Author: mreades

A couple of weeks ago, through the agency of a friend, I ended up spending the evening in a commercial kitchen preparing food.  The restaurant was closed for business that night, but had a full kitchen going for the dozen or so people who turned out to try their hands at being chefs.  We all cooked various portions of a four or five course meal. That’s me at the left in my chef’s attire chopping scallions for garnish for one of the dishes.

Sad to say, but this wasn’t the first time I’ve ever labored in the back end of a restaurant.  Both MD and I are very familiar with those duties.  One of the truly bad moves of my financial life was investing in a franchise restaurant years ago.  I still don’t know what came over me, but whatever did, it cost me a lot of money.  I distinctly remember how it all happened.  I was sitting in the kitchen of our house in Little Rock going through the mail and came upon a magazine buried in the pile.  I don’t remember now what magazine it was, but it had an article on hot new restaurant concepts.  One of the hottest, and one that was taking Dallas by storm, was a Mexican restaurant franchise called ZuZu.  ZuZu Handmade Mexican Food, to be exact.

I read the article and inexplicably reached around behind me, picked up the phone and dialed the number to get more info.  (A phone call, I might mention, that cost me hundreds of thousands of dollars before it was all over.)  The person on the other end – a honcho from ZuZu corporate office in the Rolex Building in Dallas – painted a wonderful picture of restaurant ownership, and before I knew it, MD, our eldest son and I were headed to Dallas to see a ZuZu restaurant in the flesh and try the food.

The food was dazzlingly good – all fresh, all handmade.  We tried just about everything and didn’t find anything that we didn’t love.  And much of it was low-carb, to boot.  Our eldest was just out of college and looking for something to do and our middle son was going to graduate soon.  After discussion with them, we decided to take the plunge.  Bad, bad, bad mistake on many fronts, but we learned a lot.  And that’s about the best face I can put on it.

The kids all went to Dallas and underwent the training program.  MD and I purposely avoided learning how to operate the cash register or do anything in the front of the house.  We had a large medical practice in Little Rock (a relatively small city) and didn’t want to be doing a pelvic exam or a rectal exam on someone in the morning, and then greet them that evening wearing a ZuZu hat and a big smile with ‘For here or to go?’

Consequently, whenever things went crazy – as they always do in the restaurant business – MD and I got dragooned into working the back of the house where we could do our part yet stay out of sight. One day during the first couple of weeks of being open was particularly memorable. MD and I both had presentations to make to a large medical meeting in Seattle, but the day before those presentations, we were scheduled to be on CBS The Early Show and the day before that on the Sally Jesse Raphael show.  I was busy putting together my slides for the medical presentation while MD was working on patient charts when we got the call.  MD headed to the restaurant while I stayed at the office and finished my slides.  By the time I got to the place, it was a true hellhole. MD was surrounded by piles of dirty plates, glasses, pots and pans and was deep into catching up on the dish washing so I jumped in and started prepping by chopping tomatoes, limes, onions, cilantro, you name it.  As soon as the dish washing was caught up (which took over six hours), MD started helping me prep. I was on a roll with all the stuff I was slicing and dicing, so she grabbed the peppers that I hadn’t gotten to yet and began.

As closing time approached, we began preparing the stuff for the next day.  In doing so – and I don’t remember now how I did it – I burned the bejesus out of my hand and had an enormous half-dollar size blister pop up.  After closing, MD and I got home and got into bed to get a few short hours of sleep before our 6 AM flight the next morning.  As we lay there recounting the day and wondering about our sanity for ever embarking on such a folly, MD said that her hands were starting to burn.  In just a few minutes, her hands were on fire.  She had been chemically burned by the juices from all the peppers she had prepped, and, like a sunburn, it had taken a few hours before she started feeling the effects.  She jumped up, held her hands under the cold water for about five minutes, then slathered them with a cortisone cream we had at the house.  She came back to bed and worried all night that her hands would end up red and grotesquely swollen by the morning and that she would have to appear on national TV with lobster hands along with her husband with his giant blister.  What a nightmare!

Her hands were okay by morning – a little red, but nothing all that noticeable.  I still had the enormous blister I was trying to keep intact so that the skin would act as a dressing, but I figured I could probably keep it out of sight of the cameras.  We caught our flight, went on with Sally Jesse that afternoon and the CBS morning show the next day without incident.  Then it was off to Seattle for that gig.

In addition to our labors on the above-mentioned disastrous day, MD and I have both washed thousands and thousands of dishes using the commercial dishwasher, which has a lot of hands-on effort that goes along with it.  It seemed that it always fell to me to do the prep work.  I’ve sliced and diced rosemary, cilantro, garlic, onions, tomatoes and peppers by the car-load lot. ( And along the way I developed pretty good knife skills without sacrificing any of my fingers in doing so.)  So the two of us have spent plenty of back-breaking time in the bowels of a commercial kitchen.

But never in an enormous kitchen designed to service a fairly high-end restaurant like the one we found ourselves in the other night.  I was eager to see how it all worked.

I learned plenty.  For one thing, it’s really easy to cook in a big commercial kitchen because you have everything at your disposal.  And you don’t have to dig all the stuff out when you need it – it’s already there.

If you need to quick chill something, the giant ice bath is right there.  If you need to throw an entire tray of stuff into a big fridge, you’ve got it available without having to rearrange everything so it will fit.  If you need to quickly blanch something, there is the giant strainer and the pots of boiling water are at the ready.  It really makes cooking much more hassle free than it is at home.  And the best part of all is that you have (or at least we did during this event) staff who clean up behind you.

In between my various tasks assigned tasks, I snooped around, and my worst fears were confirmed.  Before we get to that, though, let me tell you what I’ve learned about chefs.  What I’m about to say doesn’t apply to every chef who cooks, but I would guess it applies to most.

Chefs are not particularly heath conscious. They cook for flavor, not for health.  If there is a choice between making something taste a little better or making it a little more healthful, taste will win every time.  Which is fortunate in many cases because chefs – like most other people – have been brainwashed as to what is healthful and what isn’t.  Most no doubt believe that saturated fat is unhealthful, but, fortunately, that doesn’t deter them from using butter, heavy cream, bacon, and all the other tasty high-saturated  fat foods in their cooking. If butter tastes better – that’s what they use.

But many things are deep fried and cooked using vegetable oils and shortenings because these products don’t impart much of a taste.  That was the big advantage of Crisco when it came out: it was pure and while and left no taste the way lard did.  Same with processed vegetable oils today, so chefs use the heck out of it.

Part of my job was to make some egg rolls for an appetizer.  I filled them with shredded chicken, shredded crab, a snow pea, some ginger and a little salt and pepper.  Then I deep fried them.  I asked the main chef, who was keeping a watchful eye on all of us pretend chefs, what kind of oil he used in the deep fryer. (The deep fryer, like everything else in the kitchen, is running all the time, and people pop stuff into it all night long when the restaurant is busy.)  He told me it was canola oil.  I asked him if canola was commonly used in deep fryers; he said that canola was used in every restaurant he had ever worked in.

I was surprised because I wouldn’t think canola oil would hold up to a deep fryer.  I asked how often they changed the oil – he told me they did so once a week. I made a note to research it a little when I got home.

I knew polyunsaturated fat made up somewhere around a third of the fatty acids in canola oil.  Polyunsaturated fatty acids (PUFA) are the ones most harmed by heat and oxygen, so it really made me wonder why anyone would use an oil containing so many PUFA for deep frying.  I just imagined all the oxidized fats in the oil I was dropping my newly made egg rolls into.

(There is a misconception in the minds of most people about what happens to PUFA when they are kept hot and bubbling for a long time as they are in deep fryers.  A lot of people think the PUFA convert to trans fats.  They don’t.  It requires heat, pressure and a catalyst to transform normal PUFA to trans fats.  What does happen, however, is that the PUFA become oxidized.  Then when you eat them, you are consuming oxidized fats that your body has to deal with.)

When I got home after our dinner, I went to the USDA Nutrient Database to look up canola oil to see if I had remembered correctly about the percentage of PUFA. I found the following entry:

Oil, industrial, canola (partially hydrogenated) oil for deep fat frying

When I looked up the fatty acid breakdown, I discovered that this industrial canola oil made for commercial deep fat frying contained almost a third of its fatty acids (27 percent to be exact) as trans fats.  Which is why it worked for the deep fryer.  During the processing of this oil, most of the PUFA had been converted to trans fats.

I looked at the other canola oils listed in the USDA list and found this one:

Oil, industrial, canola with antifoaming agent, principal uses salads, woks and light frying

Sounds just like what you would want to eat on your salad, doesn’t it?

This particular canola oil had just a couple of grams of trans fats per 100 grams of oil, so it wasn’t nearly as bad as the deep fryer canola oil, but it still doesn’t sound particularly appetizing.

At most of the stations in the kitchen there were containers of a salt and pepper mix and containers of oil with ladles.  If frying (not deep frying, but regular frying) were to be done, you threw a ladle of oil on the grill or in the skillet.  If you were whipping up a salad dressing, you started with the oil and worked from there.  This oil is the industrial oil with the antifoaming agent.

So, the take-home message from my experience is that if you eat in a restaurant you are going to get a lot of oils that you would probably rather not have.  At worst, you’re going to get a load of trans fats; at best, you’re going to throw back plenty of omega-6s. Omega-6 fats are, for the most part, pro-inflammatory, and we get way, way too many of them in our diet as it is. Most of the readers of this blog know how harmful omega-6 fats are in large quantities, so I won’t go in to it here.  Suffice it to say, however, that the medical literature is full of articles pointing out the hazards of too many omega-6 fats.  Then there is the American Heart Association that has inexplicably come out in support of omega-6 fats for heart health (Harris, WS), which advice you can put up on your shelf right beside the advice to avoid saturated fats.

In the 6-Week Cure we wrote about how vegetable oils – at least in lab animals – drive the development of fatty liver.  Researchers give rodents large regular doses of alcohol to get them to develop fatty livers.  They have found that if they give the rodents vegetable oils, they can accelerate the development of liver disease.  If the rodents get saturated fats, however, they almost can’t get fatty livers no matter how much alcohol they take in.  Does this apply to humans?  Who knows?  These kinds of studies would be unethical to do in humans, so we can’t test to find out.  But, the evidence is clear enough in rodents that I’m not all that eager to go face down in the vegetable oil.

I suspect that one of the reasons non-alcoholic fatty liver disease is reaching epidemic proportions worldwide is the ubiquitous substitution of vegetable oils for saturated fats every where.  When we were doing research for the book, I scoured the literature to find studies in which people with fatty liver disease were treated with diet and found only two such studies.  In both of them the fatty livers of the subjects reversed quickly – in just a matter of a few days – when the subjects went on low-carb diets.  I suspect that the increase in saturated fat helped things along markedly.  And, I suspect the unwarranted avoidance of saturated fats by our bamboozled fellow citizens is one of the reasons there is so much fatty liver disease.

If you prepare your food in your own kitchen, you control exactly what goes into it.  If you go out to eat, you lose that control.  I suspect most restaurants operate about like the very upscale one I just played chef in, and so if you go to even a nice restaurant, you’re going to be consuming stuff you would probably rather not consume.  In the old days (when I was a kid, for example), going out to eat was a big deal, and it almost never happened. Everything was prepared at home.  Now people eat out more than they eat at home.

According to the National Restaurant Association, more people are dining out than ever, even in tough economic times.  On a typical day, restaurant sales in the US average $1.6 billion. The average household spent $2,698 for restaurant food in 2008.  Forty percent of adults say that eating out or getting take-out food makes them more productive in their lives. The majority of adults – 78 percent – believe that dining out with family and friends is a better way to make use of their leisure time than cooking and cleaning up.

