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

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.

The Vegetarian Myth

Before I get into a discussion of the absolutely phenomenal book you see pictured at the right, I’ve got a few disclosures to make.  First, I’m not much of a believer in the notion of man-made global warming or climate change (as they now call it since temperatures have been constantly falling instead of rising).  I’m a denier, in the pejorative term used by those who are believers.

Second, I’m not particularly pro-feminist.  And I certainly don’t hang around with any self-proclaimed radical feminists.  I have a wife who is smarter than I am, who is more talented than I am, and who, pound for pound, is probably a better athlete than I am, and I’m not bad. (In my defense, I can read much, much faster than she, but, she has better comprehension.) I long ago gave up the idea (if I ever really considered it seriously) that men are superior to women in any ways other than brute strength.  Having said that, however, I do believe that men are better suited to certain endeavors than woman and vice verse, but that doesn’t mean either men or women should be denied the opportunity to give whatever it is they want to do a whirl just because of their sex.  I guess I consider myself an egalitarian.  But from what I’ve seen of radical feminists, I’m not sure that I would count myself a big fan.

Given the above, you wouldn’t think I would enjoy and recommend a book written by a self-proclaimed radical feminist who is obviously a believer in global warming and the impending end of the earth as we know it.  I wouldn’t think so, either. Not my cup of tea even when it is sort of preaching to the choir.

But I can tell you that Lierre Keith’s book is beyond fantastic.  It is easily the best book I’ve read since Mistakes Were Made, maybe even better.  Everyone should read this book, vegetarian and non-vegetarian alike.  If you’re a radical feminist, you should read this book; if you’re a male chauvinist, you should read this book; if you have children, especially female children, you should read this book; if you are a young woman (or man) you should read this book; if you love animals, you should read this book; if you hate vegetarians, you should read this book; if you are contemplating the vegetarian way of life, you should definitely read this book; if you have a vegetarian friend or family member, you should this book and so should your friend.  As MD said after she read it, “everyone who eats should read this book.”

Anyone who has ever read a book on writing has come across the hackneyed piece of advice to cut open a vein and bleed on the page.  Lierre Keith, the author of this book, has come closer to literally doing that than almost any writer I’ve ever read.  Not only does her passion for her subject bleed through in almost every sentence, she is a superb lyrical prose stylist.  My book is dog eared, underlined and annotated from front to back – I can’t remember anything I’ve read that has contained so many terrific lines.

In fact The Vegetarian Myth is filled with so many good quotes (most by the author but some from other authors) that I was reminded of the old joke about the redneck who went to see a performance of Hamlet.  When the show let out, someone asked him what he thought of it.  Replied he:  It wasn’t nothin’ but a whole bunch of quotes all strung together.  As you’ll see when I ‘quote’ them below, The Vegetarian Myth contains quotable lines and paragraphs at about the same rate Hamlet does.

Ms. Keith was a practicing vegetarian (vegan) for twenty years, driven by her passion for kindness and justice for all creatures.  She couldn’t bear the thought of even killing a garden slug, or, for that matter, even removing a garden slug from her garden to a place where something or someone else might kill it.  Her years of compassionate avoidance of any foods of animal origin cost her her health.  Her story of coming to grips with the realization that whatever she ate came as a consequence of some living being’s having to die form the matrix onto which her narrative hangs.

You can read the first 14 manuscript pages of the book on the author’s website.  I have quoted from these 14 pages liberally below.

The introduction to The Vegetarian Myth explores Ms. Keith’s rationale for writing such a book, a book that, given her years of walking the vegetarian walk, must have been incredibly difficult to write.  She says as much with her first sentence.

She ponders the idea of factory farming, which she loathes, and the misbegotten idea that most people hold (not most readers of this blog, but most of the people in the world) that grains are good, not only for people, but for many animals as well.  And the common misconception that agriculture, the growing of annual grains and plants, is a wonderful, kind, sustainable activity.

This misunderstanding is born of ignorance, an ignorance that runs the length and breadth of the vegetarian myth, through the nature of agriculture and ending in the nature of life. We are urban industrialists, and we don’t know the origins of our food. This includes vegetarians, despite their claims to the truth. It included me, too, for twenty years. Anyone who ate meat was in denial; only I had faced the facts. Certainly, most people who consume factory-farmed meat have never asked what died and how it died. But frankly, neither have most vegetarians.

