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

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

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

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

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

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

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

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

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

Let’s look at a couple.

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

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

Here’s what they did:

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

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

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

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

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

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

What were the recommendations of the authors of the study?

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

Summary

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

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

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

Here is another.

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

The aims of the study were as follows:

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

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

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

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

The authors’ summary:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Gary Taubes continues

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

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

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

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

For maze at top
hat tip to FAILblog.org

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

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

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

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

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

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

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

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

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

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

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

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

Give me strength.

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

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

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

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

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

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

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

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

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

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

Here’s what the authors wrote:

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

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

…compliance was assessed with objective biomarkers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Three weeks later:

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

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

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

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

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

Her labs told another story.

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

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

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

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

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

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

I am eternally grateful to them.

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

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

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

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

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

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

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

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

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

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

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

Recognized?  What does that mean?

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

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

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

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

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

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

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

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

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

But as for heart disease itself:

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

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

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

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

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

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

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

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

It was unbelievable.

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

Watch and just shake your head.

Click here to view the embedded video.

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

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

This link requires requires free registration.

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

Click here to view the embedded video.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

A paper appeared recently in the prestigious Proceedings of the National Academy of Sciences (PNAS) that seems to have a whole lot of people on edge.  If you read the press accounts of this study, you might think anyone stupid enough to follow a low-carb diet would be doomed to certain death from heart attack.  But is that the case?  Or is it simply another instance of the media either failing to understand how science works or, worse, misreporting to get a better story?

I suspect the latter, but before we get into it, I need to go over a few blog housekeeping issues.

As I’m sure everyone has noticed, the look of this blog has changed – as has the look of the entire website.  Our designer and tech guys have been struggling to get everything working right, but, finally, my incessant whining got to them, and they went ahead and put the thing up in its not-completed state.  Please bear with us – it will ultimately work as it’s supposed to.  If you are having a problem, send me a description in the comments section.  Make sure you tell me what kind of computer you’re using (Mac (Intel or pre-Intel)  or PC) and which browser (Firefox, Internet Explorer, Safari, etc.) so that the gurus will know what to do to fix it.

I know the comments are screwed up right now, but don’t worry, they’ll be fixed.  Go ahead and comment away.  They’ll ultimately be up in a form you can recognize.

Once we get the blogs and website how they’re supposed to be, I’ll write a post describing all the features.

Also, our world-changing project has been slightly delayed through no fault of our own.  The new date for revelation has been pushed back from Sept 1 to Sept 15.  Sorry.  It’s been a real PITA for us, too.

Now, back to the PNAS paper.

As we all know, media reports can be totally misleading or even downright false.  Reporters have their own biases that creep into their work, and even when reporters think they are presenting the facts, they often report just one side of a story and ignore the other.  And, as we’ve seen from the previous post on the vitamin D-bate, reporters may just report a story in a way that makes for better reading without any regard for the substance of the issues.

The PNAS paper reported a study on genetically modified rodents, engineered to be more susceptible to heart disease.  As I’ve written many times in these pages, mice and rats aren’t just furry little humans – they are a different species altogether.  And although they are often used for medical experiments, the conclusions from the experiments cannot be applied to humans.  Like observational studies, rodent data can be used to establish hypotheses about human health and disease, hypotheses that can then be tested for validity.

In this case, the data on these genetically-engineered mice can’t even be extrapolated to normal mice much less humans.  Knowing just this much about the study tells us that whatever it shows has little relevance to us.  But that’s not what the media took away from the story.

The BBC came out with the following headlines that were picked up by a number of other media sources:

Low-carb diets ‘damage arteries’

And followed up with:

Low-carb slimming diets may clog arteries and increase the risk of heart attacks and strokes, a study suggests.

Diets based on eating lots of meat, fish and cheese, while restricting carbohydrates have grown in popularity in recent years.

But the Beth Israel Deaconess Medical Center in the US found such habits caused artery damage in tests on mice.

The researchers and independent experts both agreed a balanced diet was the best option.

Hmmm.  Sounds pretty brutal doesn’t it.  No hesitance there.  No equivocation.  Just a head on reporting of the facts.  I don’t think so.

Why not?  A number of reasons.  First, these researchers basically had a bias going in that low-carb diets cause heart disease even though they lower cholesterol and bring about other positive changes in lipid values, most notably reducing triglycerides, increasing HDL levels, and changing LDL particles from the small type B to the larger type A variety.  All of which changes, by the way, supposedly reduce the risk for heart disease.

The lead author of the study, Shi Yin Foo, MD, PhD, a clinical cardiologist,

first embarked on this investigation after seeing heart-attack patients who were on these diets – and after observing Rosenzweig [the researcher in whose lab she worked] himself following a low-carbohydrate regimen.

“Over lunch, I’d ask Tony [the aforementioned Rosenzweig] how he could eat that food and would tell him about the last low-carb patient I’d admitted to the hospital,” says Foo. “Tony would counter by noting that there were no controls for my observations.”

“Finally,” adds Rosenzweig, “I asked Shi Yin to do the mouse experiment – so that we could know what happens in the blood vessels and so that I could eat in peace.”

