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.

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.)

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.

How I came to be in this dreary place on a rainy day started with a story my dad told MD and me on our last trip to visit the folks in Michigan.  I can’t remember now how it came up, but he started telling us about the time he saw the remains of Adam “Eddie” Richetti, the sidekick of Charles Arthur “Pretty Boy” Floyd in a funeral home in Bolivar, Missouri.  My father grew up on a farm near a little town called Halfway, which is ‘halfway’ between Bolivar and Buffalo.  For the folks in Halfway, Bolivar was the closest ‘big’ town where everyone went to shop.  At that time, Halfway was basically a wide spot in the road.

In June 1933 ‘Pretty Boy’ Floyd and Adam Richetti (shown at right) stopped off to get their stolen car fixed at Bitzer Chevrolet where Richetti’s brother, Joe, worked as a mechanic.  As they were cooling their heels there, the Polk County Sheriff who lived in Bolivar, William Killingsworth, wandered in.  My dad didn’t know if he just happened in or if he had heard the gangsters might be there.  I suspect the former since he didn’t come in with guns drawn.  Floyd and Richetti took him captive at gun point, took Joe’s car and lit out for Kansas City.  Along the way they ditched Joe’s car, stole another vehicle, switched their hostages (they had collected another along the way) over, and kept on traveling.  Before they reached Kansas City, they let Killingsworth and the other hostage go by the side of the road, and drove off.  They reached Kansas City, and there was where the story went murky.

At the same time Floyd and Richetti were driving to Kansas City, unknown to them, an escaped fugitive was on his way there as well.  Federal agents had captured Frank Nash, an escapee from a federal prison, in a store in MD’s home town Hot Springs, Arkansas.  The agents drove him from Hot Springs to Fort Smith, Arkansas where he was passed off to other agents who took him aboard a train bound for Kansas City.  Upon arrival there, other agents arrived to transport him to the jail.  As they were getting out of the car, they were fired upon by men who jumped out of a green Plymouth parked nearby.   Nash and several of the lawmen were killed in the gun battle.

These murders took place right outside of Union Station in Kansas City and came to be known as the Kansas City Massacre.  Prior to this event, federal agents were unarmed.  As happens so often after many such tragic events, legislators stampede into making laws that are sometimes not well thought out.  In this case they decided to pass a law authorizing federal agents to carry arms, and, in the process, made J. Edgar Hoover, who then commanded a national police force of armed agents, the most powerful man in the country.

With virtually no evidence on hand, the feds put it out that Floyd and Richetti were behind the Kansas City Massacre.  By the time this announcement came out, the two were shacked up in Buffalo, NY with a couple of molls.  When they got wind that they were the suspects, they grabbed their girls and took off for Oklahoma.  On the way their car broke down in Ohio.  While there, local lawmen captured Richetti, but Floyd escaped only to be gunned down a couple of days later.

Richetti was convicted of aiding and abetting an escape and was sentenced to two years in the federal pen.  But, more seriously, he was also convicted of murder by the State of Missouri for his alleged part in the Kansas City Massacre.  Although there was virtually no evidence linking either Floyd or Richetti to the event, Richetti was sentenced to the gallows.  Instead of hanging, however, he got the dubious honor of becoming the first person to be executed in the new gas chamber at the Missouri State Penitentiary.  After he was gassed, his body was sent to his brother in Bolivar and Richetti was finally laid to rest in a cemetery in Bolivar.  During the viewing at the Boliver funeral home, my dad was one of the many people who lined up to see Richetti.

After my dad told me this story, I did a little online searching to see what I could find about Richetti and Floyd, and during my search, I came across information about other famous gangsters of the time.  I discovered that both Bonnie and Clyde were laid to rest in Dallas, Texas after they were gunned down in Louisiana.  I knew I was going to be in Dallas for our oldest grandchild’s grandparent’s day at school, so I decided to track down the final resting places of the infamous duo.

I discovered Bonnie had been laid to rest in a cemetery quite close to our son’s and DIL’s house.  Bonnie Parker now resides in the Crown Hill Memorial Park, which is at the intersection of a couple of busy Dallas streets.  MD and I set out on a gloomy, rainy day underneath a sullen sky to find her.  With our never-travel-without-it GPS device, it was easy to find the cemetery, but took some time to find Bonnie’s grave.

The Crown Hill Memorial Park is a nicely kept cemetery and is large – at least if you’re looking stone by stone on a chilly rainy day for one in particular.  After about 45 minutes of searching, we found Bonnie’s headstone tucked in behind a hedge.  In the photo below, her stone is about halfway down the left side of the long hedge in the Sunset Garden section of the graveyard.

Bonnie’s mother was most surely responsible for the wording on Bonnie’s headstone and is buried next to Bonnie.  In fact, it was Bonnie’s mother’s stone I found first because it stands up a little more than Bonnie’s and wasn’t covered with dirt.

When I finally did find Bonnie’s marker, I had to sweep the dirt off of it in order to take the photo.  As dirty as it was, it’s a wonder I was able to find it.  As you can see from the inscription on the headstone, to her mother, Bonnie wasn’t the vicious outlaw she was in reality, but was Mamma’s little girl.  Which, I suppose, is as it should be.

I wonder how many of the people Bonnie terrorized, robbed and maybe even killed would share the sentiments her mother put on her stone?

After visiting Bonnie’s grave, we fired up the GPS and headed for Clyde’s final resting place.  Our trip took us to a pretty dicey part of Dallas.  I don’t know what it was like in Clyde’s day (probably not much different, I would imagine), but today his cemetery is in a neighborhood of falling down homes and jacked up house trailers all in various states of disrepair.  The area is being encroached on all sides by various industrial operations.

The Western Heights Cemetery, Clyde’s place of interment, is as rundown as the area in which it exists.  It was the perfect cemetery to roam through on a gray, chilly day.  As you can see from the photo below, the graveyard is overgrown with knee high weeds and looks like the perfect setting for some kind of Halloween horror movie.  We had to pull the car off of a busy street onto a muddy, rutted road with a chain across the entry way.  It was a new chain, which begs the question: what happened to the old one?

Although the Western Heights Cemetery is much smaller than the Crown Hill Memorial Park, it took longer to find the grave we were searching for because of the overgrowth of weeds.  We finally found it near the edge of the graveyard overlooking the busy street we had come from.

As you can see from the headstone Clyde is buried next to his brother Marvin, aka ‘Buck,’ who was gunned down by lawmen about a year before Clyde.

Due to the overcast day, it was difficult – even with a flash – to get good contrast on the photo of the headstone (which, like Bonnie’s, was also covered with dirt and had to be swept clean).  The sentiment – Gone but not forgotten – isn’t nearly as from the heart as is the one on Bonnie’s stone.

The Western Hills Cemetery must be the final resting place of the entire Barrow clan because there were at least a half dozen Barrow stones all in the same area.

What had never occurred to me until I found these graves and subtracted dates is how young these two people were. Bonnie wasn’t quite 24 and Clyde had just turned 25.  Because of the movie and their legend and larger-than-life status, it’s hard to believe that basically they were just kids.  Mean kids, no doubt, but still, just kids.  I guess much like with people who get involved with gangs today, those who chose gangsterism as a career in the early part of the 20th century didn’t need to worry about saving for their pensions either.

As I type these words, we’re at 37,000 feet somewhere between Chicago and New York.  After all the complaining I’ve done in previous posts about my disastrous experiences with a multitude of airlines, I’ve got to say that this tour has gone without a hitch.  We’ve flown U.S. Air, American, Alaskan Airlines, and now Delta, and all flights have been on time on both ends.  We’re traveling with a crew of nine, so I am thankful for all the airlines we’ve flown and the weather gods for allowing all this to come off on schedule.

I planned to post about the different venues as we went from city to city, but as I said, the time constraints have been such that I really couldn’t do it.  I’ve got a zillion photos that I’ll post in due course and a lot of info about cooking that I’ve learned from the best.

Richard Nikoley, of the Free the Animal blog, came to the San Francisco event and posted on it, so you can read his take, complete with photos, here.

