In the Jan 9, 2012 issue of Archives of Internal Medicine in the Online First section an article appeared showing that women studied as part of the Women’s Health Initiative who were on statin drugs during the study developed diabetes at greater rates than those who were not on these drugs.  According to the statistical analysis of the authors, being on a statin increased the relative risk of developing diabetes by 48 percent!

These were observational studies and, as such, can’t be used to determine causality.  But they are interesting nonetheless because according to one of the authors there have been other clinical trials showing the same thing.  One of the authors of the study, Dr. JoAnn Manson, Professor of Medicine and Harvard Medical School commented on the findings of this study and what they mean to doctors who put patients on statins.  Dr. Manson’s commentary was provided by Medscape, a site for physicians to go to learn about the latest in medical wizardry.  The site requires registration, but if you are interested, you are allowed to register even if you aren’t a physician.

I decided that instead of commenting on Dr. Manson’s video after the fact, I would do it in real time right on the video.  This is my first effort at anything like this, so you can let me know what you think of it.  If you find it enjoyable and/or helpful, please drop a note in the comments, and I may be inspired to try it again.

You’ll notice my repeated assertions that statins don’t provide any benefits.  What I’m talking about is the fact that statins have never been shown to decrease all-cause mortality. (See the first sentence in the Lipitor product insert above.)   In other words, if you take a statin, you gain no increase in life expectancy.  If I, myself, am evaluating a drug that I might have to take, I would certainly want to make sure it didn’t simply replace one risk factor for another.

Click here to view the embedded video.

Note: The comments on this video made by me are my opinions based on my reading of the medical literature.  They are no substitute for consultation with your own physician, and should in no way be construed as medical advice.  The decision to start, continue or discontinue any drug regimen is a serious one and should be a decision made after careful discussion with your own physician.

As I mentioned in the video above, I just read a book by a cardiologist practicing the California who has dived deeply into the scientific evidence and feels the same way about the lipid hypothesis as I do.  And about statin drugs.  And this a real cardiologist.  Ernest N. Curtis, M.D. has written The Cholesterol Delusion, a book that takes a different approach to dismantling the lipid hypothesis than The Great Cholesterol Con, but is just as effective.  If you’re still in the camp that worries about cholesterol, you may take solace from the information in this terrific book.  If you need to persuade a friend or loved one, this is the book.

If you enjoy the way I sometimes dissect studies on this blog, you will love Dr. Curtis’s book because that’s what he does.  He dismembers the studies that the lipophobes rely on to maintain their fantasy that cholesterol really does cause heart disease.

Take for example the Lipid Research Clinics Coronary Primary Prevention Trial (LRCCPPT), the authors of which made the oft repeated claim that each 1 percent reduction in cholesterol gives a 2 percent reduction in cardiac risk.  Dr. Curtis eviscerates this study and describes how the authors dishonestly spun their experiment’s end result, which was essentially meaningless, in such a way that it has become one of the mainstays in the argument for cholesterol lowering.

During the study, 7 percent of the subjects on a cholesterol-lowering drug died while 8.6 percent of those on placebo died.  Dr. Curtis describes how this minuscule difference can be converted into a relative risk difference of 19 percent, which is what the authors were crowing about.  But that number isn’t nearly as important as the absolute risk, which is the difference between the 8.6 and 7, or 1.6 percent.  So those subjects on the drug (which is not without side effects and costs if the subjects had been paying for it themselves) ended up with a 1.6 percent lower absolute risk than those who didn’t take the drug.

But that’s not the end of the story.  Was the 1.6 percent difference even statistically significant?  Here’s where things get interesting.

How significant is the difference between 7.0% and 8.6%? Common sense tells us that this difference is of no practical significance.  But what about the more esoteric criterion of statistical significance?  According to the pretrial protocol, which called for a level of certainty with p<0.01, it didn’t even come close.  If one applies the more lenient criterion of p<0.05, it still fails the test when the typical two-tailed test is employed.

If one applies the p<0.05 criterion and uses the less rigorous one-tailed test, however, this difference barely qualifies as statistically significant.  This is, in fact, what the investigators did.  In one of the most flagrantly dishonest acts ever seen in a major medical study, the authors apparently changed the criteria for significance after reviewing the data.

The is absolutely shameful behavior way beyond the pale.  When researchers design a study, they set on the front end the statistical parameters by which the outcome of their experiment is to be measured.  They do this at the start so there can be no fudging at the end when the results are in.  Everyone agrees to the standards and off they go to do the study, and the outcome either reaches the level of statistical significance by the predetermined measure or not.  In this case, the standards were set, but when they weren’t reached, the standards were reduced once and then again before the results barely were able to claim statistical significance.  Shameful indeed.  And this is one of the major studies, quoted daily, showing that a reduction in cholesterol brings about a reduction in heart disease.  Jesus wept.

Why didn’t other scientists say anything about this.  One did and wrote  a withering critique in the Journal of the American Medical Association, but the journal kept it under wraps for a year before publishing.  By that time, the LRCCPPT had gotten so much coverage and the cholesterol-lowering-prevents-heart-disease mantra had swept the nation, so everyone pretty much ignored the grousing of a scientist who saw the emperor without any clothes. (You can’t tell much from the abstract I linked to, but Dr. Curtis reprints some of the juicier parts.)

This study isn’t the only one with warts all over it nor the only one routinely misinterpreted.   But it’s not surprising given the vast amount of money at stake in the business of reducing cholesterol by drug therapy whether that cholesterol reduction is important or not.

After you read Dr. Curtis’s book you will become as big a skeptic as I am of medical studies and regard them all with a jaundiced eye.

In 1976 the classic film Network starred Peter Finch as crazed anchorman Howard Beale who launched into his now-famous rant “I’m mad as hell…” on air and galvanized movie goers everywhere.  Even though Howard Beale is fictional, I often share his sentiments.

I got a call yesterday from an acquaintance who wanted to get together and talk to me “face to face.”  I’ve played golf and had a few drinks with this guy over the last couple of years, but that’s about it.  I agreed to meet him at a local coffee shop.

When we had our coffees in front of us – I, a full-strength, scalding hot Americano; he, a non-fat, decaf, double shot latte, just in case you’re wondering – we made small talk for a few minutes then he cut to the chase.  A look of despair came over him, and he confided to me that he was a type II diabetic and was in real trouble.  His doctor had been monitoring his HgbA1c levels for a couple of years, and lately they had been inexorably on the rise to the point at which drastic action was required.  What drastic action?  His doctor told him he was going to have to start insulin injections.