To the left is a graph from the USDA Economic Research Service showing the increase in the home budget dollar spent on food away from home.  It just about parallels the graph showing the development of the obesity epidemic.  I’m not necessarily making the case that eating out has caused the obesity epidemic, but I’m not sure it hasn’t played a significant role in it.  Especially now that I know what kind of oils restaurants use.

One of the statistics I read while researching for this post was that 73 percent of adults say they are trying to make more healthful choices at restaurants now than they did just two years ago.  Assuming this is true, it probably means they are ordering more salads, which seem to equate in everyone’s mind with a more healthful choice.  But if the dressings are made for the salad with the oils used in bulk in most restaurants, it’s probably not the best thing you can eat where your health is concerned.  But I always ask for my dressing on the side so that I can control how much I put on, you say?  That’s the big joke among chefs.  It’s been shown that when salads are tossed by the chef, much less dressing is used as compared to when people ask for it on the side and add it themselves.

The point of all this is that when you go out to eat, no matter how upscale the restaurant, you lose control over what goes in your mouth.  Short of bulling your way into the kitchen, you are clueless as to what oils are going into and onto your food.  If you eat out a lot, you are doubtless taking in a fair quantity of trans fats and oxidized fats and plain old omega-6 fats – all fats you can stand to do without.  The only way you maintain control is if you do the cooking yourself.  Plus, you’ll save a lot of money because it’s almost always less expensive to prepare it yourself.

One of the best things you can do for your health (and your pocketbook) is to spend more time in your own kitchen.

While on a recent whirlwind trip that included a stop in Seattle, I purchased a copy of Meatpaper at my favorite newsstand hard by the Pike Place market.  I always grab a copy of this magazine whenever I’m in Seattle because I can never find it anywhere else. Today I finally broke down and subscribed.

The quarterly Meatpaper was founded by a couple of vegetarians who made the conversion to meat eating a few years back.  (The founders say that when vegetarians cross over to the meat-eating dark side, bacon is the most common conversion food.)  It’s a difficult magazine to pigeonhole.  One would think it would revel in meat eating, and, in a way, it does.  But it does it in a daredevil sort of way, much in the way a magazine on skydiving might portray the thrill of that sport while still noting that certain death is only a chute failure away.  My take is that the writers and editors believe that meat-eating is a perilous undertaking, but one that many people choose for the taste despite the risks involved.  As anyone who had read this blog for anytime knows, my beliefs don’t quite fall that way.

The most recent issue contains a couple of articles I want to tantalize you with.  One that describes an almost unbelievably scrumptious food that I’ve yet to eat, at least knowingly, and another article I find deeply disturbing.

First, to the scrumptious.

In “Schmaltz Redux,” Daniella Cheslow briefly describes the history, disappearance and resurgence of a staple of Jewish cooking: schmaltz.  For those of you who don’t know what it is (and I was in that category until I read this article), schmaltz is basically chicken lard. Small pieces of chicken fat are cooked slowly until they resolve into an oil.  Throw in a few pieces of onion during the process, and you’ve got schmaltz, which can be used much as lard or duck confit.

To give you an example of what I mean about daredevil writing focusing not on just the delicious and nourishing virtues of schmaltz, but on the risks (non-existent, in my opinion) of consuming it.

“I love schmaltz.  But it’s very unhealthy, it’s all saturated animal fats.  I stopped eating schmaltz when my grandmother died in 1972,” said Susan Rosenthal, 59, a physician from East Brunswick, New Jersey. “I have a master’s degree in nutrition [a dead give away that the woman knows almost nothing about nutrition], so if I would have given my children schmaltz, that would have been shameful.”

Shameful indeed.

I’m sure this enlightened woman would have no qualms about giving her children all the olive oil they wanted.  But according to the USDA nutrient database of foods, olive oil contains 14 grams of saturated fat per 100 g whereas chicken fat contains 20 grams in the same amount. But 100 g is 3.5 ounces, and since schmaltz is used as a cooking oil, I suspect most people don’t eat much more than an ounce at a time, which would mean the schmaltz would give the children a little over 5 g of saturated fat while the olive oil would contain 4 g.  A difference of under two grams.  Not a huge difference in my opinion.  And since the schmaltz also contains a lot of both monounsaturated fat and polyunsaturated fat, it can’t really be characterized as “all animal saturated fats.”  But such misinformation is what comes from a master’s degree in nutrition.

The article goes on to detail a little more of the history of schmaltz and its resurgence but, at the end of the piece, once again the specter of early death from eating schmaltz rears its head.

To bring her article to a close, Cheslow offers a quote from David Sax, author of Save the Deli:

There’s something these days that’s sexy about it [making food from scratch].  I think [schmaltz] is coming back for that reason, and also people appreciate the taste, and they realize that it’s going to provide a richer experience.  Literally, figuratively, tastefully, and spiritually, it’s a heart stopper. [my italics]

Jesus wept.

I have elicited a promise from MD that when our brutal travel schedule over the next month and a half comes to a close, she will make us some schmaltz, an event I will dutifully record photographically.  Until then, however, you’ll have to make do with photos and instructions I found online.  The schmaltz in the photos in this blog post look great, but the uses the blogger makes of the schmaltz are not my cup of tea.

Now to the disturbing.

When you think Argentina, you think beef.  The Pampas, gauchos and endless herds of cattle.  For years Argentina has been one of the great beef reservoirs of the world.  But unless things change, that all may be coming to an end because the cattle are being displaced by a more profitable commodity: soy.

“Plowing the Pampas,” an article written by Nicholas Kusnetz, describes how many Argentinian ranchers are hanging up their bolas and picking up a plow.  Why?  Because soybeans are a vastly more profitable use for the land than raising cattle.

Kusnetz spoke about the switchover with scientists at a government research station in the Pampas.

Five years ago, one of the researchers told me, I would have been surrounded by pasture.  Now, nearly all the cows were crowded into feedlots.  The land was a tricolored patchwork as far as the eye could see: thousands of acres of deep green corn leaves, lighter green soybeans, and the straw-colored stubble of cornstalks that had been sprayed with Roundup to ready the field for soy.

At the station, two soil specialists showed me where they experiment with different crop rotations.  They have found that their most productive “rotation” is just the opposite: all Roundup Ready soy, all the time.  They don’t know why, they tell me, but it grows well.  They don’t see any reason to grow anything else.

“If I were a farmer,” I ask, “and I came to you for advice, what would you tell me?”

“Pure soy,” they say. “The more soy you have, the better your profits will be.”

The article goes on to describe how the economic realities are driving the ranchers to become soy farmers.  I don’t have a problem with this; you’ve got to expect that people will follow the money.  What does trouble me is that a crop with such a disastrous effect on health could be more valuable than cattle, which have been providing humans food for millennia.  But the herds are shrinking, and soon, if things don’t change, in a few years Argentina could become an importer of cattle.  An almost unthinkable proposition.

Should this disastrous end come to pass, I wonder if the grand ranches of the Pampas will still raise a few cattle along with thousands of acres of soybeans.  And will these few beef grazing in a small lot allow the farmers to continue to refer to themselves as ranchers despite the vast majority of their income coming from soy?  Probably.  I’ve seen it happen in Arkansas.

The delta lands east of Little Rock are made up for the most part of vast soybean growing operations.  The farmers who own and farm the land were descended from cotton farmers.  Cotton farming was the tradition, but economics won out, and most of the cotton fields were replanted in soy.  But old traditions die hard, and most of these farmers still keep a small patch of cotton on their land, and if asked what they do, they reply that basically they’re cotton farmers but they grow some beans on the side.

I suspect that if things continue in Argentina, many self-proclaimed ranchers will be growing a few beans on the side as well.

Sad. Very sad.

I would encourage you to subscribe to Meatpaper to keep up with what’s new and edgy in the world of meat.  I have no affiliation with the magazine nor do I get any click-through income if you subscribe.  I just like the idea of former vegetarians writing a magazine on meat and making a go of it.  And I want to help.

I’m going to start a new tradition with this post.  As anyone who reads this blog regularly knows, I read a lot.  People often ask me what I’m reading, so I’m going to start putting my current reading list at the bottom of the posts so those of you who are interested can keep up.

Survival of the Fattest by Stephen Cunnane

Atlas Shrugged by Ayn Rand.  (This isn’t a reread.  I’ve never read the thing, so I figured it was about time.)

The Plague by Albert Camus  (I’ve never read this one either, and it’s taking me forever to get through it.  But I’m almost finished.)

Predictably Irrational by Dan Ariely

One Good Turn by Kate Atkinson

The Genius in all of Us by David Shenk

The Girl who Kicked the Hornet’s Nest by Stieig Larsson (This one won’t be available in the U.S. until May 25.  A friend who visited me from the UK, where it has been available for months now, brought me a copy.)

It’s time for the 2009 bestseller list.  These are books purchased last year through this website from readers either going through the Amazon portals on the page (more about which later) or clicking on Amazon links appearing in many of the posts when books are mentioned. As always, these are all the books purchased that are not books MD and I wrote or co-wrote.

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.

Okay.  I said I was through with Anthony Colpo, but now I’m going to quote from him once again.  What gives?

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.

On to the second and, mercifully, final part of the critical review of the metabolic advantage as presented by A Colpo in his book The Fat-Loss Bible. As discussed in the previous post, our friend, like the kid to the left, is focused so intently on his refusal to believe in even the possibility of the existence of a metabolic advantage that he can’t read the literature correctly – not even the very literature he uses to try to prove his own position.  His bias has hypnotized him to the point that he can’t see anything that doesn’t confirm his what he already believes.  And this same bias prevents him from even taking a scientific approach to the problem.

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 breath.  This vapor is water that you lose every single time you take a breath.  You breathe 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.

There are a lot of disagreeable  jobs out there.  Dealing with Anthony Colpo is one of them.  Trying to make sense of thermodynamics is another.  Whereas dealing with AC is kind of like the job pictured at the left – distasteful but fairly simple – delving into the workings of the laws of thermodynamics is intellectually challenging but far from easy.  Problem is, it appears kind of easy, and everyone, it seems, fancies himself to be an expert.  (How many people have we heard blather on about how a calorie is a calorie is a calorie, thinking they are accurately stating the 1st law of thermodynamics?) But the truth is that the more you study thermodynamics and the more you seem to learn, the less you really understand.

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

I’m taking a short break from the great Anthony Colpo smackdown to report on all the goings on with the ‘wretched’ choral society and the Beatles concert.  As I’ve mentioned before, MD has been pushing for a Beatles concert since she’s been the president (her three-year term will be mercifully over on June 30, and I’ll have my wife back).  It’s all come to pass with a whole lot of help from a whole bunch of people. And, thanks to all this effort by all these people – especially Brooks Firestone – it has turned into a much, much huger event than she had ever imagined.

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

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

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

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

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

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

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

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

So, with that preamble, here it is.

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

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

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

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

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

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

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

To solve this problem, AC turns to what he calls

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Second subject:

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

Third subject:

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

Forth subject:

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

Fifth subject:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Wow!  Where do we start?

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

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

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

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

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

After going through all the data, Rabast et al conclude

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kinsell et al

Grey Kipnes

Rabast et al 1979

Rabast et al 1981

Yang et al

Bogardus et al

Hoffer et al

Leibel et al

Vazquez 1992

Vazquez 1994

Vazquez 1995

Piatti et al

Golay et al

Myashita

I’m just getting back to my desk after a several days in Puerto Vallarta, Mexico.

