Applebee's Quesadilla Burger

One of my readers sent me a link to a segment on ABC News with Charlie Gibson showing just how disgustingly slanted and inaccurate mainstream media reports can be.

Gibson leads into the segment about two reporters who underwent self experimentation on the adverse effects of unhealthy eating.  The reporters, ABC’s Yuji de Nies and Jon Garcia, set out to see what would happen if they consumed a giant meal containing over 6,000 calories.  Here is the result as they reported it.

Pretty brutal, eh?  But let’s shine the piercing light of good sense on what is going on here.  As you might expect, the reality is vastly different from that portrayed by ABC.

First off, let’s look at the actual nutritional content of the food eaten.  As reported in the piece, the total energy content of the meal was 6,190 calories, which included 187 grams of saturated fat.  These were the only parameters reported.  I took the time to go through the links in the article accompanying the video to find exactly where these foods came from.  Here’s what I found.

The burger is an Applebee’s Quesadilla Burger (served with fries, of course); the snack is The Cheesecake Factory Fried Macaroni And Cheese; and the dessert is Uno Chicago Grill Mega-sized Deep Dish Sundae (listed as cookie below).  How do I know these are the exact ones?  These were the ones referenced in the CSPI’s List of Most Unhealthy High-Calorie, Fat and Salty Restaurant Foods That May Clog Your Arteries.  After seeing the photos and comparing to what I saw on the video, these selections are the ones the reporters ate.

I then tracked down the Nutritional Facts for the foods involved (here, here, here and here) and put them into an Excel spreadsheet.  Take a look.

The first thing you might notice is that the total calorie count is 5,708, which is considerable, but is actually 482 calories fewer than the 6,190 reported.  Second, and this is a biggie, the saturated fat content of this meal is only 88 grams, not the 187 grams reported.

The reporters stretched the truth a little in that they reported as if the Mega-sized Deep Dish Sundae were a single treat to be consumed by one person at a sitting.  I’m sure it could be so eaten, but it’s actually designed for four people to share.  The Nutritional Facts list the calories per serving as 690 and the saturated fat as 17 grams.  I’ve used the amounts in all four servings, i.e., one entire four-person dessert, in my spreadsheet.

As you may have noticed, the total carb content of the meal is 745 grams, which converts during digestion to a little over three cups (3.1 cups to be exact) of sugar.  The ABC report, of course, failed to mention the carb content of the meal and ignored any immediate effect this huge intake of carb might cause.  One of the reporters, Jon, claimed that he was ’sluggish’ and ‘tired’; the implication being that this sluggishness resulted from his huge saturated fat intake.  No mention, naturally, of the enormous amount of carbohydrate and the large increase in insulin release it might cause.  From what I can see from the video, Jon looks to be sporting a little abdominal obesity, which would imply a degree of insulin resistance and hyperinsulinemia.  People with this disorder tend to over secrete insulin in response to carb intake causing an overshoot and reactive hypoglycemia (low blood sugar), which will indeed result in sluggishness.

It’s pretty impressive when the lab tech holds up the tube of blood taken after the meal and compares it to the one taken before the meal.  There is a lot of fat swimming in the serum, that’s for sure.  What the producers of this piece (and, sadly, the doctors commenting although they should know better) want you to take away from all this by the way they set it up is that all that saturated fat went directly into the blood.  And how can you argue with them?  It’s there for all to see.

Problem is, that’s what blood samples look like after almost any meal, especially one that contains carbohydrates.  The fat you see isn’t the fat the two reporters ate; it is the fat the liver has made from the carbohydrate.  It’s the same picture a tube of blood would show after either of the two doctors had eaten a high-carb, low-fat lunch.

The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route.  The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbs.  Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells.  Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature.  Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest.  The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood.  As I say, the fat in the blood you see on the video didn’t come from the saturated fat in the diet, although that was definitely the implication.

But what about the ultrasound showing the blood vessels had changed?  Wasn’t that because of the fat?

I’m afraid not.  The fat from the diet wasn’t in the blood vessels yet, so it couldn’t be the dietary fat causing the change.  So what was it?

How about a little normal physiology.  Let me explain.  The body gets blood where it needs to get it by opening certain blood vessels while closing others.  Let me give you an example.  Have you ever jumped into cold water to go swimming and noticed that not long after jumping in you have to urinate?  What happened?

Your arms and legs have a radiator effect.  Since these appendages have little padding the blood circulating there is exposed to the cold water, and if nothing is done, the cold water cools the blood creating a big problem.  Your body compensates by shutting down the circulation to the skin and areas close to the surface in your arms and legs and shunts that blood to your core.  Your core already has plenty of blood when this happens, so it has to get rid of some.  It does so by sending it through the kidneys where the liquid portion is filtered out and becomes urine.  Suddenly your bladder is full and you have to go.

The body has the ability to direct blood wherever it needs by its manipulation of blood vessel size.  Where do you think blood is needed after an almost 6,000 calorie meal?  That’s right.  The digestive tract.  It takes a lot of work to deal with 6,000 calories, and a lot of work requires a lot of oxygen, which comes from the blood.  So after a heavy meal, the body shunts extra blood to the guts where the works is being done.  It does this by opening or dilating the arteries carrying blood to the intestines and by narrowing the blood vessels in other parts of the body.

Now, think back to the video of the woman whose blood vessel (in her arm) is being examined by ultrasound.  When it’s compared to the previous ultrasound, the one before she ate, notice how much faster the heart is beating.  (The little swishing sounds you hear, each of which represents a heart beat, are spaced much closer together.)  The heart is beating faster because the body is working to digest an enormous amount of food, and this work stresses the heart in the same way that running down the street would stress the heart.  Work is work.

The digestive tract needs extra oxygen to do its work, this extra oxygen can get there only via the blood, so the intestines require more blood than normal.  This extra blood gets shunted there by opening the arteries that feed the gut and narrowing those that go other places where a lot of blood isn’t needed at the moment.  Such places as, say, a relaxed arm.

Anyone with a smattering of knowledge of normal physiology (and apparently an open mind) could predict that the artery in a relaxed arm would narrow after a heavy meal and that that artery would be back to normal six hours later (which it was so reported in this video).

What you’re seeing in this video is normal physiology at work interpreted as being abnormal by a couple of lipophobic doctors who should (and probably do) know better.  It makes for dramatic theater, but their interpretation is nothing but prevarication or ignorance or both.

But had they reported the truth, there would have been no story.  Kind of sad, isn’t it.

I have been dilatory in posting over the past few days and embarrassingly dilatory about approving comments.  I’m way, way behind, but I’ll get caught up ultimately.  So, if you have a comment doing time in comment Purgatory, don’t despair.  I will get to it.  Ultimately.

My excuse for not devoting my normal amount of attention to this blog is that I’ve been extremely busy as of late.  MD and I made a quick trip to Seattle to work on our world-changing project, then came back and spent a couple of days at the zoo that is Expo West (more about which momentarily), then the Seattle team came to us and we continued to work.  During all this, MD had a concert in which she had to perform Mozart’s Requiem and Lauridsen’s Lux Aeterna (my favorite piece of choral music) along with a couple of lesser pieces.  And tomorrow we drive back to Tahoe.  So, we’ve been busy little beavers and this blog has suffered.

Expo West has got to be the world’s largest natural foods expo.  It takes place every year at about this time in Anaheim.  And every year at about this time we drag ourselves to it.  The photo at the top of this blog represents one tiny little portion of this gathering.  To see how huge it is, take a look at the photo below of the map of the thing.

Find the red You-are-here arrow on the top middle left.  The picture at the top of this post is looking to the left from that spot on this map. And you can see only a short space down, kind of to where the aisle turns.  Imagine that view in each direction, then add a couple of floors made of several large multiple gymnasium-sized rooms, and you can kind of get the picture.  There are thousands of exhibitors and thousands of attendees.  It is one monster extravaganza of foods, supplements, beauty supplies, and anything else you might imagine having anything to do with diet, health, food and natural clothing.

I hate to go to the thing because I hate throngs of milling people and I hate the exhibitors always trying to sell you something.  But I also really enjoy it because I find new stuff and I learn a lot.  And there are the booth babes, to boot.  Although not so many this year.  Times are tough and booth babes are costly.

Each time I go to Expo West, I notice trends.  And this year was no different.  So, for what it’s worth, here are the trends I noticed after God only knows how many hours spent and miles walked traipsing through the giant Anaheim Convention Center.

Tea

There were a multitude of tea purveyors.  There was black tea, green tea, white tea, herbal teas of every description, and a dozen kinds of maté.  Way, way more tea than I’ve ever seen.  I guess the spate of recent studies that have appeared showing the purported health benefits of drinking some kind of tea has not been lost on tea vendors.  They were there in droves.  And all were babbling about studies demonstrating how tea cures this or that disease.  I didn’t have the heart to tell them that all of the studies they were using were observational studies and not worth a flip for proving that tea helps anything.

Agave

Agave was the big new product this year.  Last year there were a few vendors; this year they were everywhere.  They were selling agave syrup, agave nectar, agave crystals, agave this and agave that.  An entire other group of vendors was promoting various products sweetened with agave.  For those of you who don’t know, agave is the latest entry into the caloric-sweetener sweepstakes.  It comes in a variety of forms – syrup, nectar, crystals -  from the agave plant, a succulent plant found mainly in Mexico.  The claim to fame of this sweetener, which was emblazoned on banners, literature, labels and just about everywhere, is that it is a low-glycemic sweetener.  And it is was being touted as a great food for diabetics and any others with glucose-intolerance problems.  And it is indeed low-glycemic because it is composed of about 90 percent fructose.  If you think high-fructose corn syrup is bad at 55 percent fructose, just imagine what Agave syrup can do for you.  Yet all these ignorant people are ga ga over it as if it were the second coming.  My advice is to avoid it like death.  But be prepared to be seeing it everywhere.

Xylitol

There were a lot of products made with xylitol on display.  Products that are probably pretty good, but that I would never have imagined.  Nose spray, for example.  Xylitol is a sugar alcohol that is antibacterial, which is why it is in gums that dentists recommend.  It actually prevents tooth decay because of its antibacterial properties.  It does the same thing if sprayed into the nose, a place where a lot of bacteria live.  I saw a product made of xylitol that was to be dissovled in water and used in a Neti pot to irrigate sinuses, which, like the nose spray, makes sense.  There have been randomized control trials showing the benefit of xylitol for prevention of tooth decay and prevention of ear infections in kids.  I didn’t see any papers showing studies on the nose sprays or other products, but it’s a reasonable assumption that they probably work.  I certainly wouldn’t hesitate using them.  Based on the number of vendors I saw, expect to see a lot of xylitol-containing products in the days to come.

