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

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

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

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

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

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

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

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

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

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

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

Recognized?  What does that mean?

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

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

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

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

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

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

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

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

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

But as for heart disease itself:

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

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

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

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

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

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

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

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

It was unbelievable.

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

Watch and just shake your head.

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

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

This link requires requires free registration.

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

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

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

Let’s take a look.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Follow the money.

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

From heartwire (requires free registration):

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

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

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

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

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

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

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

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.

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.

Click here to view the embedded video.

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.

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:

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

I can’t begin to count the number of people whom I have seen in my office who have fallen off the wagon and who told me that they just couldn’t stick with their low-carb diet for any number of reasons.

A typical conversations goes something like this:

MRE: (In this drama, MRE is yours truly, the long suffering physician) So, Mrs. X, I see that you gained a little weight this week.  What happened?  Is there a problem we need to go over?

Mrs. X: Oh, no, not really.  I had to put my mother in the hospital this week, and I just couldn’t diet with all that going on.

Other answers could be: My kids all came home from summer camp, and I just couldn’t stick to it with all that going on.  Or my husband lost his job, and I couldn’t low-carb with that going on. Or I’m going through a divorce.  Or …  You get the picture.

These excuses bring to mind an absolutely wonderful book that I highly recommend, The Happiness Hypothesis.  It was written by Jonathon Haidt, an associate professor of psychology at the University of Virginia and is filled with interesting perspectives on happiness, what it takes to be happy and even the scientific basis of happiness.  The cover of the book has a sort of blurred photo taken from underwater of what appears to be an elephant with a rider on its back, which is central to Dr. Haidt’s thesis.

Dr. Haidt describes our minds and bodies (and by bodies he means not just our corporeal bodies but the working mechanisms of our bodies) as being akin to a rider on the back of an elephant.  Our conscious, thinking minds he casts in the role of the rider, and the rest of us as the elephant.  The rider can control the elephant as long as the elephant wants to be controlled.  And if the elephant is okay with being steered and directed, then to all appearances, the rider is in control.  But, if the elephant has other ideas, the rider basically just goes along for the ride.

Every time I think of this image, I’m taken back to our youngest kid’s dorm room in college where he played a bit of video he had taped from one of those Fox (I think it was Fox) shows from years ago called When Good Pets Go Bad.  It was a video of a woman who, along with her three young children,  went for a ride on the back of an elephant.  The elephant was a part of some sort of performance and had been placidly giving rides to all comers.  Once this particular family got aboard, the elephant decided it had put up with enough of this nonsense and went rogue.  It stormed out raising hell and tearing up everything in site with the poor mother and her kids hanging on for dear life. The family ended up unharmed after the rampage, but the elephant had to be destroyed.  Our kid loved the video showing all the people running in horror from this irate elephant and would play it in frame by frame mode so that he could see the looks of terror on all the faces of all those trying to flee.  MD and I, being the attentive parents that we are, must have watched this video a dozen times as he pointed out all the nuances that he loved so much, so it is firmly etched in my mind.

This rogue elephant scenario is what Dr. Haidt thinks happens to us from time to time.  Our rider (the conscious part of us) wants us to do something, but the elephant part of us doesn’t want to, and so the rider just hangs on for the ride while the elephant goes wherever it wants to go.  We can put this in dieting terms.  Our rider decides that the elephant needs to go on a diet.  As long as the elephant is up for it, the diet hums along.  But if the elephant has other ideas, the rider becomes an ornament.  If things are going well, the rider has the appearance of control; if things aren’t going well, i.e., we had to put Mom in the hospital, then the elephant takes over.  And the rider accepts it.  He says, hey, I couldn’t control this beast because we had to put Mom in the hospital, and you know how he gets when we have to put Mom in the hospital.  He wants to eat, and I, the rider, have to go along with him.

Yale psychologist Paul Bloom presents another way of looking at this situation in an enlightening article in the November 2008 issue of The Atlantic.  He puts forward the idea that we all have multiple selves that we’re constantly dealing with, arguing with and trying to fool.

Let’s say that we’ve dined large late at night and are headed for bed.  As we crawl into the sack with belly distended from a carb overindulgence and lie flat, we start getting the ol’ acid reflux feeling.  We sit up, burp, drink some water, rub our chest and grab for the Tums.  The self that is suffering says, ‘That’s it, I’m dieting tomorrow.  I can’t stand feeling like this, not for one more night.’  The next morning the self that wakes up is a different person who isn’t experiencing reflux, doesn’t have a distended belly and is hungry.  And, by God, hungry for some waffles, at that.  The feel-good morning self may not abide by the rules laid down by the refluxing self the night before.

