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

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

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

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

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

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

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

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

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

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

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

Recognized?  What does that mean?

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

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

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

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

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

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

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

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

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

But as for heart disease itself:

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

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

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

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

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

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

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

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

It was unbelievable.

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

Watch and just shake your head.

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

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

This link requires requires free registration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Now, back to the PNAS paper.

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

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

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

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

Low-carb diets ‘damage arteries’

And followed up with:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Instructor teaches Friedewald equation and bad cholesterol

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

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

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

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

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

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

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

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

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

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

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

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

And how did they fare?

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

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

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

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

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

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

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

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

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

The abstract of the study echoes this warning.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

LDL = Total cholesterol – HLD – VLDL

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

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

LDL = Total cholesterol – HDL – TGL/5

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

One more.

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

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

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

HAHAHAHAHAHAhahahahahahaha! Oh man, sometimes I crack myself up.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Nitrogen-fixation process

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

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

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

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

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

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

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

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

Fertilizer factory using the Haber-Bosch process

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

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

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

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

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

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

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

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

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

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

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

Paleolithic paintings from Lascaux cave in southern France

I imagine most readers of this blog would expect a group of subjects to do better on a Paleolithic diet as compared to a standard American diet, but there are few studies actually making the comparison. One was posted yesterday in the Advance-0nline-Publication section of the European Journal of Clinical Nutrition that shows subjects following a Paleolithic diet made major metabolic changes, and made them rapidly.

Before we get into the study, let’s make sure we’re all on the same page when we discuss the Paleolithic diet. We we say Paleolithic diet, what are we really talking about?

The Paleolithic era refers to that period of history of the genus Homo, which began more than 2 million years ago and ran until the Neolithic period started circa 10,000 years ago. The Neolithic era dates to the time when early man set down roots both literally and figuratively when he started to cultivate plants for food and domesticate animals. The Paleolithic era ends and the Neolithic era begins with the advent of agriculture.

So what did Paleolithic man eat? We don’t know precisely because Paleolithic man didn’t leave any written records, menus, cookbooks, etc. The only records Paleolithic man left are the cave paintings, of which Lascaux in France is the most famous. Virtually all of these paintings feature animals prominently, which would lead one to believe that animals figured greatly in the lives of Paleolithic people. Since they didn’t domesticate these animals, and since it seems unlikely that they kept zoos, the most obvious reason these early people focused so much artistic effort on these animals is that they ate them. Carbon-13 isotope studies bear out that idea as the same carbon isotopes found in grass are also found heavily concentrated in the bones of Paleolithic man and other known carnivores, which leads to one of two conclusions: either Paleolithic man spent his days grazing or he ate animals that grazed. I would opt for the latter interpretation.

Keep this idea of Paleolithic man as a meat eater along with the idea of the cave pictures in your mind. We’ll return to them later, but first, let’s look at this study.

Nine healthy, sedentary, non-obese subjects (6 men; 3 women) over the age of 18 recruited from the San Francisco Bay area completed the study. These subjects had their starting diets analyzed – all were on their own version of the standard American diet – and a battery of tests done on them to evaluate multiple metabolic parameters.

Once the beginning data was in hand, the researchers started the subjects on a ramp up to the full Paleolithic diet by giving them daily increases of fiber and potassium.

For the intervention phase, beginning day 1, for adaptation purposes, a series of 1-day cycle diets with gradually increasing levels of potassium and fiber were developed by the research dietitians. This was to allow the subjects’ intestinal tract and potassium handling systems to adjust to the markedly higher dietary content of fiber and potassium. ‘Ramp 1′ diet was given for 1 day, ‘Ramp 2′ diet for 3 days, ‘Ramp 3′ diet for 3 days and finally the ‘Paleo diet’ for the remainder of the study.

Once ramped up, the subjects went on the full Paleo diet for 10 days.  An interesting twist to this study was that the subjects were monitored carefully for any signs of weight loss over the course of the study, and any subjects losing even small amounts of weight were encouraged to eat more of the Paleo foods in an effort to maintain their starting weights.  Since weight loss itself can bring about metabolic changes, the researchers wanted to make sure that any changes came about as a result of the diet composition and not as a side effect of weight loss.

What did they eat?

Meat, fish, poultry, eggs, fruits, vegetables, tree nuts, canola oil, mayonnaise and honey were included in the Ramp and Paleo phases of the diet. We excluded dairy products, legumes, cereals, grains, potatoes and products containing potassium chloride (some foods, such as mayonnaise, carrot juice and domestic meat were not consumed by hunter-gatherers, but contain the general nutritional characteristics of preagricultural foods).

Hmmm. More about which later. For now, here is a layout of the specific foods the subjects ate during the ramp and the full Paleo diet.