The guy had begged his doctor for a reprieve, which he got until the end of the year, then called me in desperation.

I went through all the quotidian doctor questions and discovered that he was taking three different drugs for his blood sugar, a high-blood pressure pill, a medicine for his GERD and, it should go without saying, a statin.  I asked him about his typical diet, but I already knew the answer.  He ate pretty much what he wanted to eat, but he did try to avoid desserts because he knew sugar wasn’t good for him.  I then inquired as to whether his doctor had discussed diet with him as a part of his treatment.

He said the doctor had advised him numerous times to cut the fat from his diet.  His physician had told him that his diabetes put him at a greater risk for heart disease – which is indeed true – and that, consequently, he should cut the fat, especially the saturated fat, from his diet and live mostly on complex carbs.  He said he had tried, but just couldn’t seem to stick with it for any length of time.  With a What-can-I-do? kind of shrug, he divulged that he was a real meat-and-potatoes kind of guy who felt he would always be hungry if he couldn’t have a steak or a burger from time to time.

I asked if his doctor had perhaps suggested a low-carb diet when the low-fat diet hadn’t worked for him.  No, not really.  In fact, he, himself, had asked about the South Beach Diet since he had a friend who had done well on it.

“Absolutely not, replied his physician.  Too much fat.  Remember, you’re at increased risk for heart disease.  Besides, you don’t want to go on a fad diet.  You’ve got a serious health problem, so you need to go on a diet that might make you better.”

For the most part I face widespread medical/nutritional idiocy with a fair amount of equanimity, but every now and then, when I brood on the cost in human suffering this idiocy all too often causes, I want to do the Howard Beale and scream “I’m mad as hell.”  Problem is the idiocy is so widespread that my pitiful efforts to counter it are on par with King Canute’s trying to hold back the tide.  If I can make a little difference here and there, I suppose it’s worth the effort, so I keep trying.  But I still want to scream.

I started ruminating about all the misery this seemingly universal lack of nutritional understanding engenders when I read on Fred Hahn’s blog an email he posted from one of his readers.  In short order, I came across a brief anecdote in a book I was working through.  If that weren’t enough, I got a copy of Robb Wolf’s new book and read about his medical experiences.  Then, hard on the heels of that, the meeting with my friend almost put me over the edge.  I was ready to lean out the window and start screaming, “I’m mad as hell…”

First the email, which I have excerpted.  You can read it in its entirety here.

I also want to really thank you personally for being a part of a program that has saved my life.  That may sound dramatic, but here is my story.

I am 42 years old and 6 foot tall.  A little over ten years ago I was diagnosed with Type 2 diabetes and given medication to deal with it.  I was also told to lose some weight.  I weighed between 200 to 205 at the time.  I was also told to lower my fat intake and I could eat as much fruits and vegetables as I wanted.

Over the years, the weight stayed relatively consistent.  I am not athletic at all, but am fairly active.  However, the quantity of food has consistently gone down in my efforts to lose weight.  Additionally, my blood sugar has constantly gone up.

In these last two years, my weight started creeping up some.  As a result, I stated running fairly regularly.  It had no, or very little effect on my weight.  I pretty much stopped eating a regular dinner at night after work.  All I would eat is some yogurt or some fruit cups at night. Remember, I could eat all the fruit I wanted.  I still kept gaining weight, but my fasting blood sugar that I measured in the morning did come down a little.

On March 14th of this year, I weighed 215.  I was taking 4 different diabetes medications, one blood pressure drug, pretty much taking a Prilosec everyday for heartburn as well as Tums fairly regularly.  My doctor did not seemed concerned with the heartburn.  I assumed it was from stress at work.  I would also vomit fairly regularly.  I assumed from the various drugs, maybe stress.  My cholesterol as indicated from my blood tests when I visited my doctor were higher than recommendations as well as my blood pressure.  Neither super high, but higher than what is considered normal and healthy.

I visited all the normal diabetes type web sites and none of them said anything or recommended anything that seemed to offer anything of value.  I was mostly doing what they said.  Lots of fruits and vegetables, lots of whole grains, try to lower fats and some exercise.  Yes to all of the above.  Yet I continue to get worse.  I was beginning to believe this was just a part of aging and having diabetes.

How long was it going to be until I started having real health issues?  For the most part I very rarely get sick.  When was I going to start going blind, lose a foot or leg, have a heart attack, kidney failure, stroke out???  I was getting to be resigned that it was just a matter of time.  Inside my head I secretly hoped that I would have a fatal heart attack at a relatively young age so I would not have to deal with the real issues of diabetes.

On March 14th in a round about way, I found the Protein Power book.  It was opposite everything I knew to be true, yet it seemed more true about nutrition than anything I read before.  How could everybody else be so wrong?  I instantly started following it, cutting my carb intake to next to nothing or at least less than 30 grams a day.  Before stating this, knowing what I ate, I am fairly certain my carb intake was close to 60 to 70 percent of my total calorie intake.  I bought your book a couple weeks later.

I am sure you will not be surprised at all by the results.  As of this morning I now weigh a little over 190.  It has been close to 20 years since I have weighed that little.  I have stopped taking two of the diabetes drugs completely, one of the others I am taking 80% of what I was taking, the other I am down 30%.  I have not taken a single Prilosec or a Tums since I have started this change and this is the most stressful part of the year for me as it relates to work.  I have only vomited once and that was on March 16 or day 2.  Six weeks in, I had a doctor visit and blood test.  Blood sugar way lower, bad cholesterol way lower and in the normal range, good cholesterol way higher and also now in the normal range.

Five weeks after I changed my eating habits, I started my slow burn routines based on your book.  With some of the exercises I really struggled at first, but now am fairly comfortable with most of them.  I am still learning and refining a few things, but I can say my increases in strength are just as dramatic as my weight loss.  In the case of the chest press, the very first time I did it following your slow burn book instructions I did 3 reps at 100 pounds and was wiped out.  Yesterday, at 130 pounds I did 6 reps in a little over 2 minutes.  Time to increase the weight again.

As I said before, I was running fairly regularly for a few years.  Not that fast, and really, not that far, 3 to 4 miles in around 45 minutes.  Generally 3 or 4 times a week to do “some exercise” as recommended by my doctor and everything I had read about diabetes.  I have cut back on the running since I started your workouts, but when I do run, I run significantly farther and significantly faster than I have run in years.  I hated, hated, hated the running, but did it to do my exercise.  Now when I do run, it is almost fun.  I am so amazed at the changes in me.

