Hard at work in Seattle

Mt St Helens blog

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

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

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

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

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

Seattle skyline blog

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

Boat in winter blog

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

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

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

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

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

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

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

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

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

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

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

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

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

Odds and ends June 28, 2009

globe-trotter

Product review: Globe Trotter luggage

The photo you see above is of my beloved Globe Trotter Cetenary roll aboard.  I took it with me on this last trip to Hong Kong and London, much to the chagrin of MD, who hates this piece of luggage with a passion.

MD is a packer extraordinaire and is totally practical.  When it comes to packing, ‘cool looking’ isn’t in her vocabulary.  Since we travel so much, we have gone through many pieces of luggage over the years, and she has found the Hartmann bags best for her particular style of packing.  She can cram more into her Hartmann bags than any one believes possible.  And when she pulls her packed stuff out, it all looks great.

She has evaluated other luggage (usually at my insistence), but always defaults to Hartmann whenever she needs a new bag.  She picks the Hartmann bag she thinks looks the best, but would never, ever trade looks for utility.

I, on the other hand, will put up with a little loss in utility for a big load of cool.  And, in my opinion, the Globe Trotter luggage is maximally cool.  I’ve lusted over this stuff since the first time I read about it and saw a picture.  Every time we go to London, I would head for the Burlington Arcade where the main Globe Trotter store is housed and slobber over all the different pieces.  Finally, a few years ago, much to MD’s displeasure, I succumbed and purchased the above roll-aboard or trolley, as they call it.

Every time I try to take it anywhere, MD whines.  It isn’t divided into dual compartments- it’s just one empty box on wheels.  And it doesn’t open completely so that the top lays flat.  She feels it limits the amount that can be packed and easily retrieved, and she’s no doubt correct, but that doesn’t mean it’s worthless.  It has hard sides, so stuff is protected, and it has leather straps so it can’t pop open, and it has a great wheel system, so it’s easy to pull.  But those virtues mean nothing to her, so she always beats me down when I want to take it on one of our trips.

This time, however, I manned up and took it despite her protestations.  It functioned okay at best.  It was a real pain to get into in the overhead of the airplane, what with having to deal with the straps and the locks and the lid.  It’s much easier to simply unzip a bag and reach in.  All the gripes MD had about it turned out to be correct.  I’ve realized that Globe Trotter bags, which have been made since the late 1800s, were designed and built for a time when someone else handled all of your bags when traveling.  They’re made for durability and for unloading once you get to your destination – they’re not worth a flip if you live out of your suitcase as we often do while on the road.

I no doubt looked dashing as I wheeled my trolley across the lobby of the Mandarin Oriental hotel in Hong Kong, but that didn’t make up for the  all the downside.  Globe Trotter luggage does look great, but in this case, at least for my purposes, the looks don’t trump the lack of utility.

The placebo effect and observational studies

I got the following comment (reprinted here in part) on my last post:

Dr Mike, I must say I’m a bit uneasy about your attitude to observational studies. Doesn’t that in effect disparage most “traditional” knowledge, whether architectural (”If we build things in this way, they don’t seem to fall down”), medical (”People seem to recover from their fever when I give them this combination of herbs”), societal (”If we set up this kind of committee, things seem to function more or less peacefully and efficiently”)? I understand that an observational study doesn’t prove anything by itself but it seems that it’s a more formalized kind of traditional observation, one that, crucially, makes itself transparent and therefore open to future reinterpretation. I may be misunderstanding your stance, but I worry that in effect it negates most of humankind’s historical progress, and any kind of inquiry that doesn’t fit your preferred methods.

This commenter sets up the problem in a way that it can be explained easily.  And probably more clearly than I’ve explained it in the past.

As I pointed out in my post on observational studies, these kinds of studies are worthless for proving causality, but useful in defining hypotheses that can be tested.  Let’s take one line from the comment and is it to demonstrate what I mean.

“People seem to recover from their fever when I give them this combination of herbs.”