Bloom relates a story told by the Nobel laureate economist Thomas Schelling about his own multiple selves:

As a boy I saw a movie about Admiral Byrd’s Antarctic expedition and was impressed that as a boy he had gone outdoors in shirtsleeves to toughen himself against the cold. I resolved to go to bed at night with one blanket too few. That decision to go to bed minus one blanket was made by a warm boy; another boy awoke cold in the night, too cold to retrieve the blanket … and resolving to restore it tomorrow. The next bedtime it was the warm boy again, dreaming of Antarctica, who got to make the decision, and he always did it again.

Then Dr. Bloom goes on to tell his story of his own dual selves:

Late at night, when deciding not to bother setting up the coffee machine for the next morning, I sometimes think of the man who will wake up as a different person, and wonder, What did he ever do for me? When I get up and there’s no coffee ready, I curse the lazy bastard who shirked his duties the night before.

We are all like this.  One of our selves makes a promise that another has to keep, or, more likely, try to weasel out of.  One of ourselves gets us in a fix that one of our other selves has to get us out of. ‘What on earth was I thinking? How did that happen?’ our responsible self says when our fun-loving self does something incredibly stupid.

My responsible self says ‘No golf unless you get this project finished first.’  As the day wears on and my golf-addict self realizes that there is still enough light to get in at least 9, and it says ‘Hey, I’m almost finished, I’ll do it when I get home.’  When I get home, my tired self who wants to grab a glass of Jameson and kick back says, “Geez, why didn’t I just finish this job instead of playing golf?  I’m a member of a country club, for God’s sake; I can play any time, so why today when I had all this hanging over my head?’

And that’s the problem with all these selves.  At least all my selves, and, I suspect, most people’s selves.  These selves can outwit one another, and if the selves aren’t careful or if there isn’t a father-figure, responsible self towering above the others, not much gets done.

These two authors astutely identify the ways we as humans tend to deal with life.  And since the part of life were talking about in this post is diet, these observations apply.

Our rider says diet, our elephant, in the throes of hunger, says screw that, I’m out of here.  And the rider goes along for the ride.

Or our one comfortably-fed self gets us into a diet that our other hungry or our stressed-out self  wants no part of and so bolts.

If you believe these two psychologists, we are pretty much doomed to stay overweight, insulin resistant, diabetic, etc. because when it comes right down to it, we don’t really have any control.  What can we do as the rider of a runaway elephant?  What can we do if our good self makes the deal but the other self won’t keep it?

If you think these ways of looking at dieting are outlandish, just tell me how many times you’ve heard (or even said) these words about a specific food (high in carbs, usually):  I just couldn’t help it.  I couldn’t resist.  I gave in to the cravings. I couldn’t control myself.

Go back through the comments of the last couple of posts and read how many people wrote how they couldn’t deal with carb cravings.  Probably the most common excuse I heard for dietary indiscretion from my patients was that they just couldn’t control their diet when under some stressful situation.  The cravings got the better of them.

It sounds reasonable.  Psychologists write about elephants and riders and multiple selves fighting with one another because that’s how most people tend to react.  But it doesn’t have to be that way.  We are not that helpless.

Back in the early 1980s a psychiatrist, William Glasser, M.D., wrote a book titled Take Effective Control of Your Life that I read at the time and thought to be one of the more insightful books I had ever read.  The paperback version of that same book appeared a couple of years later under the title Control Theory.  Both editions are now out of print but pre-owned copies can be had for pennies from Amazon.  This is a book well worth reading.  And not just for dietary help.

Dr. Glasser has gone on to bigger and better things and has become famous for an an entire school of psychiatric therapy.  I’ve read most of his books, and profited from them all, but the one mentioned above is a true gem.  I don’t understand why it still isn’t in print.

The insight that Dr. Glasser had and that I recognized in myself and in my patients as soon as I read his book was that people spend all their time worrying and stressing about things they can’t control and end up ceding control over the things that they can control completely.

Going back to our example at the start of this post, my patient who put her mother in the hospital didn’t have any real control over any part of what was happening.  She couldn’t control her mother’s disease, she couldn’t really control much of anything that went on in the hospital.  But she worried constantly about these things she couldn’t control and abandoned her diet, over which she had total, 100 percent control.

