one way, then more energy to pump them back.

One of the things that happens on a high fat diet is that the body makes more uncoupling proteins. So, with carbs low and fat high, the body compensates, not by ditching fat in the stool, but by increasing futile cycling and by increasing the numbers of uncoupling proteins and even increasing the porosity of the inner mitochondrial membrane so that the protons that required energy to be moved across the membrane are then moved back. So, ultimately, just like the rocks in my example above, the protons are taken from one pile and moved to another then moved back to the original pile, requiring a lot of energy expenditure with nothing really accomplished.

This is probably all as clear as mud, but it is what happens to the excess calories on a low-carb, high-fat diet.

Cheers–

MRE

The event kicked off last night with a small reception with Sir George Martin.  About 50 people came to a wine and hors d’oeuvres at the Founders Room of the Granada theater.  Sir George gave a wonderful talk about his early career and his first meeting with the Beatles.  At that time non-Sir George was heading EMI records and his specialty was comedy records.  Brian Epstein had arranged an appointment (Martin said he still has his diary, which lists Epstein as Bernard Epstein) and when Martin told him that he wasn’t interested, Epstein looked so dejected, that Martin relented and said, “Okay, I’ll give them one hour next week.”

The Beatles came in at the appointed time, were terrible as musicians, but were absolutely charming.  Martin took them into the control room to listen to their audition recording and told them to tell him if there was anything they didn’t like.  George Harrison promptly said,”For starters, I’m not crazy about your tie.”  The other Beatles were mortified because they thought George may have blown the deal for them.  George Martin, on the other hand, thought it was hilarious.  At the end of the day, he agreed to give them a recording contract.  Then, as he said in his talk, “As we all know, the rest is history.”

He also said that after he had given the Beatles their first contract, he discovered that they had been turned down by every other record producer in England.  He had been their last resort.  Funny how things work out.

When MD and I woke up this morning, the article below was in the Santa Barbara paper. I shamelessly ripped the photo of MD and me with Sir George and put it at the top of this post.

The Dallas branch of the Eades fam flew in from Dallas for the big event, but the eldest grandchild got sick on the plane.  The two others were in fine shape, though, and ended up having their own audience with Sir George in his dressing room.  The eldest woke up in great shape this morning, so he’ll be at the big premier performance tonight.

Photo at top and in article by Matt Weir

Photo at bottom by MD Eades and her iPhone

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

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

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

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

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

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

So, with that preamble, here it is.

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

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

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

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

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

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

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

To solve this problem, AC turns to what he calls

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Second subject:

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

Third subject:

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

Forth subject:

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

Fifth subject:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Wow!  Where do we start?

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

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

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

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

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

After going through all the data, Rabast et al conclude

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kinsell et al

Grey Kipnes

Rabast et al 1979

Rabast et al 1981

Yang et al

Bogardus et al

Hoffer et al

Leibel et al

Vazquez 1992

Vazquez 1994

Vazquez 1995

Piatti et al

Golay et al

Myashita

I had a little R & R, played some golf, and just enjoyed myself in general.  Had all the same kinds of food I wrote about in a post last year, so I returned well fed.  Now I’m tanned, fed, fit and ready to type, so it’s back to the grindstone.

Thanks to the poor economy, this trip was a little more exciting than previous trips.  At least the golf part.  When we pulled the carts up to the first green on the first day we played, the caddy told us to pull off the cart path and park the carts down by the green.  When we asked why, he replied, “Banditos.”

Turns out that hard times have driven many desperate people to turn to crime to feed their families.  According to the caddy, ‘banditos’ hide in the jungle along side the cart paths and come out while the players are on the green and steal anything they can get their hands on.  A few weeks before we got there, there was an actual armed robbery on the course.  Fortunately, our trip was without incident, so I returned home with all my belongings.  Didn’t even lose anything to the airlines, which is probably a more likely way to lose valuables than to banditos on the golf course.

Aside from banditos, there are other dangers on the courses in Mexico.  I took the photo of this guy shown below as I drove by him in the golf cart.  Anywhere there is water on the Marina Vallarta course, there are crocidilos lying about.  You’ve also got to keep an eye out for snakes whenever you hunt for lost balls in the jungle bordering the courses.  And there are iguanas everywhere.