A perfect example.  Let’s say that some witch doctor sometime in the past came up with an herbal concoction that helped his ‘patients’ recover from a fever.  Over the years this herbal therapy was passed down from witch doctor to witch doctor, and it worked without fail.  A traditional doctor heard of the cure, tried it on a few patients and found that it did indeed seem to work.  Every time the good doctor prescribed this herbal remedy, patients had their fevers break and began to get well.  This doctor told other doctors, many of whom began using the herbs, and their patients, too, recovered from their fevers.  Patients swore by the stuff and rushed to their doctors to get it whenever they got sick.  Traditional doctors and witch doctors alike were in agreement that the potion works like magic.

Then comes a scientist who looks at the data and says, hey, here is a great observational study.  All the observational data indicate this stuff works like a charm, so let’s make that our hypothesis, which, simply stated, is that Herbal Mixture X reduces fever in those who take it.

Now that the hypothesis has been developed, it needs to be tested.  The best way to test it is with a randomized, double-blind, placebo-controlled study.  Our scientist recruits doctors in several clinics across the country who are familiar with the workings of Herbal Mixture X (HMX) and provides them with a study protocol and unlabeled HMX and placebo, both of which look identical.  As per the protocol, any patient who comes into the clinic with a temperature above 101 [degrees] F gets a randomly generated number and either the HMX or the placebo.  Neither the patient nor the doctor knows who is getting the real stuff and who’s getting the placebo, which makes the study double blind.  If the doctor knew who was getting the HMX, then the study would be single-blind, not double-blind, which would not remove the physician bias from the study.  The assumption is that if the doctor doesn’t know which is which, he/she will treat all patients the same and not let some subtle bias slip into the experiment.

When a patient presents to the clinic with a fever, the doctor gives either HMX or placebo and waits to see what happens.  The doctor or staff contact the patients daily and have them report their temperatures.  When temperature has returned to normal, the data point is entered on the patient’s chart.  After a specific number of patients have gone through the protocol, the codes are broken to see which patient got the HMX and which got placebo.  The scientist then crunches the data to see whether the supposed fever-lowering ability of HMX is statistically significantly different from that of placebo.  And, lo and behold, let’s say for argument’s sake there is no difference.

There is a huge outcry from all the docs who have used the treatment.  The study was flawed, they scream.  We know this stuff works.  We’ve used it for years, and we’ve seen it work.  Same goes for the patients who have taken HMX over the years: they swear by it, too.  They say, We don’t care what one stupid study showed – we know it works.

So, another group of scientists takes on the project and repeats the study.  And gets the same results.  HMWX works no better than placebo.  All the same outcries arise, and so the study is repeated a few more times, all with the same result.  Clearly, HMX works no better than placebo when compared in a double-blind, placebo-controlled study, yet thousands of doctors and countless patients firmly believe in its efficacy.  What happened?  The observational data seemed to strongly ‘prove’ that HMX worked, but the actual testing showed it to be worthless.  What’s going on here?

What’s going on and what makes HMX work is the magic of the healer telling the patient that the therapy is potent along with the patient’s belief in both the healer and the strength of the remedy.  In other words, the placebo effect.

Don’t believe me?  With the recent death of Michael Jackson, reported by some as due to an overdose of a potent painkiller, said painkiller, Demerol, is much in the news.  I just read a piece written by a doctor on the placebo effect that describes the strength of this phenomenon.  Most physicians who have been in practice for any length of time have similar stories:

Jane D. was a regular visitor to our ER, usually showing up late at night demanding an injection of the narcotic Demerol, the only thing that worked for her severe headaches. One night the staff psychiatrist had the nurse give her an injection of saline instead. It worked! He told Jane she had responded to a placebo, discussed the implications, and thought he’d helped her understand that her problem was psychological. But as he was leaving the room, Jane asked, “Can I get that new medicine again next time instead of the Demerol? It really worked great!”

A placebo as strong as Demerol?  You bet.  Happens all the time.