Do you think Dr. Foo has a little skin in this game?  Think she might have a motive for stacking the deck a little in setting this experiment up in a way that encourages a certain outcome?  This was not what you would call an unbiased quest for the truth.

I want to comment on something here as an aside.  I don’t know how old Dr. Foo is, but since she’s working in someone else’s lab, I would think she’s probably fairly new to the medical game.  She may have admitted a patient or two to the hospital with heart attacks, who, under questioning, may have admitted to following a low-carb diet at some point.  But I’m willing to put my experience with low-carb diets up against hers any day.  MD and I have followed over 10,000 patients on low-carb diets and have never had a single one have a heart attack.  So, I really doubt that Dr. Foo has admitted many – if any – patients who are actively following a low-carb diet.  But it does make for a good story.

Second, we’ve already mentioned that the mice were genetically engineered to be more susceptible to heart disease, so data generated from these rodents can’t be extrapolated even to other mice let alone to humans.

Third, the diet used wasn’t even a typical low-carb diet.  The researchers

had a diet specially made that would mimic a typical low-carb diet,” explains Foo. “In order to keep the calorie count the same in all three diets, we had to substitute a nutrient to replace the carbohydrates. We decided to substitute protein because that is what people typically do when they are on these diets.”

Oh, really?  This one statement shows Dr. Foo’s ignorance of low-carbohydrate dieting.  People don’t typically “substitute protein” when they go on a low-carb diet.  As anyone knows who has been on one, people substitute fat, the macronutrient that provides most of the calories on any low-carb diet.  The mice in this study were getting 45 percent of their calories from protein, which can be done, but isn’t what one finds in most typical low-carb diets.

MD and I have been traveling extensively lately, so I hadn’t really had the time yet to delve deeply into this study, but, fortunately, as it turns out, I didn’t have to.  Others have done it for me.

The Metabolism Society issued a press release on the paper to all its members.  You can read it in full below:

Researchers use mutant mice genetically engineered to be susceptible to heart disease to ‘prove’ carbohydrate restricted diets may harm arteries.

Defects in ApoE -/- result in defects in processing blood cholesterol.

As human studies continue to show the benefits of low carbohydrate diets and the general failure of low-fat diets, it is necessary for the nutritional establishment to find more and more obscure methods of attacking dietary carbohydrate restriction.

One method is to prepare mutant animal models, to use odd diets that humans would never consume, call them low carbohydrate diets and then show some deficit.  Because mice are not generally susceptible to atherosclerosis, it was necessary for Foo and coworkers to use an ApoE-/- mutant and a ridiculously high protein diet to vilify low carbohydrate diets which have been a useful alternative for many people suffering from obesity, diabetes and metabolic syndrome.

In keeping with the traditions in scientific research, the authors do not cite the numerous studies showing benefit of low carbohydrate diets compared to the low fat diet that has been in place during the obesity and diabetes epidemic.  That the NIH and other government agencies continue to fund this kind of biased research is probably a minor political problem in health care but should still be of concern to people who are confused about what their diet should be.

According to Dr. Richard D. Feinman, Biochemistry Professor at Downstate Medical Center in NY,  “It is a mistake to consider one experiment in a mouse mutant over riding the scientific literature where similar research trials on actual human beings clearly show benefit of carbohydrate restriction for all markers of metabolic syndrome. For some reason these studies are not the ones picked up by the media. I suppose actual advances in science aren’t hot topics for headline news stories when it concerns the proven benefits of carbohydrate restriction.

Volek JS, Ballard KD, Silvestre R, Judelson DA, Quann EE, Forsythe CE, Fernandez ML, Kraemer WJ: Effects of dietary carbohydrate restriction vs low-fat diet on flow-mediated dilation. Metabolism 2009.

Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD: Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids 2009, 44(4):297-309.

Of course, as you might expect, the press release wasn’t picked up by any of the major media outlets.

Jimmy Moore weighed in on the issue in an article in the Examiner.com in which he quotes numerous experts who have their say on this study.

And, Peter at Hyperlipid wrote two great posts taking the researchers to task and exploring  the kind of protein used and various other aspects of this study. (Here and here.)

So, I was left with nothing more to add other than to say what I’ve said countless times before:  Don’t rely on media reports to tell you anything.

(With apologies to Philip K. Dick for the title of this post.)

Instructor teaches Friedewald equation and bad cholesterol

This week sees the publication of yet another study showing the superiority of the low-carbohydrate diet as compared to the low-fat diet.  This study, published in the prestigious American Journal of Clinical Nutrition, demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL), which prompts the authors to issue a caveat.

Yes, although just about all the parameters that lipophobes worry about improved with the low-carb diet, the small increase in LDL has caused great concern and has prompted the authors to gravely announce that this small increase is troublesome and should be monitored closely in anyone who may be at risk for heart disease.  Since most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL often seen in those following a low-carb diet could put these dieters at risk.  Does it?  We’ll see.

Let’s take a look at the study. But before we do, let’s digress for just a bit and look at low-carb diet studies in general.