Sweeteners

There were a fair number of non-caloric sweeteners on display.  Most were made of combinations of RebA, the active ingredient in stevia, and other non-caloric sweeteners.  I saw a lot of erythritol and erythritol combinations as well.  If numbers of vendors are any indication, expect to see a bunch of non-caloric sweeteners hitting the shelves.

Coconut milk and oil

In what I view as an extremely positive trend, there were a zillion purveyors of coconut milk and products made from coconut milk.  In the past, there weren’t many, but this year they were everywhere.  There were a bunch of companies making ice creams and gelato made of coconut milk.  These aren’t low-carb by any stretch, but they are still more healthful (in my opinion) than regular ice cream because of all the great fats in coconut milk and oil.  I took one for the team and tried several of these, and I can tell you that they were delicious.  There were also outfits selling coconut milk that was like regular cow’s milk.  It didn’t taste quite the same, but it wasn’t far off the mark.  I thought it tasted better, but others might disagree.  The milk comes in cartons just like regular milk.  There were chocolates and any other product you could think of that would normally be made of milk or dairy made of coconut milk or oil.

Soy

In what I would consider another positive trend, there were way, way fewer companies selling soy products than ever before.  Since I’ve been attending Expo West soy has been everywhere and in everything.  All of a sudden, this year it’s kind of taken a powder.  There were a handful of people there selling soy-based products, but not anywhere near what has been there in past years.

Nuts

Every year there are people there selling nuts.  This year they wre all over the place.  I’ve never seen so many nuts on display.

Low-fat

Surprisingly there wasn’t a lot of emphasis on the low-fat nature of products.  Previously it was much more visible with banners and stickers on anything that could make the claim, but not so much this year.  Many more products were advertised as having no added sugar or sugar-free than were advertised as being low-fat.  I think the times they are a changing.

Low cholesterol

Strangely, there was more emphasis on low-cholesterol than I’ve noticed in the past few years.  More emphasis, in fact, than there was on low-fat. There were many products on display that proudly proclaimed their cholesterol-lowering properties.  The one that took the cake is pictured below.  The company makes tortilla chips that allegedly lower cholesterol.  Now you know what to do if your cholesterol is a little high: go face down in these chips.  Not!  Actually, they would probably do you less harm than taking a statin.

Meat and eggs

Yet another positive trend was the large increase in the number of vendors selling both fresh and processed meats.  Way more vendors than in the past.  And a large number selling eggs.  I saw many booths that had packets containing two hard boiled eggs and a little salt and pepper.  A good kind of fast food, if you ask me.

Resveratrol

I was expecting there to be a zillion people selling resveratrol, but there weren’t many.  In fact, I couldn’t find anyone selling just the raw stuff.  The only vendors I found selling it were selling their own proprietary versions in which resveratrol was mixed with other compounds.  Given all the press lately about resveratrol I was really surprised at how little there was.

Krill oil

All the krill oil sellers were there, and I spent a good amount of time with them.  They all had large booths, so it was apparent that krill oil has been very, very good to them all.  I finally learned all the distinctions between all the oils available and will be doing a post on them as soon as I have a little time to go over all the papers I’ve pulled to make sure I am accurate.

Vegetarian products

It’s hard to say, but if I had to bet, I would bet that there were slightly fewer this year than last.  They were still there, and they were still obnoxious, but just not in the numbers as before.  At least it appeared that way.

One of the things that constantly amazes me about Expo West and all the other natural food and health food shows I go to is how typically American all the people look who are selling this stuff.  They truly are a mirror of American.  The vast majority are overweight and they don’t look like the picture of health, yet there they are pimping products that are supposed to make the purchasers of them healthy.  If I looked like most of these people, I would hire someone who at least look lean, trim and healthy to man my booth, but these people don’t.  Most are definately not walking advertisements for their products.

Here are a couple of photos to show you what I mean. These pictures give you an idea of what a typical booth at Expo West looks like and typical people working these booths.  I didn’t pick these just because they were hawking vegetarian products, I picked them because I happened to have my camera at hand and they were right across the aisles from one another.  They were not out of the ordinary.  They look like most of the vendors.

I plan to dragoon MD into doing most of the driving tomorrow so that I can catch up on my medical reading (as much as I can anyway while keeping a close eye on the road).  When we get home, I’ll get back on my normal schedule of posting.  Hang in there ’til then.

Paleolithic paintings from Lascaux cave in southern France

I imagine most readers of this blog would expect a group of subjects to do better on a Paleolithic diet as compared to a standard American diet, but there are few studies actually making the comparison. One was posted yesterday in the Advance-0nline-Publication section of the European Journal of Clinical Nutrition that shows subjects following a Paleolithic diet made major metabolic changes, and made them rapidly.

Before we get into the study, let’s make sure we’re all on the same page when we discuss the Paleolithic diet. We we say Paleolithic diet, what are we really talking about?

The Paleolithic era refers to that period of history of the genus Homo, which began more than 2 million years ago and ran until the Neolithic period started circa 10,000 years ago. The Neolithic era dates to the time when early man set down roots both literally and figuratively when he started to cultivate plants for food and domesticate animals. The Paleolithic era ends and the Neolithic era begins with the advent of agriculture.

So what did Paleolithic man eat? We don’t know precisely because Paleolithic man didn’t leave any written records, menus, cookbooks, etc. The only records Paleolithic man left are the cave paintings, of which Lascaux in France is the most famous. Virtually all of these paintings feature animals prominently, which would lead one to believe that animals figured greatly in the lives of Paleolithic people. Since they didn’t domesticate these animals, and since it seems unlikely that they kept zoos, the most obvious reason these early people focused so much artistic effort on these animals is that they ate them. Carbon-13 isotope studies bear out that idea as the same carbon isotopes found in grass are also found heavily concentrated in the bones of Paleolithic man and other known carnivores, which leads to one of two conclusions: either Paleolithic man spent his days grazing or he ate animals that grazed. I would opt for the latter interpretation.

Keep this idea of Paleolithic man as a meat eater along with the idea of the cave pictures in your mind. We’ll return to them later, but first, let’s look at this study.

Nine healthy, sedentary, non-obese subjects (6 men; 3 women) over the age of 18 recruited from the San Francisco Bay area completed the study. These subjects had their starting diets analyzed – all were on their own version of the standard American diet – and a battery of tests done on them to evaluate multiple metabolic parameters.

Once the beginning data was in hand, the researchers started the subjects on a ramp up to the full Paleolithic diet by giving them daily increases of fiber and potassium.

For the intervention phase, beginning day 1, for adaptation purposes, a series of 1-day cycle diets with gradually increasing levels of potassium and fiber were developed by the research dietitians. This was to allow the subjects’ intestinal tract and potassium handling systems to adjust to the markedly higher dietary content of fiber and potassium. ‘Ramp 1′ diet was given for 1 day, ‘Ramp 2′ diet for 3 days, ‘Ramp 3′ diet for 3 days and finally the ‘Paleo diet’ for the remainder of the study.

Once ramped up, the subjects went on the full Paleo diet for 10 days.  An interesting twist to this study was that the subjects were monitored carefully for any signs of weight loss over the course of the study, and any subjects losing even small amounts of weight were encouraged to eat more of the Paleo foods in an effort to maintain their starting weights.  Since weight loss itself can bring about metabolic changes, the researchers wanted to make sure that any changes came about as a result of the diet composition and not as a side effect of weight loss.

What did they eat?

Meat, fish, poultry, eggs, fruits, vegetables, tree nuts, canola oil, mayonnaise and honey were included in the Ramp and Paleo phases of the diet. We excluded dairy products, legumes, cereals, grains, potatoes and products containing potassium chloride (some foods, such as mayonnaise, carrot juice and domestic meat were not consumed by hunter-gatherers, but contain the general nutritional characteristics of preagricultural foods).

Hmmm. More about which later. For now, here is a layout of the specific foods the subjects ate during the ramp and the full Paleo diet.

Table 2

The macronutrient composition of the regular diets of these subjects was 18% protein, 44 % carbohydrate and 38% fat.  The Paleo diet was 30% protein, 38% carbohydrate and 32% fat, mostly unsaturated, as the authors were quick to point out.
After the 7 day ramp period and the 10 days of Paleo dieting, subjects experienced large changes in most parameters measured.  Lipid changes are shown in the table below.

Derived from Table 3

As you can see, there were significant decreases in triglycerides, total and LDL-cholesterol with no change in HDL-cholesterol.

The body of the paper reports an insignificant decrease in blood sugar after the Paleo diet, but the units listed in the paper are incorrect, which is one of the hazards of dealing with a pre-publication paper.  All the kinks haven’t been worked out.

Fasting insulin levels plummeted by more than two thirds in (11.5 to 3.6 µU/ml) and the total area under the insulin curve was lowered by almost half.  What these figures tell us is that the diet made these subjects much, much more sensitive to their own insulin.  In other words, they required substantially less insulin to keep their blood sugars in the normal range.  Since they were producing less insulin, they had less circulating insulin, which meant less fat storage, less arterial stiffening and less of all the things that too much insulin causes.

Along with the improvements in lipids and insulin sensitivity, the subjects experienced a significant drop in diastolic blood pressure and a decrease in mean arterial pressure.  These improvements likely occurred in part because these subjects had substantially increased brachial artery diameter, a measure of arterial distensibility.  There arteries had become less stiff and more pliable over a mere 17 days of dietary change.

Urinary potassium loss increased, indicating an increased potassium intake by the subjects.  And urinary calcium excretion decreased.

Another interesting aspect of this study is that these findings were pretty much across the board.  Instead of a couple of hyper responders raising the average, either all nine or in a couple of cases, eight of the nine subjects demonstrated pretty much the same changes, indicating

consistently improved metabolic and physiological status with respect to circulatory, carbohydrate and lipid metabolism/physiology.

The authors of this paper found

in a small group of sedentary, slightly overweight, but not obese adult humans, that switching from their usual diet to a paleolithic-type diet, which contained no cereal grains, dairy [or] legumes, resulted, after only a short period of time [17 days] and without weight loss or increase in activity levels

significant positive changes in all the parameters discussed above.

I was fascinated by this study because the changes were so rapid, but I was a little put off because it could have been so much better.  I mean why didn’t they test a real Paleolithic diet?  Probably because of nutritional correctness, i.e., fear of saturated fat.