The truth is that agriculture is the most destructive thing humans have done to the planet, and more of the same won’t save us. The truth is that agriculture requires the wholesale destruction of entire ecosystems. The truth is also that life isn’t possible without death, that no matter what you eat, someone has to die to feed you.

I want a full accounting, an accounting that goes way beyond what’s dead on your plate. I’m asking about everything that died in the process, everything that was killed to get that food onto your plate. That’s the more radical question, and it’s the only question that will produce the truth. How many rivers were dammed and drained, how many prairies plowed and forests pulled down, how much topsoil turned to dust and blown into ghosts? I want to know about all the species—not just the individuals, but the entire species—the chinook, the bison, the grasshopper sparrows, the grey wolves. And I want more than just the number of dead and gone. I want them back.

After she had seen the error of her ways as a vegan and had been eating meat for two years, for reasons unknown to her, the author continued to surf the same vegan websites and message boards she had for years.  Until she read one post that was so bizarre that she finally realized the large intellectual gap that had widened between her rationale thinking and the cult like thinking of, well, a cult.  It would be funny if it weren’t so pathetic.

But one post marked a turning point. A vegan flushed out his idea to keep animals from being killed—not by humans, but by other animals. Someone should build a fence down the middle of the Serengeti, and divide the predators from the prey. Killing is wrong and no animals should ever have to die, so the big cats and wild canines would go on one side, while the wildebeests and zebras would live on the other. He knew the carnivores would be okay because they didn’t need to be carnivores. That was a lie the meat industry told. He’d seen his dog eat grass: therefore, dogs could live on grass.

No one objected. In fact, others chimed in. My cat eats grass, too, one woman added, all enthusiasm. So does mine! someone else posted. Everyone agreed that fencing was the solution to animal death.

Note well that the site for this liberatory project was Africa. No one mentioned the North American prairie, where carnivores and ruminants alike have been extirpated for the  annual grains that vegetarians embrace. But I’ll return to that in Chapter 3.

I knew enough to know that this was insane. But no one else on the message board could see anything wrong with the scheme. So, on the theory that many readers lack the knowledge to judge this plan, I’m going to walk you through this.

Carnivores cannot survive on cellulose. They may on occasion eat grass, but they use it medicinally, usually as a purgative to clear their digestive tracts of parasites. Ruminants, on the other hand, have evolved to eat grass. They have a rumen (hence, ruminant), the first in a series of multiple stomachs that acts as a fermentative vat. What’s actually happening inside a cow or a zebra is that bacteria eat the grass, and the animals eat the bacteria.

Lions and hyenas and humans don’t have a ruminant’s digestive system. Literally from our teeth to our rectums we are designed for meat. We have no mechanism to digest cellulose.

So on the carnivore side of the fence, starvation will take every animal. Some will last longer than others, and those some will end their days as cannibals. The scavengers will have a Fat Tuesday party, but when the bones are picked clean, they’ll starve as well. The graveyard won’t end there. Without grazers to eat the grass, the land will eventually turn to desert.

Why? Because without grazers to literally level the playing field, the perennial plants mature, and shade out the basal growth point at the plant’s base. In a brittle environment like the Serengeti, decay is mostly physical (weathering) and chemical (oxidative), not bacterial and biological as in a moist environment. In fact, the ruminants take over most of the biological functions of soil by digesting the cellulose and returning the nutrients, once again available, in the form of urine and feces.

But without ruminants, the plant matter will pile up, reducing growth, and begin killing the plants. The bare earth is now exposed to wind, sun, and rain, the minerals leech away, and the soil structure is destroyed. In our attempt to save animals, we’ve killed everything.

On the ruminant side of the fence, the wildebeests and friends will reproduce as effectively as ever. But without the check of predators, there will quickly be more grazers than grass. The animals will outstrip their food source, eat the plants down to the ground, and then starve to death, leaving behind a seriously degraded landscape.

The lesson here is obvious, though it is profound enough to inspire a religion: we need to be eaten as much as we need to eat. The grazers need their daily cellulose, but the grass also needs the animals. It needs the manure, with its nitrogen, minerals, and bacteria; it needs the mechanical check of grazing activity; and it needs the resources stored in animal bodies and freed up by degraders when animals die.