As we’ve discussed in these pages before, there are a couple of ways to do dietary studies in which on diet is compared to another.  You can compare a low-carb diet to a low-fat diet in a way that reflects what happens in real life.  For example, you could randomize your study subjects into two groups, then give those in one group a low-carb diet book (Protein Power, maybe) and those in the other a low-fat diet book (an Ornish or McDougal book, perhaps).  You would instruct both groups to follow their respective diets and come back periodically for evaluation.  When these kinds of studies are done, the low-carb diet invariably brings about more weight loss and greater changes for the better in just about all parameters.  But the folks who are proponents of low-fat diet cry foul.  Why?  Because in virtually all of these studies the subjects on the low-carb diet consume fewer calories than those on the low-fat diets.  Lower-carb, higher-fat diets are satisfying, and it has been shown over and over that those following such diets actually consume fewer calories while still feeling full than do those following ad libitum (eat all you want) low-fat diets.

So, the low-fatters attribute all the improvement in those on the low-carb diets as simply a result of their lower caloric intake.

If you want to eliminate this caloric-deficit difference from your study, then you design a protocol in which calories are the same in both the low-carb and the low-fat arms of the study.  This strays from the real-life way of looking at what is likely to happen when people buy diet books and follow them, but it does offer the advantage of getting rid of the calorie issue.

In these kinds of studies you randomize your subjects into either a low-carb or a low-fat diet group and put both groups on the same number of calories.  At the end of your study, you can see the differences between the two diets – if any – that are brought about without calories being an issue.

The study under our consideration today is of the latter type; it’s one in which both groups were kept on an equal number of calories, a so-called isocaloric diet.

Here’s the setup for the study titled Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo.

The researchers recruited 118 subjects who had abdominal obesity and at least one other metabolic syndrome risk factor and randomized them to either a low-carb or a low-fat diet for one year.

The diets were designed to be isocaloric with moderate energy restriction (≈6000 kJ/d [1433 kcal] for women, ≈7000 kJ/d [1672 kcal] for men). The planned macronutrient profile of the LC diet was 4% of total energy as carbohydrate, 35% as protein, 61% as total fat (20% saturated fat) with the objective to restrict carbohydrate intake to <20 g/d for the first 8 wk and to <40g/d (with the inclusion of an approved 20-g carbohydrate exchange) for the remainder of the study. The target profile for the LF diet was 46% of total energy as carbohydrate, 24% as protein, and 30% as total fat with the objective to restrict saturated fat intake to <10 g/d and <8% of total energy, with the inclusion of an approved food exchange (equivalent to the energy content of 20g of carbohydrate;) between weeks 9 and 52, so that the diets remained isocaloric.

Sixty nine subjects completed the study, and, fortunately, all the results reported in the paper were for the 69 completers, so we don’t have to worry about data contamination we would have gotten had the researchers done an intention-to-treat analysis.  We know how the people fared who actually hung in there for the entire study period, which is what we want to know.

And how did they fare?

Those on the low-carb diet lost 26 percent more weight than those on the low-fat diet (14.5 kg vs 11.5 kg), but the difference wasn’t statistically significant.  As you can see from the graph below of the weight loss between the two groups over time, the difference was widening, and we can extrapolate that the difference would have become statistically significant had the study gone on longer, but we can’t say for sure.

As for the other parameters, blood pressure, glucose, insulin, insulin resistance and C-reactive protein were the same for both groups.  There was a difference in lipid outcomes, however.

The LC [low-carbohydrate] diet also provided greater improvements in triglycerides and HDL cholesterol than did the LF [low-fat] diet, which occurred independently of differences in energy intake and weight loss. This finding is consistent with those of long-term ad libitum studies. High triglyceride and low HDL-cholesterol concentrations are 2 of the MS risk factors, a syndrome that is associated with an increased risk of type 2 diabetes and CVD. Elevated triglyceride concentrations have also been identified as an independent CVD risk factor, and the triglyceride:HDL cholesterol ratio is considered a strong predictor of future cardiac events and is a surrogate measure of insulin resistance. Our data show that the triglyceride:HDL cholesterol ratio was halved after the LC diet and was approximately double the improvement observed with the LF diet. A recent review suggests that biological markers typically associated with the MS are those improved by carbohydrate restriction, which suggests that LC diets may offer the greatest clinical benefits for overweight populations who are insulin resistant and have several metabolic risk factors.

So far, so good.  But now the other shoe is ready to drop.

Whereas the LC diet improved a range of cardiometabolic risk factors, greater increases in total and LDL cholesterol also occurred. Other studies that compared LC and LF diets reported similar findings, although the overall magnitude of the differences was smaller: 0.60 and 0.20 mmol/L in favor of the LF diet.

Let’s see how much the total cholesterol and LDL changed.

Those in the low-fat group started with an average total cholesterol of 212 mg/dl (5.5 mmol/L) and ended up a year later at same number.  These same subjects also started out with average LDL levels of 131 mg/dl (3.4 mmol/L) and ended up the same at the end of the study.  The low-carb dieters began the study with average total cholesterol levels of 209 mg/dl (5.4 mmol/L) and ended the study a year later with average total cholesterol levels of 232 mg/dl (6.0 mmol/L).  Their average LDL levels started at 124 mg/dl (3.2 mmol/L) and ended up at 147 mg/dl (3.8 mmol/L).