People do this all the time.  One of the very few things we have complete control over is what we put in our mouths.  Unless someone hogs us down, pries open our jaws and force feeds us, we have total and complete control of our eating.  Yet how many times have we heard people say (or have said ourselves), I just couldn’t do the diet with all this going on.  I lost all control.

Dr. Glasser understands about the rider and the elephant and the multiple warring selves, although he doesn’t call them such.  And he has a game plan for dealing with them, which puts the control squarely in our hands.

He explains that all behavior has four components.  He doesn’t explain these in dietary terms, but I will.

1. the physiological component
2. the feeling component
3. the thinking component
4. the doing component

We don’t have any control over the first two and only partial control over the third.  But we have total control over the fourth, the doing component.  Let’s look at how this all works with food.

Imagine you’re sitting in your office minding your own business when a co-worker comes in with a box of fresh, hot donuts, sticks the box in your face and says, ‘Have one.’  What happens?

First, your physiology kicks in.  Your pancreas says, uh oh, here comes some sugar.  Better get a little insulin cranked out to get ready for it.  You get a spurt of insulin and your blood sugar starts to fall.

Then, as your blood sugar falls, you start to feel hungry.  And your stomach starts to churn as it gets ready.  This is the feeling component.  And you have no control over this.  It all happens and it is totally beyond your control.

Then you think about how good a donut would taste.  And you imagine it.  And you say to yourself, hey, it’s only one. What could it hurt?  This is the thinking component, and you do have some control over it.  But with the physiology and feeling components hard at work, it’s difficult not to think about the donuts.  Difficult, but not impossible.

And all the above happens in just a few seconds.

Then you grab a donut and eat it.  The doing component.  You have complete control over this component.  You choose to eat the donut.  All the other components are ragging on you and you cave.  And you say you had no control, but you really did.  If someone had told you they were going to shoot you if you ate one of the donuts, you wouldn’t have eaten it.  All the other three components (at least the first two) would have been acting the same, but you wouldn’t touch the donuts.  You can control the doing component if you want to.  Problem is the other three components gang up on you, trying to disable your will.

But, this can all the dealt with.

Dr. Glasser realized that the physiology to feeling to thinking to doing progression could be reversed.  Since you have complete control over only the doing component, you’ve got to do something.  And once you do, you can foil the progression. Because if you take different action, you can drive the progression the other way.

If you get up from your desk and say, No thanks, then leave your office and go involve yourself with something else all the components start to fall in line.  Once you start doing something different, you start thinking about it, then your feelings of hunger go away and soon even your physiology falls into line.  Your liver produces glucose to make up for that the little spurt of insulin knocked down, and soon you’re back to normal.  And it doesn’t take all that long.

So, basically, we can be driven by a progression over which we have no control to abdicate the one thing we do have control over, our actual active doing.  Or we can use our ability to do something to reverse control all the components that we don’t have direct control over.

Realizing that I had this ability to control the seemingly uncontrollable made a huge difference in my life years ago and continues to do so today.  Knowing that I can control virtually any behavior, but especially my dietary behavior, by simply focusing my attention and effort onto a task or other activity has kept me on the straight and narrow multiple times when strong temptation fell in my path.

If the high-carb demon is goading you to go face down, telling you that you have uncontrollable cravings, just force yourself to go do something else.  Soon the cravings will be gone.  It takes a little practice, but it helps to repeat the mantra: I have 100 percent control of what goes in my mouth.

Take the advice of Dr. Glasser.  Start worrying less over those things you can’t control and accept that you have no control over them.  And take back control of the things you can.  If you do so, you will be a much happier person.  And a much thinner person.

Fate has dropped two studies into our hands that clearly demonstrate the superiority of low-carbs diets when matched against the high-fiber, high-cereal diet beloved of so many in the nutritional establishment and even against low glycemic index (Low-GI) diets.

In the same couple of week period two studies came out – one you’ve probably read about; the other you likely haven’t. By combining the data from these studies, we can see how these three diets match up.

The first study was published in the Dec 17 edition of the Journal of the American Medical Association (JAMA) and was a comparison of the high-cereal, high-GI diet to the low-GI diet. You can get an overview of the study by reading the JAMA press release:

IN PATIENTS WITH DIABETES, LOW-GLYCEMIC DIET SHOWS GREATER IMPROVEMENT IN GLYCEMIC CONTROL THAN HIGH-FIBER DIET

CHICAGO—Persons with type 2 diabetes who had a diet high in low-glycemic foods such as nuts, beans and lentils had greater improvement in glycemic control and risk factors for coronary heart disease than persons on a diet with an emphasis on high-cereal fiber, according to a study in the December 17 issue of JAMA.