The grass and the grazers need each other as much as predators and prey. These are not one-way relationships, not arrangements of dominance and subordination. We aren’t exploiting each other by eating. We are only taking turns.

That was my last visit to the vegan message boards. I realized then that people so deeply ignorant of the nature of life, with its mineral cycle and carbon trade, its balance points around an ancient circle of producers, consumers, and degraders, weren’t going to be able to guide me or, indeed, make any useful decisions about sustainable human culture. By turning from adult knowledge, the knowledge that death is embedded in every creature’s sustenance, from bacteria to grizzly bears, they would never be able to feed the emotional and spiritual hunger that ached in me from accepting that knowledge. Maybe in the end this book is an attempt to soothe that ache myself.

How anyone who can read these 14 pages and not purchase and read this book is beyond me.

After the introduction which deals with why the author wrote the book, The Vegetarian Myth is divided into four sections: Moral Vegetarians, Political Vegetarians, Nutritional Vegetarians, and To Save the World.

The first three of these sections are the author’s in-depth refutations of the moral, political and nutritional arguments that vegetarians are constantly putting forth.  She does a masterful job.

In the Moral Vegetarians chapter, the author addresses the moral issue of killing animals for our own food.  She beautifully makes her case by cutting to the heart of the matter:

What separates me from vegetarians isn’t ethics or commitment.  It’s information.

And while she was in her 20-year trek in the vegetarian wilderness, she shielded herself from information as most cultists do:

I was on the side of righteousness, and like any fundamentalist, I could only stay there by avoiding information.

She finally realized the truth about agriculture; she figured out that the amber waves of grain are as death dealing as any slaughterhouse.

And agriculture isn’t quite a war because the forests and wetlands and prairies, the rain, the soil, the air, can’t fight back.  Agriculture is really more like ethnic cleansing, wiping out the indigenous dwellers so the invaders can take the land.  It’s biotic cleansing, biocide. … It is not non-violent.  It is not sustainable.  And every bite of food is laden with death.

There is no place left for the buffalo to roam.  There’s only corn, wheat, and soy.  About the only animals that escaped the biotic cleansing of the agriculturalists are small animals like mice and rabbits, and billions of them are killed by the harvesting equipment every year.  Unless you’re out there with a scythe, don’t forget to add them to the death toll of your vegetarian meal.  They count, and they died for your dinner…

Soil, species, rivers.  That’s the death in your food.  Agriculture is carnivorous: what it eats is ecosystems, and it swallows them whole.

In Political Vegetarians she refutes the politics (predominantly liberal) of the vegetarian movement and describes the dark side of political meddling in our ecosystem approved of in the main by PETA and other vegetarian groups.  She follows the money.

Rice, wheat, corn – the annual grains that vegetarians want the world to eat – are thirsty enough to drink whole rivers.

The result has been an unending river of corn, drowning our arteries and our insulin receptors, our rural communities, and poor subsistence economies the world over.  The corn comes at a huge environmental toll: there’s a half gallon of oil in every bushel.  And it’s essentially a massive transfer of money from the US taxpayer to the giant grain cartels, who are able to command the price of grain to be lower than the cost of production, with all of us making up the difference – five billion dollars in subsidies for corn alone, straight into the pockets of Cargill and Monsanto.

Nutritional Vegetarians is about the nutritional inadequacies of a vegetarian and especially a vegan diet.  And she does an absolute bang up job of laying out the rationale for following a no-grain, low-carb diet.

I have a disclosure to make here.  Much of the information in this chapter is based on Protein Power and The Protein Power LifePlan.  MD and I are listed in the acknowledgments, but I swear I didn’t know this until I bought the book.  We aren’t the only ones, but there are plenty of quotes from us in this chapter.  Gary Taubes, Malcolm Kendrick and (dare I say it) Anthony Colpo are quoted liberally as well.  I would have loved this book just as much if we had never been quoted.

Ms Keith has made a few minor innocuous errors in this chapter, but, all in all, she has done a tremendous job of synthesizing the scientific information into an easy to read, informative format.