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.

A study appeared this week sure to drive members of the low-fat and vegan tribes sprinting for their Protexid.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Give me strength.

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

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

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

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

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

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

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

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

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

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

Here’s what the authors wrote:

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

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

…compliance was assessed with objective biomarkers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Then I asked myself the big question:  If I have too much insulin (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.

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

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

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

Brilliant!

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

Sounds great.  But bit of critical thinking.

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

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

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

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

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

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

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

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

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

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

Says Dr. Oz:

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

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

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

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

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

Pitiful.

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

The poem by Shelley is titled, appropriately enough, Ozymandias

OZYMANDIAS

by Percy Bysshe Shelley

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

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

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

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

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

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

Various wines for the different courses and champagne at midnight.

I’ve just now barely recovered.

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

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

What does he recommend?

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

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

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

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

Here is the energy balance equation:

Change in weight = Calories in – Calories out

Below is another way of stating the same thing:

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

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

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

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

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

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

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

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

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

A quick post just to let everyone know that I’m still among the living and that I haven’t given up posting for good.

MD and I have taken off a few days and are in Dallas with kids and grandkids celebrating Christmas.  It snowed like crazy all yesterday afternoon, and, according to the newspapers, Dallas has had its first white Christmas since 1926.  And we were here to witness it.  At left is a photo looking out the back door.  Granted, it’s not a New England eight inch snow or a Colorado two foot snow, but it’s a pretty substantial snow for Dallas.  Maybe it’s a harbinger of good things to come, although the last white Christmas preceded the year in which the Great Depression started.

I’ve been absent from posting because MD and I have been incredibly busy with Sous Vide Supreme stuff.  I just thought we were busy during the developmental stage.  The post-developmental era has consumed enormous amounts of our time.  Especially since our invention had such a nice write up in the New York Times a couple of weeks ago.  We’ve been inundated with requests for interviews from multiple media sources and for write ups for this and that.  And all that is not to mention a week’s worth of filming in Seattle.  We’re making a true infomercial on the Sous Vide Supreme with emphasis on the ‘info’ part.  So many people are unaware of what the sous vide process is, so we’re going to tell them.

We’ve teamed up with chef Richard Blais, whom many of you may know from Top Chef, Iron Chef America and other TV cooking shows.  He couldn’t be any nicer nor any easier to work with – a really great guy who can cook like you wouldn’t believe.  He will appear with MD on the infomercial that will start running early next year.  Below is a photo of the two of them camping it up on the set.

The infomercial filming went without a hitch, and the food that Richard Blais prepared in the SVS was incomparable.  On the eve of the filming my brother sent me a YouTube of an infomercial that had a few problems.  I forwarded it on to the rest of the team, and fortunately the Sous Vide Supreme functioned a little better than the popcorn popper in the video below.

Click here to view the embedded video.

We’ve also teamed up with the retailer Sur La Table.  They will be carrying the Sous Vide Supreme in their stores and in their catalog right after the start of the year.  MD and Richard will be doing demos in several of the stores, so if you want to see the SVS in the flesh, so to speak, head on over to a Sur La Table near you and take a look.

This entire sous vide experience has been different than anything we’ve ever done.  It’s really nice to see articles and reviews that are all positive instead of the hatchet jobs we’re used to getting while promoting low-carb.  No one accuses us of being purveyors of dangerous fad diets, of encouraging people to eat more artery-clogging saturated fat, of being doctors of death (which we’ve been called on live radio) or of simply trying to make a quick buck at the expense of the health of those gullible enough to follow our recommendations.  The new experience has been rewarding and a lot of fun but incredibly time consuming.  Thus my absence from my blogging duties.

But I’ve been absent in electrons only.  I’ve been flying all over the place carrying a satchel of scientific papers that I’ve been reviewing and preparing to blog about.  So I’m fully loaded with ammo and ready to write after I’ve taken a fews days of a breather.

I haven’t been totally offline, however.  I’ve been keeping up with the blogs I  read regularly and haven’t been able to resist commenting when something gets under my skin.

Food writer Michael Ruhlman did a great review of the Sous Vide Supreme, and in the comments section someone took me (and the SVS team) to task for profiteering.   As you might imagine, this kind of thing really gets my hackles up, especially since we are still way, way in the red on this project.  I kept myself in check (the good Mike won out as MD would say) and wrote a couple of mild  but informative comments.  You can read them here.

My friend Amy Alkon, the Advice Goddess, whose blog I read religiously, wrote a funny post on bacon featuring the kind of ill-disciplined child who gives the South a bad name.  Amy, who is an inveterate low-carber, wrote the post from the perspective of how much she likes bacon.  Of course some commenter couldn’t resist slamming low-carb diets in general and Gary Taubes in particular, so I couldn’t resist resorting to form (the bad Mike sort of won out on this one).  If you’re interested, you can read that exchange here (two comments). The guy turned out to be pretty nice and even sent me a friendly email via Amy.

Speaking of Gary Taubes… he tipped me off on an interesting paper on HDL that I’ll post on soon and I’ve uncovered a few others on the fallacy of the lipid hypothesis.  It looks like the mainstream is ratcheting up its jihad against low-carb again with a few spurious papers badly in need of a public dismantling.  I’ll soon be tanned, rested and ready to shred.  And to go after the statinators, the great medical menaces of our time.  Plus I’ll throw in a nice post on how long it might take the low-carb diet to become the diet recognized by all as the correct diet for most everyone.

Until then, I’m going to lay low and try to catch up on my non-scientific reading.  Speaking of which, I got a great book as a Christmas present from my grandkids today.  It is Fly by Wire: The Geese, the Glide, the Miracle on the Hudson and is about US Air Flight 5149 that went into the Hudson River last January.  Although the book extols the skill and courage of Capt Sullenberger and crew, its main emphasis is on the aircraft they flew: the Airbus 320.

Twenty five years before Flight 1549 took its plunge, a highly intelligent, charismatic French fighter pilot and test pilot named Bernard Ziegler talked the management at Airbus to let him design a plane that almost flew itself.  Ziegler recognized that pilots exhibited a bell-shaped curve in their level of skill and expertise and that some of the less skilled had ended up killing themselves along with all their passengers after getting into situations that more skilled pilots may have gotten out of safely.  He wanted to design a plane with layers of built-in redundancies that would allow all pilots, but especially those less skilled, to worry about the major goal of any pilot who is in trouble – getting safely on the ground – without  being distracted by all the little details of flying.  In other words – and in very simplistic words – if pilots could simply make the decision to land, the plane could almost fly itself.  When pilots get in tricky situations it is sometimes difficult to get out of them without stressing the plane to the point of structural damage.  As the pilots are trying to avoid disaster they have to worry not only about their main problem – a loss of power, say – but have to baby the plane to keep it from breaking up.  Ziegler fixed all that with the Airbus by designing it to perform maximally under control of multiple computers while the pilots tend to the main problem at hand.  Since the computers control these functions of the plane by electricity it’s called flying by the wire.

When Sully and crew brought the plane down safely in the Hudson, they were flying by wire.  And as the author William Langewiesche puts it

They had no choice.  Like it or not, Ziegler reached out across the years and cradled them all the way to the water. His assistance may have been unnecessary, given the special qualities of these particular two [the pilots of Flight 1549], but there is no question the practical effects were profound.  At the moment of the bird strike, when the engines lost thrust, a conventional airplane would have tried immediately to nose down.  It would have wanted to go into a sharp descent, and would have required whoever was flying to haul back on the controls with some strength and to retrim the airplane for a slower, more moderate glide, while disciplining the wings to stay level until the decision could be made to turn around.  None of this is inherently difficult, but it imposes insidious demands on the crew in an emergency, when they are already busy with more important concerns.  It is an accepted reality that the repetitive and menial jobs, associated with baseline control subtly impinge on a pilot’s capacities, and that during periods of truly high workloads, even simple thoughts are difficult to have.

Imagine trying to disarm a bomb while also having to deal with menial chores and talk on the phone at the same time.

This fascinating book doesn’t detract from the skill and heroism of the crew of Flight 1549, but explains in detail why they were able to make it look so easy.

I loved this book.  I opened it in the morning and had it finished before lunch (lunch was sous vide turkey, if you must know).  If you have any interest in aviation, Fly by Wire is a must read.  Despite the fact that the author dissects in detail a number of commercial aviation disasters in the recent past, the book actually makes one feel safer flying, especially in an Airbus 320.

This post is already longer than I had intended it to be, so I wish you all a Merry Christmas.  I’ll be back soon.

Merry Christmas from Dallas

I’ll leave you with a couple more photos.  Below on the left is my Southern grandson testing the snow barefooted.  On the right is MD slicing the sous vide turkey we had for lunch.

Last Thursday was Thanksgiving, and in the words of Arlo Guthrie, we had “a Thansgivin’ dinner that couldn’t be beat.”  Along with all the traditional Thanksgiving fare at Casa Eades, we had dueling turkeys: one cooked the traditional way and one cooked sous vide.  And let me tell you, there was no comparison.  I’m not saying this just because we’ve got a sous vide cooker for sale, either.  I’ve never had turkey that tasted so good.  Because I’m not really a big fan of turkey, I eat turkey on Thanksgiving, and Thanksgiving only.  I found our sous vide turkey to be so good, because it didn’t really taste like turkey.  At least not turkey cooked in the traditional way that I’m used to tasting.  It was like a different meat entirely.

MD has posted on how she cooked both turkeys on her blog and on the Sous Vide Supreme blog, giving precise recipes for both.  As you can see when you read the posts, cooking a turkey the traditional way is a major pain (both figuratively and literally).  It’s just not worth it when the taste and texture outcome is so much better using sous vide.  Especially since the sous vide method is so much easier and less time consuming. Vastly easier, in fact.

Lest you think this is another post cleverly designed to promote and sell the Sous Vide Supreme, let me disabuse you of that notion.  I’m going to show you how you can try the sous vide method at home without having to purchase a machine to see if it’s really for you.

Not long ago I wrote a post on how MD and I came up with the idea for what ultimately became the Sous Vide Supreme.  We wanted to try cooking sous vide, but there were no sous vide units available for the home cook, and we weren’t about to fork over $1500 for a commercial unit just to give the technique a try.  So, we cobbled together a Rube Goldberg kind of set up and tried it out.

I went back and pulled some of the photos I took of our contraption, which was made of a stock pot, a steaming basket turned upside down, and a candy thermometer.  And, the most important piece of equipment of all: constant attention.

The secret of cooking sous vide is the maintenance of a constant temperature over the cooking period.  Since most things are cooked sous vide at a significantly lower temperature than 212F/100C (the temp at which water boils), you can’t put the container directly on the stove even with the burner on its lowest setting.  The lowest setting is typically for simmering, which holds the temp right at the boiling point.  When we were trying to set up our first try, we experimented with several different ways to get the stock pot high enough up off the flame of our gas stove so that we could get the low temperatures we needed.  We found that the steaming basket (made to set inside a pan) turned upside down gave us the height we needed given the flame on our stove.

Sous vide cooking requires that the temperature be maintained precisely for long periods of time, sometimes up to 72 hours for, say, fall-off-the-bones beef ribs.  On the Sous Vide Supreme, you simply set the temp and walk away.  It’s not so easy with a homemade unit.  You’ve got to monitor it closely because temperature fluctuations of even a degree or two will make a difference in your outcome for many foods.  One of the ways you keep the temp where you want it is to use an important piece of equipment not pictured in the photo above: a pitcher of ice water.  You watch the temp carefully – you don’t have to stand there and watch it minute by minute – checking the candy thermometer every few minutes or so.  If the temp starts to drift up a little (the most common thing), you need to pour in a tiny bit of ice water to bring it down.