Table 2

The macronutrient composition of the regular diets of these subjects was 18% protein, 44 % carbohydrate and 38% fat.  The Paleo diet was 30% protein, 38% carbohydrate and 32% fat, mostly unsaturated, as the authors were quick to point out.
After the 7 day ramp period and the 10 days of Paleo dieting, subjects experienced large changes in most parameters measured.  Lipid changes are shown in the table below.

Derived from Table 3

As you can see, there were significant decreases in triglycerides, total and LDL-cholesterol with no change in HDL-cholesterol.

The body of the paper reports an insignificant decrease in blood sugar after the Paleo diet, but the units listed in the paper are incorrect, which is one of the hazards of dealing with a pre-publication paper.  All the kinks haven’t been worked out.

Fasting insulin levels plummeted by more than two thirds in (11.5 to 3.6 µU/ml) and the total area under the insulin curve was lowered by almost half.  What these figures tell us is that the diet made these subjects much, much more sensitive to their own insulin.  In other words, they required substantially less insulin to keep their blood sugars in the normal range.  Since they were producing less insulin, they had less circulating insulin, which meant less fat storage, less arterial stiffening and less of all the things that too much insulin causes.

Along with the improvements in lipids and insulin sensitivity, the subjects experienced a significant drop in diastolic blood pressure and a decrease in mean arterial pressure.  These improvements likely occurred in part because these subjects had substantially increased brachial artery diameter, a measure of arterial distensibility.  There arteries had become less stiff and more pliable over a mere 17 days of dietary change.

Urinary potassium loss increased, indicating an increased potassium intake by the subjects.  And urinary calcium excretion decreased.

Another interesting aspect of this study is that these findings were pretty much across the board.  Instead of a couple of hyper responders raising the average, either all nine or in a couple of cases, eight of the nine subjects demonstrated pretty much the same changes, indicating

consistently improved metabolic and physiological status with respect to circulatory, carbohydrate and lipid metabolism/physiology.

The authors of this paper found

in a small group of sedentary, slightly overweight, but not obese adult humans, that switching from their usual diet to a paleolithic-type diet, which contained no cereal grains, dairy [or] legumes, resulted, after only a short period of time [17 days] and without weight loss or increase in activity levels

significant positive changes in all the parameters discussed above.

I was fascinated by this study because the changes were so rapid, but I was a little put off because it could have been so much better.  I mean why didn’t they test a real Paleolithic diet?  Probably because of nutritional correctness, i.e., fear of saturated fat.

During Paleolithic times, man primarily subsisted by hunting.  The preferred food was large game animals, and Paleolithic man, a skilled hunter, wiped most of them out.   And not just the large grazing animals.  Paleolithic man completely decimated the Cave bear.  As you can see from the photo of my Cave bear skull below (from a slide I use in presentations), these were enormous animals that didn’t go down easily.  Cave bear, like all bears, had high levels of body fat, which must have been highly desired because these ferocious animals were hunted to extinction about 15,000 years ago by people wielding little more than pointed sticks.  I would have to value fat a whole lot more than I do to tackle one of these guys.  The largest bears that I could find the fatty acid composition for were polar bears, which should be appropriate since cave bear lived in northern latitudes.  Polar bears have on average 30 percent saturated fat, 50 percent monounsaturated fat and 15 percent polyunsaturated fat.  (I know these figures don’t add up to 100 percent, but they are the figures as presented in the article.)

The majority of the large animals that roamed the world are gone thanks to the depredations of Paleolithic man.  If you ever get the chance to go to the American Museum of Natural History in New York, take a stroll through the many large halls filled with the enormous skeletons of these animals that used to roam what is now the United States.  Experts estimate that it took Paleolithic man only about a thousand years to range from northern North America were he crossed the Bering strait to the southern tip of South America wiping out all the large game that existed at the time.

These large mammals that Paleolithic man decimated are now only present in skeletal form so we don’t know for sure what their fatty acid composition was.  But we do know that of those left, the larger the animals, the larger the percent body fat.  And the larger the percent body fat, the greater the percentage of saturated fat.  Given those two facts, one has to conclude that Paleolithic man consumed a large percentage of his energy as saturated fat.  We can’t look at the fat content of deer, for example, and use that to estimate the saturated-fat content of the Paleolithic diet.  Deer, as we know them today, were tiny animals as compared to those Paleo man typically dined on.

If you look at the fatty acid breakdown of the horse, a large animal (not grain fed) that we are all familiar with that is comparable in size to many of the animals Paleolithic man hunted to extinction, you find a large proportion of saturated fats.  Horse fat is about 36 percent saturated fat, 34 percent monounsaturated fat, and the rest polyunsaturated fat.  Even rabbits carry over 40 percent of their fat as saturated fat, but rabbits have much less fat per weight than the larger animals.