I’ve been lambasted by many readers over my comments on the lack of efficacy of HCG treatment for weight loss.  Many have received what they consider to be significant benefit from HCG therapy and can’t possibly believe what they were experiencing is the placebo effect.  However, based on the many studies in which HCG was compared to placebo in double-blind testing, it is no better than placebo.  But that doesn’t deter those who don’t believe.  They know it works because it worked for them.  Which, of course, is how the placebo effect operates.  According to the results of at least 20 double-blind, placebo-controlled studies, these people would have experienced the same weight loss had they been given saline (salt water) injections or drops under their tongues and been told that the therapy they were given would keep hunger at bay and make their excess weight magically disappear as it had worked for thousands of others.  Of course, the 500 kcal/day diet helps, but in the minds of those who have had success with HCG, it is the hormone that does the trick.

Fat cells and adolescence

It has long been thought that fat cell number became fixed at about the time of late adolescence, and now a study using carbon-14 labeling pretty much confirms that hypothesis.

People get fat in childhood and up to late adolescence by increasing the number of their fat cells; people who get fat after adolescence do so not by adding more fat cells, but by increasing the size of the fat cells they already have.

What this difference in method of storing fat means is that it is more difficult to lose weight after a fat childhood than after gaining excess weight as an adult.  Why?  Because obese children have a large number of normal-sized fat cells that they carry on into adulthood.  To lose weight, they must reduce normal-sized fat cells to subnormal-sized ones, a more difficult prospect than reducing the abnormally-enlarged fat cells that are a consequence of adult weight gain back to normal size.  It can be done as evidenced by all the people who were overweight as children who have lost in adulthood, but it’s a tougher row to hoe than for those who got fat as adults.

Exercise and weight loss

Gary Taubes has taken a lot of heat as have I for publishing the idea that exercise doesn’t bring about weight loss.  The body compensates for increased exercise with increased food intake, and it takes surprisingly little food to replace whatever calories were lost by exercise.  Exercise has multiple benefits, and I recommend it to everyone because of those benefits, but, sadly, increased weight loss isn’t one of them.

This concept is one like the placebo effect that many people have difficulty grasping.  I’ve had countless comments from readers who have related their own stories of how they lost weight by a rigorous exercise regimen.  And they may have, but how do they know it was the exercise that did the trick?  How do they know they were losing weight because they were exercising instead of exercising because they were losing weight?  That statement seems ridiculous on the surface because it appears so obvious that the calories expended in exercise are what causes the weight loss.  But how do we know?  Perhaps because of a change in diet the body needs to ditch a bunch of excess calories from fat stores that are being emptied and does so by increasing the desire to exercise or increase fidgeting in an effort to dissipate this energy.  The increased weight loss brought about by this increase in exercise would be perceived as being caused by the exercise whereas in reality the exercise was caused by the need to lose weight.  It’s a difficult concept to grasp, but it has pretty much been shown in controlled studies that simply increasing exercise doesn’t reliably bring about weight loss.

As I wrote above, when people exercise, they generally increase their food intake to compensate.  But it’s not just the exercises itself that increase food intake, it could be simply thinking about exercise.

Researchers from the University of Illinois reported on two studies in which they correlated food intake with advertising encouraging exercise and even with subliminal words that had exercise connotations.  People ate more when simply hearing about exercise or hearing such words as ‘action’ in the context of something else.

Wrote they:

Alarming rates of overweight and obesity in the United States have led to the development of preventive communications and interventions to promote weight loss. As weight loss is contingent on energy expenditure exceeding caloric intake, one popular approach comprises promotion of physical activity. Media and community campaigns often encourage audiences to increase their physical activity by engaging in structured exercise or active routines. The present research was designed to explore potential effects of such campaigns on eating behavior.

Their conclusion:

Overall, the findings from these two experiments are suggestive in demonstrating that exercise messages can exert inadvertent immediate effects on food intake. Such consequences may not be apparent if exercise is the only measured outcome, but could potentially jeopardize weight loss.

The body likes to keep things on an even keel and maintain homeostasis and has all kinds of mechanisms for doing so.  If you walk past a bakery and smell the aroma of freshly baked bread, your pancreas figures there is going to be some carb coming its way soon, so it releases a little insulin in anticipation.  Apparently the same thing happens if you even think about exercise.  You eat just a little bit more to compensate – even before you exercise.