So that is how you have had a part in saving my life.  I do not know how to say thank you any more than that.

Not long after coming across this email, I was reading a book on TRIZ, a methodological approach to engineering problem solving that can be applied to other realms, when I came across a report of a disturbing doctor-patient interaction.  The author is using this story to illuminate a problem solving technique called peeling the onion, which means to continue to dig deeper and deeper in the quest for a solution.  Instead of illuminating anything for me, it just made me mad as hell.

One day, I was sitting in my doctor’s office anxiously waiting to hear the results of my most recent cholesterol screening. The previous year my cholesterol had gone up just slightly, which was very depressing. I essentially had no exercise regiment prior to that, but afterward I went into fat-free mode and started walking 4 miles a day. In spite of my protests, a couple of years earlier my doctor had put me on a low dose of blood pressure medication. I don’t even like to take aspirin.

As a result of my hard work, I was certain my current cholesterol level would be outstanding. I couldn’t wait to hear the great results.

Unfortunately, the test results painted a different picture. My cholesterol level was 30 points higher.

“That’s impossible. I don’t eat beef brisket anymore… ever! I don’t eat any sausage, never go to McDonalds, buy fat-free everything, and walk 4 miles a day. It can’t be true.”

“Yeah, it sucks getting old doesn’t it? Aging is that one thing you can’t control. Even though you’re trying to eat better and exercising, which is a great thing, these efforts are obviously not enough.”

“What? Older? It has only been a year! Urrrrrrr…this doesn’t make any sense. It’s not fair.”

“I think we should put you on Lipitor.”

“No. I don’t want to take anymore meds. Let me think about it for a while. This makes no sense.”

When something makes no sense to you, your curiosity needs to kick into high gear. Well, this surely qualified as nuts to me. Yes, I was a year older, but… come on. The test results couldn’t be right. Most people would probably just do as the doctor ordered, but I almost never take anything at face value.

The author then goes on to describe how he “peeled back the onion” by doing internet searches for cholesterol and found that one of the supplements he had been taking for his joint pain – glucosamine – had been found in some cases to raise cholesterol levels.  He went off of the glucosamine, and as he tells it:

Two months later, my cholesterol was 30 points lower and back under the limit.
If I did not have a curious nature about most everything I would have been on another needless medication. It pays to peel the onion back.

I don’t think his glucosamine had anything to do with his cholesterol – the 30 point drop in his cholesterol was probably just the normal roaming range of his cholesterol levels over time. The take home lesson of this story is that this guy’s doc was ready to put him on an expensive medication with a number of pretty severe side effects because of one cholesterol reading above a particular number.  The doc wasn’t treating a patient, he was treating a lab value.  In this case the patient is a young man (mid 40s) with no history of heart disease, the very kind of patient for whom no benefit has ever been found for statin therapy.  Why, when this patient’s low-fat diet failed to lower his cholesterol, didn’t his doctor suggest a low-carb diet?  Studies have shown the low-carb diet to be more effective in solving lipid problems than the low-fat diet.  So why wasn’t it suggested.  Had this patient gone on his doctor’s statin of choice and not had his cholesterol fall, his doctor would have tried another statin.  Why not try another diet?

If you read the entire book, the author mentions throughout how his days of red-meat eating are over and makes numerous references to his much-despised (but in his mind, therapeutic) low-fat diet.  It’s really sad that he’s such a victim of medical ignorance.

I got a copy of Robb Wolf’s new book The Paleo Solution and started reading the first chapter, which describes Robb’s own story.  In short, he spent years as a vegetarian, getting sicker by the day.  All his physician’s told him that he was lucky he was able to follow the diet he was following because he would have really been much worse had he been following a standard diet.  Robb ultimately came around to the low-carb, high-meat Paleo way of eating and solved his own health problems.  When he went back to his various physicians to get blood testing – all of which was perfect for the first time – he was ecstatic.  He told his doctor he had completely changed his diet.

“Doc! Have you ever heard of the Paleo diet?” I asked.  “How our ancestors ate for millennia?”

His answer was typical of what I would encounter in the years to follow.  “That is pseudo science.  There is no proof.”

When Robb describes the remarkable difference in his health to yet another doctor, he is told:

It must be something else.

Why do these stories make me mad as hell?  Not just because the people involved suffered as a consequence of medical hubris, incompetence and intransigence, but because so many millions of others do suffer miserably and aren’t lucky enough to escape their fates as these few were.

It’s difficult to imagine the number of people who go into doctor’s offices every day with weight problems, elevated blood sugar, high blood pressure, and abnormal lipids and are told with great authority to eat less and exercise more.  If the patient asks the doctor for a specific diet, the doc usually has the nurse give the patient the standard 1800 kcal low-fat diet sheet.  Depending upon the motivation of the patient, this diet may or may not be followed.  If the patient does suck up and follow the diet, many, of not most, will fail. When these poor folks come back for their recheck, their doctor then wants to put them on some sort of drug.  Believe me, the stories above aren’t atypical.  This is happening all across the country thousands of times every single day.

And I’m mad as hell because it doesn’t have to be this way.

There is another option.  These poor people could be given a low-carbohydrate diet to try.  Most of the doctors who prescribe the 1800 kcal diet (along with a recommendation to exercise more) could give people the choice.  A low-carbohydrate diet or a low-calorie diet.  But the vast majority of them don’t.  They simply opt for the low-calorie diet, then resort to drugs when it doesn’t work.

There is plenty of good research available now showing the low-carb diet to be at least the equal of the low-fat diet in virtually every parameter with most of the studies showing the low-carb diet to be superior.  With this research backing the efficacy of the low-carb diet, why don’t more doctors offer it as an option?  Naiveté? Stupidity? Pigheadedness? Who knows?  What I do know is that it’s a real problem.

Lately the web has been full of various health gurus (mainly those involved in weight training and/or bodybuilding) making the case that the only reason the low-carb diet works is that it is satiating and spontaneously causes its followers to restrict calories.  It’s the calories, say they, not the carbohydrate restriction that does the job.  I say, So what? Who cares as long as it works?  And countless studies have shown the low-carb diet to be as efficacious (if not more so) as the low-fat diet, so why isn’t it offered as an option?

If a doctor treats a patient with a specific drug for high blood pressure, and the patient’s blood pressure doesn’t respond, the doctor switches medications.  Most doctors will fiddle with the medicines to get the problem solved.  Why not do that with diets?  Why just go with the low-cal, then move immediately to drugs if that diet fails?  Years ago, during the interim in which low-carb diets were out of favor and not much good data existed on their efficacy, I could understand it.  But why now?