The Nutritional Vegetarians section isn’t just about the science of why vegetarianism is bad and meat eating is good, it gets into the nutritional politics (as opposed to the vegetarian politics in the previous section) as well.  Ms Keith shows how we got to where we are by the nutritional strong arming by the McGovern committee back in the late 1970s.  George McGovern (a senator from a grain-producing state) and his cronies basically set the nutritional standards under which we are still oppressed.  They have been a disaster, as some scientists at the time predicted they would be.

And some scientists knew ahead of time that they would be.  Phil Handler, the president of hte National Academy of Scientists asked Congress, “What right has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?”  Dr. Pete Ahrens, an expert on cholesterol metabolism, told the McGovern committee that the effects of a low-fat diet weren’t a scientific matter but “a betting matter.”

It’s twenty-five years later and we aren’t winning this bet.  Each US American now eats sixty pounds more grain per annum and thirty pounds more cheap sugars, mostly from corn.  [Is it any wonder we’re all fat?]

The result, Dietary Goals for Americans, set in motion a cast sea change in the public’s beliefs and behaviors. … Dietary Goals was a predictable victory in a war that started ten thousand years ago.  What really won were those annual grasses that had long since turned humans into mercenaries against the rest of the planet.  We would now enshrine them like demi-gods, those whole grains and their sweet, opiate seductions, believing in their power to bestow health and long life, even while they slowly ate us alive.

I don’t think I’ve ever read a book review that was positive from beginning to end, and this one is no exception.  Based on the many comments I’ve gotten on this blog and my response to them, I’m sure many of you will find my main objection surprising.  There is too much politics in the book.  Not nutritional politics, but feminist politics.

I know, I know, I let my libertarian leanings come through in all kinds of blog posts and comment answers, but there is a difference.  My blog is just that – a weblog of things I find interesting or informative.  And it’s free.  I don’t particularly like to pay for a book (and I paid full price for this one plus shipping) on a given subject then be beaten over the head with a political viewpoint.  I guarantee you that our new book has zero politics in it.  And if people bought our book expecting to learn about getting rid of their middle-aged middles and were fed a generous dose of my politics mixed in with the information, I would expect them to be flamed.

To give the author her due in this matter, the vegetarian ideology that had her in its grasp for 20 years was intertwined with her feminist politics, so a bit of said politics are necessary to describe how she was so taken in for so long.  But I think she went a little overboard with it.

And, I think the last section of the book – To Save the World – is the weakest part of the book.  The author makes several recommendations, all of which (save one) are, in my opinion totally unrealistic.  But I’ll leave it to you to draw your own conclusions after you’ve read the book.

I’ve read that when people are asked to recall what they remember of something they read, they tend to remember the first thing in the piece and the last thing.  Most of the middle melds into a vague memory of what the article was about.  I certainly don’t want people to remember this last negative part I wrote and let it dissuade them from reading this book.  The good parts of the book so far outweigh the not-so-good parts that there is really no contest.

At a time when PETA and other vegetarian groups are mobilizing and ramping up their activity levels, a book such as this one bringing sanity to the debate is more important than ever.  And don’t think these groups aren’t becoming more active.  In the past, PETA and PETAphiles pretty much devoted their educational efforts toward the idea that eating animals was cruel.  Now they are starting to make the case that a vegetarian diet will solve the obesity epidemic.  Take a look at this billboard in Jacksonville, Florida.

whales

If you find this sign annoying, buy The Vegetarian Myth and do your part to fight back. And if you have or know anyone with a daughter who is contemplating going vegetarian (young females are the most common victims), please make this book available.  It could be the most important thing you ever do for the long-term mental and physical health of a young woman.

If you’ve made it this far in this long review, take a couple of minutes and watch this YouTube of Lierre Keith at a book event; she’s as fascinating to listen to as she is to read.

Request for help promoting our new book

I’m almost afraid to say it, but it looks like after being delayed two times our new book is actually coming out on September 8.  As we have done with all our books, we will be expected to be available for all kinds of media appearances and interviews.  It is a giant pain, but it has to be done.  It’s part of the book-writing gig.  If you don’t sign up to do the PR, they don’t sign up to publish your book. (If you want to see a little of what a book tour is like, read this piece by Joe Queenan to see what we’re up against. Sometime I’ll write a piece on the nightmare of my first three-week-long book tour and my dealings with the escorts that are a part of the book tour experience.)