Another writer who attended the San Francisco event wrote about it after.  It’s a good article but I object to the word ‘shilled.’  In my obviously biased view, ‘touted’ or ‘promoted’ or ‘recommended’ would have been much better choices.  Other press reports that are much better (from my perspective, at least) are here, here and here.

As you can see from the above articles and blog, Heston Blumenthal, chef of The Fat Duck, one of the world’s best restaurants, is traveling with us and helping us introduce the Sous Vide Supreme to the world.  Heston and team (several of whom are with us, too) did the testing of the Sous Vide Supreme in The Fat Duck Experimental Kitchen in the UK.  As one of the preeminent and most knowledgeable sous vide chefs in the world, Heston is also doing cooking and teaching demos with the unit on this tour.

At this point in my narrative breakfast arrived.  It is pictured below.  You can see to what depths airline food has fallen.

Low-fat yogurt, 2% milk, Raisin Bran, fruit, a bagel and coffee.  How nauseating.  I will admit, however, that I ate almost all of it, middle-aged middle be damned.  I did leave over half the bagel because it was totally tasteless, much like eating cardboard and as cold as stone.  I haven’t worried much about diet on this tour because we’ve been eating one meal a day – if we’re lucky – so I’ve been viewing the experience as an intermittent fast.  We get little shards of the foods prepared for the demo, but that’s about it.  The rest of the time we’re on the run and haven’t eaten much at all.

So you can see how the demo events are set up, I’ve put up the schedule and menu to the left below.

MD and I introduce ourselves and talk about how the Sous Vide Supreme was developed, much as I did in a recent blog post.  We then introduce Heston, who shows a video of the preparation of Mock Turtle Soup, which I also blogged about not too long ago.  He follows that with a short video of a dessert composed of all the essences of smoke, apples, leather and tobacco and four different whiskies – all incorporated into a flaming sorbet.  He then talks about how he started The Fat Duck with just himself, a dishwasher and a couple of waiters.  Then he moves into the different foods prepared using the Sous Vide Supreme and talks about all the extensive testing he did of the unit at The Fat Duck.  The staff passes around tasting plates of the food selections to the guests, most of whom are media people, food writers or chefs.  The food is absolutely beyond compare.  When I have more time, I’ll post a description of how each different food is prepared and show photos, of which I have a multitude.

After the event in New York is over today, MD and I have to do a little Middle-Aged Middle promotion tomorrow with some radio, then it’s off to Las Vegas (of all places) for a couple of days.  My niece is getting married there on Sunday (she lives there and is a graphic artist for one of the casino operations), so we’re stopping on the way back to attend.  Then, finally, home on Monday.  At which point, after going through all the mail and other stuff that has stacked up while we’ve been on the road, I’ll get back to more regular posting.

I got word yesterday that the 6-Week Cure blog is set up and ready to go, but so far we haven’t been able to post anything to it.  If you’ve got a 6-Week Cure question or comment, hold it for just a couple more days ‘til we get that blog up.  And if you’ve had a question languishing in the emails, we’re working on that, too.  We had an unexpected glitch, when the new email contact points got mistakenly routed to an email that we never use by the web gurus.  There they sat for about a month before we realized that was why we weren’t getting any emails from the new site.  We apologize and as soon as we get back to Casa Eades we’ll get busy answering those we can answer.

I’m working on another fun post that I’ll maybe be able to get up before we get back, but I can’t promise.  At any rate, it’ll be up soon after we’re home if not before.

Thanks for hanging in there during my absence.

As you watch this long video (and you should watch it; it’s extremely entertaining and filled with a ton of good info), there are a few things you should note.

Before we get to that though, let me fill you in on the LEARN diet.

Most of you, I’m sure, are familiar with the ultra-low-fat Ornish diet and the 30-40-30 protein-carb-fat ratio of the Zone diet, but you may not be aware of the LEARN diet.  LEARN stands for Lifestyle, Exercise, Attitudes, Relationships and Nutrition and is the brainchild of Kelly Brownell at Yale.  The LEARN diet is a low-calorie regimen that recommends 55-60 percent of calories as carbohydrate and under 10 percent of calories as saturated fat.  The LEARN program is big with academics (since it was created by one of their own) and is the diet typically used when a diet program is required as part of a study.  In fact, the LEARN manual was developed to bring some consistency to the nutritional regimens followed in research.  As a consequence of its widespread use in academia, it has also become the program that pretty much mirrors the national guidelines.  Or, to put it another way, the nutritional guidelines set by academics pretty much mirror the LEARN program.

If you look at the carb content of the LEARN program and realize that it is the basis for the national nutritional guidelines, you can LEARN why we have an obesity epidemic.  But that’s another subject.

First off, at about 17:10 in the video, Dr. Gardner talks about how Dean Ornish got mad at him for publishing this study.  (So did Barry Sears, author of the Zone, but Dr. Gardner didn’t mention him.)  Both Ornish and Sears got their noses out of joint after this study and sniffed that the study results didn’t really apply to their programs because clearly the data showed that the subjects assigned to their specific diets really weren’t following the diet as designed.  Both missed the point.

As Dr. Gardner plainly says, the study is of specific diet books and how patients lose (or don’t lose) weight following these books.  You can’t recruit a million people for a nutritional study in which you hold their hands throughout.  But you can write a book that a million or more people read and follow.  What Gardner was looking for in this study was how people would do following a diet book advocating a specific program as compared to others on different diet books promoting different diets.

As part of the structure of the study, he randomized subjects to the various diets, then had them come in weekly for eight weeks to visit with a dietitian who went over the book with them.  He relates an interesting story at about 26:10 that I’m sure is absolutely true.  Many of the people who were randomized to their particular diet were demoralized because they had already done that diet in the past and hadn’t done particularly well on it.  After going through the book with the dietitian, these same people realized they hadn’t really read the book very well – if at all – the first time through.  Once they really read and understood it, they were fired up and ready to go.  Based on may questions MD and I have received about our books, I know this only too well.

Earlier in the video, at about the 17:10 point, Dr. Gardner makes an observation that all of us using low-carb diets know well.  He is discussing how reducing carbs makes triglycerides go down and adding fat makes HDL go up.  He then says that all these people have come into the clinic he is involved with after having been on Ornish or McDougall only to find their triglycerides have skyrocketed and their HDLs have dropped off the chart.  He tells them to replace some of the carbohydrate with good quality “unsaturated fats” (sigh), and their labs revert to normal.

At about the 29:00 mark, Dr Gardner points out that as the data came in and was charted, it became apparent that it was difficult for people to stick with the Ornish or Zone diets, and when these subjects fell short of following their specific program, their macronutrient-consumption data ended up falling right smack into the middle of the LEARN data, or the national nutritional guidelines.  Those on the Atkins diet morphed a little (toward a more Protein Power sort of plan, but not quite), but not nearly as much as those on the low-fat diets did.  After a year, the data ended up showing a bunch of subjects essentially following the national nutritional guidelines and another, smaller bunch, following a semi-Atkins diet.

As Dr. Gardner points out, in virtually every parameter measured, those following the Atkins book who ended up following a semi-Atkins diet triumphed over those following the other books, all of whom ended up following the national nutritional guidelines.  Which, of course, is no surprise to most readers of this blog.

But it was a huge surprise to Dr. Gardner, a 25-year-long vegetarian.  He admitted it was a bitter pill to swallow, but the data are what the data are.  And he was man enough to admit it.  I think this study and Dr. Gardner’s engaging presentation style will start getting some notice from mainstreamers.  King Canute couldn’t hold back the tide, and I don’t think the lipophobes will be able to hold back low-carb diets forever.  This is a great video to show Doubting Thomases if they will take the time to watch it.

Aside from the finding that the low-carb diet was vastly superior, a lot of other data came to light as a consequence of this study.  Some people did great on Ornish or the Zone while others did poorly on Atkins.  Why?  You would think that since all the subjects were humans, they would all respond the same way, but they didn’t.