It seems that almost every week a new study is coming out showing the superiority of the low-carb diet.  Over the past couple of years we’ve had a trifecta of well-done studies published in major scientific journals demonstrating the effectiveness of low-carb diets.  There was even a meta-analysis published in Obesity Reviews, the most mainstream of mainstream academic journals** showing low-carb diets work better than low-fat diets.  So why don’t more doctors recommend them?

I’ve been infused with a little hope by a recent totally unscientific poll published in the Annals of Internal Medicine.  Readers (primarily physicians) were presented with the following poll.

Surprisingly, the majority answered that they would give a low-carb diet a try first.

The particular issue of the journal publishing this poll was the one containing one of the more recent papers on the benefits of low-carb dieting.  (I’ll post later on this amazing study that was designed to fail.)  As a consequence, I would bet docs taking this poll were skewed in the low-carb direction.  But who knows? I can always hope it means there is a light at the end of the tunnel, and that physicians are beginning to discard their low-fat tunnel vision.  The fact that this poll even exists in a major mainstream journal.  We should all take heart.

But until docs start changing diets that don’t work at the same rate at which they change blood pressure medicines, many, many people will suffer.  And I’ll continue to get mad as hell every time I hear about travesties such as the ones I wrote about above.  Too bad there aren’t diet reps that go into all the doctor’s offices like the drug reps do.  Maybe if there were, things would change a little faster.

Since most of you reading this blog visit your doctor from time to time, perhaps you can play the role of diet rep.  You can do it by telling your doc how your low-carb diet is working for you.  And you can provide literature just like the drug reps do to add substance to your report.  Here is a pdf file of the Obesity Reviews meta-analysis showing low-carb superiority. Meta-analysis of low-carbohydrate diets

So, be ambassadors for the low-carb diet so that more physicians might give it a try. If enough of you do that, your actions will provide a gentle but steady invigilation that will ultimately bear fruit. When physicians do gingerly recommend low-carb diets a few times, they’ll see the same astonishing results you have.  More and more will start recommending low-carb to their patients as a first line therapy, which will decrease the number of tales of woe I’ll have to sit through.  I can then dodder off into my dotage in a much more sanguine frame of mind.

If you haven’t seen it, here is a clip of the famous I’m mad as hell speech from Network.

Click here to view the embedded video.

** How mainstream is Obesity Reviews? It is the journal that published George Bray’s unfair and almost incomprehensible review of Gary Taubes’ book Good Calories, Bad Calories.

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

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

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

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

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

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

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

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

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

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

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

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

Recognized?  What does that mean?

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

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

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

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

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

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

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

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

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

But as for heart disease itself:

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

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

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

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

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

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

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

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

It was unbelievable.

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

Watch and just shake your head.

Click here to view the embedded video.

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

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

This link requires requires free registration.

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

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

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

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

Let’s take a look.

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

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

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

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

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

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

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

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.

As if trying to pull meaning out of the medical literature weren’t difficult enough as it is, a new study demonstrates yet another obstacle to easy understanding: the adherer effect.

We’ve all seen the headlines.  Statins improve bone health.  Statins prevent cancer.  Statins make us smarter.  Low-fat diets improve longevity.  All these headlines and others like them are followed by articles describing studies seeming to show that subjects taking certain medications (usually statin drugs, it seems) or following a particular diet have improvements in health and/or longevity.  The promise of these articles is that if we all take the medication or follow the lifestyle choice, we, too, will reduce our risk of [fill in the blank] or live longer.  But will we?

Maybe so.  But not for the reason most people think.

The adherer effect demonstrates that people who adhere to medical or lifestyle regimens end up with better outcomes than those who don’t…even if the regimens are nothing but placebo.

I mentioned this phenomenon in an earlier post.

Almost thirty years ago a study was published in the New England Journal of Medicine looking at this very idea. [The adherer effect]  The study that inspired the article didn’t start out looking at this idea, but one of the investigators noted a key piece of the data and published on it.  The study was looking at clofibrate, a pre-statin cholesterol lowering drug,  and all cause mortality.  Subjects were randomized into two groups – those in one group got the drug, those in the other got the placebo.  After the subjects were on either the drug or the placebo for five years, researchers calculated the mortality from the number of deaths in each group.  Turned out that the five-year mortality of those on clofibrate was 20.0 percent whereas the five-year mortality of those on the placebo was 20.9 percent, or essentially the same.  Taking the drug was no different than taking the placebo, i.e., the drug was worthless. Had one of the researchers not looked a little closer, that would have been the end of the story.

When the data were looked at from the perspective of how many people actually took the drug as prescribed, the researcher discovered that those subjects who took at least 80 percent or more of their clofibrate had a five year mortality of only 15.0 percent, substantially less than the overall five-year mortality.  Those who took their clofibrate sporadically had a five-year mortality of 24.6 percent, significantly higher than those who took it as directed, a piece of data that would seem to confirm the efficacy of clofibrate.  Right?  Not necessarily.  Let’s look at compliance with the placebo.

Turns out that those subjects on the placebo who regularly took their placebo had a five-year mortality of 15.1 percent while those who took their placebo sporadically had a five-year mortality of 28.3 percent.  What this study really showed was that there is something intrinsic to people who religiously take their medicine that makes them live longer.  There was no difference between the drug and placebo in either those who took them regularly or those who took them sporadically, but there was a huge difference in mortality between those who took either drug or placebo on schedule and those who didn’t.

Gary Taubes discussed this same study and the adherer effect in  a long article he wrote for the New York Times Magazine a few years ago:

A still more subtle component of healthy-user bias has to be confronted. This is the compliance or adherer effect. Quite simply, people who comply with their doctors’ orders when given a prescription are different and healthier than people who don’t. This difference may be ultimately unquantifiable. The compliance effect is another plausible explanation for many of the beneficial associations that epidemiologists commonly report, which means this alone is a reason to wonder if much of what we hear about what constitutes a healthful diet and lifestyle is misconceived.

The lesson comes from an ambitious clinical trial called the Coronary Drug Project that set out in the 1970s to test whether any of five different drugs might prevent heart attacks. The subjects were some 8,500 middle-aged men with established heart problems. Two-thirds of them were randomly assigned to take one of the five drugs and the other third a placebo. Because one of the drugs, clofibrate, lowered cholesterol levels, the researchers had high hopes that it would ward off heart disease. But when the results were tabulated after five years, clofibrate showed no beneficial effect. The researchers then considered the possibility that clofibrate appeared to fail only because the subjects failed to faithfully take their prescriptions.