The dark side of fiber

You just about can’t read anything these days without hearing the virtues of fiber extolled.  It seems that fiber is on everyone’s good list.  Even low-carb and Paleo diet advocates go to the trouble of making all aware that their diets contain plenty of fiber.  No one has anything bad to say about it.

Well, I do.  I can’t let one of these odds and ends posts end without linking to one of my own favorite posts from back in the days when I had only three readers.

Take a look here at a post about a pretty good study showing how fiber really exerts its effects.

My slogan has become: Fiber…who needs it?

Video fun
And, finally, I can’t quit without a video.  I saw a guy like the one in the YouTube below on the Johnny Carson Show years ago.  I was stunned back then that someone could do this, and I’m just as stunned now.  It just doesn’t seem possible.  Enjoy.

More braying from Bray

Dr. George Bray's model of obesity

Dr. George Bray's model of obesity

In July 2008 I posted on Dr. George Bray’s critique of Gary Taubes’ book Good Calories, Bad Calories that appeared in Obesity Reviews.  Included in my post was a copy of Gary’s response.  Now Dr. Bray is back with a rebuttal to Gary’s response to his (Bray’s) original critique.  In conversation, Gary told me he has elected to drop the issue because the discussion is going nowhere.  Gary makes substantive points; Bray obfuscates the issues and will continue to do so.  I, however, am not going to drop the case.  Maybe I’ll have the last word here.

I want to go over Dr. Bray’s response to Gary’s letter in some detail because it is emblematic of all that is wrong with obesity research today and clearly demonstrates why we will never get anywhere until the people of Bray’s generation fade away. I don’t know that I’ve ever seen so many instances of one writer missing the point as often as Dr. Bray does in this short reply.  The entirety of his response is an example of either shoddy thinking or intellectual dishonesty.  Or maybe both. It brings to mind Mary McCarthy’s famous quote about Lillian Hellman: “Every word she writes is a lie, including ‘and’ and ‘the’.

(You can read Dr. Bray’s original critique of Good Calories, Bad Calories along with Gary’s response in my July 2008 post.  The full-text of Dr. Bray’s letter of reply we’ll be discussing in today’s post can be found here.  You should pull it down in pdf and print it so you can follow along.)

Right off the bat, in the very first line, Bray leads off with his first porkie.

In his nearly 5000-word response to my book review, Mr. Taubes has raised a number of issues.

Gary’s response was slightly under 2000 words.  You might think this just simply a typo, and normally I would too, but the entire piece is filled with so many inaccuracies seemingly designed to denigrate Gary’s response that I don’t think so.  Why even put the number of words?  Why not simply say: In his response to my book review…?  By quantifying the number of words the way he does, Bray casts a pejorative shadow on Gary’s response from the get go.

If you read Gary’s letter, you will see that he methodically refutes Dr. Bray’s criticisms of GCBC and identifies those issues in which he feels Bray misses the point.  In his response, Bray says Gary’s critique of his (Bray’s) review of GCBC

opened the door for [him] to contrast [Taubes’] hypothesis for obesity with [his own].

It’s a kind of disingenuous way for Bray to get his own hypothesis of obesity into play in what amounts to a review of Gary’s book, but let’s take a look at what he has to say.  First, he completely simplifies and basically mischaracterizes Gary’s hypothesis of obesity.  Here is Gary’s hypothesis of obesity and his proposed treatment as interpreted by Dr. Bray:

taubes-model-of-obesity

As you can see, it appears pretty simplistic, which, I’m sure, was the intent.  Not shown are all the feedback loops and intricacies Gary has described at length in GCBC .

In referring to this diagram, Dr. Bray admits that it is based on “two sentences from the letter,” which doesn’t seem like a lot out of a 5,000-word letter (or even the 2,000-word letter that it was).  Then he goes on to use three sentences to establish the basis for the diagram.  (See what Mary McCarthy meant about even ‘and’ and ‘the’?)

