Saturated fat and heart disease: studies old and new

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

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

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

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

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

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

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

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

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

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

Let’s look at a couple.

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

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

Here’s what they did:

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

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

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

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

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

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

What were the recommendations of the authors of the study?

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

Summary

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

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

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

Here is another.

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

The aims of the study were as follows:

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

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

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

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

The authors’ summary:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Gary Taubes continues

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

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

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

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

For maze at top
hat tip to
FAILblog.org

Are all diets the same?

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

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

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

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

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

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

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

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

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

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

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

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

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

Give me strength.

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

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

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

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

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

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

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

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

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

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

Here’s what the authors wrote:

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

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

…compliance was assessed with objective biomarkers.

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

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

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

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

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

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

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

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

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

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

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

Four patients who changed my life

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

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

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

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

Then I asked myself the big question:  If I have too much insulin (and 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 a huge bestseller, 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 preparing 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 Statinator Paradox

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

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

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

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

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

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

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

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

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

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

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

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

Recognized?  What does that mean?

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

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

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

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

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

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

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

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

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

But as for heart disease itself:

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

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

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

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

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

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

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

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

It was unbelievable.

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

Watch and just shake your head.

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.)

Statinators spill the beans

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

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

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

Let’s take a look.

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

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

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

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

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

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

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

NA images2

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

NA2

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Follow the money.

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

From heartwire (requires free registration):

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

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

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

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

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

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

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

Hard at work in Seattle

Mt St Helens blog

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

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

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

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

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

Seattle skyline blog

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

Boat in winter blog

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

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

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

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

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

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

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

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

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

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

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

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

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

Rebuttal to the PCRM

eades-whisky

In my ongoing quest to become a little more technically adept, I started using Google Alerts for a number of things I’m interested in, including my own name.  (Believe me, there are a lot of people out there in the world with the last name Eades, including the Fire Chief of London.)  For those of you who don’t know, you can go to the Google main page and navigate around until you come to ‘Alerts.’  You can then sign up for these ‘Alerts’ to be delivered to you via email.  It’s a free service provided by Google, and it uses the Google system to crawl through cyberspace and find anything (blogs, articles, news reports, etc.) that has whatever word, words or phrases you submitted included and emails the link back to you.  I put a bunch of stuff in and get emails from Google throughout the day.  Most of it is stuff that is totally unrelated to anything I give a flip about, but every now and then it turns up something of interest.  Having my name listed has cost me money because one of the first things I that came back to me was an article about Eades Whisky, which I had no idea existed and which I had to try.  It is expensive, about $75 per bottle, but I ordered some.  It’s very good.  But it hasn’t replaced Jameson, however, by a long shot.

Yesterday I got back a hit about something that I had totally forgotten about:  our rebuttal to the idiotic ‘study’ presented by the PCRM (Physician’s Committee for Responsible Medicine – a name straight out of Orwell if there ever was one) a few years ago.  This group, composed mainly of militant vegetarians, came up with an insipid ‘study’ during the height of the low-carb frenzy back in 2003.  Neal Barnard, the head of the outfit, appeared on most of the morning talk shows telling how dangerous his study had found low-carb diets to be.  A couple of the national networks called MD and me asking us if we would provide a rebuttal.  We happened to be in Santa Barbara at the time, and we said sure.  Two different networks sent camera crews to interview us late in the afternoon.

As I’ve probably mentioned numerous times, we have an absolute knack for getting pre-empted whenever we get TV time.  This day was no exception.  The news teams were on their way to the little condo we had at the time to set up and shoot our rebuttal when the news came through that Michael Jackson was going to be flying in to the Santa Barbara airport to turn himself in on the child molestation charge that he later beat in court.  Of course, all the news vans and camera crews that were heading for our place were diverted to the Santa Barbara airport, and MD and I never got to rebut the PCRM idiocy on air.

A couple of days later, we flew back to our place in Santa Fe, New Mexico, and as I was walking through the door laden with suitcases the phone was ringing.  It was the guy who ran LowCarbiz.com, the now-defunct online low-carb magazine, calling me asking if we would write a rebuttal that he could publish.  I said sure, and he said he needed it fast.  I left all the unloading to MD and sat down at my computer and pounded the thing out in a couple of hours.  He published it online.  Then a year or so later the low-carb mania died off, and the magazine went down, and I figured all was lost to history.