The authors of this study bestow great significance on this fairly minor increase in LDL levels in those subjects on the low-carb diet.  In their summary of the results of this study, they list the many benefits of the low-carb diet, then end on an ominous note:

However, these potential benefits may be counteracted by the detrimental effects of an increase in LDL cholesterol, which should be monitored…

The abstract of the study echoes this warning.

However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored.

It was my impression that the tone of the authors was one of a little foreboding.  Kind of a ‘this looks too good to be true, and, hey, look at those LDL levels; it is too good to be true’ aura about it.  But is it too good to be true?  Is the rise in LDL seen in most low-carb diets the hidden stinger?  Is what all the lipophobes say true?  You know, the old ‘Well you may lose weight on those diets, but you’ll clog your arteries at the same time.’

It’s all hogwash, of course, but before we get to the heart of the explanation as to why, let me remind you that numerous studies have shown that whenever subjects go on low-carb diets, they end up increasing the size of their LDL particles.  Large, fluffy LDL particles are not only harmless, but may be protective.  If they are protective, what’s wrong with having a bit more of them?

At the same time, numerous studies have shown that low-fat diets usually decrease LDL levels, but do so while reducing the particle size.  Followers of such diets end up with lower levels of LDL made of smaller, denser, more atherogenic particles, which, in my mind, isn’t a good trade off.

The authors of our paper acknowledge this fact and cite some of this research, but they are still fixated – as are most lipophobes – on LDL levels.  They just can’t get their heads around the notion that there is more to cardiovascular risk and health than LDL-cholesterol.

Since these researchers placed so much emphasis on LDL levels in their interpretation of all the data from their study, I got to wondering how they measured LDL levels.  I looked in the Methods section of their paper and found the following:

Plasma glucose, C-reactive protein, serum lipids, and apolipoprotein B (apo B) were also measured by using standard methods (11).

The #11, of course, means that the description was in another paper that I had to go to the trouble of looking up.  I always find it annoying when authors do this when they could just as easily stick a short paragraph in their paper and save people who really want to read it critically a lot of trouble.

Tracking down the other paper in the Journal of the American College of Cardiology, I found the following:

The LDL-C was calculated according to the method described by Friedewald et al.

What this means is that the researchers did not measure LDL levels directly in their study subjects, but calculated them using the Friedewald equation.

For reasons we don’t need to go into here, LDL is fairly difficult (as compared to total cholesterol and HDL) to measure.  It can be done, but it’s expensive.  So instead of measuring it directly, most labs calculate it based on an equation derived by William Friedewald and others in 1972.

Friedewald realized that it was pretty simple to measure total cholesterol, HDL-cholesterol and triglycerides.  He knew that total cholesterol was the sum of all the various subfractions of cholesterol, which can be presented by the following equation:

Total cholesterol = HDL-cholesterol + LDL-cholesterol + VLDL-cholesterol

Rearranging this equation to solve for LDL gives us this one.

LDL = Total cholesterol – HLD – VLDL

Friedewald knew that it was easy to measure total cholesterol and HDL but difficult to measure the others.  His insight was that the triglyceride level if divided by five could give a close approximation of VLDL.  In running his experiments he also realized that this relationship held only if triglyceride levels were 400 mg/dl or under.  If they were over this, all bets were off.

So, Friedewald substituted triglycerides (TGL) divided by 5 for VLDL in the above equations, giving us the so-called Friedewald equation for calculating LDL.

LDL = Total cholesterol – HDL – TGL/5

And this is how it is still done in labs all over the world 27 years after Friedewald’s paper.   If you’ve had a lab report showing an LDL figure, I can guarantee it was calculated by the Freidewald equation and not measured directly.

What’s wrong with this if it works?  Nothing.  If it works.  Problem is, it doesn’t always work.  Friedewald himself found that in subjects with triglyceride levels greater than 400 mg/dl the equation didn’t hold.  Anyone reading this who has had a lipid test showing triglycerides greater than 400 will have note on their lab report saying that LDL couldn’t be calculated because triglycerides were too high.

I’ve always thought the same held true for triglycerides under 100 mg/dl, which would apply to almost everyone who sticks to a low-carb diet for any length of time.  Triglyceride levels of 40-90 mg/dl are not uncommon, and are, in fact, typical.  When Friedewald did his work, the triglyceride levels were mainly up in the 150 – 250 mg/dl range, and in this range his equations match pretty well to directly measured LDL levels, but all bets are off with triglycerides above 400 mg/dl and, I suspect, triglyceride levels below 100 mg/dl. MD and I did find this ourselves in a few patients that we did direct LDL measurements on in our practice.

A paper published a few years ago in a pathology journal corroborating what we found. (Full text here.)

This paper is basically a case presentation of a 63-year-old man with a total cholesterol level of 263 (all results in mg/dl), an HDL of 85, a triglyceride level of 42, and an LDL level of 170.  The LDL level was, of course, calculated using the Friedewald equation.