During Paleolithic times, man primarily subsisted by hunting.  The preferred food was large game animals, and Paleolithic man, a skilled hunter, wiped most of them out.   And not just the large grazing animals.  Paleolithic man completely decimated the Cave bear.  As you can see from the photo of my Cave bear skull below (from a slide I use in presentations), these were enormous animals that didn’t go down easily.  Cave bear, like all bears, had high levels of body fat, which must have been highly desired because these ferocious animals were hunted to extinction about 15,000 years ago by people wielding little more than pointed sticks.  I would have to value fat a whole lot more than I do to tackle one of these guys.  The largest bears that I could find the fatty acid composition for were polar bears, which should be appropriate since cave bear lived in northern latitudes.  Polar bears have on average 30 percent saturated fat, 50 percent monounsaturated fat and 15 percent polyunsaturated fat.  (I know these figures don’t add up to 100 percent, but they are the figures as presented in the article.)

The majority of the large animals that roamed the world are gone thanks to the depredations of Paleolithic man.  If you ever get the chance to go to the American Museum of Natural History in New York, take a stroll through the many large halls filled with the enormous skeletons of these animals that used to roam what is now the United States.  Experts estimate that it took Paleolithic man only about a thousand years to range from northern North America were he crossed the Bering strait to the southern tip of South America wiping out all the large game that existed at the time.

These large mammals that Paleolithic man decimated are now only present in skeletal form so we don’t know for sure what their fatty acid composition was.  But we do know that of those left, the larger the animals, the larger the percent body fat.  And the larger the percent body fat, the greater the percentage of saturated fat.  Given those two facts, one has to conclude that Paleolithic man consumed a large percentage of his energy as saturated fat.  We can’t look at the fat content of deer, for example, and use that to estimate the saturated-fat content of the Paleolithic diet.  Deer, as we know them today, were tiny animals as compared to those Paleo man typically dined on.

If you look at the fatty acid breakdown of the horse, a large animal (not grain fed) that we are all familiar with that is comparable in size to many of the animals Paleolithic man hunted to extinction, you find a large proportion of saturated fats.  Horse fat is about 36 percent saturated fat, 34 percent monounsaturated fat, and the rest polyunsaturated fat.  Even rabbits carry over 40 percent of their fat as saturated fat, but rabbits have much less fat per weight than the larger animals.

It seems pretty obvious that Paleolithic man would have eaten considerable saturated fat.  Which begs the question: Why always cut the saturated fat in experimental diets testing the hypothesis that the Paleolithic diet is more healthful?

I don’t know the answer for sure, but I expect that it’s due to the nutritional equivalent of political correctness, which I call nutritional correctness.

Researchers are simply afraid to imply that saturated fats might actually be harmless, so they go through all kinds of contortions to present their data in such a way that it couldn’t possibly present saturated fats in a positive light.  And much good research and reporting has suffered as a consequence.

A case in point is a otherwise wonderful book published 20+ years ago titled The Paleolithic Prescription.  This fascinating book goes into great detail describing the physical exploits of our ancient ancestors based in large part of reports by European explorers encountering ‘primitive’ peoples untouched by the forces of ‘civilization.’  The authors, based on the anthropological literature, describe the size of our Paleolithic forebears as being similar to our own, but their strength was significantly greater:

These people were strong – stronger by all estimates than most agricultural and industrial people (including ourselves) who lived after them.  Skeletal remains reflect strength and muscularity: the size of joints and the sites where muscles are inserted into bones indicate both the mass of the muscles and the magnitude of the force they were able to exert.  Average Cro-Magnons, for example, were apparently as strong as today’s superior male and female athletes.  Strange as it may seem, Cro-Magnons and other hunters and gatherers may have worked fewer hours per week than did the agriculturalists who followed, yet they were significantly more robust.

Think about this last sentence for a minute.  Strong, robust Cro-Magnons who settled into a life of agriculture circa 10,000 years ago, and who worked harder than their pastoral predecessors, showed a decline in strength and muscle mass.  Why?  What The Paleolithic Prescription says about energy expended is true.  The skeletal remains of agriculturalists show much more arthritic changes and incidence of joint wear implying much more regular physical activity than hunters.  So why did agriculturalists develop less muscle mass and strength?  Could it be because of a switch from diets high in fat and protein to diets low in fat and protein and high in carbohydrates?  Makes sense to me.  Same genetic material, greater exercise, different diet, yet weaker and less robust.

Getting back to my original point about this book, the authors presented a mass of data showing our Paleolithic ancestors to be more robust, healthier and able to routinely perform feats of strength that are almost unbelievable to us today.  And they dwelt on the massive amount of hunting that sustained these ancient peoples.  Then, when it came time to apply these dietary lessons to people of today, the authors tried to shoehorn their findings in a nutritionally correct regimen that followed the low-fat diet precepts that academicians are so attached to.  It’s really a shame because this could have been a wonderful book.  It’s still well worth reading, but simply ignore the dietary advice.

It would have been great had the authors of the paper above used a real Paleolithic diet for their study instead of an imaginary Paleolithic diet that conformed to the tenets of nutritional correctness.

Based on my own experience with thousands of patients, I can predict what the findings would have been.  Lipid parameters would have been improved, but with LDL staying about the same or maybe going up a little.  HDL would have gone up significantly.  Triglycerides would have fallen maybe more.  The all-important triglyceride/HDL ratio would have plummeted much more than with the faux Paleo diet.  Fasting insulin would have dropped like a rock and the area under the insulin curve would have fallen at least as much, if not further.  Blood pressure would have decreased and all the measures of vascular pliability would have improved.  All in all, my prediction is that the outcome of the study would have been better than the outcome of the study as it currently exists.

The Paleolithic diet data indicates that early man ate more saturated fat than he did carbohydrates.  And he was molded by the processes of natural selection to thrive on such a diet.  When he bolted from that meat-based diet, as he did when he settled in to life as an agriculturalist, he paid dearly for it with a devolution in health.  Since the evidence is so obvious that a diet higher in saturated fat worked wonders for Paleolithic man, it seems like some academicians somewhere would ranger up and test such a diet.  But it appears that the pox on saturated fat is so virulent that no one wants to risk it.

If such a study were done and the results tally with what I’m positive the results would be, the authors would find themselves in the untenable position of having to at least tacitly imply that saturated fats aren’t harmful.  And that could ruin an academic career.  No more invitations to present at meetings. Expulsion from the club.  People tsk tsking behind their hands.  It just couldn’t be done.

I’ve gone through and compiled a list of the most common questions and presented them to Gary.  Here are the questions followed by his responses.

The most commonly asked question was how do Asians and others living a seemingly high-carb existence manage to escape the consequences?

The Asian question first. I do address this in the book and I address it again in the afterward of the paperback. There are several variables we have to consider with any diet/health interaction. Not just the fat content and carb content, but the refinement of the carbs, the fructose content (in HFCS and sucrose primarily) and how long they’ve had to adapt to the refined carbs and sugars in the diet. In the case of Japan, for instance, the bulk of the population consumed brown rice rather than white until only recently, say the last 50 years. White rice is labor intensive and if you’re poor, you’re eating the unrefined rice, at least until machine refining became widely available. The more important issue, though, is the fructose. China, Japan, Korea, until very recently consumed exceedingly little sugar (sucrose). In the 1960s, when Keys was doing the Seven Countries Study and blaming the absence of heart disease in the Japanese on low-fat diets, their sugar consumption, on average, was around 40 pounds a year, or what the Americans and British were eating a century earlier. In the China Study, which is often evoked as refutation of the carb/insulin hypothesis, the Chinese ate virtually no sugar. In fact, sugar consumption wasn’t even measured in the study because it was so low. The full report of the study runs to 800 pages and there are only a couple of mentions of sugar. If I remember correctly (I don’t have my files with me at the moment) it was a few pounds per year. The point is that when researchers look at traditional populations eating their traditional diets — whether in rural China, Japan, the Kitava study in the South Pacific, Africa, etc — and find relatively low levels of heart disease, obesity and diabetes compared to urban/westernized societies, they’re inevitably looking at populations that eat relatively little or no refined carbs and sugar compared to populations that eat a lot. Some of these traditional populations ate high-fat diets (the Inuit, plains Indians, pastoralists like the Masai, the Tokelauans); some ate relatively low-fat diets (agriculturalists like the Hunza, the Japanese, etc.), but the common denominator was the relative absence of sugar and/or refined carbs. So the simplest possible hypothesis to explain the health of these populations is that they don’t eat these particularly poor quality carbohydrates, not that they did or did not eat high fat diets. Now the fact that some of these populations do have relatively high carb diets suggests that it’s the sugar that is the fundamental problem. Ultimately we can only guess at causes using this kind of observational evidence. To know anything with certainty we’d need the kind of randomized controlled trials I yearn for in the epilogue of GCBC.

What is your opinion on leptin in the grand scheme of obesity and fat storage?

I mostly ignore leptin in the book because I think leptin is primarily a signaling molecule and so a downstream effect. In other words, leptin is secreted from the fat cells; it doesn’t regulate directly the amount of fat that accumulates. Moreover, if the primary regulator of fat storage is insulin, which it is, and leptin is secreted in proportion to the amount of fat stored, which it is, then insulin has to regulate leptin.

Where leptin may play a primary role is in the liver. A few years ago Jeff Friedman of Rockefeller University published an article in Science showing that leptin down-regulates SCD-1 in the liver (the only place they looked), which worked in turn to increase oxidation of fatty acids. This makes sense homeostatically: if leptin is released in proportion to the fat accumulated then it is a signal of how much fat we have in reserve. So long as the mitochondria in our lean tissue and organs know that we have fat in reserve, they can continue to burn it without fear of systems failure should they run out of fuel completely. Leptin resistance would then work, like insulin resistance, to make us burn less fat and store more, while the rest of the body would have to rely on carbohydrates (blood sugar) for fuel.

In general, though, I’m interested in the cause of obesity and I don’t think discussing leptin adds much. Here’s what I say about this issue in afterward of the paperback edition of GCBC:

“Another variation on the can’t-possibly-be-so-simple argument that I have heard frequently since Good Calories, Bad Calories was published is the molecular biology theme. The last fifteen years, since the discovery of the hormone leptin in 1994, has seen obesity research become a sub-discipline of molecular biology. As a result, a search of the keyword “obesity” in the National Library of Medicine database will now identify over 100,000 relevant articles in the professional journals (nearly 20,000 review articles alone), a large proportion of which focus on the fruits of molecular biology research and the science of genomics.: It’s a burgeoning field with a cast of thousands, including the role of obesity-related gene variations known technically as polymorphisms, of signaling molecules with names like adiponectin, leptin and grhelin, of the receptors for those signaling molecules and the inhibitors for those molecules and inhibitors of the inhibitors, and so on. The obvious question is how can this research be so extraordinarily fruitful, and yet mostly irrelevant to the cause of obesity? It’s hard to imagine it’s not, and so, as I’ve frequently been told, any discussion of the cause of obesity that doesn’t discuss these molecules, receptors, inhibitors, etc. must be considered amateurish and woefully inadequate. The truth must be complicated.