But, thanks to Google Alerts, I got a ping that someone had dug this thing out and posted it on a forum.

The only link I could find to the original PCRM report was a May 2004 update that pretty much matches the original, which I have a hard copy of to compare.  You can see how scientifically valid this ‘study’ is and how worthy it is of a press release and multiple TV appearances by looking at the methods section of the ‘study’ to see how the subjects were found.

Methods

In the fall of 2002, the Physicians Committee for Responsible Medicine (PCRM) began a pilot program to test the feasibility of an online registry to identify people who may have suffered health complications related to high-protein, low-carbohydrate diets. A modest Internet advertising campaign was used to notify consumers about the availability of this registry. In November of 2003, PCRM held a news conference to highlight the health problems suffered by some individuals using these diets and to draw attention to the registry.

To report problems with high-protein, high-fat, carbohydrate-restricted diets, individuals voluntarily visited www.AtkinsDietAlert.org and filled out a form available on the site. The registry specifically inquires about the following problems: heart attack, other heart problems, high cholesterol, diabetes, gout, gallbladder, colorectal cancer, other cancers, osteoporosis, reduced kidney function, kidney stones, constipation, difficulty concentrating, bad breath, and loss of energy. In addition, many registrants indicated, in an “other problems” box on the registry, that they had experienced certain other problems while on low-carbohydrate diets. Many registrants reported more than one health concern. Through the online form, most registrants provided their contact information, age, sex, previous health concerns, length of time on the diet, reasons for choosing the diet, and other information.

The registration entries were self-reports and were not subject to verification through medical record reviews or other methods, nor was registration deemed to indicate a cause-and-effect relationship. To help clarify the possible biological mechanisms by which a high-protein, high-fat, carbohydrate-restricted diet might lead to these problems, PCRM dietitians conducted a nutrient analysis of the sample menus for the three stages of the Atkins Diet as described in Dr. Atkins’ New Diet Revolution (M. Evans & Co., 1999; pp. 257–259), using Nutritionist V, Version 2.0, for Windows 98 (First DataBank Inc., Hearst Corporation, San Bruno, Calif.).

Tells you everything you need to know about the scientific standards of PCRM.  At the time CBS, one of the network stations that had Barnard on that morning, actually stated that the ‘study’ wasn’t scientifically valid:

The online survey is not a scientific study, so there are no hard facts to say definitively that the Atkins diet is harmful. But the PCRM says there is enough evidence for concern.

But the lack of scientific validity never stops the PCRM’s Barnard from jumping in front of the camera presenting it as such.  Make sure to watch the video to observe the holier-than-thou demeanor.

What follows is our rebuttal to this nonsense.

In The Name of ‘Responsible Medicine’ The Public is Ill-Served
A LowCarbiz Rebuttal to The Physicians Committee for Responsible Medicine Report on Health Concerns Pertaining To Low-Carbohydrate Diets
By Dr. Michael R. Eades and Dr. Mary Dan Eades
© 2003 LowCarbiz/Michael R. Eades, M.D. and Mary Dan Eades, M.D.

Ten Rebuttal Points:
• PCRM uses what is at best anecdotal information and presents it in the guise of a scientific investigation.
• At least a dozen studies have been conducted recently in major medical and scientific research institutions and published in top-notch journals that confirm the lowcarbohydrate diet is superior to the low-fat diet in multiple respects.
• The respondents to the PCRM poll would represent only 0.00001125% or one onethousandth of one percent of individuals following a low-carbohydrate diet.
• Researchers from Harvard recently reported that subjects could eat 300 calories more per day on a low-carbohydrate diet than those following a low-fat diet and still lose the same amount of weight over a 12-week period.
• Dieters would prefer to lose fat rather than lean tissue, which is precisely what happens with low-carbohydrate diets.
• Virtually every study done on low-carbohydrate diets shows that weight loss is accompanied by either an improvement or no change in heart disease risk factors.
• Low carb dieters who consume green leafy and colorful vegetables and low-glycemic fruits are not at risk of osteoporosis (long-term bone loss).
• The whole idea that protein in the amounts eaten in modified low-carbohydrate diets damages kidneys is a vampire myth that refuses to die no matter how many stakes have been driven through its heart by a multitude of medical studies.
• Overall there is no evidence that meat causes colon cancer, or any other cancer, for that matter. Actually many cancer-fighting nutrients are in meat and a reduction in meat intake might be more likely to increase cancer risk.
• As the data continues to accumulate and the studies increase in number, the efficacy of the modified low-carbohydrate diet will finally be established to the satisfaction of all.