For some unexplained reason the authors of this paper decided to repeat the lab results and got the same readings.  They then wondered if his very low triglyceride readings might be having an effect, so they measured his LDL levels directly and found that instead of the 170 predicted by the Freidewald equation, his actual LDL levels were only 126.

More recently a paper appeared in – of all places – the Archives of Iranian Medicine showing the same phenomenon.  These authors tested 115 subjects with low triglyceride levels.  You can get the full text of the paper, but a line in the abstract says it all:

Statistical analysis showed that when triglyceride is <100 mg/dl, calculated low-density lipoprotein cholesterol [LDL] is significantly overestimated (average :12.17 mg/dL or 0.31 mmol/L), whereas when triglyceride is between 150 and 300 mg/dL no significant difference between calculated and measured low-density lipoprotein cholesterol is observed.

The authors of this paper derived their own equation to be used in lieu of the Friedewald equation when the triglyceride levels are below 100 mg/dl.  I suspect that if we were to apply this equation to the labs of the 33 subjects who finished the low-carb arm of the study we started out discussing in this post, whose average triglyceride levels were under 100, the LDL levels would have averaged much lower than the 147 mg/dl they were calculated to be by the Friedewald equation.  If you subtract the 12.17 mg/dl that the Iranian paper estimates as the difference from the average triglycleride levels (an admittedly extremely unscientific and non-statistically valid way to do it), you find that the average drops to 135 mg/dl, which I doubt is significantly different than the 131 average of the low-fat dieters. If you did it the right way – subject by subject and then average – I suspect it would be greater yet.

The moral of this story is that if you have been following a low-carb diet and your triglycerides are low (or if your triglycerides are just low) and your LDL reading comes out a little high – or even a lot high, don’t let anyone mule you into going on a statin or undergoing any therapy for an elevated LDL.  Demand to have a direct measurement of your LDL done.  Or if you get an insurance physical and your triglycerides are low and your LDL up a little, fight to get a direct measurement so they don’t stick you with higher premiums because they think you’ve got an increased risk for heart disease.

What we do know based on the work of many is that low-carb diets change LDL particles to the large, fluffy, harmless variety.  Thanks to these other papers we also know that the LDL levels so many people end up with on their lab reports after being on low-carb diets for a while are artificially high.

Now when you hear people say that low-carb diets may help you lose weight but run your LDL levels up and increase your risk for heart disease, you’ll know this is just so much gibberish.  Sadly, your doctor will probably spout the same thing, and it will be up to you – who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.

And if you are a researcher studying the effect of the low-carb diet on LDL, for crying out loud, hit your grant up for the extra few bucks it takes to get LDL cholesterol measured directly in your subjects so you won’t be in the embarassing position of having your data become worthless.

Echinacea for colds. Ginkgo biloba for memory. Glucosamine and chondroitin for arthritis. Black cohosh for menopausal hot flashes. Saw palmetto for prostate problems. Shark cartilage for cancer. All proved no better than dummy pills in big studies funded by the National Center for Complementary and Alternative Medicine. The lone exception: ginger capsules may help chemotherapy nausea.

Acupuncture and some of the hands-on manipulative therapies fared a little better.

As for therapies, acupuncture has been shown to help certain conditions, and yoga, massage, meditation and other relaxation methods may relieve symptoms like pain, anxiety and fatigue.

The article didn’t give a rundown of every alternative or non-mainstream therapy tested, so I don’t know what they all are, but I can add one to the list if it wasn’t tested in this $2.5B testorama.  I would add the use of HCG for weight loss.

Many practitioners are using injections of human chorionic gonadotropin (HCG) injections coupled with an extremely low-calorie diet to help their patients lose weight.  Many practitioners and many patients swear by this regimen.  But, a number of randomized, double-blind, placebo-controlled studies have shown that the HCG regimen is no better than placebo.

But if this is so, how come so many patients and practitioners believe so strongly in this HCG/diet combo?  Simple answer.  Because it works.

But if it works, why is it a worthless regimen?  Because it doesn’t work any better than placebo.

If you go to a doctor who tells you that he/she is going to start you on an extremely powerful weight-loss program that involves multiple injections along with a stringent diet composed of specific foods to be eaten on a rigid time schedule (especially if these foods add up to only 500 calories per day), you will come away convinced that you are going to do well.  Especially after you’ve paid the bill, which is considerable in these HCG centers.

If you go in for all the injections and scrupulously follow the diet, you will lose a fair amount of weight pretty quickly.  And you will develop and unshakable believe that this regimen did the trick for you.  You will tell your friends, all of whom have witnessed your rapid weight loss, and they, too, (at least those who can afford it) will go to the same practitioner and fork over for the treatment.

Problem is this treatment works the same if the patients are given a salt-water shot or an HCG shot.  There is no difference in outcome.  The HCG doesn’t do diddly.  It’s the fact that you get a shot that makes the difference.  If you simply went on the 500 calorie per day diet you would lose the same.  But it’s the magic of receiving the shot, especially after being told (as most are) at the practitioner’s office that the shot will help overcome the hunger of being on a drastically calorically-reduced diet.  And it does.  But it doesn’t matter if it’s a saline shot or a dose of HCG.  It’s the magic of having something done.