After giving short shrift to Gary’s hypothesis of obesity, Dr. Bray then goes on to lay out in great detail his own theory of obesity as represented by the Rube Goldbergesque diagram at the top of this post.  Bray’s entire hypothesis, for which he recruits leptin, insulin, the brain, glucocorticoids, and God knows what else to help make his point, is based on a faulty premise.  But it’s a faulty premise he has accepted uncritically.

His hypothetical model of obesity, he authoritatively states

starts with the First Law of Thermodynamics, which states that the change of energy in a closed system is the difference between the heat added to the system and the work done by the system.

Dr. Bray then restates this hypothesis (and the First Law) in the form of this equation:

Δ E = Heat (q) – Work (w)

Readers of this blog know this as the energy balance equation, which looks like this in its more familiar form:

Δ Weight (the Δ means change) = Energy in (food) – Energy out (exercise plus metabolism)

The fatal flaw in Dr. Bray’s hypothesis (which is a flaw we’ve discussed often in these pages) is that he doesn’t understand that the components on the right side of the equal sign are not independent variables.  They are dependent variables.  If one eats less, the rate of metabolism falls to compensate.  If one exercises more, the appetite increases, and one eats more to compensate.

Were these components truly independent variables, life would be easier (but we may not have survived).  According to Dr. Bray, Anthony Colpo, and countless others, however, these components are independent variables.  Eat less, say they, and you’ll lose weight.  Which is true, to a point.  But once the energy-out component of the equation kicks in, weight loss stalls, even if you are eating less, a fact everyone who has ever dieted knows.  Exercise more, they pontificate, and you’ll lose weight.  Which, again, works (maybe) in the very short term.  But once appetite kicks in, you unconsciously eat enough more to compensate for your increase in exercise, as anyone knows who has tried to lose weight by walking or other exercise alone without consciously restraining eating.

Now don’t get me wrong, it is possible to lose weight by decreasing food intake and increasing exercise.  It worked well in the concentration camps in WWII and in Ancel Keys’ starvation studies in the 1940s.  But in those cases, people were under lock and key.  It doesn’t work for the long term for the majority of people unless they are coerced.

This fairly obvious observation that the energy in/energy out components are not independent variables seems to elude most (if not all) obesity researchers, including George Bray.  These people persist on basing the foundation of any obesity treatment on the admonition to eat less and exercise more, which is a total folly.  Yet Bray and his ilk continue to clothe this folly in the garments of academic respectability and work to pass it off as the latest fashion in scientific thinking.

Dr. Bray believes that the reason so many people are fat is twofold. First, he thinks  humans have a ‘hedonic’ drive that inexorably pushes them to increase their food intake.  And, second, he reckons that this ‘hedonic’ drive also overrides the “appropriate negative feedback signals to stop eating.”  What stimulates this ‘hedonic’ drive?  According to Dr. Bray

It is caused by the pleasurable effects of high-fat, high-sugar foods.

Well, at least he’s half right on that one.  No one binges on pure fat.  It’s impossible because of feedback inhibition to eat a lot of pure fat at a sitting.  Try sometime to sit down and eat some butter all by itself.  See how much you can choke down.  I can guarantee you it won’t be much.  Then add a little sugar to the mix and see what happens.  Suddenly the butter is converted to frosting, and you can put away a lot of it.  What’s the difference?  It’s the sugar.  Sugar – and carbohydrates in general – override the stop-eating center in the brain.  That’s why all binge eaters binge on a combination of fat and carbohydrate.  That’s also why you can go out to dinner, eat ‘til your stuffed, not be able to eat another bite of any kind of meat or other real food, yet perk up when the dessert tray comes around.  As the old saying goes: there’s always room for dessert.  Why? Because your brain knows the stop-eating center will be overridden by the sugar and carb in the dessert.

Dr. Bray would have been more accurate had he said that the stimulus for the ‘hedonic’ drive is carbohydrate.

But he doesn’t.  He is trapped in the fat-is-bad paradigm.

In experimental animals, highly palatable food or a high-fat diet is one of the easiest ways to disturb this homeostatic system [as defined by Dr. Bray], and this may apply to human beings as well.