Since you’ve got to stay on top of it, it’s best that you limit your cooking in a homemade device to foods that don’t require a long time in the bath.  Which means you’ve got to stick with good-quality beef cuts such as rib eye, New York strips or tenderloin, chicken breasts, salmon, turkey breast, etc.  If you read MD’s post on cooking our Thanksgiving turkey, you’ll notice that she cooked the breast for 2.5 hours at 140F and the dark meat at 176F for eight hours.  If you’ve got a Sous Vide Supreme, you can stick the dark meat in, set it for 176F and get it out eight hours later.  If you’re cooking it using the homemade device, you’re going to be standing close by watching it for eight hours.  Since you probably don’t want to spend eight hours fiddling with it, I would avoid trying the dark meat of a turkey as your first outing in the homemade device.  Try the breast or, better yet, some salmon or even steak, lamb or pork chops.  You want to minimize the amount of time you have to remain vigilant in your temp watching.

Let me give you a couple of never-fail recipes so you can give it a try. And let me say that these were not the same recipes we used the first time we tried our rigged-up machine.  These are recipes that we’ve developed after a lot of bad experiences.  We suffered them so you don’t have to.

Chicken breast sous vide

The first thing you should try is chicken breast.  Why?  Because it’s easy and because the taste difference between a chicken breast cooked sous vide and one cooked any other way is so huge that you can really experience the virtue of cooking this way.

Take your chicken breasts (they can be skinless or with skins in place) and brine for for hours in an 8 percent brine.  You make an 8 percent brine by putting five tablespoons of salt in one quart of water.  Make your brine, put the breasts in, and put in the fridge for four hours.

Pull the breasts from the brine, rinse with fresh water and pat dry.

Put each breast into a food-grade plastic bag along with a big pat of butter.  (If you like it, you can add some cracked pepper or herbs to the bag at this stage)

Vacuum seal the bags with a Food Saver or one of the little hand vacuum pumps.  (You can even press all the air out with your fingers if you don’t have a pump of any kind, though you risk having your meat float and cook unevenly–and perhaps incompletely, which isn’t good with poultry–if any significant amount of air remains.)

Bring your sous vide machine to 140F and put the bags in.  Watch it like a hawk (assuming you’re using your homemade setup) to maintain that temp for about 1.5 hours.

Remove the bags, open and dump out the breasts.  They won’t look particularly appetizing, especially if they have been cooked with the skins on.  If the breasts are skinless, you can actually slice and eat just as they come out of the bag, and they’ll taste something like poached chicken, but infinitely better. But they are better yet if you sear them first to give them a little color and caramelized flavor.

To sear them, you need to put a stainless or cast iron skillet on the stove at the highest temperature you can get.  Gas or electric both work, just put the burner on its highest setting.

Leave the empty skillet on the hot burner for about ten minutes.

Add some clarified butter (ghee), which will sizzle and steam like crazy if the skillet is hot enough.

Put the breasts in the hot skillet and turn from side to side about every 30 seconds with tongs until you get a nice golden brown exterior.

Remove and eat.  You won’t be disappointed.

Steak sous vide

You can also try steak.  Here’s how we did it last night.

Get a nice cut of steak, a rib eye or porterhouse or something tender.  I wouldn’t use grass-fed beef for this experiment because you have to cook it too long to get it nice and tender.  If you use a regular grocery-store steak that isn’t too think – one inch, say – you can get by cooking for only 40 minutes to get it perfectly medium rare.

MD puts a sprinkling of sea salt on each side, a few turns of the pepper mill and a little garlic powder then puts each steak in a food-grade plastic bag and vacuum seals it.

Heat your water bath to 135F, put the bagged steaks in the bath, and watch carefully.

Pull the steaks out after 40 minutes and let them sit at room temperature for 5 or 10 minutes to drop their internal temperature just a bit.  Remove them from the bags and pat dry.  (The patting dry is actually an important part of the process.)

Do the deal with the skillet as described above for the chicken breasts.  Get it hot, add the clarified butter, then sear the steaks.

Sear them on each side no longer than about 20 seconds.  If you want, you can flip them around a bit from side to side.  You should even hit the edges of the steak with the hot skillet as well so that they are seared all around and the fat on the edges gets a nice color.

Serve immediately.

You can see from the photo on the right how the interior looks.  Perfectly medium rare from side to side with a tiny layer of caramelization on the surface.  Must be tasted to be believed.

Several of your fellow readers have used the sous vide method and posted on it.  You can read their posts here, here, here and here.

One of the nice (and sometimes aggravating) things about the sous vide method of cooking is its precision.  If you don’t like your steaks at 135F, try them at 130F or 140F.  Or even at 133F.  You can get as precise as you want.  The meat at each temperature will be a little different than when cooked a degree or two hotter or cooler.  It takes some diddling with and experimentation to find the temperature that works best for you.

Once you do, you can turn out steak after steak after steak or pork chop after pork chop perfectly cooked just as you like it.  The food will be more nutritious because nothing is lost in the cooking process, including the moisture, which is why the meat is so tender.

I’m going to reveal the only medical problem I have (at least that I know of) other than the propensity toward obesity when I eat too many carbs.  I’m going to explain how the direct response business works.  I’m going to talk about the problems direct marketers have in dealing with our servants in Washington. And I’m going to tell you how you can get the best nutritional supplement I’ve ever seen in action absolutely free.  How’s that for a pleiotropic post?

First the medical problem.  I’ll reveal it in true AA fashion.

I am a GERD (gastroesophageal reflux disorder) sufferer.

I don’t get it often, but when I do, it’s a nightmare.   As long as I stick with my own diet, I never ever have a problem.   But sometimes, what with traveling and all, I’ll stray from the straight and narrow for a bit.   The first day or two or even three after I’ve fallen off the wagon, I don’t have symptoms.  But starting about day three or four, it turns brutal.   And like most everyone else, once the let’s-eat-carbs devil is on me, I want to keep on going.   And I pay dearly.   I actually become afraid to go to bed because I know what’s going to happen.   Those of you who are fellow sufferers know what I mean.

I’ve taken to never going far without my team of GERD-preventative products, which, even though OTC, are really the only semi-sort of medicines I ever take.   I always packed the duo shown below: Tums and Pepcid AC.   Both are OTC, although Pepcid used to be prescription.   I hated to take them, but I hated the symptoms of GERD even worse.

Now for the direct response business.

A direct response company (DR) is one that sells products direct to consumer through channels other than retail stores.   Companies that sell through catalogs, online, direct mail, infomercials, Google ads, websites, etc are called DR companies.   Anyone who sells this way is said to be in DR sales.   Many companies have physical stores but still have a DR arm that sells through catalogs and online.   The little product section of our website is a DR store.

As I’ve mentioned on this blog, or at least in the comments somewhere, MD and I are part owners of a couple of DR companies that produce and sell unique, patented nutritional products.   I’ve avoided promoting any of those products on this blog because I didn’t want to contaminate it with commercial marketing. I want what I write to be accepted as my opinion based on my years of practice and my reading and understanding of the medical literature, not as an overt or even subtle effort to drive readers to buy products that I may have to sell.  Any time I do post about a product, which I did once with Pentabosol, I am always clear that I am in the business of selling said product, and I expect anyone reading what I have to say about it as coming from someone who stands to gain financially by its sales.

I will never follow the loathsome practice used by a majority of the newsletters out there that recommend products in a seemingly unbiased fashion then offer a link for readers to purchase those products from what appears to be a third party, but which, in reality, is a company owned by the newsletter publisher.  I believe such behavior is beneath contempt.

How does my GERD and my involvement in the DR business all come together in one post?

Because GERD is a problem that afflicts me, I do a fair amount of research on it.   Through this research, I’ve discovered that I’m far from alone in suffering GERD’s debilitating effects.  There are estimated to be anywhere from 25 million to 40 million fellow GERD sufferers in the US alone, numbers that get the attention of the DR marketer in me. (Not to mention the pharmaceutical companies, which is why the commercials for the little purple pill are all over TV.) For several years, I’ve been on the lookout for a natural supplement that works for GERD. If you google GERD or heartburn, you’ll find plenty of nutritional supplements, but based on my experience, none of them really work – at least not for me.  Below is a photo I took of a part of an entire section at Costco devoted to OTC reflux meds.

A few years ago I was doing my morning cruise through the medical literature when I came upon a paper by a Brazilian scientist about a natural supplement he had developed and used successfully to treat severe GERD. I read his paper his paper (pdf file) and found a follow-up paper and was intrigued. He had compared his supplement head to head with omeprazole, the generic for the drug Prilosec (and the precursor to Nexium, the little purple pill), and his supplement had won.   Moreover, he had a large number of subjects – almost 300, which is a pretty huge number for trials with natural supplements.  Usually it’s something in the range of 10-20.  He found that within 40 days ALL the subjects on his supplement had achieved complete relief from their GERD symptoms whereas only 67 percent of those on the drug had done so.  As you might imagine, this paper got my attention.

When I looked at the ingredients, it didn’t look to me as if they would particularly work to relieve GERD, but, according to his study, not only did they work, they were shown by endoscopy to actually heal ulcerations.  The follow-up paper (pdf file) had photos of the healing progression.  In doing further research on the product and the ingredients, it looked as if this product worked in a different way than all the others on the market.

Since the beginning, when people first starting treating GERD and acid reflux, they’ve used a variation of the same treatment: reducing the amount of stomach acid.  The theory is that acid from the stomach gets through a loosened lower esophageal sphincter (LES), the muscular ring that holds the bottom of the esophagus closed, and splashes onto the delicate tissues of the esophageal lining, burning them in the process.  Although new theories are emerging as to what really causes GERD, the excess acid reflux theory has held sway for ages.  According to the precepts of this theory, if you can reduce the degree of acidity of the stomach acid or cause the stomach to produce less of it, you can reduce the effects of the acid that makes its way through the LES to the vulnerable esophageal cells.

Antacids, the earliest approach developed, work by neutralizing stomach acid.  The newer drugs such as Prilosec and Nexium work by making the stomach produce less acid.  In both cases, the problem is solved by either getting rid of the acid or neutralizing it.  Which, for the most part, works to reduce or eliminate the symptoms of GERD.  But, and this is a big ‘but,’ maybe isn’t the best way to go.  Stomach acid is there in the stomach for a reason.

It’s the first line of defense against microbe invasion.  If you swallow germs, the acid works to destroy them.  When you breath in germs, they get stuck to the mucus in your respiratory tract, then the little hairs (that haven’t been burned off due to smoking) move this mucus, filled with germs and particulate matter you don’t want in your lungs, upward and dumps it in the back of your throat (you never notice this happening, but it happens 24 hours per day) from where you swallow it.  Those bugs then get killed when they hit the acid in the stomach.

When food reaches the stomach, the stomach acid acts upon it as the first phase of the digestive process.  Protein starts to be broken down in the stomach.  When the acidic stomach contents are released into the first part of the small intestine, their acidity stimulates the release of alkaline juices to neutralize them and do other work in the digestive process.  Whenever stomach acid is gotten rid of or neutralized, the very first step in the digestive process is compromised and there is a domino effect from there on.