One of the things I like about Mexico is always coming upon the unexpected.  The giant head in the photo above was half buried in the ground just off the tee box of one of the holes.  I caught a glimpse of it through the trees and couldn’t figure out what it was.  I walked around and through the brush until I could see it and snapped a photo with my iPhone.  What is it?  A football player? Why is it there in the middle of nowhere?

While I was south of the border my web guy was hard at work, which is a nice segue into a couple of blog housekeeping issues.  Those who read the comments have discovered that my comments are now up in a salmon color.  And my tech guy has installed a plug in so that I can answer specific comments and end up indented right below them so that I don’t have to use the @[insert name] business.  Anyone who wants to reply to a specific comment or even to a reply to a comment can do so by clicking the blue highlighted ‘Reply.’

This makes the entire process much, much easier for me, and will help – I fervently hope – me to keep up with the comments in a more timely fashion.

At long last the 6-Week Cure blog is finished.  All I have to do is have the tech guy click it on and you will be able to click on it from the menu at the top under ‘Blogs.’  All it is right now is an empty template.  MD and I have to populate it with a little content before it goes up.  I’m hoping it should be up with some content within a week.

I’m having trouble getting MD to focus on anything but the wretched Choral Society (of which she is the president) right now because of her big event coming up in about ten days, so if there is going to be content, I’ll have to create it.  And I’ve got a lot of other posts I want to do that aren’t 6-Week Cure posts.

MD has been working on an extravaganza that will be performed on Feb 13th and 14th in Santa Barbara that may well be the social event of the season.  I’ll post more on it as the time draws nearer, but just to give you an idea as to what’s going on, her group is singing the world premier of a choral piece written by Sir George Martin (yes, he of The Beatles fame), and, as it turns out, Sir George himself is coming from London to conduct it.  Along with the choral piece, Sir George will conduct the chorus in a version of Eleanor Rigby that he scored as a choral piece.  The rest of the performance will be Beatles tunes scored for chorus accompanied by a world premier ballet choreographed for this occasion.  So, she has a lot of work to do to pull this all together.  I suppose I’ll cut her some slack in the blog-content-creating department. At least until Feb 15.

As for my own content on this blog, the next post will be the long-awaited and promised post examining and critiquing Anthony Colpo’s Fat Loss Bible.  It will actually be a two-part post with the first part devoted to showing the errors of Anthony’s thinking vis a vis the metabolic advantage, and the second will be an in-depth look at a famous paper that Antony has dismissed out of hand but which, as you shall see, is really a brilliant study.  With these two posts, I’ll put paid to Anthony Colpo and hope to never mention him again.

I’ve been so busy lately that I haven’t posted a lot, but that doesn’t mean I haven’t been thinking about posting.  I’ve got a number of things I’ve been wanting to write about that  I plan to have up as soon as the Colpo deal is finished.  I want to add my two cents worth on a bunch of the problems some Paleo dieters seem to develop.  And I’ve got a post cooking on the thyroid and iodine.  One on fructose, and one on saturated fat.  Plus the analysis of the next stupid study that will inevitably pop up and seize the imagination of the mainstream media types who will shout it from the rooftops.

Ron Krauss and his group published a paper in the Articles in Press section of the American Journal of Clinical Nutrition (AJCN) stating there is no evidence that saturated fat intake increases the risk for heart disease.  The paper, titled Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, is not a study per se, but is a meta-analysis, a compilation of numerous studies looking at the relationship between saturated fat intake and the risk for developing heart disease.

As I’ve discussed before on these pages, meta-analyses are not my favorite types of studies.  I’ve attacked them when they’ve been used to ‘prove’ the low-fat diets are better, so I can’t very well embrace meta-analyses when they present a conclusion I agree with.  And I really can’t embrace meta-analyses when they are compilations of observational studies, which are themselves next to worthless.

For those who don’t know, meta-analyses are compilation studies in which researchers comb the medical literature for papers on a particular subject and then combine all the data  from the individual studies together into one large study.  This combining is often done to bring together a collection of studies, none of which contain data that has reached statistical significance, to see if the aggregate of all the data in the studies reaches statistical significance.  I think these types of meta-analyses are highly suspect, because they can lead to conclusions not warranted by the actual data.