As it turned out, those men who said they took more than 80 percent of the pills prescribed fared substantially better than those who didn’t. Only 15 percent of these faithful “adherers” died, compared with almost 25 percent of what the project researchers called “poor adherers.” This might have been taken as reason to believe that clofibrate actually did cut heart-disease deaths almost by half, but then the researchers looked at those men who faithfully took their placebos. And those men, too, seemed to benefit from adhering closely to their prescription: only 15 percent of them died compared with 28 percent who were less conscientious. “So faithfully taking the placebo cuts the death rate by a factor of two,” says David Freedman, a professor of statistics at the University of California, Berkeley. “How can this be? Well, people who take their placebo regularly are just different than the others. The rest is a little speculative. Maybe they take better care of themselves in general. But this compliance effect is quite a big effect.”

In the same blog post of mine I linked to above, I wrote about another study showing the adherer effect, showing graphically how potent the phenomenon is.

Previously, the study of the adherer effect has been a secondary finding in studies of various drug regimens, but now comes a paper in which the adherer effect is the primary focus of the investigation.  Based on the data in this recent paper, the effect is robust and should be accounted for in the analysis of any data generated when subjects following a particular treatment are compared to those who don’t.

The authors lay out the problem:

The healthy-user effect [the adherer effect] is a hypothetical source of confounding bias that is thought to affect observational studies of drugs, diets, screening procedures, and other health-related behaviors. This bias presumes that patients who initiate and adhere to preventive therapies are more likely to engage in behaviors consistent with a healthy lifestyle than are patients who do not initiate or adhere to such treatments. Aspects of a healthy lifestyle could include diet, exercise, moderation of alcohol, and avoidance of risky behaviors. These characteristics, which are unmeasured in typical pharmacoepidemiological databases, may be associated with morbidity and mortality outcomes in observational studies. Thus, failure to adjust for them can lead to bias in studies of preventive therapies.

The healthy-user bias has been suggested as an explanation for the discrepancy between several experimental and observational studies, including studies of the effects of long-term use of estrogen therapy and vitamin E. It has also been discussed as a potential source of bias in observational studies of the effectiveness of influenza vaccines in the elderly  and the association between use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and reduced risk of hip fracture,  Alzheimer disease,  sepsis,  cancer,  and mortality.  This bias has also been observed in randomized controlled trials in which adherence to placebo was found to be associated with decreased mortality.  Although long suspected as a source of bias, a paucity of empirical data exists on the healthy-user effect.

Here’s how the study was set up.

It was really pretty simple.  The researchers looked at a group of patients who had been prescribed one of a variety of statin drugs and followed their compliance by looking at how many times these subjects picked up their medicines in the year following their prescription.  The typical statin prescription was for 60 days worth of the medication, and all subjects had available to them a full year’s worth of medicines.  The researchers grouped subjects into two groups: one group who took the trouble to go get over 120 day’s worth of the medication (the “more adherent”) and one group of subjects who were dispensed under 120 days of meds (the “less adherent”).

All subjects entered into the study were evaluated after the one year baseline study period during which their effort to follow their prescribed statin regimen sorted them into the categories of more adherent or less adherent.  The researchers were looking to see which subjects – the adherers or the non-adherers – would develop problems that had nothing to do with the statin drugs.

We evaluated a spectrum of events after the 1-year baseline period to assess the healthy-adherer bias. The outcomes were grouped into 4 broad categories: accident events, screening events, other events not expected to be associated with statin exposure, and other events for which a possible association with statin exposure could be expected. We included inpatient and outpatient events as well as primary and secondary diagnoses.

When the data on these 141,086 subjects was crunched, it turned out that the more adherent subjects had significantly fewer accidents, especially motor vehicle and workplace accidents.  The more adherent also had a lower likelihood of developing other disorders that were not likely to be attributed to the effect of the statin drugs.

In other words, whatever characteristic it was that made subjects hang in there with their statin prescriptions also made them less likely to indulge in risky behaviors and less likely to develop all kinds of medical problems.  Why?  Probably because these people were simply more health conscious, kept themselves in better shape, and didn’t act impulsively.

The real take-home message from this study is that the adherer effect significantly affects the outcome of drug and lifestyle intervention studies.  If you see a study that says those subjects using statin drugs developed 20 percent fewer problems (of whatever kind are being studied) than those who don’t use statins, you can be sure that the adherer effect is at work.  This adherer effect is why randomized, double-blind, placebo-controlled studies are needed to determine the efficacy of any drug, and even then the adherer effect should be controlled for.

There is a big note, enclosed in a box and titled Clinical Perspective, at the end of this study that exhorts doctors to consider this adherer effect when looking at data from observational studies.  Here is the note in full.

Clinicians need to read observational studies reporting surprising benefits of drug therapy with a healthy skepticism. Observational studies of preventive medications and health behaviors are susceptible to various sources of bias, including the so-called healthy-user and healthy-adherer biases. In this article, evidence of the healthy-adherer effect is demonstrated by showing that adherence to statins is associated with a reduction in the risk of accidents (eg, workplace or motor vehicle), outcomes that would not be expected to be affected by a statin. The approximate magnitude of the adherer effect was a 15% relative risk reduction. The most likely explanation for this association is that good adherence to statin therapy is a marker for other healthy behaviors, most of which cannot be accounted for in this type of study. In keeping with this explanation, the study also shows that adherence predicts a 7% to 17% increased incidence of medical screening procedures (eg, fecal occult blood testing, mammography). Risk of myocardial infarction, which has been demonstrated to be reduced by statin therapy in randomized placebo-controlled trials, was found in this study to be reduced by 28%. This observed relative reduction must be interpreted as reflecting a combination of the healthy-adherer effect and the drug effect. Clinicians can also learn from this study that patients who follow their advice are also likely to have other healthy behaviors and a lower risk of adverse events.

It is unfortunate, but I doubt that many doctors (or researchers, for that matter) will consider the adherer effect when they read these studies.  I would bet that we will continue to see studies reported as if the positive effects found were a function of the drug or lifestyle regimen studied and not the adherer effect.

To me the saddest part of this study was the statistic that of the 141,086 subjects in this study, 49 percent were women.  The randomized, double-blind, placebo-controlled studies of statins have never shown a benefit in terms of decreased all-cause mortality in women of any age.  Which means that over 70,000 women in this study took a drug that would do them no good, but which could well cause them significant and harmful side effects.