Studies are starting to demonstrate that those who take the newer anti-GERD drugs suffer a higher incidence of pneumonias and other infections (which makes sense since the first line of defense is knocked out) and more osteoporosis and hip fractures (which also makes sense since protein digestion and absorption is affected).  As far as I know, antacids haven’t been implicated, but that’s probably because people don’t take them all the time as they do these other drugs.  Most people only take antacids as they need them, so their acid isn’t affected 24 hours per day, day in and day out.

This Brazilian product appeared to work by strengthening the LES so that the acid didn’t get to where it wasn’t supposed to be.  But the acid itself wasn’t effected, so the digestive process could perform unhindered.

I thought this could be a terrific product for DR, so I tracked the researcher down in Brazil.   He told me he had used the supplement on many, many patients besides the ones in the study and that he was shipping it all over Brazil and to people in the US and Canada.  Furthermore, he informed me that he had the worldwide patent rights on the product.   I told him I would love to work an arrangement with him to get the exclusive license to make and sell his product.  I (and my partners) flew him to the US where we put him up for a week and picked his brain on the product.  Satisfied that it was legit and that his patents were in order, we executed a worldwide exclusive licensing agreement with him.

We began to formulate a strategy to sell the product, which we named Protexid.   We decided to start with a radio infomercial because they are much less expensive to produce and can be used to work out the bugs in the presentation before jumping into the much more expensive television infomercial market.   At the same time we were in the planning stages for the radio infomercial we were working to come up with a name for the product (the name he was using in Brazil wouldn’t make any sense to an American consumer), designing the labels and accompanying literature and all the rest of the creative stuff that has to be done to bring a product to market.

Our Brazilian doctor had sent us names of clients he had in the US who had been using his product.  We got in contact with a number of these folks and found them to have been tremendously satisfied and several were willing to be testimonials for us.  Once we had all the parts of the promotion together, MD and I went to a studio and recorded the radio infomercial.  We stayed in the booth for two days making a number of iterations of the program.  Once finished we got the shows transcribed and sent the scripts to the attorney whose job it is to keep us out of trouble with all the government regulatory agencies.   MD and I are old hands at this, so we pretty much know how to do these things on the fly and stay in the clear.  Consequently, we were expecting a few little cuts here and there, but nothing that would substantively alter what we were trying to say.   We’re we ever in for an eye opener.

Here comes the part about our friends in Washington.

When we spoke with the lawyer, we found that our show had been cut to the bone.   GERD is a disease, and if you make disease claims – as in, it relieves the symptoms of GERD – you are making a disease treatment claim, which runs you afoul of the FDA.   The only way you can make a so-called disease claim is to go through the same kind of extensive FDA-approved studies as drugs have to go through.   If you try to make a disease claim without doing this, you get hammered by the FDA.   Then there are all the FTC regs.   About half the time you can’t say one thing because the FDA won’t let you and the other half you can’t something else because the FTC won’t let you.   After our lawyer – who really is reasonable – got through with our show, it turned out that the only claim we could actually make was the following:  Protexid may offer relief from occasional heartburn.   Nothing about GERD, nothing about acid reflux, nothing about the long term problems with untreated GERD, and nothing about how our product stacked up against a prescription drug.   All in all, our program had been totally emasculated.

We had no way to explain how phenomenal Protexid really is without risking serious problems from our government watchdogs.  Which is extremely frustrating when you’ve got a product that works as well as this one and that so many people could benefit from.

And it works extremely well.

As we were fiddling with all the work necessary to get this project moving, I was going about my business doing all the things I normally do including tending to this blog.   Over the first couple of months or so that we had the product I had an episode or two of GERD, but dealt with them with Tums and Pepcid AC as usual.   I didn’t use our own product for a couple of reasons.   First, the samples we had gotten from the Brazilian doc had been made in China and I wasn’t about to take them.  Second, when I got GERD, I got it bad (for some reason, I never have a slight case or a touch of it; I always have the full-blown version), and I wanted to take something I knew worked, not something I had never taken before.  So even when we had our own US manufactured product, I didn’t take it myself.

I’ve had tons of experience with natural supplements, and they all pretty much work the same.   You take them for several weeks or a few months and you build up levels that actually start to work.  Krill oil had been the perfect example.   I took a krill oil/fish oil/curcumin combination to relieve my aches and pains from playing too much golf so I could quit taking all the ibuprofen I was taking.  After about a month and a half I was pretty much ache and pain free.   Now I take only a single krill oil softgel and one curcumin daily to keep myself that way.  But it initially took almost two months for the natural supplement combo I was using to kick in and do its thing.   Which, in my experience, is pretty much the standard course with natural supplements: many work, and work well, but it takes time.

When I have an episode of GERD, I don’t have time to wait.   I want relief now.   I don’t want to lay awake all night in agony and do so for two months while I’m waiting for the natural supplement to kick in.  Thus I never used our own product the couple of times I needed something.

Until one time MD and I went on a several-day-long trip, and I forgot to take my Tums and Pepcid.  A couple of days into the trip, I could tell I was going to get GERD that night. (Most of the time I can tell when it’s going to happen; occasionally it sneaks up on me.)   I was desperate.   I was getting ready to head off to find a drug store and get the stuff I needed, but MD brow beat me into taking a Protexid.  I took one capsule (the standard dose) at bedtime and experienced no GERD.  I wrote it off as a fluke.  But then I tried it again the next night and, again, no symptoms. I tried to test it by eating a bunch of junk that I knew would normally do me in.  One capsule at bedtime and nothing.   This is what the Brazilian doctor had told me, but I simply hadn’t believed him.  Once I saw how well it worked for me, I became almost a religious convert.  I knew a few guys I played golf with who had GERD.  Most took prescription drugs daily for the condition.   I got them to try the product.  In every case, they got complete relief with one capsule at bedtime. I was stunned that it worked so well.

I have had probably 30 people that I now know first hand who have taken this product with success equal to mine.   One guy – a surgeon – ditched drugs he had been taking for years and got total relief.   He feared he was going to have GERD one night, and so took one of his prescription drugs that night in addition to the product.   He didn’t have symptoms and we don’t know if he would have on the product alone or not.   But that’s as close as we’ve come to a treatment failure with his product.

In fact, in all my years of medical practice, I have never seen a natural supplement that works like this one.   It works quickly and it takes only one capsule at bedtime, not the large doses throughout the day that are associated with most natural supplements.   It is the only supplement I’ve ever seen that has truly drug-like effects in terms of speed of action and efficacy.

So we’ve got this great product and we can’t really tell people via paid advertising how it really works.  We ran our emasculated radio infomercial, but, as expected, it didn’t do squat.  The people who purchased the product were happy, but not nearly enough bought it to make continuing to run the show profitable.  We cut our losses and shut down.

We were approached by another company that wanted to promote our product via television infomercial, so we negotiated a sub-licensing agreement with that company.   This outfit went over the moon in making claims about Protexid (in our licensing agreement, of course, we made sure we were exempt from any liability for claims this company made), yet they, too, were unsuccessful in making the promotion a success.  They spent even more money and tried again with even more aggressive claims and got very little return.  They finally gave up and returned the rights back to us.

Why didn’t these shows work?  We knew ours didn’t work because we couldn’t really describe how effective the product really is.  But how about the other show?  The one that took it over the moon in terms of claims?  Why didn’t it sell there? I’ve got my suspicions as to why that I’ll talk about it a bit.

Right now we’re scratching our heads about what to do with this phenomenal product. I put it up on the catalog part of our website, but no one really knows what it is, so we haven’t really sold much Protexid that way.

Which brings me to the point of this meandering post.  We’ve worked on this project for going on three years now and the Protexid we’ve got left is going to expire soon.  It really isn’t going to expire in terms of efficacy, but it’s going to expire based on the dates the manufacturer printed on the bottles.

There are two versions.  The first, pictured to the right, is the original that is the product used in the published study.  It’s in a blue bottle and is called Protexid. (In case you’re wondering, Triparadol is what the name is in Brazil) The other is in an orange bottle and is called Protexid ND.  The Protexid ND has lower doses of a couple of ingredients and seems to work as well as the regular strength product.  I’ve used both – I use whichever I happen to have at hand when I need it – and haven’t seen a difference.  The Brazilian doctor uses the lower dose all the time and in his follow-up paper he used the lower dose, but we made the higher dose so we thought we could use the first paper that compared Protexid to the prescription drug.  Had we used the first published paper to support the claims for the product with the lesser dosage, we would have been hammered.

We have about 80 of so bottles of the blue, full-strength Protexid, but it expires at the end of November.  We have more bottles of the Protexid ND, which expires at the end of December 2009.  I don’t know off hand how many Protexid ND we have, but substantially more than the other.  As I say, as far as I can tell, they both work the same.

Get it free!

Anyone who wants to try this product can get it absolutely free by ordering on our website.  The price should be set at $0.  All you will have to pay is the shipping and handling, which is minimal.  Please, though, no more than two per person.  That’s TWO per person.  It can be one of each or two of one kind, but not two of both kinds.  I want to make sure that everyone who wants to try Protexid gets a chance, and there really is a limited amount left.  No obligations on your part.  You don’t have to sign up for more.  Just grab it and run.  So, if you or someone you know has the problem, give it a try.

I don’t think Protexid will ever be a good infomercial product because due to government regulations it can’t be promoted in a way that explains what its real benefits are.  And without the explanation no one really wants to purchase a product that ‘may offer relief from occasional heartburn.’  And the obvious problem with GERD is that it hurts and that some people actually spit up acid and burn their throats.  These problems can be solved with prescription medicines – or, as in my case, with OTC meds.  But without the explanation as to why these aren’t the best solutions, why would anyone have the impetus to pay for Protexid when prescription drugs that relieve the symptoms can be had for the price of a co-pay.

So we are changing course to look at selling Protexid into the retail market and/or through health practitioner’s offices. I have a friend who is a naturopathic physician who works in an integrative pharmacy, which is one that does compounding and sells a lot of nutritional supplements along with prescription medicines.  She tells me that almost 70 percent of people who come into the pharmacy (who aren’t coming in specifically to get a prescription filled) are looking for something for GI problems, and that most of those are having problems with GERD.  The pharmacy in which she works is in an upscale part of Los Angeles, and she says most of the people coming in have a prescription for Nexium or one of the other similar drugs, but are looking for natural alternatives.  This is the group we need to be marketing Protexid to, but our whole team are skilled only in the DR way of marketing.  None of us have a clue as to how to get a product into a pharmacy.  I’m constantly amazed at the collective wisdom of people who read this blog.  Maybe someone out there is experienced in retail placement or other means of distribution that they could direct me to.  If so, I would love to hear from you.

And if anyone has used this Protexid ( you know who you are) and wants to tell about the experience – good or bad – send it to the comments, and I’ll post for all to read.

Until we get our marketing strategy worked out, we’re probably not going to manufacture any more Protexid, so gets yours free while they last.

One last thing.  I’ve given Kristi, our long suffering assistant who works for slave wages, time off for good behavior, so she is leaving tomorrow for Thanksgiving with relatives.  She may not be able to get some of these orders out until Monday.  Thanks in advance for your patience.

As anyone who regularly reads this blog can tell, I’ve been a bit hit and miss in posting lately.  The bride and I have been swamped with work on the Sous Vide Supreme project.  MD has been working with chefs to develop recipes along with creating a bunch herself; she has been editing a book on sous vide for the home cook written by yet another sous vide expert; she’s been posting on the Sous Vide Supreme blog (eggs the sous vide way); and, as you can see at the left, she’s been talking sous vide to anyone who will listen.  All this while she prepares for performing the Messiah in about two weeks.  I’ve been heavily involved in the business end of things, which is a never-ending task.  Plus, I’m the taster-in-chief.  Neither of us dreamed that this would turn into such a time-gobbling project after the development of the machine.  But it has.  It seems that we are spending twice as much time now working in some capacity on  Sous Vide Supreme than we ever did before – even when we were at our busiest.  I’m going to have to work harder on my time management if I expect to keep up with all the other projects – including this blog – that I have going.