MD and I have been in discussion with our publisher and have gotten permission to excerpt part of the book, which I will do on this blog soon.  The book is about the weight gain that seems an inevitable part of moving into and through middle age and how this weight is different from that gained in the younger years.  It’s a kind of bad news, good news story because middle-age weight comes from a more dangerous kind of fat (the bad news), but a kind of fat that is fairly easy to lose (the good news).  But despite its being easier to lose, it still requires some effort…and a little different approach.  And, surprisingly, most of this fat can be lost in a 6-week window.  That doesn’t mean that we promise that all weight will be lost in a 6-week window, but most of the middle-aged weight can be ditched or at least significantly shed in this time period – thus the title.

Since we don’t have an active practice right now, most of the subjects we’ve given the diet to are former patients, friends and relatives.  We have had almost unbelievable success with those who gave the program a fair try.  We had one middle-aged friend who had struggled with lipid problems for years.  Despite our telling her not to worry and not to go on a statin because those drugs have never been shown to be beneficial for women, she was worried.  Her doctor was hectoring her, telling her that she would have to go on a statin if her lipids didn’t come into line.  She had an appointment in two weeks, so she went on the first two weeks of the program, then went to her doctor.  Not only did she lose eight pounds in her first two weeks, her lipid numbers plummeted.  Her total cholesterol fell from 240 to 174; her triglycerides dropped to below 100; and her HDL ran up to 60.  Happily, this all happened during the editing phase of the book, so we were able to include her story.  Other subjects have done as well if not better.

Another story is that of a business associate of ours who has gradually gained weight over the past 15 years who tried the plan.  She has tried diets of one kind or another for about 10 years.  She loses a little, but it’s been a tough slog for her.  She went on the new program and also lost eight pounds the first two weeks, which was a much greater loss than she had ever experienced.  A 60-year-old friend of ours easily lost 20 pounds over the course of his 6-week effort and had remarkable improvement in his lipids.  His wife had been on an HCG program that we had tried to talk her out of.  When she saw her husband lose substantially faster than she did, and without going on a 500 calorie diet, she switched to our program and her weight loss picked up and her measurements improved dramatically.

We have had multiple successes like the ones above, but, as I said, all are friends, relatives or business associates.  And they are not people who are keen on giving their testimonials to various media sources.  The first lady, mentioned above, works in the entertainment business – she was the director of a popular sitcom that most readers of this blog would probably be familiar with.  She doesn’t mind telling her story, but she doesn’t want her picture shown.  We found this out when the PR department of our publisher contacted us about some major interest in our book by a major women’s magazine.  They had read an advance copy of our book and were interested in making it a cover story.  They asked if we had any success stories they could interview and build a story around complete with photos.  We said sure and started calling all our ‘patients.’  Each one declined to be interviewed or would be interviewed but didn’t want her actual name used.  All refused to have their photo appear in the article.  So, we were left holding the bag, so to speak.

So, here is my request.  If any of you out there who are middle-aged and overweight would like to try the program, we will send you an advance copy of the book.  The deal is that you must be willing to have your real name and photo used by any media that approach you. This could be magazines, newspapers, online articles, and/or radio. You must also be willing to go on TV with us (or by yourself) – either national or local – and tell your story.  Should a TV appearance be required, generally all your expenses will be picked up by the television station, and if not, then you need not appear.  All you have to do is read the book, follow the program, keep us updated about your progress and tell anyone from the media who might contact you how you fared on the regimen.

Our publisher will let us recruit only 20 people for this project, so we can’t make it available to everyone who wants to do it.  We will select the 20 people from the applications we receive.  I have no idea how many that might be: it could be five or it could be 50.  I just don’t know.

I’ve set up a gmail account for anyone who is interested.  Please send an email giving your particulars, i.e., age, sex, weight, dietary history (what kind of diets you’ve been on, when and with what degree of success), medications, other disorders (diabetes, heart disease, kidney disease, etc.), contact info and a photo if you have one.

Send to:

6weekcure at gmail dot com

Put ‘6weekcure’ in the subject line of your message.

We’re also looking to recruit a few people in other categories for some more immediate media exposure.  So, if you have used the shakes for weight loss that I have given the recipe for multiple times in the comments section of this blog, send an email to the above gmail address and put ‘Shakes’ in the subject line.

If you have been on an all-meat diet and done well, drop us a note and put ‘All meat’ in the subject line.