This intrigued Dr. Gardner, so he began slicing and dicing the data to see what he could come up with.  At about the 40:00 point on the video, he discussed a few papers showing that people who are insulin sensitive actually do better on high-carb diets than they do on low-carb diets, whereas those who are insulin resistant do just the opposite.

I pulled all the papers he discussed and plan on reading them over the next ten days while I’m spending (literally) about 24 hours in an airplane seat.  (As part of our Sous Vide Supreme tour, MD and I leave tomorrow for Dallas, then Vancouver, Seattle, San Francisco, Chicago, New York, and Las Vegas, so I’ll have plenty of time to read.) I do find this information fascinating, but I have a few reservations as well.  There are very few moderate to significantly overweight people who aren’t insulin resistant to some degree, so I’ll be curious to see how the authors of these papers define insulin resistance.

Based on my own experience with a whole lot of patients, there are a few, but not many, overweight people–usually women, but occasionally men–whose lab reports show normal insulin sensitivity. I treated them with a low-carb diet, and they did well.  But I didn’t randomize these apparently insulin-sensitive overweight patients into two groups and put one group on a low-carb diet and the other on a low-fat, high-carb diet, so I can’t really say the ones I treated did better than they would have on a low-fat diet.

What I do know, however, is that those who have been overweight and insulin resistant, and who lose their weight and restore their insulin sensitivity with a low-carb diet, will regain in a heartbeat if they go on a high-carb diet for maintenance.  So, it’s hard to reconcile this fact that I know from hands-on experience with the data Dr. Gardner presented.

It could have something to do with the genetics that prevent the development of insulin resistance in the first place.  I’ll post on my thought about this paradox after I’ve read the relevant papers and reflected on them.

I had only one real objection to this presentation.  At the end, during the Q & A, someone asked a question about ketosis, and Dr. Gardner was clearly in above his head.  He did make the distinction between the ketosis one experiences on a low-carb diet and the dangerous ketoacidosis that those with uncontrolled type I diabetes are subject to, but he seemed to be uncertain as to whether low-carb ketosis was harmful over the long run.  He did remark that everyone is in ketosis part of the day, but then he kind of tossed it off by saying that the people on the Atkins diet weren’t really following it that closely and so weren’t really in ketosis for that long.  I wish had addressed the ketosis situation head on.  There is no danger in being in ketosis for extended periods of time.  Ketones are normal fuels of respiration and don’t pose any problems over the long haul.  In fact, some research has shown that ketones are a preferred fuel of many organs including the heart. (Veech et al)

As I’ll be traveling a lot the next 10 days, and since I don’t know my exact schedule even yet, I can’t promise a lot of regular posting.  But I will check the blog often and put up the comments as they come in.  If any of you have experience with trying a low-fat diet after losing on a low-carb diet, I would love to hear about it.

I had hoped to have a new blog for The 6-Week Cure up by now, but our tech people have been working on other projects and unable to get to the blog. They have been working on the Sous Vide Supreme website, which just got up late last night in it’s full and operational form. Now they have one more Eades-related project to do, then they can do The 6-Week Cure blog. I hope it won’t be much longer.

I’ve had no end of comments stacking up that I will deal with as soon as this post is posted, so if you’ve had a comment languishing in ‘awaiting-moderation’ purgatory, it should be up soon. I’ve promised this before and failed, but my time commitments are now such that I’m going to have to stick to it: I can no longer answer specific comments. I’m going to post them as they come in, and if I feel the need to answer a specific one, I’ll do it as I did in in Tim Ferriss’s blog and do so with a comment of my own.

Numerous people have written comments/questions asking about why they’ve stalled or why they’ve gotten diarrhea or why they’ve gotten constipated of why [fill in the blank] on The 6-Week Cure. It is extremely difficult to answer these types of comments because I don’t (and can’t possibly) know the whole story of what is going on. In the office when these kinds of questions arose, our staff was trained to ask specific questions to ferret out the problems. MD and I could go over with patients an entire list of questions to figure out what is happening, do appropriate lab tests, examine the patients first hand. But we don’t currently have a clinical practice and we can’t do that over the internet. Many of the questions we asked in person are basically designed to tease out what the patients are really doing. Many people think they are following a specific program to the letter, when the truth is that they are not. They have misunderstood something or only heard part of what we told them to do or are confused or have had any number of things happen that are causing them not to be adhering to the regimen we thought (and they thought) they were adhering to. If we can’t figure out what specific diet our patients are following, we can’t possibly figure out why they are having whatever problem it is they are having.

I’m sure most of the people who have written asking questions about their experience with The 6-Week Cure think they are following the program exactly as presented in the book, but it has been my experience that as often as not they aren’t. Let me give you a couple of examples that I know about personally so you can see what I mean.

Out of the many people (friends, relatives, etc.) that MD and I know personally who are on the 6-Week Cure, two spring to mind who demonstrate clearly how easy it is to misread or misunderstand instructions as written. The first is a lady who has done well on the program, but who kind of over thought what she read – or we didn’t write it clearly enough. This lady is very smart and runs a successful company employing hundreds of people. She read the part in the book about adding a pasteurized egg to the shake and followed the instructions to the letter. Before I tell you what she did, however, I want to clarify what the whole pasteurized-egg-in-the-shake deal is. We’ve had a number of questions about this, so it obviously isn’t as clear as it should have been.

In the book we make the case that dietary cholesterol is important to the body for numerous reasons and we recommend that people get some good, unoxidized cholesterol in their diet daily. A raw egg is a great source of good-quality cholesterol, so we recommend the option of adding a raw egg in one of the shakes each day for those who don’t get cholesterol from another source. We give this recommendation only for those who, for whatever reason, don’t eat red meat or don’t get their cholesterol from other sources. If you do eat red meat for your meal or if you eat eggs as part of your meal, you don’t need to add the egg to your shake. It’s primarily intended for those who don’t eat red meat or eggs for their meal. And even for those, it is only one egg per day, not one egg per shake.

Since we advocate adding one raw egg (or egg yolk) to one shake per day (for those who don’t get the red meat), we have to advise that the egg be pasteurized for safety’s sake. Most people can eat raw eggs that are not pasteurized without incident, but there is a slight risk of food poisoning. The risk is much higher for those who are immuno-compromised, who shouldn’t be exposed to the possibility (remote) of infection from consuming eggs that aren’t pasteurized. Since we have no way of knowing who is buying our books and reading them, we have to err on the side of safety and recommend that the eggs be pasteurized to cover all contingencies.

Our friend read this as that she needed an egg in each shake (despite the fact that she almost always ate red meat as her daily meal) and so, like many people who have written to us, she used one raw, pasteurized egg per shake. But she went further. She decided that since we said the eggs should be pasteurized in the shell that we meant that she should add the whole egg – shell and all – to her shakes. Which she did. She was throwing an entire raw egg into her blender and whirring it up. She didn’t have a problem, but in conversation with MD, she mentioned that she really had to run the blender a long time before she could get all the shell ground down to where she could drink the shake without crunching on egg shells. MD, of course, told her that she didn’t have to consume the whole egg complete with shell, that just the contents of the shell would do.

Neither MD nor I could have imagined that someone would throw an entire egg in the blender, but this very intelligent woman had done so.

Another friend who is extremely bright made a mistake that was a little more consequential, at least in terms of his weight loss.

This friend is a pretty good size, muscular guy who was a world class college athlete. He, like many of us, put on a little belly as he aged. He decided to go on The 6-Week Cure. He called and peppered us with a bunch of questions about protein powder and leucine before he started. Once he got started, he did fine, but he also said that there was no way he could get three shakes down per day. Two, max, is what he could consume, and even then, he had trouble with the two.

He progressed fine on the program although he wasn’t losing weight as quickly as he figured he would (nor as fast as we assured him that he would), but he was losing around his waist and he was happy. He had some blood work due to be drawn, so he decided to stay on the shakes and a meal regimen for longer than just the first two weeks. He stayed on it almost a month so that he could get the maximum effect before his labs were drawn. When he got his labs back, all of his lipid parameters had improved, so he was thrilled.