Twitter

The sous vide time commitments have put a real hickey on my reading.  I’ve probably read less over the past four months than in any four month period of my life.  Instead of five or six books per week, I’m down to about two or three max.  I hate it.  I’m trying to keep up with my daily medical/scientific journal trawl, but that has even slacked off a bit.  When I do find something of interest, instead of blogging on it as I used to, I stick it up on my Twitter page.  I probably post 10-15 times per day on Twitter, so if you want to keep up on a moment-by-moment basis, follow me on Twitter.  If you have a problem thinking of yourself as a Twitter person, give it a try.  I dipped my toes in the Twitter waters with great hesitation, and now I love it.  I’ve found it extremely valuable because I find all kinds of new stuff daily.  You’ve got to be careful who you follow, however, or you can waste a ton of time.  If you get started, start following people who provide you with information you can use.  I avoid following people who do nothing but tell me what they ate for breakfast that day or what movie they’re going to see that night.  Sign up an give it a go. You don’t have to write anything (or tweet, as it’s called) if you don’t want to.  You can simply lurk and be the beneficiary of a ton of good info.   The Twitter people take you by the hand and get you squared away.  It takes all of about two minutes – if even that.  Literally.

Comments

I have fallen way, way behind on dealing with comments.  As I wrote a while back, I had to stop answering individual comments, and I’ve pretty much stuck to my guns on that.  Problem is, I had about three hundred comments stacked up before I started doing that.

When comments come in and I post them, they go up in by date.  So back when I was spending half my day dealing with them, I would often come across a comment that required some thought and a detailed answer.  If I didn’t have time to deal with it right then, I put it off until later.  Often when later came, I had 20 or 30 more that came in after the one requiring the time.  I didn’t want to answer those and put them up ahead of the one I hadn’t answered, so I simply didn’t deal with any of them.  Now I’ve got about 340 of them stacked up and it gives me heartburn whenever I even get on my blog administration screen.  The sad thing is that some of these comments go back months and months.

I’ve been wracking my brain trying to figure out what to do with them, and I’ve finally come to a decision.  I’m simply going to post them as they are.  I’m going to post about 30 of them per day until they’re all up.  Why not all at once?  Because I know many of you are set up to get comments emailed to you when I post them.  I don’t want to clot email accounts with 340 emailed comments all at once, especially since some of these comments are lengthy.  So, I dole them out over the next 10 days or so while keeping up with the new comments as they come in. I won’t start this process for a few days to get those of you who don’t want even 30 of them a day coming in to unsubscribe.

Since many of these hoarded comments contain very good questions, they are a trove of subjects for future blog posts.  As I post them, I’m going to reread them and clip those that would make for good posts into Evernote or my new favorite plaything DEVONthink that I’m just starting to feel my way along with. (See this great Steven Johnson (whom I follow on Twitter) article about the virtues of DEVONthink.)  After I’ve got these blogworthy comments in a format in which I can find them instantly, I’ll start working through them and posting.

Bloggers and the Federal Trade Commission (FTC)

I don’t know how closely blog readers attended to the recent announcement by the FTC that they were going to start riding herd on bloggers, but the bloggers went ballistic.

Among its other duties, the FTC patrols the universe of advertising in this country looking for anyone or any company engaging in, as they term it, deceptive practices.  In other words, the FTC is on the prowl seeking out advertisers who make false claims in order to stop them and punish them.  Which all sounds good in the abstract, but in reality is a whole other story.

As I pointed out in an earlier blog, it’s a valuable exercise to read Kevin Trudeau’s first book to see how the FTC operates.  The nutritional and health information he presents is total garbage, but his description of the practices of the FTC is right on the money. (I’ve got to admit that some of the nutritional and health information presented in Trudeau’s first book (the only one I’ve read) is accurate, but I write that off to the law of averages.  He presents so much information that odds are some of it just happens to be true.  So, if you read the book and come across something that is nutritionally accurate, don’t write me about it.  I know a few things are there, but not enough to justify reading the book other than the first part, which is an excellent treatise on the FTC.)

The FTC has the power to absolutely ruin anyone and/or any company it chooses to go after.  If you read the first part of Trudeau’s book, you’ll see how.

So, the FTC opined that they planned on monitoring bloggers to see if they disclosed the fact that they were paid to do reviews on products.  Apparently, many bloggers make money by doing paid reviews on products without disclosing such, and the FTC doesn’t like it.

I’ve never reviewed products for pay, but I have read enough about it to know how it works.  Companies provide bloggers products, then pay these bloggers for reviews of the products.  I guess the fact that bloggers are given the products and possibly paid for the reviews as well might induce them to write positive reviews of products that they thought sucked.  And I assume that’s what the FTC is concerned about.

The FTC’s actions certainly got the blogosphere in an uproar.  So much so, in fact, that the FTC started to crawdad, which I never thought would happen.  Just goes to show that if you turn the spotlight of public awareness on even the most aggressive and powerful of all government agencies, you can get results.

Not that I fear the FTC on this (at least not at this point), I’ll go ahead and disclose where I get dinero from this blog.  Virtually all of the money that comes to me through the blog comes from readers buying products through Amazon.com.  When they buy a book I recommend or go through one of the book thumbnails of Protein Power or the 6-Week Cure up at the top right or any of our other books I have up on the site, I get a little bit of lucre for it.  And I get a little more if they buy anything else after entering Amazon through one of the portals in this blog.  In a good month, it’s enough to cover my hosting and web guy expenses; in a bad month (as this one is turning out to be), it’s about enough to cover the hosting of the site and maybe an hour or so of the web guy time.

Google ads

I get a little income from Google ads, but I’m trying to get them off the site.  I’ve had several web guys working on the site over the years, and I guess code for these Google ads is stuck all over the place.  I get rid of them in once place, it seems they pop up somewhere else.  When I had Google ads everywhere, I made about $150 per month, which, in my opinion, isn’t enough to justify tacky-ing up the site with a zillion ads.  Plus, I don’t have time to go through and spend time trying to figure out which ads to block.  Many people, I’ve learned, don’t realize that these ads aren’t part of the site, and they wonder why, when I’ve just spent 2000 words bashing statins, an ad for a statin pops up.

A while back I was having lunch with Mark Sisson of Mark’s Daily Apple when he asked me what kind of a deal I had going with Atkins Nutritionals.  I told him I didn’t have any kind of deal going with them whatsoever.  I asked him why he asked.  He told me that he gets my blog posts by email, and that at the bottom of each one is a banner ad from Atkins.  I was embarrassed to say that I didn’t even know you could get the posts by email and that I didn’t have a clue why the Atkins ads were there.  I went home and pulled up the blog (I usually never look at the actual blog – only the admin page), and sure enough, there was a way I could get the posts by email.  I signed up to get my own posts, wrote one, and sure enough, here it came with an Atkins ad at the bottom of it.  I thought I had it all taken care of, but I just looked moments ago and there is still a banner ad at the bottom of the emailed post.  I’ve added it once more to the list of things to have my guy deal with when I get with him on Monday.

Book recommendation

While on the subject of Amazon.com, books and book recommendations, I might as well recommend one.
I finished a terrific book not long ago called A Colossal Failure of Common Sense: The Inside Story of the Collapse of Lehman Brothers. As the title implies, this is a treatise about the fall of the House of Lehman, one of the country’s oldest investment banks, and is written by one of the vice presidents who names names and points the finger.

Not only is this book chock full of great information about how Lehman Bros, Bear Stearns, Goldman Sachs and others operate, it is extremely well written.  The ‘author’ realized he didn’t have the skills to tell his own story in a readable manner, so he hired a writer.  But he didn’t just go out and hire one of the non-fiction write-for-hire folks that are swarming around out there, he hired Patrick Robinson, a best-selling thriller writer.  As a consequence, the book is absolutely gripping. Not only do you learn a ton about how the financial crisis developed, you learn it in a gripping, racing-through-the-pages fashion.  You’ve heard people say about certain books that they read like a novel.  Well, this one does.  I had real trouble putting it down.

After reading this book, you will know exactly why we’re in the boat we’re in now and will be stupified at the mismanagement at the top.  As I read through and learned about the perfidy of Moody’s, Standard & Poors, and the other financial rating outfits that gave the most worthless financial instruments triple A ratings, I was stunned that these companies hadn’t been prosecuted.  Without their complicity, the whole house of cards couldn’t have been erected because no one would have purchased the products.  I was interested to read in today’s Financial Times that at least  Ohio is going after them.  I suspect Ohio won’t be the last.  According to the author, these companies made billions while failing to do their due diligence before passing out AAA ratings like they were candy at Halloween.

Not long after I read the book, I came upon a piece by Calvin Trillin in the editorial section of the New York Times that summed up the situation nicely.  The problem was the enormity of the amounts of money waiting to be made drew smart people to Wall Street.  A funny but insightful short essay.

After you read the book and Trillin’s piece, take a look at this video I posted about a year ago.  It will make it all that much more funny.  And sad.

The 6-Week Cure blog

All I can say is that it’s about up.  And apologies for not having it up sooner.  I hope we’ll have it operational this week and populated with a few posts.

Another vegetarian myth

I wrote in a bookish post (or maybe in answer to a comment on a bookish post – I can’t remember) a while back that I had read most of the mystery novels out there and was looking for a new series to sink my teeth into.  Someone suggested the DI Charlie Priest mysteries by Stuart Pawson.  I got one and liked it, so I’ve been motoring through those as time allows.

The last one I read was Deadly Friends about a murdered doctor, a serial rapist and a host of other minor villains. At a point about midway through, DI Priest and one of his underlings are walking around scoping out a pharmacy prior to entering to get info about the dead doctor.  All these books – at least the four or five I’ve read so far – are written in the first person, so everything is from Priest’s perspective.  Here’s what he says:

We completed our circuit of the block.  Passing the back of the butcher’s I tried not to inhale and wished I had the willpower to go vegetarian.  Trouble is, I like my steaks.

AAARRRGGGHHHH!  Even in mystery novels I’m being reminded of how deep the vegetarian mantra has wormed its way into our collective brains.  How many times have we all heard variations on this theme?  One of the ideas the vegetarian movement has managed to get firmly implanted in the minds of many is that vegetarianism is a more healthful way to eat.  I’ve heard numerous people wistfully say they really would like to be able to follow a vegetarian diet because it’s so much more healthful, but they just like meat too much to do it.

The truth is, as we all know, that vegetarian diets are decidedly less healthful than diets containing animal protein. But the great unwashed masses don’t seem to have figured this out.

But I’ve got to hand it to the vegetarian brigade: they’ve managed to successfully propagandize most of the population.  And they’ve done so without any real science behind them.  The most they can point to is a sheaf of observational studies that don’t prove squat.

The low-carb/Paleo movement, on the other hand, is producing more data almost daily that a lower-carb, higher-fat, higher-protein diet is infinitely better for a majority of the population.  But, we don’t get the message out as well as the other side does, I suppose.  I went to a Borders Books the other day and found an entire collection of free booklets written for children telling of the horrors of factory farming and encouraging them to go vegetarian.

We are starting to make some inroads into this nonsense, however, with the help of some former vegetarians who have seen the error of their ways.  If you haven’t read Lierre Kieth’s book yet, add it to your Christmas list.