MD and I thank you, in advance, for being willing to help.

Addendum:  We have received over 300 requests from people wishing to try the program in our book.  Since our publisher is providing us with only 20 copies, we have to terminate the offer at this point.  We will go through the 300 plus submissions and contact all those who wrote shortly.  Thanks for all your interest.

Low-carb lite…sort of

English breakfast at our hotel.  A good low-carb diet.

English breakfast at our hotel. A good low-carb diet.

It was bound to happen.  Forever the low-fat diet promoters, whenever asked about low-carb diets, would always say: Show me the studies.  Well, we showed them the studies, the vast majority of which demonstrated the superiority of low-carb diet, but they didn’t like what they saw.  So they demanded more.  The rallying cry became: Show me the long-term studies.  Now that those are in, the anti-meat folks are running out of options.  But one of their own great lipophobes (Lipid  = fat; phobic = fear of.  Lipophobe = fearer of fat.), David Jenkins, has come to the rescue.

Since the low-carb diet has proven so effective, opines he, why not make it even more so by making a vegetarian version?  Then dieters can have all the advantages of a low-carb diet along with all the advantages of a plant-based diet.  That is, assuming there are advantages to a plant-based diet, more about which later.

Although the low-carbohydrate diet has proven itself a cut above the low-fat diet in virtually all parameters measured, in one little measurement it has fallen short, at least in the minds of the lipophobes.  A number of studies of subjects following low-carb diets show that LDL-cholesterol levels don’t fall to the levels found in subjects following lower-fat, higher-carbohydrate diets.  And this troubles the lipophobes mightily.

To a lipophobe, LDL-cholesterol is all that matters.  These people have bought in to the premise that LDL-cholesterol is a major driving force behind the development of heart disease, and in their minds, anything that doesn’t lower LDL-cholesterol levels is a very bad thing, indeed.  It doesn’t matter to them if a particular nutritional regimen improves every other parameter relating to general health and even cardiovascular health, if that regimen doesn’t also lower LDL-cholesterol levels, it is suspect.

It matters not to them that there is no evidence showing that LDL-cholesterol levels cause or worsen heart disease; they believe with all their hearts that it does.  In their fat-deprived brains, the lipid hypothesis isn’t a hypothesis at all.  It is fact.

And so they set out to test the hypothesis that a low-carb diet without meat could achieve the Holy Grail of lipophobery: a lowered LDL-cholesterol.

The study published in this week’s Archives of Internal Medicine was picked up and reported on by multiple media outlets. It starts out with an opening statement laying out the problem of low-carb diets from the lipophobe’s perspective.  Remember as you read this that virtually none of the statements presented as facts have ever been proven to be so.

There is a dilemma relating to the proportion and source of fat, protein, and carbohydrate that constitutes the optimal weight loss and cholesterol-lowering diet. Newer dietary approaches for the prevention and treatment of chronic disease increase the consumption of fruit and vegetables but reduce meat consumption either directly as part of the dietary strategy or displace meat by advocating increased intakes of fish, poultry, and low-fat dairy foods. Running counter to this advice has been the promotion of low-carbohydrate diets with increased meat consumption for body weight reduction and also in the longer term for the prevention and treatment of diabetes and coronary heart disease (CHD). These diets not only challenge the concept that red meat intakes should be reduced but also reverse the dietary macronutrient profile with fat and protein as the major macronutrients and carbohydrates as the minor macronutrient. Such low-carbohydrate diets have been shown to be effective in inducing weight loss, reducing insulin resistance, lowering serum triglyceride (TG) concentrations, and raising high-density lipoprotein cholesterol (HDL-C) concentrations. However, the higher meat diets have not resulted in lower low-density lipoprotein cholesterol (LDL-C) concentrations, but have tended to increase LDL-C concentrations except when vegetarian sources of fat and protein were included. This lack of a benefit for LDL-C control is a major disadvantage in using this dietary strategy in those already at increased risk of CHD.

There it is, the sticking point for lipophobes and the low-carb diet.  It doesn’t matter what kind of good results those following low-carb diets achieve, in their minds all that matters is the LDL-cholesterol.  Read that last sentence again.  After all the description of the multiple benefits of low-carb dieting, it all boils down to LDL.