In this study, those who dropped out of their statin regimen because of intolerable side effects would be considered to be less adherent or non adherers.  My guess is that many of these ‘non adherers’ who dropped out because of side effects were really ‘adherers’ by nature.  Had these drop outs due to side effects been controlled for, I would bet that the difference between the less adherent and the more adherent would have been much larger than the data showed.

Snake oil comes in many guises, most of which exist to reduce the contents of one’s purse.  Last week an Associated Press writer detailed how the government spent $2.5 billion of our money to test various so-called alternative health remedies, most of which would be considered snake oil by mainstream medicine, and came up virtually empty handed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

One more.

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

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

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

HAHAHAHAHAHAhahahahahahaha! Oh man, sometimes I crack myself up.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Nitrogen-fixation process

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

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

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

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

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

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

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

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

Fertilizer factory using the Haber-Bosch process

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

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

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

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

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

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

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

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

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

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

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

I’ve had a number of people email me about a new study appearing in the Archives of Internal Medicine purportedly showing that statins really do provide benefit to those who take them regularly.  As you can see from the heading of an email piece I pasted above, even Medscape is all over this article and blasting it out to physicians all over the world.

I’m sad to say that this is the same kind of paper I would have been taken in by 20 years ago before I really understood how to read the scientific literature critically.  In fact, I would have used it myself to justify giving statins to all kinds of people, and I’m sure other physicians are doing so right now.  But I would have been in error to base my prescribing on this paper, and all the other docs out there giving statins like they were candy are in error as well.

If you don’t want to read a dissection of this study, let me just tell you up front that it doesn’t really mean a thing.  It certainly doesn’t prove that you should rush out and get started on statins.  If, however, you do want to learn about how perniciously deceptive these kinds of studies are and how to analyze them, read on.

Here’s the deal.  Researchers went back and combed through the records of a large HMO in Israel and pulled those of patients who had been prescribed statins from 1998-2006.  Since the HMO provided the statin prescriptions, there were records of how many of these people who were prescribed statins actually filled their prescriptions (and, one would assume, took the medications).  Then the researchers figured out how many of those people prescribed statins died.  The final step was to compare the list of those who died with the list of those who took their statin prescriptions (or, more accurately, those who filled their statin prescriptions).  After crunching all this data, it turns out that those patients who filled over 90 percent of their prescriptions were 45 percent less likely to die than those who filled under 10 percent of their prescriptions.  Which, to the uncritical reader (including, obviously the Medscape writers and the peers who reviewed this piece for the journal in which it was published), this appears to be pretty persuasive evidence that statins confer some kind of benefit in terms of preventing death.  After all, those that took them lived while those who didn’t died.

As I say, these kinds of studies are pretty beguiling.  But do they really mean anything?

Before we get to the specifics of this study, let’s contemplate this type of study in general to see why the data they generate is often misleading.

The gold standard for scientific studies is the randomized, double-blind, placebo-controlled trial.  In this type of study, researchers randomize the study population into two similar groups and give the members of one group the drug being studied and the other a placebo.  Double blinded means that neither the researchers nor the subjects know who got what.  At the end of the trial, the data are analyzed to determine if the study drug really showed any difference in efficacy as compared to the placebo.  If it did, then it can be said that the drug works to treat whatever condition was being studied.  Or that it decreases all-cause mortality, if that is the end point of the study.

It’s impossible to do these gold standard studies with diet and/or exercise because a) they involve lifestyle changes and b) they can’t be double blinded.  When it comes to diet and exercise, there are basically two ways studies can be done.  Researchers can allow subjects to self-select which arm of the study they want to be in.  Or researchers can put subjects into one arm or the other.  Neither of these choices is optimal, but they are all that are available.

If I decide that I’m going to compare a very-low-carb diet to a very-low-fat diet, I can recruit volunteers and ask them which diet they would prefer.  If readers of this blog were recruited into such a study, I would assume most would opt for the very-low-carb diet.  Those who are fans of Dean Ornish would opt for the other.  What you end up with is people in each arm of the study who are already believers in the diet they will be following, and they will be more likely to remain on the diet until the end of the study.  At the end, the data will be a little polluted because it really doesn’t prove that one diet is superior to the other – it only proves that people who self-select into that diet do better on that diet than people who self-select into the other.  The last it an important point, especially when applied to exercise.  More about which in a moment.

The other way to study diet is to gather a group of people together and randomize them into one diet group or the other.  That takes the self-selection bias out of the equation.  But it creates other problems.  If a person committed ideologically to a low-carb diet gets randomized into the low-fat group (or vice verse) there are problems with compliance.  Most nutritional studies randomized this way end up with large numbers of dropouts.  If you do an intention-to-treat analysis of the data (which includes the drop outs), you usually find little difference between the two diets.  If you look at only those subjects who hung in there for the duration on whichever diet they were randomized onto, it raises the issue of whether these subjects may have been the same ones who would have self-selected themselves into this same diet if given the chance, which then creates the same problems as self-selection.  These issues make diet studies difficult to do and difficult to interpret validly.  It’s even worse with exercise.

I get a ton of email and comments from people who can’t come to grips with the idea that there is no proof that exercise brings about weight loss.  I say this because it is difficult to come by this proof.  Even those who are adamant that exercise brings about weight loss agree that pretty intensive exercise is required to do so.  The typical prescription to just get out and move a little more virtually everyone realizes is worthless.  Most people believe that it’s intensive exercise that does the trick.  Maybe so, but how do you prove it?

If you randomize people into an intensive exercise group and another into a no exercise group to see which loses the most weight (assuming diet is held constant), how many of those sedentary people are going to stick with the intensive exercise for any length of time.  They will be the dropouts.  If you allow people to self select, all the people who enjoy exercise will put themselves into the exercise group while those who hate it will put themselves into the sedentary group.  Then if those in the exercise group do lose weight, how can you tell it’s the exercise and not due to some other component of a person who will commit to an intensive exercise program that brings about the weight loss?  The answer is that you can’t tell.  Which is why the notion that exercise brings about weight loss is similar to a particular religious belief: it is accepted as an article of faith, not as a product of scientific investigation.

You can send me a comment (as several people have done) telling me how you were stuck in your weight loss efforts at 220 pounds and then you decided to start high intensity interval training.  After a couple of months of this, you lost 25 more pounds.  Therefore that’s proof that exercise brings about weight loss.  Wrong!  That’s proof that in you exercise brought about weight loss.  There may be something different about you that allows you to commit to such a regimen that others might have difficulty following AND allows you to lose weight.  This sounds ridiculous, but it is true.  And it is the key to understanding why this statin study is bogus in terms of whether or not taking statins makes people live longer.