I’m girding my loins for all the hostile comments I’m sure to get from angry vegetarians.  These comments will be from vegans telling me how healthy they are and how many miles they can run and how they could kick my butt in any endeavor I might wish to engage them in.  And they’ll reference the idiotic China Study and a host of other meaningless observational junk.  But wait.  I don’t have to gird my loins.  I’m not dealing with these comments any more.  I’m just posting them as they come in.  Give it your best shot.

To see under what conditions our genome developed, read on.

The hunter-gatherer lifestyle

Just to wrap this long, meandering post up, I want to end with a link to a great article in the December 2009 National Geographic.  And to bring this post full circle, I’ve got to let you know that I found this article on Twitter.  I wouldn’t have discovered it otherwise. At least not as quickly as I did.

The long article is about the Hadza who follow a hunter-gatherer lifestyle in remote Tanzania.  The area the Hadza roam is being encroached upon by all kinds of agricultural and tourist businesses, and the author doubts these indigenous people can maintain their lifestyle for much longer.
The men hunt and the women gather.  The Hadza went on a nighttime baboon hunt and took the author along.  His account of the hunt makes for a riveting read.  Once killed, the Hadza haul the baboon back to what serves as a camp and prepare to serve it up.  I’ll leave you with the author’s description of the meal.

Ngaola skins the baboon and stakes out the pelt with sharpened twigs. The skin will be dry in a few days and will make a fine sleeping mat. A couple of men butcher the animal, and cuts of meat are distributed. Onwas, as camp elder, is handed the greatest delicacy: the head.

The Hadza cooking style is simple—the meat is placed directly on the fire. No grill, no pan. Hadza mealtime is not an occasion for politeness. Personal space is generally not recognized; no matter how packed it is around a fire, there’s always room for one more, even if you end up on someone’s lap. Once a cut of meat has finished cooking, anyone can grab a bite.

And I mean grab. When the meat is ready, knives are unsheathed and the frenzy begins. There is grasping and slicing and chewing and pulling. The idea is to tug at a hunk of meat with your teeth, then use your knife to slice away your share. Elbowing and shoving is standard behavior. Bones are smashed with rocks and the marrow sucked out. Grease is rubbed on the skin as a sort of moisturizer. No one speaks a word, but the smacking of lips and gnashing of teeth is almost comically loud.

I’m ravenous, so I dive into the scrum and snatch up some meat. Baboon steak, I have to say, isn’t terrible—a touch gamy, but it’s been a few days since I’ve eaten protein, and I can feel my body perking up with every bite. Pure fat, rather than meat, is what the Hadza crave, though most coveted are the baboon’s paw pads. I snag a bit of one and pop it in my mouth, but it’s like trying to swallow a pencil eraser. When I spit the gob of paw pad out, a young boy instantly picks it up and swallows it.

Onwas, with the baboon’s head, is comfortably above the fray. He sits cross-legged at his fire and eats the cheeks, the eyeballs, the neck meat, and the forehead skin, using the soles of his sandals as a cutting board. He gnaws the skull clean to the bone, then plunges it into the fire and calls me and the hunters over for a smoke.

Pity the poor lipophobes and statinators.  They’ve just taken another grievous wound to their favorite theory and haven’t even got sense enough to know it.  In fact, not only do they not have sense enough to realize they’ve taken the hit, they’re actually crowing about it.

The current issue of the Journal of the American Medical Association (JAMA) has an article titled Trends in High Levels of Low-Density Lipoprotein Cholesterol in the United States, 1999-2006 that puts another major dent in whatever validity remains of the lipid hypothesis of heart disease.

I’m going to start categorizing the types of findings published in this paper under the rubric of The Statinator Paradox.  I find it interesting that whenever scientists discover data that shows the opposite of what their hypotheses predict, they don’t conclude that their hypotheses might be wrong; instead they deem the contradiction a ‘paradox’ and bumble on ahead with their hypotheses intact.

The lipophobes hold the hypothesis dear that saturated fat causes heart disease.  When the data began to surface that the French eat tons more saturated fat than do Americans yet suffer only a fraction of the heart attacks, the French Paradox was born.  Nothing wrong with our hypothesis, it’s just those pesky French people who are somehow different.  It’s a By God paradox, that’s what it is.

Same thing happened with the Spanish.  Researchers looked at the food consumption data in Spain and discovered that Spaniards had been eating more meat, more cheese and more dairy while decreasing their consumption of sugar and other carbohydrate-rich foods over a 15-year period.  And, lo and behold, during this same period, stroke and heart disease rates fell.  Can’t be.  Saturated fat causes all these things.  But the data show…  Thus came the Spanish Paradox.

Statinators and lipophobes believe with all their little fat-free hearts that LDL-cholesterol is bad and is the driving factor behind heart disease.  So whenever I come upon data that gives the lie to this notion, I’m going to start calling it the Statinator Paradox.

This JAMA paper is a classic case of the Statinator Paradox.

Researchers using the NHANES data looked at the change in the prevalence of elevated LDL cholesterol and found that it fell substantially from 1999-2000 to 2005-2006.  In a period of about six years the prevalence of high LDL cholesterol dropped by a third, which is a lot of drop in a fairly short period of time.

And since everyone knows that high LDL cholesterol causes heart disease, it should go without saying that during this same time period there occurred a significant decrease in the prevalence of heart disease.  Right?  Uh, well, no, not really.  If anything, the prevalence of heart disease actually increased.  But not to a statistically significant degree.  So statistically there was no difference in the prevalence of heart disease during a time in which high LDL cholesterol levels were falling.  But if high LDL cholestrol causes heart disease…? It’s the ol’ Statinator Paradox writ large.

It was fun reading this paper because a basically fairly simple project was cloaked in all the regalia of academia and academic speak.

It starts out with a great opening sentence that is a paragon of academic weaselry:

High total blood cholesterol is recognized as a major contributing factor for the initiation and progression of atherosclerosis.

Recognized?  What does that mean?

I could substitute words in this sentence and come up with the following:

The policies of Barrack Obama are recognized as a major contributing factor in the initiation and progression of socialism in America.

What does that mean?  Depends upon whom you say it to.  If I were to shout this sentence at a Sarah Palin campaign event, I would be cheered loudly.  If I said it at a Nancy Pelosi event, I would be tarred and feathered.  Since the ‘truth’ of the sentence is a function of the bias of the person hearing it, it’s not a meaningful sentence.  As written, the sentence doesn’t mean squat, which makes it perfect for academic writing.

The authors, I’m sure, are believers in the lipid hypothesis but just can’t muster the gumption to write ‘high total blood cholesterol IS a major contributing factor…’  Instead they use the word ‘recognized,’ which makes the sentence meaningless and lets them off the hook should the lipid hypothesis ever blow up in their faces.

In setting up the study, the researchers went through a lot of rigmarole to allocate subjects to three different categories depending upon their degree of risk for developing heart disease.  In determining this risk, researchers used the Framingham risk equation, which relies to a great extent on cholesterol levels to allocate that risk.  Which is strange since the Framingham Study has never shown elevated cholesterol to be a risk factor for heart disease.

Once subjects were divvied into these three groups, the researchers measured LDL-cholesterol levels and calculated what percentage of subjects in each group had high LDL-cholesterol levels.  The threshold as to what was high varied as a function of the risk level of the group as a whole.  The bar for what was high was lowest in the high risk group and highest in the low-risk group.  In other words, if subjects had multiple risk factors, then an LDL-cholesterol level of anything over 100 mg/dl was considered ‘high,’ whereas in subjects in the lowest risk category, an LDL-cholesterol level over 160 was considered ‘high.’

Researchers calculated as a percentage the number of subjects who had high LDL-cholesterol in each risk group and did the calculations again six years later.

The weighted age-standardized prevalence of high LDL-C levels among all participants and among participants in each ATP III risk category decreased significantly during the study periods.

Which is what they were crowing about.  Our therapy dramatically decreased the number of people at risk for heart disease.

But as for heart disease itself:

No significant changes were observed in the prevalence of CHD or CHD equivalents from 1999-2000 to 2005-2006.

So what did our researchers conclude from the fact that there were one third fewer people with high LDL-cholesterol yet there was no decrease in heart disease?

They concluded the obvious.  There were still two thirds of people with LDL-cholesterol levels that were too high.  And, no doubt, these people were not on statins.

Don’t believe me?  Here it is in their own words.

However, our study found that almost two-thirds of participants who were at high risk for developing CHD within 10 years and who were eligible for lipid-lowering drugs were not receiving medication.

So, let me see if I’ve got this straight.  This study shows no evidence that lowering LDL-cholesterol levels decreases the prevalence of heart disease.  And what we conclude from this data is that we simply need to treat more people.  Brilliant!

As I was reading this paper online, I got a bing alerting me that I had an email from Medscape bringing me the latest in mainstream medical thought.  I opened the email and began scrolling through the various articles displayed when my eye fell on one titled “Lipids for Dummies.”

I clicked on it, and what opened was a video of a statinator of the deepest dye interviewing an alpha statinator about how to best deal with the risk of heart disease.

It was unbelievable.

Here in a short interview is everything that is wrong with mainstream medicine today.  We have two influential doctors at the pinnacle of their academic and clinical prowess – no doubt on the payrolls of multiple pharmaceutical companies – who are absolutely full of themselves blathering on about expensive treatments that have no true scientific grounding.  And their BS is being disseminated to practicing doctors everywhere. Instead of ‘Lipids for Dummies’ this interview should have been called Dummies for Statins.

Watch and just shake your head.

Click here to view the embedded video.

These guys aren’t really talking about reducing the risk for heart disease or early death; they’re discussing how to use extremely expensive medications that are not particularly benign to treat lab values.  As I’ve written countless times, statins can quickly and effectively treat lab values, but there is little evidence they treat much else.  So if you want to have lab values that are the envy of all your friends, statins are the way to go.  But if you want to really reduce your risk for all-cause mortality, you might want to think twice before you sign up for a drug that will cost you (or your insurance company) $150-$250 per month, make your muscles ache, diminish your memory and cognition, and potentially croak your liver.

If you wonder who underwrites these kinds of interviews, take a look at the actual Medscape link in which the video is embedded.  See if you, like Sherlock Holmes, can figure it out.

This link requires requires free registration.

(If I weren’t so pleased with a nice Sous Vide Supreme review we got today, this kind of nonsense would make me contemplate seppuku.)

Oftentimes people become so fixed in their thinking – and in their belief that everyone else thinks the same way – that they unwittingly raise the curtain and expose the wizard of their flawed thinking, showing it for what it really is.  Statinators have done just that in an article in the current issue of the Journal of the American College of Cardiology (JACC).

The study, Effects of High-Dose Modified-Release Nicotinic Acid on Atherosclerosis and Vascular Function, compares the increase in carotid artery plaque over a 12-month period in subjects taking niacin versus those taking a placebo.  It turns out that those subjects taking the niacin experienced a shrinkage of their plaque whereas plaque grew larger on those taking the placebo. The revealing hitch in this study is that both groups were on statins, which means the group on statins alone was the placebo group.  Therefore the data from this study shows that statins alone do not reverse the growth of plaque (at least not plaque in the carotid arteries) despite lowering LDL levels.  Taking the logic a little further, the data from this study gives weight to the idea that a lowered LDL doesn’t reduce plaque growth.

There is a lot we can glean from this study and the from the authors’ commentary on it.

Let’s take a look.