It seems pretty obvious that Paleolithic man would have eaten considerable saturated fat.  Which begs the question: Why always cut the saturated fat in experimental diets testing the hypothesis that the Paleolithic diet is more healthful?

I don’t know the answer for sure, but I expect that it’s due to the nutritional equivalent of political correctness, which I call nutritional correctness.

Researchers are simply afraid to imply that saturated fats might actually be harmless, so they go through all kinds of contortions to present their data in such a way that it couldn’t possibly present saturated fats in a positive light.  And much good research and reporting has suffered as a consequence.

A case in point is a otherwise wonderful book published 20+ years ago titled The Paleolithic Prescription.  This fascinating book goes into great detail describing the physical exploits of our ancient ancestors based in large part of reports by European explorers encountering ‘primitive’ peoples untouched by the forces of ‘civilization.’  The authors, based on the anthropological literature, describe the size of our Paleolithic forebears as being similar to our own, but their strength was significantly greater:

These people were strong – stronger by all estimates than most agricultural and industrial people (including ourselves) who lived after them.  Skeletal remains reflect strength and muscularity: the size of joints and the sites where muscles are inserted into bones indicate both the mass of the muscles and the magnitude of the force they were able to exert.  Average Cro-Magnons, for example, were apparently as strong as today’s superior male and female athletes.  Strange as it may seem, Cro-Magnons and other hunters and gatherers may have worked fewer hours per week than did the agriculturalists who followed, yet they were significantly more robust.

Think about this last sentence for a minute.  Strong, robust Cro-Magnons who settled into a life of agriculture circa 10,000 years ago, and who worked harder than their pastoral predecessors, showed a decline in strength and muscle mass.  Why?  What The Paleolithic Prescription says about energy expended is true.  The skeletal remains of agriculturalists show much more arthritic changes and incidence of joint wear implying much more regular physical activity than hunters.  So why did agriculturalists develop less muscle mass and strength?  Could it be because of a switch from diets high in fat and protein to diets low in fat and protein and high in carbohydrates?  Makes sense to me.  Same genetic material, greater exercise, different diet, yet weaker and less robust.

Getting back to my original point about this book, the authors presented a mass of data showing our Paleolithic ancestors to be more robust, healthier and able to routinely perform feats of strength that are almost unbelievable to us today.  And they dwelt on the massive amount of hunting that sustained these ancient peoples.  Then, when it came time to apply these dietary lessons to people of today, the authors tried to shoehorn their findings in a nutritionally correct regimen that followed the low-fat diet precepts that academicians are so attached to.  It’s really a shame because this could have been a wonderful book.  It’s still well worth reading, but simply ignore the dietary advice.

It would have been great had the authors of the paper above used a real Paleolithic diet for their study instead of an imaginary Paleolithic diet that conformed to the tenets of nutritional correctness.

Based on my own experience with thousands of patients, I can predict what the findings would have been.  Lipid parameters would have been improved, but with LDL staying about the same or maybe going up a little.  HDL would have gone up significantly.  Triglycerides would have fallen maybe more.  The all-important triglyceride/HDL ratio would have plummeted much more than with the faux Paleo diet.  Fasting insulin would have dropped like a rock and the area under the insulin curve would have fallen at least as much, if not further.  Blood pressure would have decreased and all the measures of vascular pliability would have improved.  All in all, my prediction is that the outcome of the study would have been better than the outcome of the study as it currently exists.

The Paleolithic diet data indicates that early man ate more saturated fat than he did carbohydrates.  And he was molded by the processes of natural selection to thrive on such a diet.  When he bolted from that meat-based diet, as he did when he settled in to life as an agriculturalist, he paid dearly for it with a devolution in health.  Since the evidence is so obvious that a diet higher in saturated fat worked wonders for Paleolithic man, it seems like some academicians somewhere would ranger up and test such a diet.  But it appears that the pox on saturated fat is so virulent that no one wants to risk it.

If such a study were done and the results tally with what I’m positive the results would be, the authors would find themselves in the untenable position of having to at least tacitly imply that saturated fats aren’t harmful.  And that could ruin an academic career.  No more invitations to present at meetings. Expulsion from the club.  People tsk tsking behind their hands.  It just couldn’t be done.

At Fat Head the Movie premiere

A couple of years ago I got an email from a guy named Tom Naughton asking if he could come interview me for a movie he was making that was supposed to kind of be a counterpoint to Morgan Spurlock’s Super Size Me! I hadn’t seen Spurlock’s film at the time, but I knew enough about it that I was wary of anyone who wanted to make a film maybe showing fast food places in a positive light.  I wrote Tom back and suggested we talk.  Once he had me on the phone, Tom was able to make me realize that his film was not pro fast food, but was pro personal responsibility.  And that it was pro low-carb, since the diet he went on and lost weight on eating at nothing but fast food restaurants was a low-carb diet.