One dietary strategy aimed at improving both diabetes control and cardiovascular risk factors is the use of low-glycemic index diets, but there is disagreement over their effectiveness, according to background information in the article.

David J. A. Jenkins, M.D., of St. Michael’s Hospital and the University of Toronto, and colleagues assessed the effects of a low-glycemic index diet vs. a high-cereal fiber diet on glycemic control and cardiovascular risk factors for 210 patients with type 2 diabetes. The participants, who were treated with antihyperglycemic medications, were randomly assigned to receive 1 of the 2 diet treatments for 6 months.

In the low-glycemic index diet, the following foods were emphasized: beans, peas, lentils, nuts, pasta, rice boiled briefly and low-glycemic index breads (including pumpernickel, rye pita, and quinoa and flaxseed) and breakfast cereals (including large flake oatmeal and oat bran). In the high-cereal fiber diet, participants were advised to take the “brown” option (whole grain breads; whole grain breakfast cereals; brown rice; potatoes with skins; and whole wheat bread, crackers, and breakfast cereals). Three servings of fruit and five servings of vegetables were encouraged on both treatments.

The researchers found that hemoglobin A1c (HbA1c; a substance of red blood cells tested to measure the blood glucose level) decreased by -0.50 percent absolute HbA1c units in the low-glycemic index diet compared with -0.18 percent absolute HbA1c units in the high-cereal fiber diet. Significant treatment effects were observed for high-density lipoprotein cholesterol (HDL-C) and the low-density lipoprotein cholesterol (LDL-C):HDL-C ratio. HDL-C increased in the low-glycemic index diet group by 1.7 mg/dL and decreased by -0.2 mg/dL in the high-cereal fiber diet group. The LDL-C:HDL-C ratio showed a greater reduction in the low-glycemic index diet group compared with the high-cereal fiber diet group.

“Lowering the glycemic index of the diet improved glycemic control and risk factors for coronary heart disease (CHD). These data have important implications for the treatment of diabetes where the goal has been tight glycemic control to avoid complications. The reduction in HbA1c was modest, but we think it has clinical relevance,” the authors write. “Low-glycemic index diets may be useful as part of the strategy to improve glycemic control in patients with type 2 diabetes taking antihyperglycemic medications.”

“Pharmacological interventions to improve glycemic control in type 2 diabetes have often failed to show a significant reduction in cardiovascular events. In view of the 2- to 4-fold increase in CHD risk in participants with type 2 diabetes, the ability of a low-glycemic index diet to address both glycemic control and CHD risk factors increases the clinical relevance of this approach for patients with type 2 diabetes, such as those in this study, who are overweight and also taking statins for CHD risk reduction.”

The gist of this study is that diabetic subjects on the low-GI diet improved minimally as compared to those on the high fiber, high-GI diet.  As I’ve written in this blog and lectured on numerous times, I’m not a big believer in the virtues of the glycemic index.  As this JAMA study demonstrates, subjects switching to lower-GI carbs while keeping their overall carb intake the same gain slight improvement, but not enough, in my estimation, to make the change worthwhile.  In my opinion it is the overall carb intake that counts more, not simply switching to lower-GI carbs.

At about the same time the JAMA paper came out, a study performed at Duke University comparing a low-GI diet to a real low-carb diet appeared in the online journal Nutrition & Metabolism. Here is the Duke press release about that study:

LOW CARB DIETS PROVE BETTER AT CONTROLLING TYPE 2 DIABETES

Which works better at controlling type 2 diabetes: a diet low in carbohydrates or one that focuses on carbohydrates with a low glycemic index? That’s what Duke University Medical Center researchers sought to uncover when they compared the two over a six-month period.

Their findings, published online in Nutrition and Metabolism, indicate that a diet low in carbs with the lowest possible rating on the glycemic index scale leads to greater improvement in blood sugar control, according to lead author Eric Westman, MD, director of Duke’s Lifestyle Medicine Program. And, patients who followed the diet experienced more frequent reductions, and in some cases elimination, of their medication used to control type 2 diabetes.

“Low glycemic diets are good, but our work shows a no-glycemic diet is even better at improving blood sugar control,” he says. “We found you can get a three-fold improvement in type 2 diabetes as evidenced by a standard test of the amount of sugar in the blood. That’s an important distinction because as a physician who is faced with the choice of drugs or diet, I want a strong diet that’s shown to improve type 2 diabetes and minimize medication use.”