“Again the counter-argument seems itself simple and straightforward: if you’re hit over the head with a hammer, it will cause both pain and inflammation. The mechanisms of pain and inflammation have also yielded up a wealth of knowledge to the tools efforts of the molecular biologists. These physiological phenomena are understood to be mediated via signaling pathways and molecules (in this case, prostaglandins, tumor-necrosis factors, etc.) that emerge in response to the damage done. The more researchers learn about these responses and the molecules involved, the more complex the pathway from hammer to pain and inflammation to healing will appear. But the relevant fact to all those immediately involved is that both the pain and ensuing inflammation were caused by the hammer and perhaps the person who swung it. Everything else is downstream and may be relevant only to the question of which drugs will best deal with the pain and perhaps accelerate the healing process. “

A number of questioners asked why you think it is more difficult to lose weight the second or third time around on a low-carb diet?  And why it seems more difficult to lose on low-carb with increasing age?

I’m curious whether this is in fact true. Another possibility is that it’s more difficult to lose weight on low-carb as we get older; that the carbs effectively do chronic damage to our tissue and so the longer we’ve been overweight or obese, the harder it is to lose weight. I can imagine a scenario in which the fat tissue becomes hypersensitive to the insulin we secrete, or the pancreas becomes hypersensitive to the carbs and secretes even more insulin, or the insulin resistance in the lean tissue becomes less tractable, and so the longer we remain fat, the more our fat tissue compensates when we restrict carbs. It’s also possible that repeated low carb dieting somehow exacerbates this process, but I’d want to see definitive studies (and on all this speculation) before I believed it.

Several people asked for a comment on any important studies that you may have left out of GCBC.

The issue isn’t leaving out studies so much as not wanting to get into the he-said, she-said game of quoting particular studies that support my preconceptions. In this business, you can always find studies that support a particular hypothesis, or at least seem to if you selectively interpret the data. So when I had to make a point about the efficacy of a particular treatment — exercise, for instance, or semi-starvation diets — used meta-analyses or Cochrane Collaboration systematic reviews, which are designed to minimize author bias, to make the general points. When I discussed the saturated fat/cholesterol/heart disease hypothesis in the first few chapters, I did indeed mention virtually every study and certainly every meaningful clinical trial, because I knew if I left anything out I would be accused of cherry picking the data (which, of course, I was anyway). I did omit much of the observational epidemiology on the nature of a healthy diet because I find it meaningless and impossible to interpret correctly, in part for the reasons I discussed above about the Asian diet issue.

When I cut the book down from the initial 400,000 word unfinished draft, a lot of what was removed were indeed the counter- and counter-counter arguments. For instance, obesity researchers will argue that obesity causes hyperinsulinemia, not the other way around. That way they can still say that obesity is caused by over-eating and once we get fat, that causes insulin resistance and jacks up insulin levels. I spent, literally, months writing a lengthy section explaining how this view came about and what the evidence actually did and did not demonstrate. Then when I realized the book had to shrink dramatically, and with the benefit of sage advice from my editor, I decided that it was unnecessary to explain why the mainstream researchers would disagree with my take and then spend yet more space explaining why they were wrong to disagree. One thing I did cut from the book that I regret was a section linking gout to fructose and uric acid, and discussing the history of gout and how it’s frequency in populations and socioeconomic groups paralleled the spread of sugar. Nobody had ever made that point before and I wanted to make it, considering that people have been speculating on what aspect of diet or lifestyle causes gout back to Hippocrates. Still, my friends rightly argued that when your book is a few hundred thousand words long, you can’t afford to keep a section about gout, even if a lot of people get gout these days and, of course, they’re more likely to get it if they’re overweight or obese. Along these lines Dan Harrington asked why his gout goes away on the Atkins diet and that’s my answer: no sugar, primarily, means no fructose and so no fructose-induced hyperuricemia. In other words, fructose raises uric acid levels and gout is caused by the elevated uric acid in the blood stream.

It is true that you can find studies in the literature that seem to contradict the hypotheses in GCBC but are not mentioned in the book, When Gina Kolata reviewed my book in the NY Times, she evoked a study by Jules Hirsch and Rudy Leibel, then both at Rockefeller, suggesting that nutrient composition of the diet has no effect on weight. As I explained in a letter to the Times, the study failed to refute the carbohydrate/insulin hypothesis of weight regulation for a variety of reasons — the subjects, for instance, could have gained as much as 15 pounds a year on one particular diet composition but not another, and the study would not have detected it. And the subjects, almost exclusively, were lean middle-aged individuals. What we’re interested in here, though, is why why people predisposed to obesity get fat, and that may not be something you can study in people who have remained lean into their 40s and 50s. Would Leibel and Hirsch have obtained a different result if they had used, say, obese subjects who had first been slimmed down by some kind of diet (Atkins or a starvation diet)? These types of subjects are considered pre-obese, since they’re so highly likely to go back to being obese. And if Leibel and Hirsch had used them, they might have found that they stay relatively lean on a low carb diet and put on weight easily on a high carb diet. Anyway, rather than get into this kind of too-and-fro in the book, I made the decision not to mention these types of ambiguous studies. I would like to think that had there been a single compelling study refuting the hypothesis — or better yet, two, since you’d like to see things replicated in science — I wouldn’t have written a different book.

What you think of a Slow Burn type of exercise and low-carb dieting?  Do you still stand by your notion that exercise doesn’t help people lose weight?

I haven’t looked into the science behind slow burn exercise (although I know Mike has) but I now do it regularly (with Fred Hahn in Manhattan at Mike’s recommendation) and it seems to be helping my lower back pain immensely. I can let you know next spring whether it helps my softball game, where my ability to hit with power has been deteriorating sadly with the advancing years. What fascinates me about it is the weird confluence of the desire for self-improvement with what seems to be deep-set sadomasochistic tendencies. It’s torture when you do it, and then you look forward to going back.

As for exercise, I do not believe that it causes long-term fat loss. I think it might be helpful in a weight loss program only because it gives you a kind of positive feedback that dieting per se does not. You can feel good after a work-out, while it’s hard to feel too good after a meal that didn’t include either the calories or the carbohydrates you preferred. On the other hand, since it does make you hungry — work up an appetite — I worry whether for some or even most people the psychological benefits could be counterbalanced by the drive to consume even more calories than you might have expended during the work-out.

Are you familiar with the work of Dr. Jan Kwasniewski, and, if so, what do you think of it?

I am not.

What kind of response have you gotten from the medical/scientific community about GCBC?

In general, I think it’s safe to say that I’ve been ignored. If obesity researchers have read the book, they haven’t bothered to tell me. When GCBC was published we sent out 150 copies to obesity researchers, authors of obesity task force reports, foundations that fund obesity research, everyone at NIH who funds obesity research, etc. etc. I heard back from 3 or 4 thanking me for sending them the book. Two followed up to tell me they had read it. Some later told me outright that they didn’t have the time to read a 500 page book, and particularly so when they already know what I think because of the 2002 NYT Magazine article and don’t particularly agree. That said, I may be making some progress in getting people to pay attention.

Whenever I do hear from someone who is sympathetic, I ask them to try to set up a lecture at their institution. Often I ask them to contact other researchers they might know and get me lecturers at those institutions. Through this kind of networking, I’ve been invited to lecture at some of the more influential obesity research centers and at least some of those people have taken my arguments seriously. A few months ago, I heard from some contacts at the NIH, that I might be invited down to lecture to the nutrition coordinating committee at NIH, which would be a big step forward, but the fact that I haven’t heard anything since then (August) makes me pessimistic.

When I do give these lectures a common response that I get from nutritionists and obesity researchers, and one that I find profoundly disturbing, is that they find what I say interesting but don’t see it as anything they should think about further. In other words, they have their schtick (as my wife, an almost-academic calls it); whatever research they get their funding to pursue, and even though in theory we’re all in this to cure and prevent obesity and chronic diseases, their schtick may have nothing to do with my schtick. If they’re studying, say, genetic strains of obese rats or questionnaires to improve the accuracy of diet assessment in epidemiologic studies, what does that have to do with my argument that obesity is caused by carbohydrates? So they listen politely, ask a few intelligent questions (in an ideal world) and then go back to their research, because that’s how they make a living. They don’t say to themselves, I’m going to read Taubes’s book and, if I find it compelling, switch my research over to studying the efficacy of carbohydrate restriction. And even if they did, they wouldn’t get funding to do so because they’d have no track record in that field.

So, bottom line, at the moment is that I know of a handful, maybe as many as a dozen researchers, who find the arguments in the book compelling and are doing what they can, in their limited spare time, to help get the message out and maybe get us to the place where the hypotheses are taken seriously and are rigorously tested. The rest either don’t care or don’t know GCBC even exists or just think what I say is wrong and so not worth further discussion, either because they read the book or some of it and think its crap or because they think its crap based solely on what they know about me or heard about the book and so don’t have to read it.

What’s next?  Another book?

What am I doing next? As suggested by many readers, I am going to write a short, easy-to-read version of the weight section of GCBC. It won’t be a diet book — no recipes — but it will be far more of a self-help book than GCBC. I might also do a weightier (no pun intended) serious investigation into the sugar and corn syrup industries; their history, political influence, lobbying, etc — that would be interwoven with a more intensive look at the potential health effects of sugar and HFCS and fructose particularly. The first book will definitely be done; the second depends on getting the funding to do so. I’d also like to get back to straight science writing for a while, since I do enjoy writing about good science, which is how I started my career, and it would be a pleasant change from the mainstream nutrition and health nonsense.

How about a blog?

As for a blog, I just haven’t got the time at the moment, although I always hope that that will change in the future.

Many wrote that GCBC had changed their lives.  Can you think of a book that has changed your life?

Did any books change my life? Yes, All the President’s Men, by Woodward and Bernstein. I read it in my last year of college or my first year of graduate school and it made me decide that I wanted to be an investigative reporter rather than go to business or law school, which was the direction I seemed to be headed.

What do you know about Dr. Simeon’s HCG protocol?

Mostly nothing.

What led you to the idea that saturated fat doesn’t cause heart disease?

It was a progression of steps. Back in the late 90s, I was reporting a story for Science on the salt-hypertension controversy and one of the worst scientists I ever interviewed (and having written a book about cold fusion, Bad Science, I had interviewed quite a few terrible scientists) took credit not just for getting Americans to eat less salt, but getting them to eat less eggs, meat and butter, too. I literally got off the phone with this guy and called my editor at Science and said, “when I’m done writing about salt, I’m going to do a story on dietary fat. I don’t know what the story is, but if this guy was involved in any substantive way, I know there’s a story to be done.” So that’s what I did. I finished the salt story and then spent a year working on the fat story, which was published in Science.