This lack of a benefit for LDL-C control is a major disadvantage in using this dietary strategy in those already at increased risk of CHD.

A major disadvantage they say.  Will someone show us, please, all the evidence that there is a disadvantage?  Gary Taubes wrote an entire book about the lack of evidence of any advantage to achieving a lower LDL and the lack of data showing saturated fat causing any increase in risk for heart disease, but that information is lost on these guys.

The authors of this paper are going to fix the low-carb diet problem.  Here’s what they did in their own words.

In view of the apparent success of low-carbohydrate diets for weight loss and the demonstration that relatively high-carbohydrate diets low in animal products lower CHD risk factors, we determined the effect of a low-carbohydrate weight-loss diet, without the use of animal products, on serum lipid concentrations compared with a higher carbohydrate diet.

Let’s take a look at what they did.

They recruited 50 subjects, 47 of whom actually started the study.  The researchers randomly assigned the subjects to either a low-carbohydrate or a high-carbohydrate, calorie-reduced diet of a one-month duration.  Couriers delivered the food, all of which was prepared in a metabolic kitchen, to the subjects, all of whom presented themselves to the clinic weekly for evaluation.

Here is a description of the diets:

Metabolically controlled diets in which all food was provided were consumed by the participants. The low-carbohydrate diet provided the minimum level of carbohydrates currently recommended (130 g/d) and eliminated common starch-containing foods, such as bread, baked goods, potatoes, and rice. The protein content was provided by gluten (54.8% of total protein), soy (23.0%), fruits and vegetables (8.7%), nuts (7.5%), and cereals (6.0%). Gluten was provided in the nut bread and wheat gluten (also called “seitan”) products and, together with soy, in burgers, veggie bacon, deli slices, and breakfast links. In addition, soy was provided as tofu and soy beverages. Nuts included almonds, cashews, hazelnuts, macadamia, pecans, and pistachios. The fat was provided by nuts (43.6% of total fat), vegetable oils (24.4%), soy products (18.5%), avocado (7.1%), cereals (2.7%), fruits and vegetables (2.3%), and seitan products (1.4%). The diet was designed to provide 26% of calories as carbohydrates, 31% as protein, and 43% as fat. The high-carbohydrate diet was a low-fat lacto-ovo vegetarian diet (58% carbohydrates, 16% protein, and 25% fat) using low-fat or skim milk dairy products and liquid egg whites or egg substitute to ensure a low–saturated fat and low-cholesterol intake. All diets were provided at 60% of estimated calorie requirements using the Harris-Benedict equation with allowance for exercise.

The low-carbohydrate diet featured viscous fiber-containing foods, including oats and barley, for the relatively limited amount of carbohydrates allowed, and the production of a “no starch” high-protein bread made entirely from ground almonds, hazel nuts, and wheat gluten. The carbohydrate foods and low-starch vegetables, emphasizing okra and eggplant, provided 6 to 7 g of viscous fiber per 2000-kcal diet. The bread was provided as part of the diet.

Whoa there!  Did we read that correctly?  Did it say that the low-carbohydrate diet contained 130 grams per day of carbohydrate?  It sure did.  Doesn’t sound much like a low-carbohydrate diet to me.  It takes a restriction of carbohydrates down to the 50 or so gram per day level to get the real benefit of low-carb dieting, the so-called low-carb magic.  Anything much above that is simply a low-calorie diet with a little less carb.

What were the results of this experiment after both groups were on their respective diets for a month?  Well, it’s hard to say for sure because of the way the data were looked at.  Fifty subjects were recruited, but only 47 actually started the program.  Of these 47, only 44 completed the study (22 in each group).  But the data were evaluated using an intention-to-treat analysis, which, at best, gives less than valid answers.

Here is the chart showing the study outcomes:

veg-low-carb-diet-blog

If we ignore the fact that these data were derived using an intention-to-treat analysis and take them as presented, we can see that the lower-carb veggie diet out performed the higher-carb, lower-fat diet in a number of parameters.  Let’s look at those that were statistically significant (a P value of less than 0.05).

Satiety was greater in the higher-fat diet.  As you can see, subjects on the low-calorie, high-carb diet got hungrier as the study progressed.  Those on the lower-carb diet got minimally less hungry as compared to the start of the study, which isn’t a surprise as fat is filling.