Eight-four volunteers with obesity and type 2 diabetes that were randomized to either a low carbohydrate ketogenic diet (less than 20 grams of carbs/day) or a low-glycemic, reduced calorie diet (500 calories/day). Both groups attended group meetings, had nutritional supplementation and an exercise regimen.

After 24 weeks, their glycemic control was determined by a blood test that measured hemoglobin A1C, a standard test used to determine blood sugar control in patients with diabetes. Of those who completed the study, the volunteers in the low-carb diet group had greater improvements in hemoglobin A1C and diabetes medications were reduced or eliminated in 95 percent of the volunteers, compared to 62 percent in the low-glycemic group. The low carb diet also resulted in a greater reduction in weight

“It’s simple,” says Westman. “If you cut out the carbs, your blood sugar goes down, and you lose weight which lowers your blood sugar even further. It’s a one-two punch.”

While the diet is easy for some to follow, it is not easy for everybody. “This is a therapeutic diet for people who are sick,” says Westman. “These lifestyle approaches all have an intensive behavioral component.  In our program, people come in every two weeks to get reinforcements and reminders. We’ve treated hundreds of patients this way now at Duke and what we see clinically and in our research shows that it works.”

The gist of this study is that those diabetic subjects following an honest-to-God low-carb diet achieved dramatic improvement as compared to those who simply switched to a low-GI diet, but kept their carb intake high.

Now, as you might expect, knowing as we all do the propensity for the mainstream media to ignore studies showing the superiority of the low-carb diet while glorifying carbs, the New York Times picked up on the JAMA press release, but ignored the Duke press release.  If you read the gushing Times article, it makes it sound like the low-GI diet absolutely stomped the high-GI diet. The truth is a little different, however, because the differences between them were minimal.

I went to the trouble of pulling the data from both studies and putting it in spreadsheet form so that it could be compared side by side. Then I decided to go to a little more trouble and display it graphically so that the differences could be seen much better.  What follows is a series of graphs comparing the high-GI diet on the left to the two low-GI diet groups in the middle (JAMA low-GI study on the left and the Nutrition & Metabolism low-GI diet study on the right) and to the low-carb diet on the right. The light-colored bar represents the value at the beginning of the study for the parameter under question and the darker-colored bar represents the changes after 6 months on the various diets.

First, let’s look at the amount of weight lost by the subjects over 6 months on the various diets.

As you can see, the subjects on the low-carb diet lost the most weight despite the fact that they were not counting calories, only carbs.  This is especially impressive when you consider that all the groups except for the low-carb group were encouraged to count calories and reduce food intake.  The low-carb group was instructed to restrict carbs to below 20 gm per day but to otherwise eat all they wanted.

Let’s look next at HgbA1c, a measure of blood sugar control.  The lower the HgbA1c, the lower the blood sugar.  Since all the subjects in both these studies were diabetic, all started with high HgbA1c levels.

The low-carb diet brought about a much greater lowering of HgbA1c than did either the high-fiber, high-GI diet or the low-GI diet, both of which are routinely recommended for people with diabetes.  Makes you wonder, doesn’t it?

Next, let’s consider total cholesterol.  It’s a pretty much meaningless number, but it was included in the data, so I’ll include it here.

In these studies the low-GI diet held its own with the low-carb diet in terms of total cholesterol lowering.  But since total cholesterol is only a lab parameter and doesn’t really have a lot to do with health, it really doesn’t matter.  What does matter, if anything does, is what that total cholesterol is made of.  Is it made of LDL-cholesterol, the so-called ‘bad’ cholesterol or is it made of HDL-cholesterol, ‘good’ cholesterol?  Let’s look.

Both the low-GI diets lower LDL cholesterol better than does the low-carb diet.   But it doesn’t beat it by all that much.  The data from these studies don’t show how much of the LDL-cholesterol is small particle size and how much is large particle size.   As readers of this blog know, small, dense LDL-cholesterol particles are associated with increased risk for heart disease, whereas large, fluffly LDL-cholesterol is protective.   Particle size wasn’t measured in these studies but other parameters were that are stand-ins or markers for particle size.   It’s well known that when triglycerides go down, LDL-cholesterol particle size goes up.  We’ll look at triglycerides shortly to see what happened with them, but before we do, let’s take a look at HDL-cholesterol.