The story made the point that there was virtually no evidence that a low-fat diet prevented heart disease, but let open a window for saturated fat having some deleterious effect. Then a couple of years later, I was reporting the New York Times Magazine story that would become “What If It’s All A Big Fat Lie?”, when I heard about these five clinical trials comparing low-fat, calorie-restricted diets to Atkins diets. Since the Atkins diet is a high-fat, high saturated fat diet and it improved cholesterol profiles in all these trials, that pretty much clinched it. I’ve been arguing since that these diet trials have to be perceived as tests of the hypothesis that saturated fat is a “bad” fat, although the medical establishment still prefers to ignore that fact.

Is there anything new or updated in the paperback version of GCBC or is it the same as the hardback?

It’s the same as the hardback, but there is a 3000 word (or thereabouts) afterward that’s worth reading.

I tried to come up with a selection of questions that represented the majority of questions asked.  I know that some went unanswered, but when Gary agreed to do this I promised him that he wouldn’t have to answer an exhaustive list that would require days of time.  So, I’m sorry if any specific question went unanswered, and I hope you understand.  Thanks to everyone for the terrific response.

Dinner tonight at Casa Eades

Last Sunday the New York Times published a color spread on the US Department of Agriculture (USDA) data on the changes in food consumption in this country between 1970 and 2006, which got me to musing.

To the uninformed, which, sadly, probably means most people working in the nutrition industry and even those employed in a nutritional capacity at the USDA, these changes (all save two) seem to be in a positive direction. The intake of dairy products has decreased; the intake of vegetables has increased; the intake of red meat has fallen; the intake of fish, chicken and skyrocketed; the intake of fruit is up; the intake of grains has increased markedly; and the intake of vegetable fats has almost doubled. The only two negatives are that sugar and sweeteners have increased and overall food consumption has gone up by about 11 percent, or an addition 1.8 pounds per person per week.

At the same time all these positive changes have been taking place, changes that all the (misinformed) people in the mainstream nutritional biz have been advocating, there has been an enormous increase in the rate of obesity. According to the Centers for Disease Control (quoted in the Times article) the rate of obesity has more than doubled since 1970, which is interesting because up until 1970 the rates of obesity hummed along at about the rate of 15 percent for decades.

What has happened since 1970 to cause this enormous societal change?

If asked, people give many answers: too much saturated fat, too much refined carbohydrate, too much food, etc.

I have my own opinions, which I will elaborate. I believe that the obesity epidemic has probably been driven by several dietary changes that have occurred since 1970. These changes are an increase in fructose and vegetable oil consumption and a decrease in saturated fat consumption. I believe that another contributing factor is the increased overall consumption of carbohydrates, which leads to an increased food consumption in general.

I want to emphasize that these are my opinions based on a pretty good knowledge of nutrition, metabolism, biochemistry, and physiology.

First, a sort of no-brainer. Since the USDA came out with the idiotic Food Pyramid that we all loathe, there has been a major strategy in the food industry to move away from fats and toward carbohydrates. We have all seen this in various food consumption statistics. And we can tease it out from this Times piece if we look at which foods have increased and which have decreased in the diet. There has been a large increase in carbohydrate consumption as evidenced by the large increase in grains, vegetables, fruits and sweeteners.

Forgetting about all the metabolic events that carb intake precipitates that we all know cause obesity (i.e., increased blood sugar, increased insulin, etc.), let’s focus on simply one of the brain processes that carbs affect. The satiety center, located in the hypothalamus, is the part of the brain that tells us when we’re full. Unfortunately, it runs about 20-30 minutes behind our actual eating pattern, so we can stuff food in for a good while before our brains tell us we’ve had enough. Fortunately, it works a little more quickly (thanks to the help of cholecystokinin and some other gut hormones) when we eat primarily fat. If you eat a big steak, you feel full more quickly than if you eat a lot of carbs. Carbs tend to override the satiety center, allowing you to eat more. Let me describe a situation we’ve all experienced, and you’ll see what I mean.

Your at a restaurant. You’re just at the end of a big meal and you’re stuffed. One of your dinner partners asks you to try a bite of his wonderful swordfish. It’s the best he’s ever tasted, he tells you. You say, I just can’t eat another bite. If I do, I’ll be sick. Then appears the waiter with the dessert tray, loaded with wonderful gooey treats. You look them over and say: I’ll take the carrot cake (or the chocolate mousse or whatever). How can you eat this calorically-laden dessert when you’ve just refused a bite of meat because you were so full? Because your brain’s satiety center is overridden by the carbs. And you haven’t even eaten the carbs yet. But experience has taught you that no matter how full you seem to be, there is always room for carbs. And fat, since most desserts are pretty high in fat as well. But it’s the carbs that do the satiety-center-blunting trick. It’s the reason dessert is always at the end of the meal. If you ate the dessert first, you would never be able to eat all the steak. And this carb overriding of the satiety center is why people don’t binge on steak, eggs and bacon. They binge on cake, chips, cookies and other high carb treats because they can stuff them without their satiety center telling them they’re full.

Since we’ve (as a nation) significantly increased our carb intake, it only makes sense that we’ve also increased the overall amount of food we eat. Carbs let us do that without even trying.

We have definitely increased our intake of fructose since 1970. I used the figures in the Times article to make my own calculations. Considering that table sugar is one half fructose and high-fructose corn syrup is 55 percent fructose (the most commonly used variety; some go as high as 90 percent fructose), I calculated that we ate about 50 grams of fructose per capita per day in 1970. By 2006 that figure had increased to 75 grams, a 50 percent increase. And we’ve got to bear in mind that these are average figures. I eat maybe 3 grams of fructose per day, and MD eats the same. That means that two other people out there are eating their 75 grams plus our extra 72 to make the averages come out as they do. I would suspect that most of the people reading this blog eat very little fructose, leaving a lot of other people to consume their share to keep the averages up.

But even 75 grams of fructose is a helluva lot. A little fructose – the amount you might find in a piece of fruit, for example – actually helps with glucose metabolism. It more or less primes the pump so that less insulin is required to reduce blood glucose. Large amounts of fructose are a different story, however. Fructose bypasses the enzyme phosphofructokinase, which is the rate-limiting enzyme in the glucose metabolism pathway. Consequently, large amounts of fructose are shunted past the sugar-regulating pathways and into the fat-formation pathway instead. The liver converts this fructose to fat, much of which, unfortunately, remains in the liver. ( Here is a nice paper on fructose metabolism. Ignore the idiotic conclusions, which is just another ad hoc attempt to make the data fit a preconceived notion acceptable to all academics.)

With continued consumption of large amounts of fructose, fat tends to accumulate in the liver leading to a condition called non-alcoholic fatty liver disorder (NAFLD). At this point, not only are we in an obesity and a diabetes epidemic, we are in an epidemic of NAFLD. Studies on ‘normal’ adults have shown that a little more than a third have significant fat accumulations in their livers. Even worse, 15-20 percent of children show the same thing.

NAFLD is the same disease people get who chronically over consume alcohol. Under the microscope NAFLD looks exactly the same; pathologically it acts the same. The only way to differentiate is by history of alcohol consumption: if there is fat in the liver and no history of chronic alcohol abuse, then NAFLD it is.

NAFLD has the same progression as the alcoholic variety. First, an accumulation of fat that becomes inflamed leading to a condition called non-alcoholic steatohepatitis (NASH), which means a non-alcoholic inflammation of fat in the liver. This condition can then progress to liver fibrosis, then to cirrhosis, then, ultimately, to liver cancer. Not all NAFLD follows this complete progression just as not all alcoholics get cirrhosis, but enough follow it to not make you want to get NAFLD if you can help it.

And one of the big ways not to get it is to avoid fructose.

By increasing fat in the liver, fructose also increases circulating insulin levels, which can lead to hyperinsulinemia and insulin resistance. How? Because a liver full of fat doesn’t work as well as a non-fatty liver. One of the jobs of the liver is to metabolize hormones and clear them from the circulation when their work is done. When you consume carbs or protein you stimulate the release of insulin to deal with them. Once insulin has done its job, the liver breaks it down to its amino acid components and puts them back in the circulating amino-acid pool. If the liver is filled with fat, it can’t do this as well. Insulin stays elevated (and in a diabolical twist even stimulates more fat synthesis in the liver) and tends to downregulate the insulin receptors, making them less responsive. The entire process can lead to insulin resistance, hyperinsulinemia and ultimately to obesity.

Below is a nice chart showing how the increase in obesity has paralleled the rapid increase in sugar consumption. Remember that table sugar is half fructose. Also remember that correlation is not causation. But in this case we do have the biochemistry of why worked out.

From Johnson RJ et al, AJCN 2007; 86:899-906

What about saturated fat? How does a decrease in saturated fat cause obesity. First, the decrease in saturated fat has tracked with the increase in vegetable oils, which are typically rich in omega-6 fats. Omega-6 fats have been shown in numerous studies to be proinflammatory. They have also been shown to worsen alcoholic fatty liver disease, and, one would assume, NAFLD as well. I haven’t seen any studies showing a worsening of NAFLD with increased consumption of vegetable oil – it hasn’t been studied as far as I know. (Maybe one of you readers can dig up a paper.) But it has been shown repeatedly with alcoholic liver disease, and since NAFLD is basically the same disorder, it makes sense that vegetable oil would worsen NAFLD as well. And if vegetable oil indeed does worsen NAFLD, then it promotes obesity by the mechanism described above.

Saturated fat is a healthful food. Read this article by Mary Enig that describes in detail the health benefits that come from eating saturated fat. I’ll address a couple of different issues.

Saturated fat is, well, saturated. That means that every carbon in the fatty acid chain has a full complement of hydrogens attached to it. There are no double bonds. In the picture below you can see a saturated fatty acid on top and a monounsaturated (one double carbon-carbon bond) fatty acid on the bottom.

Double bonds make fats unstable. These double bonds are the places that free radicals strike to convert unsaturated fats into peroxides, or oxidized fats. The more carbon-carbon double bonds a fatty acid has, the more susceptible it is to oxidation. Oxidized fats don’t function as well as non-oxidized fats. They make faulty cell membranes and less than optimal membranes for all the organelles within the cell. Oxidized fats can themselves become free radicals attacking adjacent fats and damaging them, or worse, starting an entire free-radical-fat-damaging cascade. All these forces work even more effectively at higher temperatures, so unsaturated fats shouldn’t be used for cooking. Unless, of course, your goal is to eat oxidized fats.