On November 20th, the Physicians Committee for Responsible Medicine (PCRM) released a report entitled Analysis of Health Problems Associated with High-Protein, High-Fat, Carbohydrate-Restricted Diets Reported via an Online Registry. The report, which dresses, speaks and behaves like something that might appear in a bona fide medical journal, examines a host of health problems consumers have suffered allegedly as a result of their following a high-protein diet.

We find this report interesting on a number of fronts, not the least of which is in the way PCRM uses what is at best anecdotal information and presents it in the guise of a scientific investigation.

Over the past twenty years when we and other physicians who use low-carbohydrate diets to help our patients lose weight, normalize blood lipids, stabilize blood sugars, reduce their high blood pressure and generally improve their health reported our clinical experience with thousands of such patients we have often been greeted by groups such as PCRM – which view science through a vegetarian or low-fat lens — with cries of “Anecdotal! It’s only anecdotal evidence. If your low-carbohydrate regimen is so good, where are the clinical studies?”

In the last couple of years, however, at least a dozen studies have been conducted in major medical and scientific research institutions throughout the world and published in top-notch medical and scientific journals that confirm what we and others have been saying for years—the low-carbohydrate diet is superior to the low-fat diet not only for weight-loss but for improvement of virtually all of the components of the metabolic syndrome as well.

It is a delicious twist of fate that the tables have turned on PCRM and the group’s fellow travelers who, now, faced with this ever-growing body of credible scientific literature must themselves resort to the worst kind of anecdotal reporting: using a group of respondents to the PCRM website—and an extremely small group, at that—to imply that low-carbohydrate diets are a hazard to the entire population of dieters who follow them.

PCRM reports that “in the fall of 2002, [PCRM] began a pilot program testing the feasibility of an online registry for identifying people who may have suffered health complications related to high-protein, low-carbohydrate diets.” After one year of a “modest internet advertising campaign” by PCRM to “notify consumers of the availability of this registry” a total of “188 individuals reported experiencing problems with high-protein, high-fat, carbohydrate-restricted diets.”

At whom was this “modest internet advertising campaign” directed? How is the PCRM online registry found? The PCRM report doesn’t say, but one supposes the campaign was directed to and the registry found by people who have a predisposition to the PCRM philosophy. So it is reasonable to assume that people finding the PCRM online registry would have an axe to grind with the low-carbohydrate, non-vegetarian diet and lifestyle and would be more prone to report problems.

Even if we make the unlikely assumption that these respondents are all enthusiastic followers of low-carbohydrate lifestyles who have run afoul of their diets, the PCRM numbers are so tiny as to not even approach significance: 188 respondents in one year. The most recent and credible survey we’ve read estimates that there are somewhere in the neighborhood of 32 million people following some version of a low-carbohydrate diet in the United States alone (the PCRM report doesn’t say whether the respondents to their registry were from America only or from throughout the world). Even if that 32 million number is halved, it would mean that the respondents to the PCRM poll would represent only .00001125% or one one-thousandth of one percent of these people following a low-carbohydrate diet, a number easy to not get too excited about. (One wonders what kind of numbers PCRM would have garnered had they put out the request for positive experiences on a low-carbohydrate diet.)

When we look at the problems that the majority of this one one-thousandth of a percent of people report we find that the majority of them suffer from constipation (44%), loss of energy (42%), and bad breath (40%). Not exactly the kind of serious medical problems calling for “the urgent need for monitoring” nor the proposal that our “public health authorities begin tracking the use of high-protein, high-fat, carbohydrate-restricted diets used for weight loss or maintenance and record adverse events” as the PCRM report recommends.

PCRM applied its anecdotal analysis to “health problems associated with high-protein, high-fat, low-fiber, carbohydrate-restricted diets” without really specifically defining the macronutrient composition of these diets. One of the problems in the medical literature is that there is no definition of a “high-protein” diet or a “carbohydrate-restricted” diet. Many studies refer to a diet composed of 40% carbohydrate as a low-carbohydrate diet, which it is when compared to one containing 55-60% of its energy as carbohydrates, but this really isn’t a low-carbohydrate diet as used by the vast majority of followers of low-carbohydrate diet plans.