Which is why in the $2.5 billion tests, the manipulative therapies worked and the others didn’t.  There is something about having a procedure done that makes you feel like your getting a more powerful treatment.

I can’t tell you how many people came in to see me when I had a regular medical practice who demanded a shot because they were convinced that shots worked better than oral medications.  For some things they do, but for most, they don’t.  But you couldn’t convince most of my patients of that.

There are a few of what many would consider alternative medicines that do work.  I posted on one that does here.  But, as the large conglomeration of studies reported on by the AP showed, most don’t.

As you might imagine, the report of the failure of most alternative therapies was like catnip to mainstream physicians, researchers and writers.  They were absolutely giddy with joy.  Here are just a few representative comments:

Well, since I’ve been bagging on the alt-med nonsense lately, I simply couldn’t pass up this headline.  And folks… the headline says it all… “No Alternative Cures Found”… Zilch… Nada… Zip… Zero!  Despite their inability to understand the most basic aspects of science and the associated math, I think that zero is a number that even alt-med woo-meisters can grasp

(Woo is the derogatory term these mainstreamers have come up with for any treatment or therapy not taught in traditional medical schools or developed by Big Pharma.)

I never thought I’d see it, but I have. After an a decent article on the infiltration of quackademic medicine into American medical centers and a very good article on cancer quackery, Marilyn Marchione of the AP has done it again:

AP IMPACT: $2.5B spent, no alternative med cures…

I’ve documented the woo funded by NCCAM on multiple occasions. I mean, NCCAM is funding studies of that woo of woos, homeopathy, fer cryin’ out loud! I”m [sic] glad that the mainstream media is finally noticing.

One more.

Here’s a shocker for you: after a decade and 2.5 billion (with a b, folks) dollars spent, a government study shows that almost no alternative medicines worked.

So, they used actual scientific testing processes instead of anecdotes, and found that most of these simply don’t work. Like I said: shocker.

… the studies have shown that most of these remedies don’t work. And will this change the minds of their advocates?

HAHAHAHAHAHAhahahahahahaha! Oh man, sometimes I crack myself up.

This is just one more arrow in our quiver, but the alternative medicine believers will continue to move the targets around. Stay vigilant, and remember: people waste money, people get sick, and people die because of this antiscientific thinking. That’s why testing this, publicizing it, and fighting the misinformation is so important.

Believe me, this is just a small sampling of what I came across on the internet when I searched for links to the AP article.

Hostile and condescending as the tone of these remarks is, the people who made them are pretty much on the money.  These treatments need to be evaluated in the harsh glare of double-blind, placebo-controlled studies.   Now they have been, and, just as with the HCG regimen for weight loss, they’ve been found lacking.

But that’s not necessarily the end of the story.  We don’t know the details about these studies.  Was there just one study for each alternative therapy?  Or were there multiple studies, each of which demonstrated no effectiveness?  If just one, then the above criticisms may not be valid.

Absence of evidence is not necessarily evidence of absence.  Just because we can’t get a positive result in one study doesn’t mean there isn’t a positive result to be had.  Science is the continual testing of hypotheses until the evidence is overwhelming that the hypothesis is valid or it isn’t.  But even overwhelming evidence doesn’t always prove out in the long run.  Newton’s laws were held to be valid after centuries of testing, then Einstein came along.

What interests me so much about the glee with which these mainstreamers greet the failure of alternative medicine (at least the failure shown by $2.5B worth of research) is that the vast majority of these same folks believe in the notion that people are overweight because they eat too much and exercise too little, an idea that scientifically holds little water.  A myth, really.  But they all believe it because on the surface it seems to make sense to them.  All the scientifically valid arguments that, say, Gary Taubes makes fall on deaf ears.  (Here is a video of a recent lecture Gary gave to doctors at Dartmouth.  Do you think any of them were moved to give up their antiquated views by the science presented?  It’s highly doubtful.)

And while most of the people pooh poohing woo are doing so, they are out pushing statins for all their worth.  And statins – other than for a small group of people – have the same efficacy as the alternative medicines they are so quick to disparage.  Let’s see, how did that one writer put it?  “…Zilch… Nada… Zip… Zero!”

That’s right.  The category of drugs that are the top selling drugs worldwide have no efficacy in terms of reducing overall mortality, at least as shown by randomized, double-blind, placebo-controlled studies, in any group except men under the age of 65 who have been diagnosed with heart disease.  This doesn’t mean men under 65 who have elevated cholesterol, but men under 65 who have actually been diagnosed with heart disease or who have had a heart attack.  And even in that group, the efficacy is questionable.

The mainstreamers such as those quoted above don’t question the effectiveness of statins even though at least $2.5 billion has been spent to test them and found them lacking, but readily discount alternative medicines simply because they don’t fit with their belief system.  Based on the evidence at hand, I wouldn’t give people Echinacea, shark cartilage and all the rest because the studies show they don’t work better than placebo, but for all the same reasons, I wouldn’t give a patient a statin either.  In fact, I would probably give the Echinacea before I gave the statin because, as far as I know, no one has died taking Echinacea, of which the same can’t be said of statins.