Saturated fats have no double bonds. They are immune to free radical attack. They are immune to heat damage. You can cook with them, you can hit them with a hammer, you can throw them on the floor and jump up and down on them. And they stay the same. Saturated fats are stable fats.

Most people don’t realize this, but the body has the ability to convert saturated fats to unsaturated fats. But the body doesn’t have the ability to convert unsaturated fats to saturated ones. The body can make saturated fats (palmitic acid, a 16-carbon-chain fatty acid) from excess carb consumption, but it can’t make a saturated fat out of an unsaturated one. If nature hadn’t wanted us to have saturated fat, why did she make us so that we make our own if we eat too many carbs. Could it be that during our evolutionary past the only time we might over consume carbs would have been when there was no meat available…and we needed the saturated fat? Sounds reasonable to me.

We have enzymes called desaturases that desaturate, i.e., add carbon-carbon double bonds, fats. We can take unsaturated fats and make them more unsaturated. And we can take saturated fats and make them unsaturated. But we can’t go the other way. In order to have saturated fats that provide the necessary structural stability that only saturated fats can provide is to get them in the diet, which we can do by eating saturated fats or by eating a whole lot of carbs. Since over consuming carbs comes with its own set of problems that we would rather avoid, that leaves eating saturated fats.

So how does avoiding saturated fats lead to obesity. In my opinion in a couple of ways. First, indirectly, by having them replaced by vegetable oil, particularly hydrogentated vegetable oil, i.e., trans fat. Due to their stability, saturated fats have cooking properties that no other natural fats have. Food chemists have created trans fats to have the same cooking properties – and in some situations even better cooking properties – as saturated fats. But the addition of trans fats to the diet creates a host of other problems. The medical literature is crawling with studies showing that trans fats drive the development of obesity.

The other reason is that saturated fats compose the lion’s share of normal membranous fats and of the brain. When membranes don’t work as well, especially mitochondrial membranes, our energy storage and regulation system doesn’t work as well. Anything that impairs membrane functioning impairs signaling function. If signaling function falls off, then various hormones, neurotransmitters, etc. lose function. As insulin loses function, more insulin is required, more insulin leads to more downregulation of receptors, all of which ultimately leads to obesity.

Even overeating carbs doesn’t help even though saturated fats are produced as a result. Carbs stimulate the production of palmitic acid, a 16-carbon chain fat. For proper membrane function and signaling we need shorter-chain saturated fats as well. These we can’t make – we get them from diet only. We can make shorter fats longer with elongase enzymes, but we can’t make longer fats shorter. We’ve got to get them via mouth.

Since this is speculation on my part – educated speculation, but speculation nevertheless – we may ultimately find that there are other reasons for the obesity epidemic instead of these or in addition to these. In fact, I can think of a few other minor causes, which I’ll save for a later post.) But I’ll bet that when all the work is done – which may not be for a hundred years given the academic climate of today – I’ll bet these ideas will be close to the mark.

What we have to keep in mind here is that nutrition is a science (or at least should be) and science is about generating hypotheses, making predictions from our hypotheses, and then seeing if they hold true. The relevant hypothesis here — i.e., what we’ve believed for the past 30-odd years — is that saturated fat causes heart disease by elevating either total cholesterol or LDL cholesterol, specifically. So our prediction is that the diet with the higher saturated fat content will have a relatively deleterious effect on cholesterol. We do the test; we repeat it a half dozen times in different populations. Each time it fails to confirm our prediction. So maybe the hypothesis is wrong. That seems like a reasonable conclusion. No one is proving anything here — as some of your respondents like to decry — we’re just looking at the evidence and trying to decide which hypotheses it supports and which it tends to refute.

The knee-jerk response — as exemplified by quite a few respondents — is to assume that sometime in the not-too-distant past, maybe the 1960s or 1970s, before this low-fat dogma set in, such trials, or far better trials, were done and found the opposite — that the higher the saturated fat in the diet, the lower the cholesterol and the better the cholesterol profile. Or the higher the saturated fat, the greater the mortality. But that’s simply not the case, as I point out in my book. In fact, I’ve been criticized (by Gina Kolata, among others) for going on and on in the book about all the different studies. But I did so precisely because I didn’t want to be accused of cherry picking the data. (I was anyway, but that’s just the nature of this business.) When Ancel Keys, for instance, reported in the 1950s reported that saturated fats raised total cholesterol, which they did in his studies, he based it on comparisons of butter fat to polyunsaturated oils in studies that lasted only two to nine weeks. (He also reported, curiously enough, that the saturated fats had no significant effect on LDL.)

These latest trials just happen to be the best data we have on the long-term effects of saturated fat in the diet, and the best data we have says that more saturated fat is better than less. It may be true that if we lowered saturated fat further — say to 7 % of all calories as the American Heart Association is now recommending — or total fat down to 10 percent, as Dean Ornish argues, or raised saturated fat to 20 percent of calories, as Keys did, that we’d see a different result, but that’s just another hypothesis. The trials haven’t been done to test it. It’s also hard to imagine why a small decrease in saturated fat would be deleterious, but a larger decrease would be beneficial.

Gary’s full commentary here.

In scrolling through the ever-increasing list of comments to this Tierney post, it appears that there has been an outbreak of good sense. There are still a host of overbearing, know-it-all, self-righteous idiots out there (witness the comments below), but, thankfully, they are in the minority.

Bull. Utter Bull. When will the public stop trying to blame their waistlines on some mythical nutrient (or lack thereof) and realize that food…real actual food that does not come from a box, is the only thing you should eat. Eat Food. Not Much. Mostly Plants. How hard is that to recognize?

I noticed a few regular commenters on this blog had commented there, too. All were in the good sense camp.

I suppose that I shouldn’t be too hard on these commenters who are, I assume, just people out there with opinions based on little knowledge and a lot of prejudice when those who should know better make equally idiotic comments.

Here is Robert Eckel, M.D., former president of the American Heart Association (AHA) and professor of Medicine at the University of Colorado medical school, commenting on this study to Medscape (a site available to physicians only) and rejecting the idea that saturated fats could possibly be harmless (or, God forbid, beneficial). Before you read the comments of this influential physician/scientist, go back and read Gary’s comments (or reread GCBC) about how there is no evidence that saturated fat causes heart disease.

Anything that would endorse the Atkins-type of food-intake pattern would not be something that the AHA would back. Saturated fats raise LDL cholesterol — I don’t think many people would disagree with that. . . . At this point limiting saturated fats is still a position the AHA would claim, and I think that’s consistent with the National Cholesterol Education Program guidelines, the American Diabetes Association, the US Department of Agriculture. I don’t think there is any major professional organization at this point that’s willing to throw in the towel on saturated fats and say they are unimportant.

Uh, earth to Bob, earth to Bob, I think a lot of people who actually bothered to read the scientific literature would disagree that saturated fats do squat in terms of causing heart disease. If all you talk to is other statinators and lipophobes who are willing to believe the worst about fats without a shred of evidence other than these shared conversations, then I guess you could come away with this idea. But not if you read the scientific literature, which I always thought was what scientists did. This example glaringly demonstrates the point Gary made in GCBC when he wrote that nutritional science as practiced today can’t really be called science.

Dr. Eckel does make another strange point that I found intriguing in his diatribe against the findings of this study. He first adopts the Ornish argument that you can’t really call the low-fat diet a low-fat diet because it isn’t low-fat enough to qualify as a real low-fat diet. But Eckels morphs this argument into one that says this diet isn’t really an AHA diet because the AHA changed its dietary guidelines. Said he:

The AHA updated its dietary guidelines in 2005, which are quite different from the diet that’s quoted here. The dietary fat restriction at 30% of calories is no longer part of the AHA guidelines, and the saturated-fat content has been reduced from 10% to 7% and the cholesterol content from 300 to 200 mg/day. I think it’s a little bit unfair to kind of generalize that the AHA, number one, stands for a low-fat diet; that’s no longer the case.

Hmmm. Number one. Unfair to generalize that the AHA stands for a low-fat diet. Please.

And number two? Hold on to your seat. Here’s where it really gets interesting. The number two reason that the low-carb, higher-fat diet shouldn’t be compared to the AHA diet:

And number two, there is some kind of mysterious benefit of being on the Mediterranean and low-carb diets over time that doesn’t necessarily at this point have any explanation.

Jesus wept.

I am not making this up. That is a direct quote. Make of it what you will. I suppose the fact that insulin is a fat-storage hormone and that it decreases on a low-carb diet doesn’t “necessarily…have any explanation” in Dr. Eckel’s world, but I’ll bet that any low-carb newbie could probably set him straight.

One of the questions many people had about the Israeli study was why the recommendation to follow a vegetarian low-carb diet instead of a more meat-heavy low-carb diet? And, in view of this recommendation, what was the final diet the subjects on the low-carb arm consumed? [full text of the study]

Eric Westman, M.D. from Duke University corresponded with the lead author of the paper and asked these questions. Here is the response:

Hello Eric,

This is kind of funny that some could think of a “vegetarian low-carb” diet. Is it a new suggested strategy? could be interesting idea but this wasn’t the case here. Our low-carb diet was based on Atkins, the participants read the book and the recipes were more or less comparable to what you know in the states. Beef is the main red meat. What could be different? People here would not mix in the same meal meat and butter, a salad is considered a very rich one and not a lettuce based, and the main dressing is olive oil. As for beverages, same industry that makes money everywhere.

For example, a plate could include : fish or fried/not bread coated chicken/or red meet, broccoli and mushrooms coated with eggs, roasted eggplants, vegetable salad (peppers, cucumber, green leaves, not lettuce) with olive oil dressing. I understand that some of the low-fat people find it hard to believe that such a low-carb diet was tremendously favorable within 2 years in a well designed study, but these are the facts and the science of tomorrow, with the next long term studies in the pipeline, may confirm or not these findings.

Best regards, Iris [Shai]

As I mentioned in my previous post, I figured it had something to do with the dietary restrictions followed by observant Jews. For those who don’t know, one of the major dietary restrictions is the avoidance of mixing meat and dairy products. Observant Jews go to great extremes in adhering to this tenet of Jewish law. They have separate dishes, silverware, and pots and pans for meat and for dairy. Those who can afford it have two dishwashers – one for meat, one for dairy. Kosher restaurants are either meat or dairy. If you go to a dairy kosher restaurant you can have all the milk, butter, cream, ice cream, cream sauce, etc. you want. You can have pasta, fish (not considered meat), and pretty much anything not made of meat. Cheese, although obviously a dairy product, is often missing because cheese is made using rennet, which is an animal product and considered meat. At a kosher meat restaurant you can eat all kinds of meat (as long as it’s kosher), but you can’t have butter or cream for your coffee or any kind of cream sauce. Or anything made from milk or cream. You can have faux dairy products, i.e., margarine and trans fat-laden non-dairy creamer for your coffee or in desserts. There are pretty high rates of heart disease in Israel, and many believe one of the causes is the large amount of trans fats Israelis consume in an effort to follow Jewish law.