Dr. Bray seems to believe that we live in a toxic world in food terms.  We are unable to help ourselves, and are therefore destined to be fat because of our ‘hedonic’ drive.  We are helpless.  There is no cure save eating less and exercising more, which even he more or less admits doesn’t work despite his entire model being based on the idea.  As I have discussed in another post, Dr. Bray is a major proponent of drug therapy to treat obesity.

In a way, I agree with him about the idea that we live in a toxic world, one with all kinds of the wrong kinds of food available to tempt us 24/7.  Problem is that Bray and his ilk are a major part of the reason we live in such a world.  But that’s a topic I’ll leave for a future post.

Dr. Bray makes a bizarre case for why he thinks the majority of dietary studies show better results in those subjects following low-carb diets than in those consuming low-fat regimens.  I’m going to use his own words, so you won’t think I’m making this up.

the principal studies that directly support this model [Taubes’ theory on low-carb dieting] included the word ‘Atkins’ in their clinical trial. When similar low-carbohydrate diets were tested without using this ‘name’, the low-carbohydrate diets had no more effect than those to which they were compared.

There you have it.  All you have to do to make a diet work is include the name ‘Atkins’ in the title.  I wish MD and I had known that when we wrote Protein Power.

What is truly ironic about this nonsense is that in this very same issue of Obesity Reviews containing Bray’s rebuttal is a long review article titled Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities.  This article takes an in depth look at studies comparing low-carb diets to low-fat diets.  Here is the conclusion as written in the abstract:

There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year.

Dr. Bray lists five other issues about Gary’s letter to which he wishes to respond, but before he gets to the list, he makes one last flippant point.

I thus conclude that if any diet ‘cured’ obesity as their proponents often claim, there would be no obesity and thus no need for the next diet. Yet the past 150 years, since the publication of Banting’s first popular diet, have seen a continuing stream of new diet books.

The reason, of course, is that we dieting fish all swim in waters that have been polluted by Bray and his brethren, more about which in a later post.

Now to the list.

1.    Near the end of the letter, Mr Taubes suggests that my review of his book may be a ‘conflict of interest’. He says ‘I [Bray] may be defending what my scientific research has led me to believe’. If this is a conflict of interest, then all scientists have a conflict of interest.

This first short point of only three sentences tells you everything you need to know about Dr. Bray’s scientific credibility.  I have no problem with the first sentence.  The second sentence is purportedly a quote from Gary Taubes letter.  It isn’t.  It is a paraphrase…sort of, but put in quotation marks.  This is a real no no.  It was done so for a particularly egregious reason, which was for a set up for Bray’s final sentence.  But that sentence even further diminishes his credibility.  Scientists are supposed to constantly challenge their own hypotheses, not accept them as fact simply because they’ve spent their careers enraptured with them.   All true scientists don’t have this conflict of interest.

2.    The first paragraph of his letter dealt with lipoproteins that I said he had not covered. The issue was not the lipoproteins but their receptors, from which we have learned so much in the past 30 years.

This one is a real copout.  In Bray’s original critique he wrote:

As I read through Good Calories, Bad Calories, I found a number of errors of omission or commission that are important when relating diet to heart disease.  There is no mention in the Diet-Heart section of low-density lipoprotein-cholesterol (‘bad cholesterol’) or of high-density lipoprotein-cholesterol (‘good cholesterol’).

The issue may have been the receptors and not the lipoproteins, but as you can see from his direct quote above, that’s not how Bray characterized it.  Gary set him straight with a list of about two dozen pages and groups of pages where LDL and HDL were mentioned, yet Bray weasels instead of admitting his mistake.  When I read his first letter, it made me wonder if he had even read the book.

3.    In his letter he mentions doubly labelled water only to conclude that we knew this already from the 19th and early 20th century and he did not need to discuss it in his book. I would submit that we did not know that people under-report their intake by as much as they do and that overweight people under-report more than normal-weight people do.

Okay.  There’s a total non sequitur.  What does the second sentence have to do with the first?  Weird.  Was Bray on dope when he wrote this?