In conversation with MD and me over dinner, he started talking about how expensive it was to do the shakes. MD asked him what kind of protein powder he was using, assuming that that was where the expense came in. He told her it wasn’t the protein powder that was expensive – it was the coconut milk. It was costing him a fortune even through he was buying it by the case. Buying it by the case?

MD, thinking there must be some miniature-sized cans of coconut milk she didn’t know existed, asked him what size cans he was getting. He told her he was getting the normal sized cans available at his natural food grocer. Then she asked him how much he was using.

“A can per shake, just like the instructions say,” he replied.

A can per shake?!?! MD was incredulous. “The instructions don’t say a can per shake. You are supposed to be using an ounce of coconut milk per shake, not an entire can,” she told him.

‘Hmmm,” said he. “No wonder my shakes were so thick I could eat only two per day.”

Indeed. Especially since each can contains 14 ounces of coconut milk, meaning that each of his shakes contained 14 times the recommended amount.

And no wonder he wasn’t losing as fast as he thought he should have been. As you can see from the nutritional facts from a can of the coconut milk he was using, at two cans per day, he was getting an extra 26 ounces (2X13) of coconut milk per day, which meant he was getting an extra 1560 calories per day along with an extra 91 g saturated fat and an extra 52 g of carb. And he was still losing weight, not to mention improving his lipid values! Who says saturated fat makes your lipids worse?

These two really smart people misread the instructions and didn’t really follow the program as written, even though they thought they were following it to the letter. I’m sure they aren’t the only people who have unknowingly veered from the path as presented. Had one of them – the guy with the can of coconut milk – written me through this blog and asked why he wasn’t losing as fast as I said he should be, I could have racked my brain trying to figure out why, when the real reason was that he was using the wrong amount of coconut milk. I can attest from the comments and letters we’ve received that he isn’t alone in having a hard time getting all three shakes in each day, so there may be others out there making the same unwitting mistake, and it would previously never have occurred to me to ask ‘how much coconut milk are you using in your shakes?’

So, the point is, if you are having a problem or not getting the results you think you should, go back to the book, look up the recipes, and make sure you are making them exactly as written. If you have questions about the recipes, go to the forum and ask your dieting compatriots. They will be more than willing to give you the benefit of their experience. You can post a comment here, and if I get a bunch asking the same question, I’ll do a short post or a comment of my own about it. But for the next few weeks, I’m not going to be able to be as responsive as usual, so the forum is probably your best bet for quick answers.

While writing this post I got word that a rudimentary 6WC blog should be up in a day or two.  Don’t hold your breath because I’m not holding mine.  But keep checking because hope springs eternal.

One final note.  If you have gout or want to learn more about gout, take a look at this post on Tim Ferriss’s blog.  He published one of the many parts left on the cutting room floor when Good Calories, Bad Calories got edited down to publication size.

For those of you unfamiliar with sous vide, it is a French term meaning ‘under vacuum’ and refers to a method of cooking in which vacuum-packed foods are cooked in a water bath creating a taste and flavor that can’t be replicated any other way.  Though many of you may never have heard of the term ‘sous vide,’ it’s a good bet that you have tasted food prepared using the ‘sous vide’ method, especially if you have eaten at a fine restaurant.

Why on earth would two physicians who made their reputations caring for overweight patients and writing books about diet and nutrition veer off in the direction of manufacturing a kitchen appliance?  As is always said in situations such as this one, it’s a long story.  But not really that long, so I’ll tell it.

A couple of years ago I was trolling through the internet looking for something – I don’t remember what – and I came upon an article about the sous vide method of cooking.  I read about it and did a little more research.  Once I understood the concept, it all made perfect sense to me, so I did what I always do in cooking situations: I dragooned MD into doing all the work.  I did help a little, but she was the real technician in putting our first sous vide contraption together.

So you’ll understand how sous vide works, I’ll digress a little from the story of our development of the Sous Vide Supreme to explain.

Say, for instance, you want to cook a perfect medium rare steak.  You throw it on a very hot grill (or skillet) and try to guess the amount of time it will take for the extreme heat to penetrate the steak until it raises the temperature in middle of the steak to 134 degrees F.  Often you miss and either under cook or (more commonly) overcook the steak.  You can be more precise if you use a meat thermometer and pull the steak off the grill when the temperature reaches 134 degrees.  This meat-thermometer technique is obviously a more accurate way to ensure the perfect medium rare steak, but it has its drawbacks.  If you pull the steak off the grill when the center is at 134 F, the steak continues to cook and will end up more well done than medium rare.  If you pull it off at, say, 128 F, you are playing the guessing game again, hoping that it will cook to the 134 F on its own.

And we’re not even talking here about the problems you run into if you are cooking several steaks of differing thicknesses, a situation that multiplies the probability of having a not-quite-right outcome – at least with some of the steaks.

If you use either of the above methods precisely, you end up with a perfect medium rare steak…right in the middle.  The center of the steak is medium rare, but it gets more and more well done as it gets closer to the surface.  You have what looks kind of like a target with the perfect medium rare center being the bulls eye with the rest of the target being progressively more well done as it gets nearer the edges.

Sous vide solves this problem.  You season your steaks however you like them seasoned, then you put them in vacuum bags and seal them.  (You don’t have to have an expensive machine for this.  You can find vacuum bags and pumps for just a few dollars at most grocery stores.)  You then put the seasoned, sealed steaks into a sous vide water bath set for 134 F and walk away.  You can leave them in for an hour or eight hours – the time doesn’t really matter that much because as soon as the steaks reach 134 degrees throughout, they are perfectly medium rare and they don’t get any more well done beyond that point.  So if you’re having a dinner party and your steaks are in a sous vide cooker awaiting the meal and the pre-dinner chit chat runs a half hour (or an hour or two hours) over, it doesn’t matter.  You take the steaks out, remove them from the bag, finish them off for about 30 seconds, and you’re finished and have perfect medium rare steaks.  And it doesn’t matter if some of your guests want thick fillets while others want thinner sirloins and yet others want rib eyes – they all come out perfect at the same time.

Sous vide is the perfect method for cooking tougher cuts of meat.  Grass fed beef, though tasty, isn’t always the most tender of selections.  If, however, you put a couple of grass-fed beef steaks in a sous vide bath before you go to work, by the time you get home, they are as tender as a mother’s heart while still retaining all their taste.  MD blogged about flank steak cooked sous vide a while back.  You can cook flank steak, which is really tasty but tough, using the sous vide method and have a meat that is as tender as filet but with all the taste of the flank steak and best of all, not overcooked.

Here is a link to a full-page Wall Street Journal article from about a year and a half ago that describes the sous vide process and has a pretty good video showing how it works to cook a steak.

But it’s not just for steak. You can use the Sous Vide Supreme to cook any kind of meat and vegetables.  And can even use it to make ice cream base, béarnaise sauce, creme anglaise and anything that requires a precise temperature to cook properly.  Vegetables cooked sous vide are out of this world.  For instance, if you cook beets the traditional way by boiling them, you’re left with a lot of beet-colored water in the pan after you’ve removed the beets.  This beet-colored fluid contains flavonoids, carotenoids and other beneficial nutrients that you would prefer not to lose. If you vacuum seal the beets and cook them sous vide at 185 F, you end up with beets that are unlike any beets you’ve tasted before.  They look the same, but taste much more beet-y, because they have retained all the nutritious fluid that you previously threw down the drain after boiling.  The beets are tastier, have a better consistency and are more nutritious than beets cooked any other way.  It works the same with all veggies.

When MD built our first home-made sous vide contraption on our stove, she used a stock pot that she had to put up on a scaffold she built out of odds and ends she rounded up from the kitchen.  She had to get the pot above the flame because even at its lowest setting, the fire was hot enough to simmer water, which meant that the temperature was 212 F, way, way too hot for sous vide.  She had to get the bottom of the pot high enough, so that the temperature in the water in the pot was around 140 F (at that point, we thought 140 was the temperature required for a perfect medium rare steak).  It was no mean feat to do so.  She had to keep a candy thermometer in the pot and keep adding little bits of cold water and even ice to keep the water at 140 F. (I now wish that I had photographed this early contraption, but, alas, I didn’t, so you’ll just have to imagine it.) After keeping a couple of vacuum-sealed steaks submerged at roughly 140 F for a couple of hours (which required her constant attention), MD pulled them out, finished them off on the grill for a few seconds, and we cut into them.  We learned a couple of things.  First, 140 F is too hot for medium rare, and, second, finishing is an important part of the process.