John Tierney in his New York Times blog posted an interviewed with Gary Taubes about the findings of this low-carb study with respect to saturated fats. Here is what Gary had to say:

These trials are fundamentally tests of the hypothesis that saturated fat is bad for cholesterol and bad for the heart. They’re not just about which diet works best for weight loss or is healthiest, but what constitutes a healthy diet, period. (This is the point I made in my Times Magazine story six years ago). Specifically, these low-fat/low-carb diet trials, of which there are now more than half a dozen, test American Heart Association (A.H.A.) relatively low-fat diets against Atkins-like high-saturated-fat diets.

In this last test, the A.H.A. diet was about 30 percent calories from fat, less than 10 percent calories from saturated fat; the low-carb diet was almost 40 percent calories from fat, around 12.5 percent saturated fat. In this particular trial, as in all of them so far, the high-saturated-fat diet (low-carb or Atkins-like) resulted in the best improvement in cholesterol profile — total cholesterol/H.D.L. In this Israeli trial, the high-saturated-fat diet reduced L.D.L. at least as well as the did the A.H.A. relatively low-fat diet, the fundamental purpose of which is to lower L.D.L. by reducing the saturated fat content.

So here’s the simple question and the point: how can saturated fat be bad for us if a high saturated fat diet lowers L.D.L. at least as well as a diet that has 20 to 25 percent less saturated fat?

It could be argued (and probably will be) that the effect of the saturated fat is confounded by the reduction in calories, but the A.H.A. diet also reduces calories and in fact specifies caloric reduction while the low-carb diet does not. It will also be argued, as Dean Ornish does, that the source of the saturated fat was not necessarily meat or bacon, but beans or other healthy sources.

But the nutritional reason why meat has been vilified over the years, is that it’s a source of unhealthy saturated fat. It’s not that meat per se is bad — unless you buy the colon cancer evidence, which has always seemed dubious — it’s that the saturated fat in meat makes it bad. So the argument about the source of the saturated fat is irrelevant.

The question hinges on whether saturated fat raises cholesterol and causes heart disease. One way or the other this trial is a test of that hypothesis. It’s arguably the best such trial ever done and the most rigorous. To me that’s always been the story. If saturated fat is bad for us, then these trials should demonstrate it. They imply the opposite.

Why does the A.H.A. continue to insist that saturated fat should be avoided, if these trials repeatedly show that high saturated fat diets lead to better cholesterol profiles than low-saturated fat diets? And how many of these trials have to be done before the National Institutes of Health or some other august institution in this business re-assesses this question? After all, the reason the food guide pyramid suggests we eat things like butter and lard and meats sparingly (and puts them high up in the pyramid) is that they contain saturated fat. This is also the reason that the A.H.A. wants to lower even further what’s considered the safe limit for saturated fats in the diet.

More here.

It’s nice to know that at least one person at the New York Times has good sense (nutritionally, at least). Tierney had a piece in today’s Science section that debunks a handful of what he considers scientific myths that people spend time worrying about. I don’t know if I agree with him that all these ‘myths’ are really myths, but I completely agree with his take on the hot dog.

Killer hot dogs. What is it about frankfurters? There was the nitrite scare. Then the grilling-creates-carcinogens alarm. And then, when those menaces ebbed, the weenie warriors fell back on that old reliable villain: saturated fat.

But now even saturated fat isn’t looking so bad, thanks to a rigorous experiment in Israel reported this month. The people on a low-carb, unrestricted-calorie diet consumed more saturated fat than another group forced to cut back on both fat and diet, but those fatophiles lost more weight and ended up with a better cholesterol profile. And this was just the latest in a series of studies contradicting the medical establishment’s predictions about saturated fat.

If you must worry, focus on the carbs in the bun. But when it comes to the fatty frank — or the fatty anything else on vacation — I’d relax.

On a you’ve-just-got-to-shake-your-head note, go back to the Tierney piece containing the long quote from Gary and read through the hundred plus comments that follow. Doing so gives you an idea of the total nutritional ignorance out there. These are the misinformed people that politicians and bureaucrats pander to when establishing the nutritional guidelines. A sorry state of affairs indeed.

I’ve linked below to a video of a mainstream cardiologist being interviewed as to her thoughts on the best diet for a healthy heart. Listening to her, it’s easy to see what’s happened to mainstream thinking.

For years mainstream thinking was that the low-fat diet was the be-all and end-all for preventing heart disease. Whenever anyone brought up the idea that low-carb diets may be as effective if not more so than low-fat diets, that idea was dashed with the old ‘Show me the studies’ song and dance that the mainstream knew how to perform so well. As Gary Taubes presented so beautifully in Good Calories, Bad Calories, those studies had already been done years before, but were unknown to the mainstreamers of today. But over the past few years numerous studies have accumulated showing that the low-carb diet at the very worst equals the performance of the low-fat diet and at the very best stomps the performance of the low-fat diet in reducing putative risks for heart disease. Now, what is the mainstream to do?

This video answers the question. The mainstream has retreated to the all-things-in-moderation mantra. Let’s eat less and exercise more and we’ll all be thin and happy. And let’s don’t forget to cut sodium from our diets as well. Even though sodium is the most abundant electrolyte in our bodies, we need to be careful. And let’s forget about all those studies showing that salt intake doesn’t do squat in terms of increasing high blood pressure. Let’s just pretend those don’t exist.

Watch this woman’s response when asked about low-carb, high-protein diets. She stammers and stutters for a moment as you can see her try to access the hard drive in her brain for info on low-carb diets. Aha, she’s found it! She trots out the myth that protein is bad for the kidneys. But she’s obviously been around long enough and been hit with the info showing that protein intake has no harmful effect on normal kidneys. So she cleverly makes the case that people who go on low-carb diets are overweight, therefore most of them have high blood pressure and/or diabetes that often accompany obesity. And since both diabetes and high blood pressure are associated with slightly impaired kidney function, it isn’t a good idea to increase protein intake. A clever one, this.

She ignores the fact that low-carb diets are the best diets around for rapidly lowering blood pressure and normalizing blood sugar. And she ignores the fact (or, most likely, is ignorant of it) that low-carb diets are not necessarily high protein diets. If anything low-carb diets are high-fat diets and moderate-protein diets. This is the kind of person who, if asked about a diet of hamburgers, French fries and a Coke, would say that it’s a bad diet. If asked if it would harm the kidneys, she would say no, but it still isn’t a good diet. Now if you ask her about a the same hamburger with the bun removed, a salad instead of the fries, and an unsweetened ice tea or bottled water, she would probably say that said diet was one of those dangerous high-protein diets and would harm the kidneys.

Here is a paper from Nutrition & Metabolism showing how a low-carb diet was used to treat kidneys damaged from diabetes. Based on this paper and my own years of experience, I can tell you that low-carb diets do not cause kidney problems, even in people with less-than-perfect kidneys.

The mainstream is definitely bunkering down into the low-calorie mode because they just can’t bring themselves to even consider the low-carb diet after all the years they scorned it. It’s really too bad they can’t look on the data in an unbiased way.

Here is a link to the video.

It’s beyond my abilities to embed the thing, so you’ll have to go to the link. If the video that opens isn’t the correct one, go to the right of the video and click on the one that says: Is there a single save your heart diet?

According to this expert, the answer is yes and it’s the low-calorie diet.

Jesus wept.

A couple of times per year my friend puts on seminars for people wanting to learn about how the media work. He invited me to one a few years ago in Las Vegas, and I can tell you, it was an eye-opening experience. The program started with my friend asking the attendees to write a few sentences describing what they thought constituted ‘news.’ Before you read on, stop for a moment and come up with your own definition of news. Have you got it? At this meeting virtually everyone (including yours truly and his lovely wife) came up with something on the order of: ‘News is when something happens of sufficient importance to the readers or viewers of a particular media format in a defined local (could be local – could be national) that it requires reporting.’

My friend gathered the papers and started reading them to the group. One after the other was a variation on the theme above. After he had read a dozen or so, he looked at the crowd and said: “Let me define news for you. News is what the media wants you to know.”

In the previous post I wrote the media wanted you to know that the Atkins diet was dangerous, so that’s how they reported it. A reported went in to an oral poster presentation, a tiny sub-meeting of the larger overall meeting, and reported on non-peer reviewed data in such a way as to make a perfectly safe and sensible way of eating, practiced by literally millions of people over the last 30 years, appear to be a danger to health. That’s news because that reporter and his editors said it was.

I’m stressing this because the American Heart Association (AHA) also reports the news, which, in its case, is what it wants people to know. The AHA has an entire publicity arm that sends reports out to doctors all over the world telling them what the AHA wants them to know. And guess what? In none of these reports is the study on the Atkins diet mentioned.

I got these reports by email for every day of the conference. You can click on them by day – Sunday, Monday, Tuesday and Wednesday – to see what the AHA wanted doctors interested in this conference to know. If you burrow down into all the links and follow where they lead, you’ll find that none of them (at least none that I could find) lead to the Atkins diet presentation. Probably because the study wasn’t very important relative to the others, and because any one with a modicum of scientific understanding would see right through it.

But not the public. Members of the public aren’t trained to even find the relevant study much less analyze it critically. So that’s where the reports were sent. To the public. Not to the doctors. I find it interesting to say the least.

One other thing, then we’re through with this travesty of a study. A number of people wrote comments wondering about the inflammatory markers that went up in the folks who went on the pseudo Atkins diet. Here is the full text of a study done by Jeff Volek and his group at the University of Connecticut showing that real low-carb diets bring about a decrease in inflammatory markers. And here is another demonstrating that real low-carb diets bring about improvements in atherogenic lipid profiles in subjects who do not lose weight. So, it’s the diet that does it, not the weight loss that usually accompanies such a diet.

Today I’ve been inundated with comments, emails and even a phone call or two about the ’study’ that hit the news this morning allegedly showing that the Atkins diet causes blood vessel damage, and increase in ‘bad’ cholesterol and increased levels of inflammation. I figured I would take this opportunity to describe how this kind of information gets out there and discuss this ’study’ in particular.

To begin with, this isn’t really a scientific study published in a peer-reviewed journal. It was a brief presentation (about 15 minutes including questions) made at the annual scientific meeting of the American Heart Association in Orlando, Florida a couple of days ago. To better understand where presentations like this one fit in the hierarchy of the scientific world, let’s take a look at how these huge meetings are organized.