If alternative medicines are going to be held to scientific standards, so should be pharmaceuticals.  Snake oil is snake oil no matter what its bottle it looks like.

In the fall of 1898 Sir William Crookes (right) gave his inaugural address as the incoming president of the British Academy of Sciences.   Unlike the typical such speech, this one was prophetic and alerted the British populace for the first time to a real and growing problem.  And the populace began to worry, because Sir William was the Al Gore of his day, alerting his country (and the world) to a looming danger.

Other than prophesying disaster, however, there were a few notable differences between Sir William and Al Gore.  First and foremost, Sir William was a true scientist, not a bloated former politician with no technical training.  He was the inventor of the predecessor of the tubes later used in televisions and radios and had discovered and added thallium to the periodic table.  The second major difference is that his worries were valid.  They weren’t concocted from a gibberish of people hoping to cash in on the public’s fears of an imaginary melting of the earth, but were born of a serious concern for the continued success of the human race.  Or at the very least, the continued success of the people of Great Britain.

Sir William Crookes was deeply (and rightfully) concerned that the world would soon run out of the ability to fertilize crops, and that, as a consequence, millions would die.  At that time Britain was importing guano (the droppings of sea birds) from islands off the coast of Peru and from the nitrate fields of Chile, but those sources were finite, and Sir William realized they would at some point run out.  (He predicted sometime in 1930 as doomsday.)

To those of us today who can go to our local hardware or garden store and grab all the fertilizer we can afford to pay for, this hand wringing seems a bit melodramatic, but at the time, it was of real concern to many scientists.  The world’s population was growing rapidly, and, like today, the vast majority of the world’s population depended upon grains – mainly wheat – for sustenance.  Most grains suck nitrogen from the soil to fuel their growth, and once that nitrogen is gone, it takes a long time to get back.  And until it does, most any crop grown in nitrogen-depleted soil fails to thrive, and yield per acre falls dramatically.

The fact that nitrogen is lacking in the soil seems strange since we all walk around breathing air that is about 80 percent nitrogen.  But the nitrogen in the air can’t get into the soil in a form plants can use unless it is ‘fixed.’  Which I guess isn’t so strange when you consider that we ourselves need nitrogen to grow and repair our tissues, but we can’t get it from the air we breathe either.  We have to get it from the protein in our diets.

Nitrogen-fixation process

Bacteria that live symbiotically with the roots of certain clovers and legumes (the so-called green manure) are able to fix nitrogen from the air and covert it to the form plants can use.  Over the years farmers had figured this out and planted clovers and legumes in fields for a year or two to replace the nitrogen and make the fields fit to grow cash crops.  Or they could use manure or compost – both traditional sources of nitrogen – to replace that needed for growth, but they needed a lot because these were not particularly rich in fixed nitrogen.  Consequently, crop rotation and spreading manure/compost wasn’t a particularly efficient way of keeping a profitable farming business growing.  A more rich and readily available source of nitrogen was needed.

When enormous deposits of guano -  about 10 stories high, extremely rich in nitrogen, and taking literally centuries to accumulate – were discovered off the coast of Peru, a bustling shipping business grew up hauling the stuff from there to Britain.  As those supplies started to dwindle, explorers found fields of nitrites in Chile that began to replace the guano.  But, as Sir William observed, those sources were finite as well, and would at some point be gone.  If nothing was done or no other sources discovered by time the Chilean fields ran out, then the world would be in real trouble.

Sir William pointed out that the populations of all the great wheat-eating peoples, the Brits, the United States and Europe mainly, would outstrip their grain of choice, resulting in the deaths of thousands and perhaps even millions.  He announced in the most racist of terms (common at the time) that if a solution of this problem weren’t discovered, and discovered fairly quickly, “the great Caucasian race will cease to be foremost in the world, and will be squeezed out of existence by races to which wheaten bread is not the staff of life.”

“It is through the laboratory,” he pontificated, “that starvation may ultimately be turned into plenty.”

I don’t know what the population at large thought about Crookes’ speech, but the scientific community took it seriously.  In Germany, a Jewish scientist named Fritz Haber, after years of work, developed a desktop working model of a machine that could convert the nitrogen from the air into ammonia, which is basically the form needed for both fertilizer and gun powder.  Other scientists thought Haber’s contraption was interesting but impractical in that the temperatures and pressures required couldn’t be produced with the technology available then in any kind of industrial-sized plant.  One non-naysayer was Carl Bosch, an engineer at BASF, the giant German chemical company.  Bosch thought he could make Haber’s machine work, and after intense effort he succeeded on a giant scale. Now Haber-Bosch machines use about one percent of the earth’s resources and provide the nitrogen that sustains around 40 percent of the earth’s population.  That’s the good news.  The bad news is that these machines allow us to live in a carb-dominant world, rich in wheat and corn. Had this technology never have been invented, who knows how the nutritional history of the world would have progressed.

The Alchemy of Air by Thomas Hager is the fascinating story of the development of the Haber-Bosch system as told through the lives of the main players.  The secrecy, the infighting, the suicides, the war-time intrigue – all provide high drama in this fascinating story.  What I found particularly interesting – not to mention germane for us today – was how Bosch, who could apparently do just about anything chemical engineering-wise, developed a method to make gasoline out of coal.  By the end of WWII, 35 percent of Germany’s gasoline and all of its gunpowder came from plants developed and built by Bosch.  Why aren’t we looking at this technology that’s already existent to help wean ourselves from foreign oil?