Total cholesterol and LDL-cholesterol both fell to a larger extent on the lower-carb diet.  Finally, a low-carb diet in which LDL-cholesterol dropped.  I’m sure the researchers were orgasmic.

As anyone with any experience with low-carb diets would predict, triglycerides fell markedly as compared to those on the control diet.

All the lipid ratios were improved more on the low-carb diet.

Apo B (a measure of LDL particle number) fell to a greater extent on the low-carb diet and the apo B to apo A1 ratio was lower on the low-carb diet, a fact the researchers made much of.

Both the apo B concentration and the apo B–apo A1 ratio fell significantly more for the low-carbohydrate vs the high-carbohydrate diet…

Most low-carbohydrate diets have not reported the effects on apolipoproteins. The reduction in apo B and the apo B–apo AI ratio observed in the present study is a further confirmation of the potential CHD benefit that might be expected from this dietary approach to body weight reduction. In some studies, the apolipoprotein concentrations have been claimed to have greater predictive value for CHD events than more conventional lipid variables.

This emphasis on the apo ratios is interesting.  Apo B is the protein associated with LDL-cholesterol and apo A1 is the protein associated with HDL-cholesterol.  One of the big bugaboos about low-fat, high-carbohydrate diets is the fact that although these diets generally bring about a fall in LDL-cholesterol, they also bring about a greater decrease (percentage-wise) in HDL-cholesterol.  This study is remarkable because HDL-cholesterol fell in the low-carb arm whereas in most low-carb diets HDL-cholesterol goes up.  HDL-cholesterol is fat dependent (probably saturated-fat dependent if you want my opinion), and since most low-carb diets are high-fat diets, HDL-cholesterol goes up in subjects following them.  I’m sure these researchers desperately wanted the same to happen here, but, alas, it didn’t.  HDL-cholesterol fell just as it did in the high-carb arm. They are trying to cover for this by focusing attention on the apo B to apo A1 ratio, which did fall, meaning, basically, that LDL-cholesterol levels fell more than did HDL-cholesterol levels.  On a good quality low-carb diet you would typically find that LDL-cholesterol levels stay about the same (or maybe fall a little or even rise a little) while HDL-cholesterol levels go up.

I find the last sentence in the above quote really intriguing.

In some studies, the apolipoprotein concentrations have been claimed to have greater predictive value for CHD events than more conventional lipid variables.

Since apolipoprotein levels are indicators of the various cholesterol particle sizes, I would say this is a great understatement.  Virtually all of the research on this subject has shown that low-fat, high-carbohydrate diets – even though they reduce LDL-cholesterol – end up resulting in LDL-cholesterol of the small, dense particle size, which is much more atherogenic than the larger, fluffier particles found in subjects after following low-carb, higher-fat diets.  To report that this is the case in just some studies is disingenuous to say the least.  But to report it otherwise would give the lie to the notion that LDL-cholesterol levels by themselves amount to much of anything.  And we wouldn’t expect a true lipophobe to do that, would we?

When we slice and dice all the data from this study, what do we find?  We find that a lower-carb diet (not a low-carb diet, but a lower-carb diet) so complicated it basically requires a metabolic kitchen to prepare provides the same benefit as a real meat-based low-carb diet with the only difference being that the plant-based lower-carb diet gives a little lower LDL-cholesterol reading.  When you consider that this lower LDL-cholesterol reading came at the expense of a reduction in HDL-cholesterol and a major effort required to prepare the diet, one has to ask if it is really worth it?

I would bet that if the plant-based lower-carb (130 g/day) diet were compared with a meat-based real low-carb diet (50 g/day or under), the real low-carb diet (such as the one pictured at the top of this post) would win across the board.  The LDL-cholesterol number may not go down as much, but who really cares?  LDL-particle size would be larger (I calculated particle size in this study, and there was no change) and all other parameters would probably be improved more.

Maybe someday someone will do such a study and prove me right.  Or wrong.  In any case, this study has some value in that now maybe all those docs who have shied away from prescribing low-carb diets to their patients because of ungrounded fear of a minimal increase in LDL-cholesterol will give this version a try.  For all its faults, it’s better than the low-fat, high-carb diet.

*Lipid  = fat; phobic = fear of.  Lipophobe = fearer of fat