Other papers report data on diets containing 5-10% of calories as carbohydrate and call them low-carbohydrate diets, which they certainly are, but not the same low-carbohydrate diet as those containing 40% carbohydrate. Another complicating factor is that most researchers use percentages of macronutrient composition to define their study diets whereas we and others who prescribe low-carbohydrate diets along with virtually everyone who follows some form of a lowcarbohydrate diet use absolute grams of usable carbohydrate to set the parameters of the regimen. Anyone following a low-carbohydrate diet knows how precisely many grams of carbohydrate per day he or she is taking in but doesn’t have a clue as to what percentage of caloric energy that represents. Another problem is that these diets are referred to in a number of ways—high protein diets, low-carbohydrate diets, high-fat diets, carbohydrate-restricted diets, etc. Although these terms are used interchangeably they really aren’t. A low-carbohydrate diet doesn’t have to be a high-protein diet; a high-fat diet isn’t necessarily a low-carbohydrate diet; and, nor is a high-protein diet necessarily a high-fat diet. In order to bring clarity to this dietary debate, a definition of just what a low-carb diet is needs to be established.

PCRM and other groups and individuals who are anti-low-carbohydrate diet typically define the low-carbohydrate diet as the Atkins Diet, which in its original form was an extremely low, almost no carbohydrate, very high-fat diet that bears little resemblance to the low-carbohydrate diets recommended by us and others (including the current Atkins plan). Most people on lowcarbohydrate diets focus on limiting their intake of carbohydrates to 30-70 grams per day and let the fat and protein content of their diet fall wherever it may within this carbohydrate restriction.

Compared to the standard American diet, most people following a low-carb diet end up consuming significantly fewer carbohydrates, about the same or marginally higher amounts of protein and fat, and a smaller number of total calories.  (There is little question that the reduction in calories drives the weight-loss engine of the low-carbohydrate diet, a point seized on by PCRM and others as somehow being a slight to the lowcarbohydrate diet. More about this later.)

The vast majority of medical studies published within the past few years have used this modified low-carbohydrate diet as the basis for comparison. Unfortunately, although this modified diet is substantially different from the original Atkins Diet, PCRM and others along with help from the media persist in referring to it as the Atkins Diet. An example: a recent research paper in the New England Journal of Medicine describing the effectiveness of our specific version of the lowcarbohydrate diet, which is substantially different from the Atkins Diet, in reducing weight and improving health was hailed by the media as the “vindication of the Atkins Diet.” Before we move into what the research data shows about the effectiveness of the modified lowcarbohydrate diet, let’s take a look at just how surreal this entire debate has become.

The PCRM report states that “high-protein, high-fat, low-fiber, carbohydrate restricted diets, such as the Atkins Diet, when used for prolonged periods, are expected to increase the risk of multiple chronic diseases and other health problems.” One would assume that according to PCRM that the low-carbohydrate diet would be worse than the standard American diet, but if we look closely is their assumption valid?

A typical American lunch, one eaten by hundreds of thousands, if not millions, of people in this country every day is a hamburger, fries, and a soft drink. To modify this basic lunch to fit the low-carbohydrate regimen dieters would remove the bun from the burger, avoid the fries and have a salad instead, and drink water or some other non-caloric beverage. In the eyes of the PCRM these simple modifications have converted this typical American lunch into a “dangerous” high-protein diet destined to ruin the kidneys, destroy the bones, and permanently damage the hearts of anyone who follows it. In making these modifications, however, lowcarbohydrate dieters get rid of the trans fats and refined carbohydrates in the bun, miss out on the large amount of fat (including trans fat) and high-glycemic carbohydrates in the fries, pass up the quarter of a cup of high-fructose corn syrup in the soft drink, and get a fair amount of carotenoids, flavinoids, lycopenes, fiber, and other anti-oxidants and phytonutrients in the salad. And, significantly reduce the caloric content of the lunch. You will note that the protein content remained unchanged. One would think that the PCRM would applaud these modifications, but instead they decry them. Surreal indeed!