MD with my invaluable technical advice fiddled with our device for another few runs of steaks before she hit on the way to cook them perfectly.  Once she did, and once we tasted them perfectly done, I was sold.  I decided that we needed to purchase a sous vide unit for our house.

I got online and searched.  What I discovered to my absolute amazement is that there was not a sous vide unit made for the home kitchen.  There were several companies making sous vide units for restaurant use, but the price of them would knock your socks off.  The least expensive one – and it was tiny – ran to over a thousand dollars.  Most costs many thousands of dollars.  I kept thinking that there had to be a home sous vide unit somewhere, but search though I did, I couldn’t find one.

The light bulb went on.

I reasoned that I couldn’t be the only one who wanted a home sous vide unit.  And of such thoughts are opportunities made.  I figured it couldn’t be that tough to make a unit, since, after all, they were nothing but sophisticated Crock Pots.  So I thought.  As it ends up, nothing is further from the truth, but I didn’t know that at the time.

During my online searches for some kind of home sous vide machine, I came across countless articles on sous vide cooking.  One of these articles contained a quote by Nathan Myhrvold – the retired Chief Technical Officer of Microsoft who has devoted his post retirement to cooking, photography* and various other endeavors – a sous vide expert who figured prominently in the Wall Street Journal article mentioned above, and who is the go-to guy whenever a writer needs a comment about sous vide.  When I read these words, I knew  there was a real opportunity.

Most dedicated home cooks purchase laboratory water baths, which are available on eBay, says Myhrvold.

“I believe someone will produce a home sous vide machine in the not-to-distant future,” says Myhrvold.  Basically, “a Crock-Pot with [a] very accurate thermostat.”

Knowing as I did Nathan Myhrvold’s status in the food world, I reckoned he would know if someone was already working on one, and since he didn’t mention it (and since I’m an eternal optimist), I figured there wasn’t anyone working on one.  So, it was full speed ahead.

What I didn’t realize was that Nathan Myhrvold was wrong.  Not about the no-one working on one, but about the technology required.  He made it sound easy.  But, as it turns out, a sous vide cooker is much, much more than a Crock-Pot with a very accurate thermometer.  To be able to cook sous vide, the temperature can’t fluctuate more than a half a degree in either direction.  For example, eggs cooked at 63 degrees C (you can set the Sous Vide Supreme for either C or F) are totally different from eggs cooked at 62 or 64 degrees.  Try to cook perfect eggs by setting a Crock-Pot at low, medium or hot, the temperature selections available for most.  You can’t do it.  The maintenance of a specific temperature for hours (and even days) is an absolute necessity in cooking sous vide, and that was what we set out to do in developing our machine.  This kind of temperature control can’t be maintained with a simple thermostat mechanism.

Once we decided to make the leap and try to develop a home sous vide unit, it dawned on us that neither of us knew anything about the appliance business.  So we hadn’t a clue as to how to launch such a venture.  But we allowed as how there were bound to be people who did.  So I set about finding them.

Through a business acquaintance, I got introduced to an entrepreneur and businessman who had some experience in the small appliance development business. (A pedigree in small appliance development would be more correct.  He took The Juiceman and The Breadman from concept to success and was also an executive VP at Salton with the George Foreman Grill.)

Bob Lamson, who is now a partner in the business and a great friend, is just the kind of guy I enjoy being around.  I, of course, don’t think he is nearly as smart as I am, but he may disagree.  He is trained in philosophy, has a undergraduate degree from Yale, has a Ph.D. in economics from the University of Washington, ran for US Congress as a Democrat (and almost won), is the author of a book on the economics of the defense industry, and was in a small high school philosophy study group with Barrack Obama’s mother.  As you might imagine, Bob and I have many spirited conversations about many, many topics, which keep all our get togethers stimulating. He is a Seattle resident of long standing, thus our many trips to Seattle where a branch of the Sous Vide Supreme offices are located.

MD and I (MD mainly) came up with the specs for a home sous vide unit, and Bob, who knows everyone involved in the appliance business the world over, after gathering bids, recommended an engineering and design firm in London that got started on the design work.  After much back and forth, and many prototypes, we finally got the design we wanted and a prototype that worked like a charm.

After a lot of consultation, we concluded that if we had any hope of bringing our product to market at a reasonable price for the home consumer, we were going to have to have it made in China, a situation about which I had considerable angst.  We were confronted with the reality that if we made it somewhere else, our appliance would be too costly, and if we made it in China, it would, well, be made in China.  Bob assured us that many Chinese factories were state of the art, and that it was just a matter of selecting the right one.  Bob had had many products made in China (just about everything, I discovered, including the Macbook Pro I’m typing these words on is made in China) and had had no problems.  He told us he would go to China himself and check out any factory we might end up using.  MD and I decided to go as well.

I was in for a huge surprise.  During my years as an engineer I visited many factories, so I have a pretty good feel for what US factories look like.  The factory we decided to work with in China was a marvel of high technology.  In their showroom were many of the products we’re all familiar with here in the US, and as we were shown through the huge work spaces, there were all these same familiar products rolling off the assembly lines.  The testing facilities were beyond compare, and the engineers were terrific.  In fact, the engineers there solved many of the temperature-control and cooling problems that had been plaguing us.  Whenever we found anything problematic, the folks at this factory were immediately responsive in getting it fixed.  After spending a couple of days at the facility, meeting the engineers, and watching the testing processes, we felt more than comfortable using this factory for our product.

What we didn’t realize when we started this venture was that the difficulty in achieving the precise temperature control necessary to sous vide cooking meant that each and every machine had to be calibrated by hand after it came off the line.  The engineers at the factory developed a system to do this that required filling each machine with water and testing multiple temp settings without the process adding huge amounts to the cost of the system.  I found the Chinese engineers easy to work with and incredibly understanding of all the hassle required to bring a product to market in the US.

After designing, building and working all the kinks out of our Sous Vide Supreme, one hurdle remained for us.  We had to get it approved by Underwriters Laboratories (UL).  No UL approval, no US sales.  It was as simple as that.  No retail stores will touch an appliance that isn’t UL approved, and let me tell you, UL approval isn’t easy to come by.  The UL people visited the factory in China, worked with the engineers, made suggestions as to how we could improve our machine, and finally granted us the coveted UL Approved moniker just a couple of weeks ago.  It was this approval I was waiting for before I wrote this post.  I didn’t want to alert the world as to what we were doing until we had this final and most important process firmly in hand.

I can’t begin to tell you what an enormous project this has been.  You don’t really know (I certainly didn’t) what’s involved when you go down to buy a small appliance at your local department store.  We’ve had to hire designers to create logos, do artwork for the box; we’ve had to come up with how-to-use manuals (which are a part of getting a product through UL) and cooking instructions. We’ve had to test multiple iterations of the machine and tweak each one until we got it right.  We’ve had our units tested in major test kitchens here and in Europe, and worked with famous chefs to get it right.  We’ve had to deal with trans-oceanic freight companies and packing and shipping facilities in the US and China.  We ourselves have cooked a zillion different foods in our own test kitchen. It’s been a seemingly never-ending process as you can tell by how long I’ve been putting off the great revelation.  But now it’s done and ready to go.

Our PR firm, Duo PR, is sending us out on a cooking/demo tour that should start on October 18 if all goes well.  Most of the gigs we’ll be going on will be private affairs for potential retailers, but if any are public, I’ll post them so that any of you who have the opportunity and so desire may come to one of the events.