4.    Mr. Taubes say ‘the goal of science is to determine causality…’

(What Gary actually wrote was ‘The goal of science is to correctly determine causality,’ but who’s counting?)

Then Bray wades into this strange discourse about the theories of Karl Popper, whom he misnames as Hans Popper.  (Does this guy ever bother to look anything up?)

This is significantly different from the views of Hans Popper, the philosopher of science, whose search is for ‘reality’ rather than ‘causality’. Popper says ‘there is a reality behind the world as it appears to us, possibly a many-layered reality, of which the appearances are the outermost layers. What the great scientist does is boldly to guess, daringly to conjecture, what these inner realities are like. Popper also espouses the concept of ‘falsification’, which is at the heart of rationalist thought. To quote him again –’a false theory may be as great an achievement as a true one. And many false theories have been more helpful in our search for truth than some less interesting theories which are still accepted’.

If you can make sense of this gibberish, you’re a better man than I am.  All I know is that Bray misses Popper’s point about falsification in a major way.  (We discussed Popper and his theory of falsification in an earlier post.  And it ain’t anything like Bray makes it out to be. I seriously doubt he has even read Popper’s work.)

The last sentence of the above paragraph I find particularly interesting.  Writes Bray, apropos of nothing really:

And many theories have been more helpful in our search for truth than some less interesting theories which are still accepted.

I don’t know about the search for truth, but I can tell you that the inability of Bray and the rest of the academic obesity ‘experts’ to shake loose from their own ‘less interesting theories’ have led us into the obesity epidemic we’re in the throes of now.

Dr. Bray’s fifth comment, which I’m not going to reproduce in full, is a world-class case of totally missing the point.  After commending Gary for proposing an experiment to validate his hypothesis, he goes on to quote Gary’s rebuttal letter:

He says ‘the positive energy balance hypothesis of obesity asserts that the only way to lose excess fat is to eat less and/or exercise more – that without consciously inducing a negative energy balance we will not lose weight’. His hypothesis is ‘the carbohydrate/insulin hypothesis asserts that if we restrict carbohydrates in the diet/and or improve the quality of the carbohydrates consumed then insulin levels will be lowered, reducing the accumulation of fat in the fat tissue independent of the nutrition state of the subject’. I would take exception to his use of the word ‘consciously’ in his statement of the energy balance hypothesis. For example, the current level of oil prices may increase human energy expenditure through more walking as it decreases automobile use. This is not a ‘conscious’ choice in the sense used above but would have the same effect.

Say what?!?!?!

Let me get this straight.  Dr. Bray thinks if we walk more because we decrease automobile use as a consequence of the high price of gasoline that we’ll lose weight because we are unconsciously exercising instead of volitionally exercising?  As I say, he misses the point, which is that the two components on the right side of the energy balance equation are not independent variables, but are dependent variables.  It doesn’t matter if one walks as a part of exercise or because one can’t afford the gas, the body compensates by increasing food intake.

Dr. Bray ends his response by resorting to the old conservation of energy principle, which all the eat-less, exercise-more folks hew to.  They seem to believe that no one who advocates low-carb diets can understand the laws of thermodynamics when it is they themselves who don’t understand them as applied to diet.  There is nothing inconsistent with Gary’s theories of the cause and treatment of fat accumulation and the laws of thermodynamics.  It’s Bray and friends’ lack of understanding of these laws and/or their refusal to accept the dependent nature of the energy in/energy out components of the energy balance equation that are the heart of the problem.

This entire rebuttal of Dr. Bray’s reminds me of my own favorite lines from Good Calories, Bad Calories.  They are my favorite because I’ve seen first hand what they describe.

The institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades.  For this reason, it is difficult to use the term “scientist” to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book.  It’s simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created, as a result, can reasonably be described as science, as most working scientist or philosophers of science would typically characterize it.  Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but “the results of their enterprise,” as Thomas Kuhn, author of The Structure of Scientific Revolutions, might have put it, “do not add up to science as we know it.”

The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of all, that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.

Is it any wonder that Dr. Bray didn’t enjoy the book?