We can certainly see where some of the gain in total cholesterol came from in the low-carb group.   It came because they increased their HDL-cholesterol so much.   The other groups either held steady or went up minimally whereas the low-carb group showed a huge increase in HDL-cholesterol, which also correlates with larger LDL-cholesterol particle size.

What about triglycerides?   Most readers of this blog can predict what happened there.  Let’s look.

As we would expect, there was a significant reduction in triglyceride levels in the low-carb group as compared to the others.   This lowering of triglyceride levels is important for a couple of reasons.   First, lower triglycerides correlates with greater insulin sensitivity.   And, second, it correlates with larger LDL-cholesterol particle size.   So, the slight increase in LDL-cholesterol we saw with the low-carb diet in a previous graph probably comes from an increased amount of large, fluffy LDL-cholesterol particles.

If we look at the important triglyceride/HDL ratio we see some major improvement in the low-carb group.

As expected, we find a humongous lowering of the triglyceride/HDL ratio with the low-carb diet.  The lower this ratio, the better, so the low-carb diet has brought about major improvement compared to the others.

Looking at the two other measurements both studies included, we find that blood pressure improved more on the low-carb diet than on the others.   First, we’ll look at systolic pressure, which is the first or top number in the blood pressure reading.   If your blood pressure is 120/75, the 120 is the systolic pressure.

Once again the low-carb diet brings about great results.  If we look at the more important diastolic measurement, we find even better news.

Yet again the low-carb diet emerges the champion.

These graphs should give you an idea of how much more potent the low-carb diet is as a tool to deal with diabetes than are low-calorie, high-fiber, high-GI diets and low-calorie, low-GI diets, both of which are the mainstays of mainstream diabetic diet therapy.

Remember, all of these studies were done on diabetic patients and all were conducted over a 6 month period, so were are comparing apples with apples here.  Based on the data shown in these graphs, the low-carb diet emerged the champion by a long shot. If these graphs told the whole story, the low-carb diet would be the hero.  But the graphs don’t tell the whole story.  Why not?  Because large numbers of subjects in all these study groups were on oral anti-diabetic medicines and/or insulin.  What happened to medication doses as these subjects progressed through the 6 month study.

The JAMA paper tells us the following about the subjects in the high-fiber, high-GI and the low-GI diets:

…of the 11 participants who reduced their diabetes medications, all 6 who had clear evidence of hypoglycemic symptoms or low blood glucose levels were taking low–glycemic index diets.

So, 11 study subjects were able to reduce their medications during the study.  This doesn’t seem like a lot when you consider that out of 210 study participants 208 were on diabetic medications at the start.  Virtually all were on antidiabetic meds of one kind or another and 11 of them were able to reduce these medicines.  Eleven out of 208 means that 5 percent of the subjects on these two diets reduced their diabetic drugs.

If we look at the low-carb study, we find a much greater rate of success:

Twenty of 21 (95.2%) LCKD [low-carb diet] group participants had an elimination or reduction in medication, compared with 18 of 29 (62.1%) LGID [low-GI diet] group participants.

To really get a feel for what happened with these subjects, let’s look at a table from the study showing insulin and medication reductions in those subjects who were on insulin therapy before starting the study.

A quick study of this table shows us that 3 subjects out of 29 taking insulin in the low-GI group reduced or discontinued insulin whereas 8 out of 21 reduced or eliminated insulin in the low-carb group.

I would say that given the substantial improvements in virtually all the parameters demonstrated by the graphs combined with the enormous difference in improvement in those taking medications, the low-carb diet didn’t just perform as a star, it was a super star.

It’s saddens me to think about how many doctors don’t know or understand these data and will continue to treat their patients in a much less effective manner, no doubt leading to more complications, greater medication usage and shorter lives.  It really is a shame.

I’ve just discovered that the soft-cover version of Good Calories, Bad Calories is out.  I guess it has been out for a few weeks, but I just discovered it was available.  If any of you have been waiting for the paperback before reading this terrific book, now is the time to get it.

Since GCBC came out a year or two ago, I’ve gotten countless comments asking me what Gary thinks about this topic or that one.  And I’ve gotten comments from folks asking me to ask Gary a question for them.  I was going to interview Gary and post his responses to my questions when it occurred to me that you all might like to ask questions of him directly without having them come through me.  I contacted Gary this weekend to see if he would be willing to answer specific questions from people on this blog.  He very generously agreed to do so.