To give you an example of what I mean, let’s assume that we have a study looking at a flipped coin.  If a researcher flips a coin 10 times and comes up with 6 heads and 4 tails, runs this through a program checking for statistical significance, he/she will discover that the 6-4 ratio isn’t a statistically-significant difference because of the low number of overall flips (10).  Now, let’s say that 50 researchers did the same kinds of study and some found that their coins came up heads 6 times out of 10 or 4 times out of 10, etc.  If a researcher then wants to ‘prove’ that heads comes up more times than tails on a coin flip, he/she can gather all the studies showing heads come up more times than tails, add them together in a meta-analysis and come up with 25 studies, each with 10 flips, showing that heads came up 63 percent of the time.  Now we’re talking 250 flips and we would probably reach statistical significance.  We know that over the long run a flipped coin is going to come up heads about 50 percent of the time and that the more the times it is flipped the more likely the number of heads will close in on the 50 percent figure.  But, the meta-analysis that selected the studies showing the 63 percent heads is statistically significant because the studies were cherry picked.

Researchers using meta-analyses set up selection criteria to pick which studies will be included in their final product, which leaves the door open for all kinds of mischief.  For example, let’s say a researcher wants to make the case that low-fat diets reduce cancer. He/she would create a set of criteria, do a literature search for all the studies that meet those criteria, then do a statistical analysis of all the data.  If the data demonstrate that low-fat diets are linked to lower rates of cancer to a statistically significant degree, the researchers submit their paper for publication.  But let’s say that when the data is crunched, it doesn’t show any such relationship?  It’s easy to go through all the studies and find which ones strongly show the opposite of what the researchers want to show and then figure out how to change the study-selection criteria in such a way as to keep those studies from being selected, run the whole process again, and repeat until enough studies are found to make the meta-analysis show the link between low-fat diets and lower rates of cancer.

Sad to say, this is often how it is done.  Which is why I don’t give a lot of credence to meta-analyses.

But having said all this, I’m still happy to see a researcher with the academic credentials of Ron Krauss coming out with a meta-analysis showing no correlation between saturated fat intake and cardiovascular disease risk.  And getting it published in the AJCN, probably the world’s most prestigious nutritional journal, no less.  It’s called putting your money where your mouth is.  Many academics whom I’ve spoken with admit that there is no correlation, but wouldn’t risk their academic reputations doing a meta-analysis to ‘prove’ it.

I’ve had many people tell me that it’s really nice to finally see some studies coming out vindicating saturated fats.  Or at least not attacking them.

I have to tell them that pro-saturated fat studies have been around for years.  Not just observational studies or meta-analyses, but real controlled studies looking at death rates from heart disease as a function of fat intake.

Let’s look at a couple.

Over 40 years ago, way back in 1965, there were two studies published showing that heart patients – the kind of people who today assiduously avoid saturated fat – who ate saturated fat were more likely to survive than those who didn’t.

One paper titled Low-Fat Diet in Myocardial Infarction, published in The Lancet, looked at the survival of subjects who had suffered heart attacks who went on either low-fat diets or their regular high-saturated-fat diets.

Here’s what they did:

264 men under the age of sixty-five, who had recently recovered from a first myocardial infarction and who had been in the Central Middlesex, Edgeware General, or West Middlesex hospitals took part in the trial.  On leaving hospital they were allocated at random to one of two groups at each hospital.  One group was placed on a low-fat diet, which the other group continued with their normal diet.

The trial, which ran from 1957 to 1963, was managed by four research medical registrars working at the three different hospitals.
What was the low-fat diet?

Patients in the diet group were allowed to take 40 g fat daily [under 20 % fat].  The daily allowance included 14 g (1/2 oz) butter, 84 g (3 oz) of meat, 1 egg, 56 g (2 oz) cottage cheese, and skimmed milk.  The nature of the fat consumed was not altered, nor were any additional unsaturated fats given.  The diet was often unpleasant, [my italics] and where possible, it was modified to suit individual tastes.

The body of the article states that the control subjects on their regular diet consumed about 2.5 times the fat eaten by those on the low-fat diet. (106-125 g for the former; 44-45 g for the latter.)  I ran the saturated fat calculations on the low-fat study diet and found that it contained about 30 g saturated fat, which is about 13.5 percent of total calories.  Most ‘experts’ today recommend keeping saturated fat under 10 percent of total calories.  Given how the data was presented in this paper, there was no way to tell how much saturated fat the control group got, but we can estimate their total fat intake to be about 46 percent, which was the average fat content of the typical American diet when I first got into this biz way back in the early 1980s just as the low-fat jihad was kicking off.  I would guess that the control diet contained 60-70 g of sat fat or about 25 percent of calories.  You can see the difference in fat intake in the graph above on the left.