If you want more information about the Sous Vide Supreme, here is the website of our company, Eades Appliance Technology, aka EAT.  Sign up where indicated and we’ll email you information as it becomes available.  And, BTW, the ‘Eades’ in Eades Appliance Technology means a bunch of Eadeses, not just MD and me.  We’ve tapped our family for legal advice, financing, food tasting and creative assistance.  So it is truly a family enterprise plus Bob, Mo and the rest of the staff at the Sous Vide Supreme office in Seattle.

Since this blog isn’t really a blog to sell stuff – other than an occasional recommendation here and there – I’m not going to be writing much on the Sous Vide Supreme.  I’ll have links to the website on the links, and I’ve started a Twitter account so I can put up links on sous vide cooking.  But other than those, this is pretty much it. (I may have one other major announcement, if we can get the legal-contractual issues worked out, but that should be it.) Many people have wanted to know what we’ve been working on so mysteriously, so this is it.  In fact, this is the very first piece to go out into the world about the Sous Vide Supreme. Other than the team working on it, you are the first in the world to be learning about this product.

Next post I’ll be back to the nutritional stuff.

Here are a few photos of MD cooking steaks in one of the sous vide machines in our kitchen.

Here you see a couple of units on our counter so you can get the feel for the size. To the right are cooked, vacuum-sealed steaks pulled from the water bath ready to be finished. The steaks are lying in the inverted top of the Sous Vide Supreme. This top as tray was one of MD’s innovative brainstorms.

In this close up of the perfectly medium rare steaks, you can see that they have been seasoned before being put in the vacuum bags. They are now ready for the skillet. But first, you’ve got to put some butter in the skillet and heat it until the butter is foaming. Then you put the steak in and leave it for just about 20-30 seconds on one side, then flip and sear on the other side for only a few seconds.

One steak in the pan searing on one side and about ready to be flipped.

Two steaks cooked perfectly. I wish the photo were as perfect as the steaks. I intended to take a picture of the steak after it was cut, but my hunger got the best of me and I forgot.

* Nathan Myhrvold took the photos I displayed in a previous blog post.

In April 1995 an article appeared in the journal Current Anthropology that was an intellectual tour de force and, in my view, an example of a perfect theoretical paper.  “The  Expensive-Tissue Hypothesis” (ETH) by Leslie Aiello and Peter Wheeler demonstrated by a brilliant thought experiment that our species didn’t evolve to eat meat but evolved because it ate meat.

The ETH is an example of the kind of scientific detective work that I love.  In fact, this paper is one of my all time favorites.  (An amazing bit of trivia about this paper is that it almost didn’t get published.  I had the opportunity to talk with Leslie Aiello at a meeting a few months ago, and she told me that the journal was reluctant to publish the paper because they thought it too technical for their readers.  I suspect they also found it too controversial.  Now I’m sure they’re glad they published because I would imagine it is the most cited of all the papers ever published in Current Anthropology.)  The authors methodically lay the scientific foundation for their experiment, then, like Sherlock Holmes, progress step by step, accumulating little pieces of data until they reach the ineluctable conclusion that meat eating made us human. I would like to walk us all through their thought processes as laid out in their brilliant paper.

Let’s start with the problem.

For years anthropologists have speculated about why humans developed such large brains so quickly – from softball size to what we have now in just a short 2 million years.  Below is a graphic showing hominid/human brain growth over time.

A number of hypotheses have arisen to answer this question.  Some say that humans developed large brains because they had to contend with problems involving group size, others posit that large brains came about as a consequence of developing complex foraging strategies, others yet say the development of a social or Machiavellian  intelligence was the driving factor.  And even others say that the complexities of learning to hunt expanded brain size.

Any or all of these hypotheses may be valid, but the problem isn’t really as much a matter of why as it is a matter of how.  Other primates deal with groups and have complex foraging strategies; and many deal with social problems within their groups, and some even hunt.  Yet they still have small brains.  (Granted, their brains are larger for their size than those of other mammals, but primates sport small brains as compared to humans.)  How did the human brain grow?

This isn’t an easy question to answer because of the thermogenics involved.  Brains consume a large amount of fuel and, consequently, throw off an enormous amount of heat for their size.  The metabolic rate of brain tissue is nine times that of the average of  the metabolic rate of the rest of the body.

So what? you may say.  So we’ve got a big, hot-running, energy-burning brain.  What difference does that make?  It’s reflected in our overall metabolic rate, right?  Well, sort of, and therein lies the crux of the problem.  As we will see below, our total metabolic rate – even with our huge brains – is the same as that of any other animal our size. Or to say it another way, animals our size with much smaller brains have the same metabolic rate that we do with our huge brains.  This fact was the starting point for the authors of the ETH.  So let’s start there as well.

In keeping with a great scientific tradition, Aiello and Wheeler were able to see what they saw because they stood on the shoulders of giants who came before them.  In their case the giant was Max Kleiber, an animal physiologist working at the University of California at Davis, who published a groundbreaking paper in 1947 and a scholarly text titled The Fire of Life in 1961.  Kleiber’s work involved the meticulous measurement of the metabolic rates of numerous animals, including humans.  As he plotted the various metabolic rates, he discovered an extremely strong correlation between the mass of an animal and its metabolic rate.  Kleiber found that this relationship held constant across numerous species.  His October 1947 paper in Physiological Reviews simply titled “Body Size and Metabolic Rate” was a classic.  By using the equations Kleiber worked out, the metabolic rate of virtually any animal could be determined simply by knowing the animal’s body size.  Or, as Kleiber put it in the paper:

Does a horse produce more heat per day than a rat or do some rats produce more heat than do some horses?  Almost anybody who understands what is meant by “heat production per day” will not hesitate to give the correct answer and will even be convinced that the daily rate of heat production of men or sheep is greater than that of rats, but smaller than that of horses.  Thus most people (among those who understand the question) are convinced that in general the bigger  homeotherms produce more heat per day than the smaller homeotherms, that, in other words, the metabolic rate of homeotherms is positively correlated to body size.

The answer to the next question: “does a horse produce more heat per day per kilogram of body weight than a rat?” requires some biological training.  Most biologists, however, will not hesitate to answer that the rate of heat production per unit body weight of the big animal is less than that of the small animal.

The positive correlation between metabolic rate and body size, and the negative correlation between metabolic rate per unit weight and body size, establish two limits between which we expect to find the rate of heat production [basal metabolic rate] of a horse if we know the rate of heat production of a rat.  We expect the metabolic rate of the horse to be somewhere between that of the rat, and that of the rat times the the ratio of horse weight to rat weight, provided of course that we do not regard these two correlations as simply accidental.

If we are firmly convinced that the metabolic rate of horses, and other homeotherms of similar size, is never outside these two limits, then we admit to recognize a natural law between body size and metabolic rate.

This natural law, carefully calculated by Kleiber, is now known as Kleiber’s law.  Below is Kleiber’s law graphed out by him as it appeared in his seminal paper.  And this is exactly as it appeared in the journal, but with the addition here of colors for better legibility.  Since their was no Excel nor graphics software in Kleiber’s time, the graph was hand drawn and appeared in the pages of Physiological Reviews as such.  How times have changed.

As you look along the line running from lower left to upper right, you can find rats and horses and a host of other mammals including humans.  Over the years, mammals that Kleiber didn’t have the opportunity to work on have been measured, and they all fit nicely along Kleiber’s line, following Kleiber’s law.  Because of this tight correlation, Kleiber’s equations can be used to precisely estimate the metabolic rate of any animal just by knowing its size.

Aiello and Wheeler used Kleiber’s law as the jumping off point for their grand thought experiment.

Since all animals measured have conformed to Kleiber’s law, Aiello and Wheeler postulated that animals now extinct – including our human and pre-human predecessors – would have fallen along the same line. Using skeletal remains paleontologists have been able to calculate body sizes of extinct animals along with pre-Homo and early-Homo species.  Then using Kleiber’s law, it is possible to closely estimate the metabolic rates of these creatures.  And here’s where it gets interesting.

According to Kleiber’s law, an australopithecine weighing 80 pounds would have the same metabolic rate as a human weighing 80 pounds despite the disparity in brain size between the two.  The much larger brain of the human would have 4-5 times the metabolic rate of the brain of the australopithecine, yet would have the same overall metabolic rate.  What gives?