If a technical book is more your style, then grab a copy of Enriching the Earth by Vaclav Smil.  You will learn more about the science of ‘fixing’ nitrogen and less about the personal dramas of the main players on the stage.  I read both and found them complementary to one another.  If you read both, you will know just about everything there is to know about fertilizer and nitrogen. But if you just read one, make it The Alchemy of Air.

Below is a photograph of a Haber-Bosch plant operating in the United States today.

Fertilizer factory using the Haber-Bosch process

Let’s jump subjects and move into the world of fiction.  Mystery fiction, to be precise.  I’ve been doing a lot of traveling lately, and I catch up on my ever-growing stack of crime novels while on the airplane.  I enjoy all kinds of mystery fiction, but lately I’ve had a run of British police procedurals along with an Italian one and a few German ones thrown in the mix.

I just finished Peter Robinson’s All the Colors of Darkness, which I found so so.  I thought it a wee bit contrived, much more so than his previous books, which are good books to start with if you’re unfamiliar with the British police hierarchy.  The author was born and grew up in the UK, but has lived in Toronto for years. He writes with the knowledge that his readers won’t be up with all the British police jargon, so he goes easy on them.

Despite my ho hum feelings about this book, I did find a paragraph that caught my eye.  The paragraph describes a lazy, off-duty Saturday morning routine (which, after this setup, you know ain’t going to last long) followed by Detective Chief Inspector Alan Banks, the protagonist of the series:

Banks stopped at the newsagent’s and bought The Guardian, which he thought had the best Saturday review section, then headed to the Italian café for his espresso and a chocolate croissant.  Not the healthiest of breakfasts, perhaps, but delicious.  And it wasn’t as if he had a weight problem.  Cholesterol was another matter.  His doctor had already put him on a low dose of statin, and he had decided that that took care of the problem and allowed him to eat pretty much what he wanted.  After all, he only had to be careful what he ate if he wasn’t taking the pill, surely?

I suspect the author of this series takes a statin.  From his photos he doesn’t appear to be overweight.  I would be willing to bet that he, like his character, takes a low-dose statin (what with all the statinators around, who doesn’t these days?) and probably doesn’t watch what he eats because the statin makes him feel safe.  Bad mistake, probably, but one I’m sure more than a few who feel themselves invincible on statins make. (Who would’ve thought I could dredge an anti-statin blog out of a mystery novel?)

If you want to get started reading Peter Robinson, find a few of his earlier books.  Try Gallows View or Hanging Valley or Past Reason Hated.  Any of his books are a good introduction for the US reader into the intricacies of how the UK police works.

I read recently the second novel in Susan Hill’s mystery series, The Pure in Heart, which is a much different kind of book than the Peter Robinson books.  Susan Hill is a prolific writer of note who sticks mainly to contemporary fiction with the occasional ghost story thrown in.  The detective novel is a departure from her normal course of work, but she adds her own creative touch to the genre.  If you decide to read this book, read the one before it, The Various Haunts of Men, first or you will learn something in The Pure in Heart that will give away a big part of the plot in the previous book.  As I say, these aren’t your regular mysteries, but that’s what makes them nice.

If you want a mystery that’s a series you can get into and that is quick and fun to read, have a go at any of the novels by Andrea Camilleri about Sicilian police inspector Salvo Montalbano.  I’ve read most of these books and just finished the most recent one, August Heat.  With this series, you can start anywhere.  These novels will certainly show you the difference between the police systems in the UK and in Italy. I don’t know where I would rather be arrested, but I do know that I wouldn’t want to have been arrested in Germany in the 1930s.

If you really want to go back to pre and post WWII Germany, read the wonderful series of books by Philip Kerr about Berlin detective Bernie Gunther.  I am currently reading The Rise and Fall of the Third Reich (I always have a long, serious book going that I dip into read a little of daily. Right now I have two: The Rise and Fall and Dawin’s On the Origin of Species.), and Kerr’s novels describe pre WWII Germany to a tee.  If you want to see what life was like for Fritz Haber, Carl Bosch and others living in Germany as Hitler came to power, you’ll do no better than to read these novels.  The first three books in the series, referred to by aficionados as the Berlin Noir trilogy are March Violets, The Pale Criminal, and A German Requiem.  You can get all three now in one large paperback, but I would save it for last.  As far as I’m concerned, the best way to read these books is from last, to second to last, then the trilogy.  In other words, in opposite order in which they were written.  Start with the last book, A Quiet Flame, move on to the next-to-last one, The One From the Other, then finish with the trilogy.  You won’t be disappointed.

As I’m sure most of you know, I read a lot.  I’ll be happy to post from time to time about some of the books I enjoy if most everyone is game.  Let me know in the comments if you like these little book reviews.  And, please, feel free to recommend any of your own favorite books.

Thanks to ALLIED 2008 151 for the photo of the fertilizer plant

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.