The patients on the low-fat diet had pretty close counseling during the course of the multi-year study, and, consequently, they hewed fairly closely to their diet.  The researchers knew this because the study group consumed about 400 fewer calories per day as compared to those subjects on their regular diet and lost weight.  The researchers also used serum cholesterol levels as a measure of compliance to the diet.  In 1965 it was well known that reducing fat in the diet, especially saturated fat, made cholesterol levels go down.  As you can see from the chart on the right, cholesterol levels went down on the low-fat diet and stayed there.

What did the researchers find after observing these subjects for years?  They found that putting people on unpleasant low-fat diets didn’t help them live any longer nor avoid another heart attack.  Over the course of the study, the same number of subjects died in both groups.

What were the recommendations of the authors of the study?

It is concluded that in men under the age of sixty-five who have survived a first myocardial infarction, a low-fat diet does not improve their prognosis.

Summary

A controlled diet of a 40 g low-fat diet was carried out on 264 men who had survived a first infarction.  Despite a lowering of the blood-cholesterol and a greater fall in body-weight in the treated group, the relapse rate was not significantly different in the two groups.

A low-fat diet has no place in the treatment of myocardial infarction.

Ah, how things have changed since 1965.  And not for the better.

Here is another.

A paper published in the British Medical Journal (BMJ) in 1965 titled Corn Oil in Treatment of Ischemic Heart Disease looks at the differences in the rates of death or a second heart attack in patients following one of three diets: Their regular diet (control diet), a high-olive-oil diet, or a high-corn-oil diet.  After determining the caloric intake of the control group, the researchers had subjects in the other two groups restrict their intake of fat from foods as much as possible and replace it with supplements of either olive or corn oil in amounts calculated to match the calories they reduced by getting rid of animal fat.  The subjects getting one of the two oils ended up getting about 80 g per day.

The aims of the study were as follows:

Our purpose was to study the effects of prescribing a vegetable oil and a restricted fat diet to patients with ischaemic heart disease.  The primary interest was in an unsaturated oil with a cholesterol-lowering effect.  But large doses of any oil may have secondary effects on diet and nutrition, so that differences between an unsaturated-oil group and a control group might be due to these secondary effects rather than to unsaturated fatty acids as such.  It could, for example, be relevant that mortality from heart disease is low in Italy and Greece, whose inhabitants consume much olive oil; this oil has no major effect on serum cholesterol level, its main fatty acid (oleic acid) being only mono-unsaturated.  The trial was therefore designed to study the effects not only of a more highly unsaturated oil (corn oil) but also of olive oil.  It seemed likely that if any differences emerged between the olive-oil and corn-oil groups these would reflect the specific effects of polyunsaturated fatty acids.

After starting the diets to which they were randomized, the subjects were followed closely for two years.  As with the last paper, the researchers used serum cholesterol levels to monitor compliance with the diet.  You can see the differences in serum cholesterol in the three groups in the chart below.  Note that the cholesterol levels in the control group did not change a significant amount, which would be expected.  The same held true for the olive oil group: no significant change.  But those subjects in the corn-oil group dropped their cholesterol levels significantly.

Over the course of the study a number of patients died or had a second heart attack.  The researchers knew which subjects were on the control diets but were blinded (as were the subjects) and so didn’t know which were consuming the olive oil or the corn oil.

When the codes were broken and the data analyzed, it turned out that 75 percent of subjects following their standard high-fat, high-saturated-fat diets were remaining alive and free from a second heart attack whereas only 57 percent of subjects on the olive oil had done so.  The group with the worst outcome was the corn-oil group.  Only 52 percent of those subjects remained alive and heart-attack free.

The authors’ summary:

Eighty patients with ischaemic heart disease were allocated randomly to three treatment groups.  The first was a control group.  The second received a supplement of olive oil with restriction of animal fat.  The third received corn oil with restriction of animal fat.  The serum-cholesterol levels fell in the corn-oil group, but by the end of two years the proportions of patients remaining alive and free of reinfarction (fatal or non-fatal) were 75%, 57%, and 52% in the three groups respectively.

It was concluded that under the circumstances of this trial, corn oil cannot be recommended in the treatment of ischaemic heart disease.