Send your questions in via the comment section.  I ask on Gary’s behalf that you ask no personal medical questions, but questions about the science and the history of the science behind the way we eat today and the way we probably should be eating.  I promised Gary that he wouldn’t have to answer questions by the score, so we’ll see what comes in.  He and I will look at the questions and answer those that are a) the most common, b) those of the most general interest, and c) those that he feels are particularly important.

I know I don’t have to tell the readers of this blog not to be shy, but I will anyway.  Don’t be shy.  Get those questions in. If you’ve had a question that’s been gnawing at your brain, now’s the time to ask.

I’m heading off for a 9 hour drive to make it home in time to do my civic duty tomorrow, so I’ll be out of the loop for a while.  I can post comments through my Blackberry, however, so don’t hesitate to ask the question you would like to ask.

Note: I have closed the comments on this post.  Since Gary agreed to answer a number of questions, I think 101 is probably enough.  Thanks for all your interest and intelligent questions.

Imagine my surprise today when I got my emailed weekly version of Medscape Internal Medicine and found not just a lukewarm recommendation for the low-carb diet, but an enthusiastic one.

Medscape is a subscription service available only to physicians and is as mainstream as it gets. The lead article in this weeks issue is not really an article, but a video lecture.   One Dr. Sandra Fryhofer lectures the mainstream docs subscribing to Medscape on what the above study shows.   She points out the weaknesses of the low-fat diet and is positively enthusiastic about the low-carb diet.   She does issue a disclaimer, i.e., that the study was partially funded by the Atkins Foundation, but that’s about all.

She does get into the energy balance equation and the idea that it’s impossible to lose weight without exercise, but aside from that and he kind of condescending manner, the video is a real endorsement for the low-carb diet.   And – and I still can’t believe this – it’s being beamed out to mainstream physicians everywhere.

Since Medscape is a subscription service (it’s free, but you have to prove you’re a licensed physician to get the service), I figured they wouldn’t look kindly on my posting my username and password on this blog so that readers could see the video for themselves.   But I desperately wanted you all to see it.   So, I worked all afternoon trying to copy the video from the Medscape site and convert it to a form that I could post here.  After about four hours of trolling sites telling me how to do it in language I didn’t understand, I decided to see if I could somehow upload it onto YouTube.   Another zero there.   Finally, I called our youngest kid (he of the roughly sutured head) who is sort of a computer whiz and asked him if he could get ‘er done.   He fiddled with it for a while then put out the call to all his buddies for help.   A few moments ago I got an email from him telling me that his girlfriend found it already up on YouTube.   So, had I looked there first, I might have saved myself a lot of wasted effort.

Take a look and see if you don’t think Dr. Fryhofer is pretty enthusiastic about the low-carb diet.   I still can’t figure why this particular study would have rung her chimes, but I’m glad it did.   You can use this video as part of your armamentarium when you try to persuade your own doc why you want to go on a low-carb diet.

Enjoy.   Maybe the tide is starting to turn.

Click here to view the embedded video.

I’ve been on a low-carb diet, and I’m afraid my cholesterol is going to be up a little and my doctor will want to put me on a statin.  How can I show him/her that I’m really on the right track?

Another common variant:

I want to go on a low-carb diet, but I’m sure my doctor will be against it.  What should I tell him/her?

I’m always puzzled by these comments.  I’ve been on the other side of countless doctor-patient conversations, so I know how doctors (at least this one) think.  And I’ve been in countless doctor-doctor conversations, so I know how doctors think about their patients.  While there are a few old, crusty it’s-my-way-or-the-highway types still out there, it’s been my experience that most doctors are willing to work with their patients.

The important thing to remember is that you – not your doctor – are the one ultimately in control of your health.  I can guarantee you that if you have been reading this blog for any length of time or have roamed through and read in the archives, you are much more nutritionally savvy than the vast majority of doctors out there.  The old saw is absolutely true: doctors get very, very little nutritional training in medical school and even less in their post-graduate training.  In my own case, I got exactly one lecture on nutrition in medical school, and that was from a registered dietitian, which should tell you all you need to know.  And it wasn’t even a lecture on nutrition; it was a lecture on how to write orders for various diets for hospitalized patients.

Virtually all of my nutritional knowledge was self taught.  And most doctors don’t bother – I didn’t bother for the first five years of my practice.  I said all the same ignorant things and gave the same terrible advice that most doctors still give today.  Had statins been available then, I would have been giving them to everyone who walked through the door with elevated cholesterol levels.  I would have been telling patients that these drugs were a gift from the gods and that the evidence was conclusive that they worked.  And I would have been dead wrong.