Almost thirty years ago a study was published in the New England Journal of Medicine looking at this very idea.  The study that inspired the article didn’t start out looking at this idea, but one of the investigators noted a key piece of the data and published on it.  The study was looking at clofibrate, a pre-statin cholesterol lowering drug and all cause mortality.  Subjects were randomized into two groups – those in one group got the drug, those in the other got the placebo.  After the subjects were on either the drug or the placebo for five years, researchers calculated the mortality from the number of deaths in each group.  Turned out that the five-year mortality of those on clofibrate was 20.0 percent whereas the five-year mortality of those on the placebo was 20.9 percent, or essentially the same.  Taking the drug was no different than taking the placebo, i.e., the drug was worthless. Had one of the researchers not looked a little closer, that would have been the end of the story.

When the data were looked at from the perspective of how many people actually took the drug as prescribed, the researcher discovered that those subjects who took at least 80 percent or more of their clofibrate had a five year mortality of only 15.0 percent, substantially less than the overall five-year mortality.  Those who took their clofibrate sporadically had a five-year mortality of 24.6 percent, significantly higher than those who took it as directed, a piece of data that would seem to confirm the efficacy of clofibrate.  Right?  Not necessarily.  Let’s look at compliance with the placebo.

Turns out that those subjects on the placebo who regularly took their placebo had a five-year mortality of 15.1 percent while those who took their placebo sporadically had a five-year mortality of 28.3 percent.  What this study really showed was that there is something intrinsic to people who religiously take their medicine that makes them live longer.  There was no difference between the drug and placebo in either those who took them regularly or those who took them sporadically, but there was a huge difference in mortality between those who took either drug or placebo on schedule and those who didn’t.

Lest you think this was a bizarre one-of-a-kind study, another study published a few years ago in The Lancet showed a virtually identical outcome.  Patients taking a medication for congestive heart failure were compared to those taking placebo.  Those taking the drug (Candesartan) showed no difference in mortality compared to those taking placebo.  But when compliance was evaluated, those taking either the drug or the placebo as directed had much lower mortality than those taking either one sporadically.  In fact, as you can see from the graph below, the mortality curves were almost identical.

From Lancet (2005); 366(9502):2005-2011

So there is something about adherers to a drug regimen that promotes longevity as compared to non-adherers.

Getting back to our statin study, how do we know that the decreased risk of death in those who religiously stuck with their statin prescriptions as compared to those who didn’t came about because they were adherers and not because of the statins?  We don’t.  In fact, based on the two studies I detailed above, it’s much likelier that the decreased mortality in those who took all their statins came about not because of the statins, but because those who stuck with them are adherers and have what ever quality it is that adherers have that makes them live longer.  And, if this is the case in this study as in the others, the statins don’t really do anything at all.

Despite its not really proving that statins confer greater longevity, the study does provide some interesting admissions and entertaining confabulations.

First, the study authors admit that there is no gold standard, randomized controlled study data showing that statins are of benefit in preventing death except for one group of people (and they even get that wrong).

The beneficial effects on cardiovascular mortality of treatment with statins to decrease levels of low-density lipoprotein cholesterol (LDL-C) have been established in several long-term, placebo-controlled trials.

The value of primary prevention with statin therapy in the reduction of overall mortality has recently been questioned.

A pooled analysis of 8 randomized trials in primary prevention populations showed that statins did not reduce overall mortality, indicating that lipid-lowering therapy with statins should not be prescribed for true primary prevention in women of any age or in men older than 69 years.

What they’re saying here is that statins have been shown to reduce mortality from heart disease in those who have elevated LDL, which is true.  But this decrease in deaths from heart disease is compensated for by an increase in deaths from cancer and other causes, so there really isn’t a gain.  You’re still dead.  Just maybe not from heart disease, but what difference does it make.  Are you going to spend $200 per month for the rest of your life and stay on medications that may make you feel lousy and lose your memory just so you can die of something other than heart disease?

In the last paragraph in the quote above, the authors confess that the data from actual randomized control trials show that statins confer no all-cause mortality benefits to women of any age and to men over 69.  They are playing a little fast and loose with the truth here because as I have posted before, the gold standard trials have shown no benefit for women and no benefit to men over 65 or to men under 65 who have never had heart disease.  The only improvement in all-cause mortality has been in men under 65 who have been diagnosed with heart disease, and even that benefit is so small that many people question if the extra cost and side effects of the statins are worth it.

So the authors of this study acknowledge that there has never been a randomized control trial that has shown any benefit to taking statins, but that doesn’t stop them.  They forge ahead trying to figure a reason that all these clinical trials haven’t shown an advantage.

Because clinical trials do not usually include individuals with multiple comorbid conditions or those receiving an extensive list of medications, there are considerable concerns regarding the applicability of findings from randomized clinical trials to the general population of patients seen in routine clinical practice.

Aha! They are saying that because the randomized controlled trial didn’t show what they wanted them to show – that statins worked for everyone all the time (thus the “considerable concerns”) -  that they need to figure out a better way to study them, one that involves patients with a lot of problems so that they don’t have to randomize them and confront failure yet again.

In light of the controversy surrounding lipid-lowering treatment for reduction of mortality among primary prevention populations, we undertook the present study to evaluate the effect of statin therapy in a large and diverse cohort of patients treated for dyslipidemia in a single health maintenance organization.

Interesting take.  There is no controversy.  The randomized controlled studies clearly show very little benefit to statin therapy in terms of decreasing all-cause mortality, the one statistic that really counts.  The controversy arises because the statinators simply don’t want to believe what these carefully performed trials tell them.  They by God want statins to work.  And they’re going to keep looking and fiddling with the data until they get a study that tells them what they want to hear whether the data is valid or not.

It’s pitiful that they are so desperate.

Don’t fall for the false promise of this or any other version of an observational study.  These kinds of studies do not prove causality.  Nor do they prove that a drug regimen works.  The patients in this study who religiously took their statins had better all-cause mortality than those who didn’t.  But, as we saw above, adherers always have better all-cause mortality than non-adherers.  In this case, was it that the adherers lived longer or was it that statins conferred some sort of benefit.  We can’t tell.  But we do know that in the real studies, the randomized control trials, statins didn’t do squat, so my vote would be that what we’re seeing here is an adherer effect and not a statin effect.

My advice is to continue to regard statins with a jaundiced eye.  So far, we haven’t seen any evidence that justifies the expense and the side effects of these drugs.