Weight Loss

The caloric restriction that is a by-product of carbohydrate restriction accounts for the majority of the weight loss found with low-carbohydrate diets. Most, but not all. A recent review of lowcarbohydrate diets in the Journal of the American Medical Association stated that virtually all of the weight loss brought about by these diets came as a result of caloric restriction and when compared with low-fat diets there was no difference in efficacy as long as the two diets were equal in calories. A careful review of the individual studies comparing low-fat to low-carbohydrate diets almost always shows that over the course of the diets the people on the low-carbohydrate diets consume slightly more calories than those on the low-fat diet. A couple of recent studies showed a more pronounced and significant difference in the weight loss verses caloric intake between the two diets. One study done at the University of Cincinnati demonstrated greater weight loss in a group of women following a low-carbohydrate diet containing slightly more calories than a low-fat diet. Researchers from Harvard recently reported that subjects could eat 300 calories more per day on a low-carbohydrate diet than those following a low-fat diet and still lose the same amount of weight over a 12-week period. Where does this extra weight loss come from? It is known that dietary fat increases the production of mitochondrial uncoupling proteins, and there is some evidence that carbohydrate restriction might increase the proton leak across the mitochondrial membrane. Either or both of these actions would increase the loss of energy without reducing the caloric intake, but both these mechanisms as well as other theories need more study for clarification.

Clearly, low-carbohydrate diets give more weight loss bang for the calorie buck, but even if they didn’t, even if the weight loss were the same with low-fat and low-carbohydrate diets of equal caloric content, the low-carbohydrate diet would still be the diet of choice for other reasons. As everyone who has ever dieted knows, it’s not just the amount of weight that is lost that is important, but where this weight loss comes from. Everyone would agree that dieters would prefer to lose fat rather than lean tissue, which is precisely what happens with low-carbohydrate diets. Studies done at the University of Illinois, the University of Connecticut and other research institutions have shown that subjects following a low-carbohydrate diet lose more fat and less lean body tissue than those subjects following a calorically equivalent low-fat diet. In fact, in some cases, subjects on low-carbohydrate diets even gain lean body mass while losing fat on lowcarbohydrate diets, a finding virtually never observed in subjects following low-fat diets.

Cardiovascular Disease

It would seem a bad bargain to trade weight loss for a substantially increased risk for heart disease, which is the case that the PCRM makes in its report. While conceding that lowcarbohydrate diets are effective for bringing about weight loss, the PCRM cautions that these diets are “associated with increased risk of…heart disease.” A strange statement since the very studies the PCRM references as showing that the low-carbohydrate diets “facilitate modest short term weight loss” also demonstrate that low-carbohydrate diets improve lipid profiles and enhance insulin sensitivity in their followers, both changes that are known to substantially reduce the risk for heart disease. Virtually every study done on low-carbohydrate diets shows that weight loss is accompanied by either an improvement or no change in heart disease risk factors.

Few, if any, studies of low-carbohydrate diets show a worsening of heart disease risk factors. Most authorities agree that excess body fat is a risk factor for heart disease; so even the studies that show no improvement in other risk factors in subjects on low-carbohydrate diets actually do demonstrate a lowered cardiovascular disease risk implicit in the weight loss they bring about.

Osteoporosis

PCRM is on a little more solid footing when it claims that the Atkins Diet can cause bone loss, but PCRM misses the point entirely when considering the modified low-carbohydrate diet we and others recommend and that most people now follow. Studies going back almost a century describe the bone loss that can occur in people following a predominately meat diet. A diet high in meat alone creates a mild metabolic acidosis in the human body. This metabolic acidosis or excess acid created by the metabolism of meat has to be buffered or neutralized, which the body does by leaching calcium from the body’s storehouse of calcium, the bones. On a day-to-day basis the amount of calcium lost from the bones in this way is insignificant, but over a decades-long period of time can result in osteoporosis. Meat, however, is not the only food that produces such a response. Along with meat, the other two main offenders are grains and cheeses, especially hard cheeses. That’s correct: eating grains causes a metabolic acidosis just as meat does. When you consider the cheeseburger, a staple of the American diet, it’s easy to see why osteoporosis abounds. So, the PCRM correctly points out that the Atkins Diet, which in its original version recommended primarily meat and cheese, could cause osteoporosis if followed for the long term. But what about the modified low-carbohydrate diet? Does it do the same? Most plant foods, other than grains, bring about the opposite metabolic situation; whereas meat consumption causes a metabolic acidosis, green leafy and colorful vegetables and low-glycemic fruits bring about a metabolic alkalosis. The reduction in acid-producing grain consumption along with the alkaline response of the very plant foods recommended on the modified version of the low-carbohydrate diet offsets and neutralizes the acidity from the meat so that there is no net metabolic acidosis and no long term bone loss.