Which brings me back to my first point.  You are in control of your own health.  And you likely know at least as much about nutrition as your doctor does.  So, why worry about what he/she thinks or says about nutritional issues? Besides, he/she is working for you, not the other way around.

But, it’s pretty apparent that many people are concerned about this issue, so let me tell you how to go about discussing diet with your doctor.

First, don’t bring a copy of Protein Power or some other diet book in and tell your doc to read it.  Just seeing a diet book makes the ‘fad diet’ warnings go off in a doctor’s head.  Plus, your doctor will never read it, so you’ll be wasting a perfectly good book. And don’t bring in magazine articles or copies of posts from this blog because they will scream the same ‘fad diet’ message.

Instead, bring in a short medical article.  I’m going to give you one you can print and use.  I’ll describe it a little later.  I’m going to provide you with a published case report, which is about all most physicians can read.  It will probably surprise you to learn that most practicing physicians don’t know how to and virtually never do search the medical literature.  (Academic physicians do know how to use the medical literature, but for the most part, don’t know how to take care of patients.)  So, if you bring in a long New England Journal of Medicine article, it will never get read.  A case report is what you want.

Then tell your physician that you’ve had friends or family that have been successful on this diet and that you are planning on giving it a short-term try.  And that you want your physician to monitor you.

If it’s a statin issue, you can do the Nancy Reagan and just say no.  Or you can say that you’ve done so well on your diet in other respects that you want to give it a little more time.  Or you can leave with the prescription and simply not get it filled if you don’t want to take the drug.  If you continue on the diet, your cholesterol will probably fall before your next visit anyway, and you can say that you decided to give your diet a little more time to work.  (If you want a lot of information to really discuss statins with your doctor, simply enter ’statin’ or ’statins’ in the search function of this blog and you’ll find plenty.)

I’ve got an interesting (and short) case report in my files that was published in the journal Aviation, Space, and Environmental Medicine, the official journal of the Aerospace Medical Society and sort of the unofficial NASA journal. Here is a downloadable pdf file of this paper suitable for presentation to your physician.pp-diet-in-an-aviator-av-spc-envir-med-2001

The paper presents the case of a 54-year-old army helicopter pilot with high-blood pressure (controlled with medications), obesity, diabetes, and elevated cholesterol.  When he presented for his annual flight physical, his blood sugar problems had worsened from glucose intolerance to diabetic proportions, and he was removed from flying status.  This pilot decided to go on Protein Power, and his flight physicians monitored him. Here is the brief history of his dietary journey:

After documenting normal renal function, that patient adopted a recovery plan of exercise and a high-protein diet.  His exercise consisted of walking 2 mi 3-4 times per week.  He kept his daily carbohydrate intake below 30 gms, but otherwise did not count calories.  In a 3-mo period of time, he lost 35 lbs.  His cholesterol was lowered to 204, his triglycerides [which had been greater than 500] lowered to 238, his fasting blood sugar lowered to 100, a 2-h post glucose load lowered to 122, and he discontinued his hypertension medication and remained normotensive.  The patient has continued the high-protein, low-carbohydrate diet with a gradual increase in the amount of calories from carbohydrates and for 1 yr has maintained quarterly hemoglobin A1C in the low 5 range.  He reports feeling better than he has in many years and has successfully returned to flying.

The article goes on to describe specifically the Protein Power diet in a comprehensive way.  It’s a much better short description of our own diet than one I could have probably written.  The paper then confirms the data we presented on the superiority of the low-carb approach with one other paper (there were more out there at the time, so I don’t know why they quit with just this one) that you can read in full text or download in pdf here.

This is the kind of case report you can simply give your physician and tell him/her that you are going to try this diet.  Your doc probably will read this one since it’s only two pages and reads like one doc writing to another, which is what a case report really is.

When you do go on the diet, your results should speak for themselves.  Your physician will then be as surprised as the docs were who wrote this case report.  Why do I know they were surprised?  Because you only write case reports on unusual or surprising findings.  You’ll never see a case report that says the patient came in with strep throat, we treated him with antibiotics, and he got well.  That’s an everyday occurrence.  It’s only the stuff that makes you sit up and take notice that inspires a written case report.  Your doc will be pleasantly surprised at your outcome just as these doctors were surprised at this aviator’s outcome.

Then maybe, just maybe, your doctor will want to know more.  And then you can give him or her the book.