That’s precisely what the authors of “The Expensive-Tissue Hypothesis” wondered.

Because the human brain costs so much more in energetic terms than the equivalent average mammalian brain, one might expect the human BMR [basal metabolic rate] to be correspondingly elevated.  However, there is no significant correlation between relative basal metabolic rate and relative brain size in humans and other encephalized animals.

Where does the energy come from to fuel the encephalized brain?

The authors postulated a solution.

One possible answer to the cost question is that the increased energetic demands of a larger brain are compensated for by a reduction in the mass-specific metabolic rates of other tissues.

In other words, if one organ – the brain, for example – is chewing up a lot of energy and contributing a disproportionate amount of the basal metabolic rate for the animal as a whole, then maybe another organ or group of organs are consuming less energy to compensate.  The heart, the kidneys, the liver, the skeletal muscles, the GI tract – all consume energy and contribute to metabolic rate.  Maybe one of these organs became smaller as the brain became larger over time.

We can hone our analysis a little finer if we begin to look at an energy-balance equation, but an energy-balance equation of a different kind.  I have written a number of times in this blog about the energy-balance equation that applies to weight loss: change in weight equals energy in minus energy out.  That is not the equation we’ll be talking about here.  The other energy-balance equation says that the total metabolic rate is the sum of all the metabolic rates of the various organs and tissues in the body.  If you add the metabolic rates of the kidneys, the heart, the brain, the muscles, the digestive tract and so on together, you will get the total metabolic rate of the body, which makes sense because it is the sum of the parts.

Total BMR = brain BMR + heart BMR + kidney BMR + GI tract BMR + liver BMR + the remainder of the body’s tissues.

The authors of the ETH set out to look at the metabolic rates of the various organs.  By a diligent search of the literature, they found that along with the brain, the the heart, the kidneys, the liver and the gastro-intestinal tract account for the vast majority of the total BMR.  They dubbed these organs as ‘expensive tissues’ because they consume a large amount of energy as compared to their size.  (Surprisingly, muscle mass doesn’t contribute all that much to the total metabolic rate (skin and bone contribute even less), which gives the lie to that old notion — that I, myself, have fallen prey to — that replacing fat with muscle increases metabolism significantly.)

Aiello and Wheeler reasoned that if the total metabolic rate stayed the same while the energy-expensive brain grew over time some other expensive tissue had to get smaller.  There could be no other solution.

But which of the expensive tissues got smaller?

Aiello and Wheeler examined the data on the metabolic rates and sizes of the various expensive tissues and learned that for a 65 kg primate, the heart, the kidneys, and the liver were approximately the same size as those of a 65 kg (143 lb) human.  The greater metabolic rate of the large human brain was compensated for by a GI tract significantly decreased in size.  It turns out that the GI tract of a 65 kg human is just a little over half the size of the GI tract of a similar sized primate.

The combined mass of the metabolically expensive tissues for the reference adult human is remarkably close to that expected for the average 65-kg primate, but the contributions of individual organs to this total are very different from the expected ones.  Although the human heart and kidneys are both close to the size expected for a 65-kg primate, the mass of the splanchnic organs (the abdominal organs) is approximately 900 g less that expected.  Almost all of this shortfall is due to a reduction in the gastro-intestinal tract, the total mass of which is only 60% of that expected for a similar-sized primate.  Therefore, the increase in mass of the human brain appears to be balanced by a almost identical reduction in size of the gastro-intestinal tract.

Below is a graphic from the ETH showing the sizes of the different organs as based on predictions from a 65-kg primate and the observed size in humans.

So we know that as humans evolved larger brains they simultaneously co-evolved smaller guts in order to maintain a set BMR.  And this is where the story gets interesting. Why?  Because

the logical conclusion is that no matter what is selecting for brain-size increase, one would expect a corresponding selection for reduction in the relative size of the gut.

Some researchers believe that increasingly complex activities drove the brain to enlarge.  As the authors of the ETH summarized it:

The relationship between relative brain size and diet is often mentioned in the literature on primate encephalization and is generally explained in terms of the different degrees of intelligence needed to exploit various food resources.  For example, [some] have argued that a relatively large brain and neocortical size correlates with omnivorous feeding in primates , which requires relatively complicated strategies for extracting high-quality foodstuffs.  Alternatively, [others] have suggested that frugivores have relatively large brain sizes because they have relatively larger home ranges than folivores, necessitating a more sophisticated mental map for location and exploitation of the food resources.

But it doesn’t matter whether our brains got big because our predecessors were socialized, developed complex foraging strategies, lived in and had to deal with groups or were skilled hunters, in order to obey Kleiber’s law, something had to force our guts to get smaller at the same time.  What could that be?

According to Aiello and Wheeler, it is increased diet quality that allowed the gut to get smaller while still absorbing the necessary nutrients to fuel the metabolism.  As they put it

The results presented here [in the ETH] suggest that the relationship between relative brain size and diet is primarily a relationship between relative brain size and relative gut size, the latter being determined by dietary quality.  This would imply that a high-quality diet is necessary for this encephalization, no matter what may be selecting for that encephalization.  A high-quality diet relaxes the metabolic constraints on encephalization by permitting a relatively smaller gut, thereby reducing the considerable metabolic cost of this tissue.

What the authors are saying is that it doesn’t matter how much more brain power was required, the brain couldn’t enlarge without something else giving.  What obviously gave was the size of the GI tract, and the only way a smaller GI tract could provide the fuel for the body was to have a higher-quality diet. How did the our most ancient relatives the early hominids increase the quality of their diets?

A considerable problem for the early hominids would have been to provide themselves, as large-bodied species, with sufficient quantities of high-quality food to permit the necessary reduction of the gut.  The obvious solution would have been to include increasingly large amounts of animal-derived food in the diet.

Increasing the amount of easily-digested food of animal origin allowed us to shrink our guts while expanding our brains.  Had we remained on a diet high in vegetation, we would no doubt not have been able to expand our brains irrespective of how much more thinking those brains would have needed to do.  It just wouldn’t have been possible to do so without violating Kleiber’s law.

Take the gorilla, for example, almost pure vegetarians that spend their entire ‘working’ day foraging and eating, which they have to do to get enough calories to maintain their enormous bulk.  They have large guts and pay for it by having small brains.  Even smaller than that of our most primitive ancestors, the australophthecines.

Gorilla has one of the lowest levels of encephalization of any haplorhine primate, and the much higher level of encephalization of all the australopithecines suggests a diet of significantly higher quality than that of this genus.

Which makes sense when you consider that carbon 13 isotope analysis has shown that Australopithecus africanus (the species that came right after Lucy) consumed meat.  As you go up the lineage from Australopithecus and through Homo, you find that more and more meat was consumed the higher up the tree you go.

It’s easy to see that, as compared to humans, chimps and gorillas have large, protuberant bellies, which supports the fact that they have larger GI tracts, but what about our ancient ancestors.  All we have to go on are skeletal remains, which show nicely that their heads (and brains) were much smaller than ours, but what about their guts?  How do we really know their guts were larger?  According to Kleiber, they would have to be, but how to we really know they were?

The large gut of the living pongids gives their bodies a somewhat pot-bellied appearance, lacking a discernible waist.  This is because the rounded profile of the abdomen is continuous with that of the lower portion of the rib cage, which is shaped like an inverted funnel, and also because the lumbar region is relatively short (three to four lumber vertebrae).

The drawing below from the ETH shows the inverted-funnel shape of the ribcage of the chimpanzee on the left.  You can mentally draw the lines downward from these ribs and envision the pot-bellied look of the abdomen that these primates evidence.  Looking at the image on the right, you can see that Australopithecus afarensis (Lucy’s species) has the same inverted-funnel shaped rib cage, indicating a large belly and a low-quality diet.

The drawing in the middle is of a modern human.  If you extrapolate the lines down from the human rib cage, you can see that they lead to a more narrow waist.  Makes you think more of a lean, rangy wolf or other slim-waisted carnivore, whereas the other two don’t.