Impaired Renal Function

Fear of kidney damage has long been the bugaboo of people following low-carbohydrate diets. It’s doubtful that anyone pursuing a low-carbohydrate diet for any length of time hasn’t been told at least once that his or her kidneys are in danger. Here again the PCRM doesn’t disappoint; the group is right there leading the chorus. And PCRM doesn’t beat around the bush: “Highprotein diets are associated with reduced kidney function,” so says its report. No equivocation there. But once again PCRM has missed the boat. If we are to believe PCRM, we had better leave the buns on our burgers and eat every fry in the box to protect our kidneys. Studies from around the world have shown that the amount of protein contained in the modified version of the low-carbohydrate diet does not harm the kidneys. Even studies in patients with diabetic kidney disease show they will harm their kidneys more by increasing their carbohydrate intake and running up their blood sugars than they do by increasing their protein intake. In the late 1980s a group did an extensive study in Israel comparing the kidney function of people of all ages who ate a high meat diet with the kidney function of those on a vegetarian diet. The study showed that although both groups suffered a slight reduction in kidney function with age (it’s a sad fact of life—as we age function of just about everything including the kidneys decreases) the degree of loss of function was indistinguishable between the groups. Another recent study of kidney disease in diabetics performed at the University of California in San Francisco demonstrated that caloric reduction was a more potent force in protecting damaged kidneys than restriction of dietary protein. In fact, this study used a low-carbohydrate diet to restrict the calories. The whole idea that protein in the amounts eaten in modified low-carbohydrate diets damages kidneys is a vampire myth that refuses to die no matter how many stakes have been driven through its heart by a multitude of medical studies.

One last point on this subject, an admittedly anecdotal one, but illustrative. The one group of people who eat more protein than any other single group is serious body builders. These people eat anywhere from three times to eight times the amount of protein recommended in any lowcarb diet, and do so for long periods of time. What does this do to their kidneys? It must not do much because it’s never been reported in the medical literature. If the PCRM were correct about protein damaging kidneys there would be lines of body builders queuing up outside of dialysis centers all over the world.

Colorectal Cancer

The idea that meat intake definitively causes colon cancer is another vampire myth that refuses to die. Studies have indeed shown that increased intake of meat might cause colon cancer, but so have an equivalent number of studies shown that refined carbohydrates might cause colon cancer. The studies that the PCRM mustered for its report of course show an increased risk, otherwise PCRM wouldn’t have mustered them. When a situation exists where there are dueling studies it’s always prudent to look at a meta-analysis, which is a study of all the studies. Dr. Michael Hill, a British epidemiologist, performed and published such an analysis. He reported that overall there is no evidence that meat causes colon cancer, or any other cancer, for that matter, and stated that since many cancer-fighting nutrients are in meat, a reduction in meat intake might be more likely to increase cancer risk than reduce it.

By a curious coincidence the day the PCRM chose to release it’s report bashing low-carbohydrate diets was the same day pop star Michael Jackson surrendered to authorities in Santa Barbara County. Upon his release after posting bail the singer was reported by his attorney to have said: “Lies run sprints, but the truth runs marathons.” It remains to be seen how this aphorism applies to Mr. Jackson himself, but there is little doubt that the endurance of the modified lowcarbohydrate diet makes it the major contender for victory in the dietary marathon. As the data continues to accumulate and the studies increase in number, the efficacy of the modified lowcarbohydrate diet will finally be established to the satisfaction of all.

Until then, however, the PCRM and other such groups with a political agenda will continue their feeble attacks on a diet that has helped millions. The weakness of PCRM’s data even it admits publicly. Buried near the end of the PCRM report under the heading “Limitations,” PCRM writes: “The key limitation of this report is that adverse health effects were self-reported and are not likely to have the same prevalence in the general population. Data collection was Web-based and no attempt was made to assure a representative sample.” And yet the PCRM finds these data of a magnitude to require the “urgent need for monitoring” by our “public health authorities.” The PCRM report and the disproportionate amount media attention it garnered are merely a sprint.©2003 LowCarbiz/Michael R. Eades, M.D. and Mary Dan Eades, M.D.

What I find particularly enjoyable about this whole fiasco is that if you Google it, you find our rebuttal much more often than the PCRM idiocy that started it in the first place.  I guess it’s only fitting that it turned out to be a sprint indeed.

Hat tip to Google Alerts and to Cooking TLC