The annual Scientific Sessions of the American Heart Association is an enormous meeting with thousands and thousands of attendees. This year’s meeting, which is still going on, is being held at the giant convention center in Orlando, Florida. When the organizers of these kinds of meetings start working on putting them together – which they do years in advance – they begin to contact all the big guns for the major lectures. These lectures are presented during the prime times of the conference when nothing else is going on and they can be attended by all attendees. These lectures held in the huge auditorium are usually by well-known, established researchers who present the data from many years of their work on specific inquiries.

Scheduled in around these giant lectures are concurrent meetings, which are held in small conference rooms holding 50-60 or so people. (The photo at the top of this post shows the typical size of one of these sessions) These smaller lectures compete with other lectures taking place at the same time. Usually there are four or five sessions going on at once, which is a major pain if you’re an attendee because invariable two lectures you want to see are going at the same time. (Fortunately, in our case, MD can go to one and I go to the other, so it’s not so bad.) These lesser presentations are often, but not always, made by graduate students or newly minted Ph.Ds or physicians doing postdoctorate work.

At the bottom of the food chain in terms of importance are the poster presentations. These are usually held in a large room and involve a bunch of people with posters describing work that they have done or research in progress.

In between the poster presentations and the concurrent lectures are oral poster presentations. These are lectures about work in progress or small or preliminary studies that have been done but haven’t been published. The ’study’ in question is an oral poster presentation.

When the organizers of these meetings are in the preparation stage they send out a call for abstracts. They get inundated with abstracts and arrange them sort of in terms of significance with the most interesting or scientifically significant ending up being presented as a concurrent lecture. The next down the list are the oral poster presentations, then finally the posters.

The important thing to understand about these presentations is that they are not peer reviewed as they are if and when they show up in a scientific journal. They are sort of peer reviewed on the spot in the sense that other researchers familiar with the specific field ask questions of the presenters or of the people with the posters. But that’s it. There is no scientific review of the data as there is when it is published in a journal. So people can present all kinds of data with no one looking it over other than the folks who ask questions. And sometimes the exchanges at these meetings can become spirited to say the least, which means that those lecturing are often present data much at odds with what other scientists have found doing the same kind of studies. That’s why it’s always good to take anything that comes from a meeting like this one with a huge grain of salt.

If you take a look at the monster program for the 2007 Scientific Sessions of the American Heart Association (click here) you can find the presentation in question on page 407. It is session #3610. You should roam through this program a little just to get a feel for the scope of a meeting of this size and to see just how much is going on at once, which puts perspective on any given oral poster presentation.

These giant meetings are open to the press, members of which get these huge programs just as do the scientific attendees. The folks with press passes go through these programs looking for lectures that they think will give them a headline. They don’t care how insignificant the talk is, who is giving it, whether it’s a poster or an oral poster presentation – they are looking for headlines. And what better headline than that there is a problem with low-carb diets or even better, the Atkins diet itself.

So the stage is set. I would imagine that of the 30 or 40 people (if that many) who attended this talk a large number had press passes. These media types stay after and talk to the speaker to get a few quotes, then head off to the press room, dash off a few hundred words, send it to their service, and head back off for another headline-grabbing talk (or the bar).

Now that you know the genesis of the news report about this oral poster that many of you have read and maybe worried about, let’s take a look at the study itself.

I emailed the publicist for the University of Maryland Medical Center for an abstract of this talk, and he kindly sent it to me within minutes. (I’ve converted it to PDF for you: miller-2007-aha-abstract-diet.pdf.) Remember, this is all there is. Just an abstract, not a real paper. We can tell only a little about what really went on in this study. But let’s take a look.

The people doing this study were obviously tired of hearing about the supremacy of the low-carb diet as a weight-loss tool, and they probably didn’t want to do yet another study comparing the low-carb diet to the low-fat diet for weight loss or lipid improvement or blood sugar normalization or blood pressure lowering because they knew what that outcome would be. Those studies have been done again and again and the low-carb diet always comes out on top. So, these researchers decided to take a different tack.

They wanted to see what happened when subjects stayed on the diet after reaching maintenance, so they took 18 subjects (they started with 26, but only 18 made it through the entire study) and put them on one of three diets: the Atkins diet, the Southbeach diet or the Ornish diet. The subjects stayed on one of these diets for 4 weeks, then followed their normal diets for 4 weeks, then went on another of the three diets for 4 more weeks, then off for 4 weeks, then on to the last of the three diets for 4 more weeks. But the researchers didn’t put the subjects on the weight-loss versions of these diets, they put them on maintenance versions. They did this by weighing the subjects at the end of each week and adjusting their caloric intake so that they neither gained nor lost weight.

By keeping the weight of the subjects stable, any changes wrought by the various diets could be attributed to the diet and not to the lost weight. Many people believe the changes brought about by low-carb diets occur not because of the diet but because of the weight loss the diet induces. And since in most studies subjects on the low-carb arm lose more weight than those following low-cal diets, it seems reasonable to suppose that it is the lower weight and not the diet composition that results in the better lipids, normalized blood sugars and lowered blood pressure commonly seen in the low-carb group.

In this case the weights stayed the same for all the subjects during the various diets, and as you can see from the abstract, the LDL levels went up (although not significantly) in the Atkins group while LDL levels dropped in the other two groups. The abstract says that the researchers drew blood at the end of each 4 week phase on the different diets, and I assume that they also drew blood at the start of each 4 week dietary trial, but the abstract doesn’t say. For all I know, they could have drawn blood for baseline values at the very start of the study and compared the lab values at the end of each 4 weeks to this baseline number, which would make the later numbers suspect. This is one of the problems with ’studies’ like this one. These questions would all have to be answered before such a study could be published in a peer-reviewed journal. But in a conference, pretty much anything goes. It would be left up to an attendee to ask such a question.

Along with the LDL levels, the researchers also looked at a number of fairly arcane measures of inflammation: ICAM2, SELL and SOD1. As far as I know, these are not lab studies that the average doctor can order, but are ones that are done in research facilities for research purposes. In any case these indicators went up on the Atkins diet and stayed the same on the Southbeach and Ornish diets.

Finally, the researchers performed a brachial artery reactivity test (BART), which is a somewhat controversial but nevertheless commonly used test to measure endothelial function. (About halfway this old post is a description of how BART works. If you want a more detailed explanation with a discussion the controversial nature of the test, read this full text article.) As to the outcome of BART, the abstract simply reports the following:

BART testing revealed a significant inverse correlation between flow-mediated vasodilation and intake of total fat, saturated fat and monounsaturated fat.

We’re not told if this correlation holds irrespective of which diet the subjects were following or if these were the numbers while they were following the Atkins diet. From the wording of the abstract one would have to think that these values were reported for all the diets. If so, then the researchers have extrapolated from these numbers that the Atkins diet causes more endothelial dysfunction simply because it contains more fat and certainly more saturated fat than the other two diets.

Based on the abstract we find that

In the absence of weight loss, the high fat Atkins diet is associated with increased LDL-C, reduced endothelial vasoreactivity and increased expression of biomarkers of atherothrombosis. As such, these data suggest that isocaloric conversion to the Atkins diet may negatively impact cardiovascular health as compared to the South Beach or Ornish Diet.

Now, let’s probe a little deeper. And we don’t have to get very deep to see a major flaw in this study.

Before we get to the major flaw, though, let’s look at the LDL changes. As far as I’m concerned, they are a big Ho Hum. I mean, who really cares? How many studies do we have to look at to know that when you cut fat from the diet LDL levels decline? We already have dozens showing us this same finding. Dozens of other studies show us that when fat, particularly saturated fat, is increased in the diet that not only do LDL levels rise a little but HDL levels rise a lot. (I posted about this in the past.) So what little risk we might seem to accrue because of increased LDL levels is more than offset by the greater increase in HDL levels. It even gets better. The majority of studies have shown that when LDL levels increase due to high-saturated-fat, low-carb diets, the LDL particle size increases, making the LDL non-atherogenic. And while LDL levels fall with low-fat, high-carbohydrate diets, the LDL particle size decreases and becomes the small, dense type, which is highly associated with cardiovascular disease.

So, this study tells us that when the subjects went on the Atkins diet their lipid profiles actually improved as compared to the other two diets. Why didn’t the researchers just say that? One wonders. One also wonders why – if they went to the trouble and expense to check ICAM2 and the other markers of inflammation – they didn’t bother to check HDL levels or LDL particle size, especially since LDL particle size is lipid parameter that has the strongest correlation to the development of cardiovascular disease.

Back to the major flaw. The abstract doesn’t say how much these subjects weighed. So we can only assume. Let’s assume that they were average weight and required 24oo kcal per day to maintain their average weight. While these subjects were on the Atkins diet part of the study the abstract tells us that they were consuming 50 percent of their calories as fat. Let’s think about this for a minute and do a few back of the envelope calculations. Fifty percent of 2400 calories is 1200 calories. So 1200 calories were fat and 1200 calories were other than fat. Since other than fat means carbs and protein, that means that the other 1200 calories were divided between these two macronutrients. If we assume that 20 percent of calories were protein that calculates out to about 120 grams of protein per day, which is a fair amount and probably more than they actually got. But let’s assume 20 percent. That leaves 30 percent of calories as carbohydrate. Thirty percent of 2400 kcal comes out to 720 calories as carb. And since a gram of carb is 4 calories, dividing it out gives us 720/4 or 180 grams of carb per day. Does that sound like the Atkins diet to you?

Let’s give the researchers the benefit of the doubt and say that they had the subjects on 30 percent protein (180 grams), which I doubt because they would have been scared to death to give someone 180 grams of protein. But let’s assume they bucked up and did it. Running the same calculations on 20 percent of carbs gives us 120 grams of carbs per day – that’s a full 24 teaspoons of sugar’s worth of carbohydrates per day. Or two potatoes and a serving of pasta. Is that the Atkins diet?

See what I mean. It was a flawed study. I already linked to this post above, but it discusses the same issues, i.e., blaming a lab finding on saturated fat when the diet is full of carbs.

What do we care that a low-carb diet showed an increase in inflammation and worsening endothelial function when what was tested wasn’t really a low-carb diet?

In summary: no complete study, no peer review and no Atkins diet. Yet it made the news big time.

Now that you know the story, go back and read the press report of this oral report of a poster. See if your take home message is any different now.

Oh, and one other thing. According to the abstract the study started out with 26 subjects, but only 18 completed it. That’s a dropout rate of over 30 percent. One wonders why these subjects dropped out? And from which dietary protocol? It would be interesting to know, but I can make a pretty good guess.