Researchers randomized 71 subjects–all of whom were on statins and all of whom had low HDL-C and either a) type II diabetes with coronary artery disease or b) carotid or peripheral atherosclerosis–into two groups.  The researchers did magnetic resonance imaging (MRI) studies of the carotid arteries of both groups, then started the subjects in the study group on niacin while the subjects in the other group got a placebo.  Subjects in both groups continued with their statin therapy.  At six months and one year later, MRI studies determined the degree of carotid atherosclerosis and whether it had increased, decreased or remained the same.

After one year, it was found that the subjects receiving the niacin along with their statin significantly reduced their carotid atherosclerosis as compared to those subjects on placebo.  And remember, the placebo group of subjects were also on statins and still experienced an increase in their carotid atherosclerosis.

Almost 90 percent (63) of the 71 subjects were males with an average age of 65.  As I’ve discussed previously, there is no evidence that statins provide any benefit in terms of decreased overall mortality to females of any age or to men over the age of 65 regardless of their state of health.  The only group that statins has shown to provide any benefit for in terms of decreases all-cause mortality (the only statistic that really counts) is men under the age of 65 who have been diagnosed with heart disease.  Even in that group, benefit is so small as to be questionable.  Knowing this, we can say (assuming an equal distribution of under 65 and over 65 to get an average of 65 years old for the group as a whole) that the majority of people in this study were taking statins unnecessarily.  Those males in the study who were under 65 and who had been diagnosed with heart disease were really the only ones who (according to all published research) may have received long-term benefit from the statin therapy.  This aside has nothing to do with study or its outcome, it’s simply my commentary on the widespread overuse of statins. So back to the study…

The authors reported on changes in blood values, blood pressure and body weight between the groups:

In the NA-treated [niacin-treated] group, mean HDL-C increased by 23% and LDL-C was reduced by 19% at 12 months. Triglycerides, apolipoprotein B, and lipoprotein(a) were significantly decreased by NA compared with placebo. CRP was decreased by NA compared with placebo (p = 0.03 at 6 months, p = 0.1 at 12 months). Adiponectin was significantly increased at both 6 and at 12 months (p < 0.01). From the safety perspective, minor transient elevations were noted in creatine kinase and liver enzymes, but no significant, sustained elevations (>3× the upper limit of normal for 2 weeks) were observed in any subjects. Fasting glucose did not change significantly, but glycated hemoglobin showed a small increase in the NA group versus placebo (p = 0.02 at 6 months, p = 0.07 at 12 months). Blood pressure and body mass index did not change significantly in either group.

As any of you who have taken niacin will understand, about 10 percent of the subjects dropped out because they couldn’t tolerate the flushing, itching and GI side effects of the niacin. (Some people have had good luck with taking niacin as inositol hexanicotinate, marketed as ‘No-flush Niacin’ though the tolerance for this form isn’t perfect either.)

Those subjects who were able to tolerate it had niacin (nicotinic acid) added to their statin dose and experienced a slight decrease in carotid plaque volume.  Meanwhile those on statins alone had their plaque volume increase.  Below is a representative MRI showing the difference:

To the untrained eye, these kinds of studies are difficult to read.  Even to the trained eye, they can be misread, so there have been computer programs designed to calculate the plaque area so that it can be quantified.  You can see the results graphically below:

Before we all start thinking the combination of statins and niacin (nicotinic acid in the graph) is the second coming as far as atherosclerosis treatment is concerned, let’s be aware of a couple of facts.  First, these differences in plaque volume don’t really mean squat in terms of blood vessel functionality.  As the authors stated:

Neither aortic distensibility nor flow-mediated dilation of the brachial artery was significantly altered by [niacin] treatment.

The terms “aortic distensibility” and “brachial artery dilation” are measures of arterial function, and neither changed.  Also, as you can see from the MRI above, the differences in plaque size don’t seriously compromise the open area in the artery through which blood flows.

The fact that none of these indicators of functionality changed and the plaque shrinkage didn’t make a measurable dent in the blood-carrying capacity of the arteries means that none of these subjects really got any short term benefit from the therapy in terms of true risk reduction.  Maybe subjects who were worse would have, but we don’t know.  And maybe if the therapy continued for the long term, really remarkable changes between the two groups would begin to become manifest. But we don’t know that for sure, either.

What I found the most interesting about this study is what it didn’t say.  Or, I guess, a better way to put it is what it said, but probably didn’t intend to say.

If you were to ask any statinator worth his/her salt what it would take to really significantly reduce the risk for heart disease, he/she would tell you to try to get LDL-cholesterol levels below 100 mg/dl.  If you then asked, “Well, what about if we got those levels to 80 mg/dl, what then?”  You would be no doubt told that the risk for heart disease would then be minimal.

Well, the subjects on placebo – those on the statin alone – in this study had their LDL-cholesterol levels below 100 mg/dl.  In fact, at baseline their LDLs averaged 84 mg/dl and fell to 80 at six months and one year.  Yet their plaque continued to grow.

We can conclude from this study that reducing LDL to these low levels doesn’t stop plaque growth.  We might also conclude that LDL levels may not have a whole lot to do with heart disease.  We can’t really make that conclusion definitively from this data, but it sure adds strength to that hypothesis.

In an JACC editorial (available by subscription only) about this study, the author begins thus:

Despite the substantial clinical benefit offered by potent low-density lipoprotein (LDL)-reducing therapeutics such as statins, a majority of patients will still experience major cardiovascular events.

Hmmm. Let’s tease out all the information loaded into this one sentence.

Despite “substantial clinical benefit” provided by statins means the substantial treatment of lab values, i.e., LDL-cholesterol lowering.  Statins lower LDL-C; no one denies that.  But to what end?  The last half of the sentence tells us:  A “majority of patients will still experience major cardiovascular events.”  If what you’re trying to do is reduce LDL levels, sounds like statins are the drug of choice.  But if what you’re trying to do is reduce heart disease, maybe not.

We know for certain that statins reduce LDL, so the sentence also tells us that LDL may not have squat to do with heart disease, since significantly lowering it obviously doesn’t accomplish a lot.

Now, here’s how the authors of the paper started out in their introduction:

Atherosclerosis is a systemic condition in which coronary, carotid, and peripheral arterial disease frequently coexist.  In patients with atherosclerotic disease, low-density lipoprotein cholesterol (LDL-C) reduction with [statins] has consistently shown reduction in major cardiovascular events and mortality.  However, treatment of LDL-C with statins prevents only a minority of cardiovascular events.

Another few sentences filled with interesting truths.  What the authors say about statins reducing “major cardiovascular events and mortality” is true as long as the word ‘mortality’ is associated with ‘cardiovascular.‘  In those who take them, statins do indeed reduce the incidence of cardiovascular events and deaths due to cardiovascular events.  What isn’t said in this sentence is that the decrease in cardiovascular deaths the statins prevent is more than made up for by deaths from other disorders that statins likely cause. As far as your risk for death is concerned, taking statins is a zero-sum game: you don’t die from heart disease but you do die from something else within the same period.  What you want to do is not to die.  Or at least not for a long time.  You want to decrease your all-cause mortality, i.e., deaths from all causes, not simply switch from one form of death to another.

Also in the above paragraph, the authors – statinators to a man (or woman), I’m sure – state that treatment with statins “prevents only a minority of cardiovascular events.”  From this last sentence, we can once again draw the conclusion that – at least in the minds of true believers of the lipid hypothesis – lowering LDL doesn’t do diddly to reduce heart disease.  Yet they all continue to try to treat it by lowering LDL.

I’m glad researchers are looking at niacin as a supplement to be used in the treatment of heart disease.  As I’ll discuss below, they have ulterior motives in doing so, which is why they combined niacin with a statin instead of having an arm of the study with niacin alone.  About 12 or 13 years ago MD and I found ourselves FAB (flat-a**ed broke) after sending three children through expensive private universities.  We had just written and published Protein Power, but it hadn’t started to sell, and we didn’t know if it ever would.  Our agent approached MD (who can write like the wind) about being the ghostwriter for one of the major university family medical guides (I can’t tell you which one, but it’s one of the Harvard-, Johns Hopkins-, Mayo Clinic-type of giant family medical guides than many of you may have in your homes) for a nice chunk of change.  She didn’t want to do it, and I didn’t want her to do it, but we decided that she should because it would probably make Protein Power a success.  Why did we decide this?  Because that’s how fate works.  We reasoned that if we didn’t take the deal, Protein Power would die on the vine, and we would be wishing that we had taken it.  If we took it and Protein Power took off, then we would be wishing that we hadn’t taken the ghost writing deal and could buy our way out.  We took it, Protein Power took off (thank God), and MD bought out of her contract after having written about four fifths of the book.

During this awful project, I did a lot of the research and MD did all the writing.  Plus MD did all the teleconferences with the major university honchos whose names are actually on the book.  After each of these conferences she would run for the wine, because these guys (all were guys) were so detached from reality that it was impossible to deal with them.  They were so hidebound in their mainstream way of thinking that no amount of reasoning could dissuade them.  Which is why MD didn’t want her name anywhere on the book.  She didn’t want to be associated with such idiocy when she had had years of hands-on clinical practice teaching her that most of what these people – who probably hadn’t treated patients in years, if ever – believed was bunk.

Where this dreary tale is leading is that during the research for this book, we determined from all the published data out there that niacin was the only substance that had ever been shown to actually reduce all-cause mortality in cardiovascular patients.  That was in the mid-to-late 1990s and now they’re just getting around to evaluating it again.

So why after all these years are they now looking at niacin in conjunction with statins in this study?

Follow the money.

Robin Choudhury, in whose lab this study was done, is on the payroll of several statin manufacturers, including Merck.  The study was underwritten by Merck, the maker of Mevacor and Zocor.  Okay, so why would statinators and statin manufacturers want to add what is basically a nutritional supplement to their beloved statins?  A discussion in an online cardiology site tells the tale.

From heartwire (requires free registration):

The paper comes as anticipation builds for the ARBITER-HALTS 6 study results. ARBITER-HALTS 6 is an imaging study comparing changes in carotid intima-media thickness in patients treated with ezetimibe (Zetia, Merck/Schering-Plough) or extended-release niacin; market analysts are already predicting a win for niacin. As previously reported by heartwire, ARBITER-HALTS 6 was stopped early: full results will be presented Monday, November 16, 2009 at the American Heart Association meeting in Orlando, FL.

So, it appears that extended-release niacin is going to kick tail when compared heads up to Zetia, or at least that’s the way the market is betting it.  And that’s usually because the market has info that the rest of us don’t.  If niacin is the clear winner, the press will be all over it and many people (and their physicians) will be wanting to switch from other cholesterol-lowering drugs to niacin.

With this study in hand, Merck and the other statin manufacturers can say, “Don’t give up your statins; the science shows that statins plus niacin is the effective combo.”  Just keep your statin and add some niacin. And prescription niacin, to boot, so it all stays in the Big Pharma family.

Which is why – as heartwire reported – this paper is coming out now: to beat the rush.

We’ve learned a couple of things from this study.

First, we’ve learned that we have here a randomized, double-blind, placebo-controlled study showing that statins reduce LDL but don’t stop the progression of atherosclerosis, which, after all, is why we would take them.

And we have learned from reading between the lines in this study that statinators don’t really believe their own hype.  As Samuel Johnson said about second marriages, the statinator’s reliance on statins as a cure all for heart disease “is a triumph of hope over experience.”  Things haven’t really changed since MD wrote the family medical guide. If you’re worried about heart disease, take some niacin, the only substance yet that has been shown to decrease all-cause mortality. And it doesn’t have to be the prescription variety.