The authors conclude:

If an encephalized animal does not have a correspondingly elevated BMR [which according to Kleiber, it can’t], its energy budget must be balanced in some other way.  The expensive-tissue hypothesis suggested here is that this balance can be achieved by a reduction in size of one of the other metabolically expensive organs in the body (liver, kidney, heart of gut).  We argue that this can best be done by the adoption of a high-quality diet, which permits a relatively small gut and liberates a significant component of BMR for the encephalized brain.  No matter what was selecting for encephalization, a relatively large brain could not be achieved without a correspondingly [sic] increase in dietary quality unless the metabolic rate was correspondingly increased.

At a more general level, this exercise has demonstrated other important points.  First, diet can be inferred from aspects of anatomy other than teeth and jaws.  For example, an indication of the relative size of the gastro-intestinal tract and consequently the digestibility of the food stuffs being consumed is provided by the morphology of the rib cage and pelvis.  Second, any dietary inference for the hominids must be consistent with all lines of evidence.  Third, the evolution of any organ of the body cannot be profitably studied in isolation.  Other approaches to understand the costs of encephalization have generally failed because they have tended to look at the brain in isolation from other tissues.  The expensive-tissue hypothesis profitably emphasizes the essential interrelationship between the brain, BMR, and other metabolically expensive body organs.

I hope you are now armed with enough knowledge to be able to see through these articles and/or charts that are all too common showing how the GI tract of humans is closer to that of a gorilla than it is to that of a cat or some other carnivore.  It seems to me that Aiello and Wheeler have pretty thoroughly demolished the notion that humans are actually designed by the forces of natural selection to be vegetarians.  Based on the data and the argument they present, it is actually the opposite:  we evolved to be meat eaters.

It was our gradual drift toward the much higher quality diet provided by food from animal sources that allowed us to develop the large brains we have.  It was hunting and meat eating that reduced our GI tracts and freed up our brains to grow.  As I wrote at the start of this post, the evidence indicates that we didn’t evolve to eat meat – we evolved because we ate meat.

Lierre Keith had it right in The Vegetarian Myth:

The wild herds of aurochs and horses invented us out of their bodies, their nutrient-dense tissues gestating the human brain.

If we evolved because we ate meat, why would we want to stop now?

Note: I found the full text of this article available on Scribd.  If it gets taken down, let me know, and I’ll put it up here.  I’m just trying to save space on my server.

Painting at top: Monkey Before Skeleton by Gabriel Cornelius von Max

I’m getting a lot of comments on these last posts from people who have read our new book and have questions. I don’t want this blog to transmogrify into the blog for the 6-Week Cure, so after much consultation with the bride, we’ve decided to start another blog for the 6-Week Cure that we’ll both moderate. Problem is, we’re still in the throes of getting the current blog and website as it should be, so it may be a day or two before we get the thing up. On the 6-Week Cure site we will post the schedules for any media appearances and book signings we will be forced to do, so anyone interested can keep up there. We will also answer the questions that come in and use the questions to develop an FAQ. And we will use the blog to disseminate any messages or info we need to get out that is specific to readers of the new book.

Speaking of which…a journalist from First magazine is interested in talking to women who have done the 6-Week Cure, and who would be willing to give testimonials and allow their names and photos to be used in a magazine article. If you are interested, you can contact Lisa Maxbauer at lisamaxb (at) yahoo (dot) com. You can check out her Twitter site at twitter.com/FIRSTmagLISA as well.

I’ll have the meat-eater post up as soon as I’ve got a little consolidated time to finish it.

And the post immediately after the meat-eater post will be the post on our change-the-world project MD and I have been working on for a year and a half.

Feel free to comment on this post about what you would like to see on the 6-Week Cure blog.  Thanks.

Due to other commitments tomorrow and Monday (see below for the Monday commitment) I more than likely won’t be able to get the promised post up before Tuesday.  I was working away on it this afternoon (actually alternating between writing the post and dealing with comments) when my bride came in and whined for me to go to a movie I didn’t really want to see.  But, being the dutiful and obliging spouse that I am, I went.  And I was glad I did.

MD just finished the book Julie & Julia and was hot to see the movie.  I hadn’t read the book, and don’t plan on it, so I was lukewarm at best on the idea.  But I’m glad I relented because the movie is one of the best I’ve seen in a long while.  MD and I related to it on a number of levels.  We written books and have been through all the publisher snafus that Julia experienced.  We know what it’s like to have a cooking show.  And we’ve been through the blogging experience.  But, unlike the heroine of the blog and book, we’ve actually met Julia.

In the summer of 2000, a couple of friends of ours who own Al Forno, a famous restaurant in Providence, RI, arranged for MD and me to be a part of a huge fundraiser for the Providence Public Library.  It got worked out in such a way that MD and I attended as – get this – celebrity chefs.  Chefs? I still don’t know how it happened because our cooking show hadn’t even been conceived of at that time and we had just published The Protein Power LifePlan a few months earlier.  But there we were as celebrity chefs with – get this, too – Emeril Lagasse, Jacques Pepin, and Julia Child.  And, as they say, that’s not all.  We were there with Billy Joel as well.  Yep, Billie, Emeril, Jacques, Julia, MD and me – the celebs brought out to raise money for the Providence Public Library.  It was kind of surreal.

When I was introduced to Julia, I told her I was delighted to meet her and that my wife and I lived in her home town.  I knew she lived in Santa Barbara, and MD and I had been living there for about a year at the time – if you could call it living there.  We actually lived primarily in Incline Village, Nevada and Santa Fe, New Mexico, but we did spent a fair amount of time in Santa Barbara, where we lived aboard a sailboat in the marina when we were in town.  So, I was more or less honest when I said we lived in Santa Barbara.

Julia Child was a big woman.  And I don’t mean fat, I mean big.  She’s well over six feet tall and is imposing even stooped a bit as she was then at age almost 90.  As we shook hands she replied to my remark about living in her home town in her wonderful, warble-y, quivery voice, “Which home town? Santa Barbara or Cambridge, Massachusetts?”  And she moved when she spoke just as Meryl Streep portrays her in the movie.

Until that moment, I hadn’t realize she lived anywhere but Santa Barbara, but it just so happened that MD and I had just purchased a condo in Cambridge a few months before.  Our eldest son, wife and first grandchild were moving to the Boston area for a year while our son clerked with a federal judge.  We bought the condo and they rented it from us.  So, I answered her that we lived both places.  Which, of course, was a stretch since we lived part time on a boat in one and owned a rental condo in the other, but, hey, I was among real celebrities so I had to act the part.

In the years between that first meeting and her death, we saw her a dozen or so times around Santa Barbara.  She frequented a lot of the same restaurants we did and was a regular at the farmer’s market.  But other than the time we chatted a bit at the Providence Library shindig, neither MD nor I ever spoke with her again.  We would say hello if we passed one another, but that’s it.  I’m sure she didn’t have a clue we had met before.  Having had the interaction with her that we did, made the movie a little more poignant for us.  I now wish we had made the effort to get to know her while we had the chance.

Julia had to deal with her publisher and with promoting her various books.  And we do too.  One of the things authors agree to when they sign a publishing contract is to make themselves available for various publicity events.  MD and I have done the book tour routine (which is miserable), appeared on countless TV shows and radio shows, and shown up for innumerable book signings.   None of these PR events are particularly fun, but the most loathsome PR event of all takes place this coming Monday.  It is the dreaded radio satellite tour.

There is a certain type of PR agent that books these kinds of things, which involve scheduling numerous radio shows one right after the other with military precision.  The shows start on drive time radio on the East Coast and move west with the sun.

We will start at 6:50 AM Eastern, which is 3:50 AM our time, and be on the radio pretty much non-stop throughout the day.  A number of you have asked in the comments if we are going to be appearing anywhere.  Right now, this is all that is scheduled.  I’ve posted the schedule below so that if we’re on a station in your neck of the woods, you’ll be able to listen should you chose to.

It will be a grueling day for us, but somehow we’ll manage to keep our good cheer through it all.  A thousand cups of coffee will help.  Hope you get to listen in to part of it.