I posted last year about all the trouble Pfizer got into by using Robert Jarvik, the developer of the artificial heart, as their spokesman for the most commonly prescribed statin drug Lipitor.  Pfizer has taken a new tack and is now bombarding the airwaves with yet another commercial for Lipitor using as their spokesman an actual victim of a heart attack.

They chose a 58 year old California ad man and talent agent named John Erlendson who did indeed have a heart attack at age 57, and who was not taking any cholesterol-lowering medicines prior to that.  As opposed to the Gollum-like Jarvik, Mr. Erlendson comes across as a sincere guy who is genuinely distraught over his medical condition.  He is easy to empathize with.

Pfizer spent $181 million advertising Lipitor last year, and if the frequency with which they are running their new ad is any indication, I’m sure they are not pinching pennies with their ad budget now. It’s difficult to have a television on for half an hour and not see Mr. Erlendson at least once.  But, hey, what’s a measly $181 million when you’ve got sales of $12.7 billion?  I’ll take that deal any day.

This recent ad is a prime example of how viewers are manipulated by clever ad people.  You’ve got to be able to interpret the ads just like you do the medical literature.  I want to walk through this ad with you, but first, just take a minute and watch it.

Click here to view the embedded video.

Makes you want to run out and grab some Lipitor quick, doesn’t it.  You don’t want John Erlendson’s fate to befall you, and based on his oozing sincerity, neither does he.

You know how the ad makes you feel.  Now let’s look at it line by line to see what it really says.

Mr. Erlendson looks out from the screen and says:

Talk about a wake up call.  I had a heart attack at 57.

Okay.  I’ll buy that.  It would be a wake up call.

My doctor told me I should have been doing more for my high cholesterol.

As it turns out, Mr. Erlendson did have high cholesterol before his heart attack, and his doctor probably did warn him about it. (Of course, 50 percent of people who have heart attacks have normal or low cholesterol, so his being high is not the danger sign so many think it is.)

What was I thinking?

What indeed?

But now I trust my heart to Lipitor.

There are several implications in the above dialogue that we all accept subconsciously.  First, that high cholesterol was the cause of this man’s heart attack.  Second, that had he taken Lipitor he would have prevented his heart attack.  And third that you, the viewer, can protect yourself against Mr. Erlendson’s fate if only you take Lipitor before it’s too late.

Notice how cleverly they got this message across without actually saying it?  That can’t make the claim that high cholesterol causes heart disease because, although the vast majority of people seem to believe it, that relationship has never been proven.  Pfizer would have had the FDA all over them had they tried to actually make the claim that Lipitor would have prevented Mr. E’s heart attack because they have no way of knowing that.  Based on the randomized clinical trials for statins, Mr. Erlendson was not in a high risk group, so there is no evidence that a statin drug would have done him any good whatsoever.  And the FDA would never have allowed Pfizer to actually say anything remotely like: Take Lipitor and protect yourself from Mr. E’s fate.  But, because of how cleverly this ad was written, this all comes across without it being said, so the FDA can’t lay a glove on them.

Next in the commercial, Mr. Erlendson carries on in the background and the announcer comes on in a voice over.

When diet and exercise are not enough, adding Lipitor may help.

Really?  Rubbing Vick’s Vapor Rub on your chest ‘may’ help too.  ‘May’ is a real weasel word that ad people use all the time.  They say ‘may,’ the listener hears ‘will.’

Interestingly, during the voice over part of the commercial Mr. Erlendson can be seen in the background riding a bike, which implies that he probably was exercising yet still had his heart attack. Or it implies that now that he’s on Lipitor, his life has changed for the better.  I can’t figure out which.

The voice over continues:

Unlike some other cholesterol-lowering medications, Lipitor is FDA approved to reduce the risk of heart attack, stroke and certain kinds of heart surgeries if you have several common risk factors for heart disease.

There is an entire daisy chain of weasel words.  The ad doesn’t say that Lipitor will reduce the number of heart attacks, stroke, etc., it says that it will reduce the risk IF you have several common risk factors.  No one knows what causes heart disease, so no one really knows what the risk factors are.  So we’ll take a bunch of what we think are risk factors, put them in tiny print at the bottom of the ad, and tell you that Lipitor reduces these risk factors.

Here is my favorite.

Lipitor has been extensively studied with over 16 years of research.

Yes, but has this 16 years of research shown anything worthwhile?  It has shown that Lipitor and other statin drugs don’t reduce all-cause mortality (the statistic you should really care about) in women of any age, in men over 65 and in men under 65 with no history of heart disease.  Only in men under 65 who have actually had a heart attack have statins shown any benefit in reducing all-cause mortality.  And even that is minimal.  Mr. Erlendson falls into this last group, so he is one of the few people who may actually get some benefit from a statin.  But he didn’t fall into this group before his heart attack because he had no history of heart disease before his heart attack.  High cholesterol is a lab finding, not a history of heart disease.  In sum, the 16 years of Lipitor research have been pretty fruitless.  But that’s not the message you take away from this ad.

Then the voice over drones quickly through all the problems that one can experience with Lipitor.  Then it’s back to Mr. Erlendson.

I learned the hard way, but you may be able to do something.

There is our friendly weasel word ‘may’ yet again.  Implies, once more, that Lipitor will save your butt.

Then back to the voice over.

Have a heart to heart with your doctor about your risk and about Lipitor.

Okay, so the next time you go to your doctor, you inquire about your cholesterol and ask if Lipitor would work for you.  After all, you don’t want to learn the hard way like John Erlendson, do you?  Your doctor, being brainwashed as they almost all are, gives you a prescription for Lipitor because, hey, why not, it’s so good they’re talking about putting it in the drinking water.

You go away with a $150 a month drug habit that does you no good whatsoever.

The creative people at Pfizer have put together an ad that says nothing, but implies everything.  They stay out of hot water with all the regulatory agencies, yet the viewer takes away the exact message that the advertiser could never get by with saying explicitly.  Is it any wonder that half the country is on a statin?  Ain’t Madison Avenue grand?

And, by the way, you, too, can be in a Lipitor ad.  Click here to find out how.

The last few studies I’ve posted on here seem to have been designed by their authors to show that low-carb diets aren’t all they’re cracked up to be. Of course none of these studies have used real low-carb diets – they’ve all used diets that are called low-carb, but really aren’t. They’ve set up a low-carb straw man, knocked it down, then crowed about it. These antics have left us all longing to see a study using a real low-carb diet.

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.