In this same issue of the BMJ appeared an editorial about this study.  The author of this editorial points out that

the patients treated with corn oil had the worst experience, though initially their outlook was apparently similar to that of the other groups.  There is a 1-in10 to 1-in-20 chance that corn oil had a deleterious effect; the probability of its having any beneficial effect is remote.

This came at a time when corn oil was being touted on advertisements everywhere as the best oil to prevent heart disease because it is polyunsaturated.

The editorial goes on to grumble about the outcome and discusses a few other studies with conflicting outcomes.  The writer finally declares that maybe the problem is that this and other studies have been done on subjects who already have heart disease.  Maybe that’s too late in the game to make a difference.  (The outcome of this study wouldn’t indicate that, but the writer didn’t let that fact get in the way of his opining.)

Maybe it doesn’t help to lower cholesterol or increase polyunsaturated fats in those already afflicted; maybe what really needs to be done is to increase polyunsaturated fats and lower cholesterol levels in healthy people with no sign of heart disease.

A different approach, and a formidable one, is the prevention of ischaemic heart disease by altering the diet of healthy people.  A study of the organization of such a scheme in the U.S.A showed that it was practicable, and an anti-coronary club for men has been in existence in New York since 1957.  Its 814 members take a “prudent diet” in which fat is moderately reduced and equal proportions of saturated, monounsaturated, and polyunsaturated fats are eaten.  Already there is evidence  that the development of “coronary events” is being prevented.  Again, we await confirmatory evidence.

What the editorialist is waiting for is evidence to confirm his bias that reducing fat generally and saturated fat specifically (while increasing polyunsaturated fat) and the lowered cholesterol levels arising from such changes will prevent the development of heart disease.  Unfortunately, for him, this confirmatory evidence was not forthcoming.

From Gary Taubes’ Good Calories, Bad Calories (pg 36 hardcover):

Overweight Anti-Coronary Club members were prescribed a sixteen-hundred-calorie diet that consisted of less than 20 percent fat.

[It was reported] in February 1966 that the diet protected against heart disease.  Anti-Coronary Club members who remained on the prudent diet had only one-third the heart disease of controls.  The longer you stayed on the diet, the more you benefited, it was said.  But in November 1966, just nine months later, the Anti-Coronary Club investigators published a second article, revealing that twenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent.  Eight members of the club died from heart attacks, but none of the controls.

Like the maze shown at the top of this post, the people who have a bias against fat are trying to make things more complex than they are.  The simple solution is to look at the mortality, which no one wants to look at because it doesn’t confirm their bias.  They all want to look at more complex issues that have little bearing on the most important issue – whether one lives or dies.

Even the authors of the study showing the members of the Anti-Coronary Club members dying at enormously higher rates than non-members and dying with heart attacks want to look at other more complex information.

Gary Taubes continues

This [the deaths by heart attack of the club members] appeared “somewhat unusual,” Christake [the author of the paper] and his colleagues acknowledged.  They discussed the improvements in heart-disease risk factors (cholesterol, weight, and blood pressure decreased) and the significant reduction in debilitating illness “from new coronary heart disease,” but omitted further discussion of mortality.

Classic behavior from someone whose mind is made up.  Ignore the evidence denying your hypothesis and focus on that confirming it.  Instead of focusing on which people actually die of heart disease, let’s spend our time running through the maze looking at how our beloved low-fat diet reduces supposed risk factors. Which brings to mind a wonderful Winston Churchill quote:

However beautiful the strategy, you should occasionally look at the results.

How many people have died or been incapacitated with heart disease since 1965 when the evidence above was presented?  How many fathers, mothers, aunts, uncles, grandfathers and grandmothers could have had more years of productive lives if only the people who do these studies had looked at just the two mentioned above and taken the tack that maybe they had been going down the wrong path?  Had they done that instead of ignoring these results and continuing to try to prove an hypothesis that can’t be proven, how many lives might have been saved?  I’m glad it’s not on my conscience.

For maze at top
hat tip to FAILblog.org

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

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

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

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

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

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

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

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

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

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

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

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

Give me strength.

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

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

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

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

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

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

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

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

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

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

Here’s what the authors wrote:

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

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

…compliance was assessed with objective biomarkers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Three weeks later:

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

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

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

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

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

Her labs told another story.

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

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

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

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

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

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

I am eternally grateful to them.