He came to visit with all his movie making paraphernalia and we set to the interview, which I wrote about in a previous post.  We kept in contact over the intervening years, and I watched multiple versions of the film as it evolved and got better and better with each new iteration.  Finally, Tom called to tell me Fat Head was finished.  MD and I attended the premiere of the movie a few weeks ago (we are pictured above with Tom at said premiere), and I can tell you that folks were laughing their heads off.  It’s a very funny movie made by a guy who is a professional comedian.  Along with being funny, however, the film is exceedingly thought provoking.  I can’t imagine anyone who might be anti low-carb watching it and coming away feeling the same.

Tom has been dogged in his mission to actually get this film made and distributed.  And he has succeeded in a world where few do, the world of the independent filmmaker.  He has a distributor (which is the movie equivalent to a book agent) and has already had the film picked up in some foreign venues.  Today, Feb. 3, Fat Head goes on sale at Amazon.com. I urge you to click here to get a copy and watch it.  You’ll be glad you did.

One of the questions I’m asked constantly by people who have achieved success on low-carb diets is what can we all do to help spread the word?  I always tell them to buy books (and not just mine) and give them away or loan them out.  The response I almost always get is that no one will read a book.  Well, they will probably watch a movie, especially one as funny and entertaining as Fat Head.  Even if you don’t buy one to give to someone, buy one for yourself because the movie is a real treat.  Can you think of a  better way to spend a pleasant hour and a half than to watch a bunch of low-fat twits get pilloried?  Plus, Tom has witnessed firsthand the power of the low-carb diet to improve health and bring about weight loss, and has not just exulted in his own success, but has put his money where his mouth is.  He has financed every cent of this movie out of his own hip pocket.  And, as we all know, movies are not inexpensive to produce.  He has done a great service for the low-carb community, and we need to do our part to help pay him back. And to encourage others to take the risk to move the ball closer to the goal.

If you want to get a little taste of what the movie is all about and watch some video clips, check out the website.

To get an even more in depth take on the movie, here is an interview I did with the filmmaker himself.

Q:  What inspired you to make a film challenging Super Size Me?

A:  I actually didn’t set out to take on Super Size Me.  I began this project thinking it would be maybe a half-hour humor piece about how we treat fat people in American society.  I watched Super Size Me as part of my research.  And to be honest, I thought Super Size Me was very well done and very amusing, but at the same time a couple of things about it really bugged me.  One was the overall premise, that it’s McDonald’s fault people are getting fatter.  That’s ridiculous.  Ronald McDonald can’t force you to eat anything, and most people eat at McDonald’s once in awhile, not everyday.

But what really bugged me was when I realized Spurlock’s math didn’t add up.  I spent a good part of my adult life as a serial dieter, so I have a pretty good idea what the calorie counts are at McDonald’s.  When Spurlock’s nutritionist told him he was consuming 5000 calories per day, alarm bells went off in my head.  There’s no way you can consume that many calories at McDonald’s if you’re following his supposed rules.

Q:  So in your opinion, Super Size Me is essentially dishonest.

A:  Yes, it’s dishonest.  Long before I saw it, I heard people talk about how Super Size Me shows what would happen if you just ate three meals per day at McDonald’s.  But that’s not what it shows.  It shows what would happen if you decided to stuff yourself like crazy so you could gain weight and make a movie about it.  You could stuff yourself at a vegan restaurant and gain just as much weight, if that was your goal.

Q: You did exactly the opposite:  you ate nothing but fast food for a month and lost weight.  How did you manage that?

A:  I did it by intentionally ignoring the standard-issue nutrition advice.  My doctor of course warned me that if I was going to live on fast food, I should eat as many salads and grilled chicken breasts as I could so I wouldn’t consume too much fat.  But I knew better.  I ate a lot of fat, because fat is what keeps you feeling full and satisfied.  But I did limit my carbohydrates to about 100 per day, because that’s the real key to losing weight, at least for me.

Q:  You say you ignored the standard advice because you knew better.  How did you know better?

A:  Personal experience for one.  Low-fat diets never worked for me.  I’d lose a little weight and then stall, plus I’d end up feeling lethargic and depressed.  The first time I really lost weight and felt good doing it was when I tried The Zone diet, which was the first time I seriously cut down on my carbohydrates.

Q:  The Zone diet isn’t exactly a low-carbohydrate diet.

A:  No, but keep in mind, I’d been living on a more or less vegetarian diet because I thought it was good for my health, so I was eating a lot of rice and potatoes and pasta.  That seems crazy to me now, because of course I kept gaining weight in spite of working out regularly and walking several miles per week.  I just figured it was because I was getting older.

So when I finally tried The Zone diet, I was consuming maybe 170 carbohydrates per day, which isn’t exactly low, but it was a lot lower than I’d been consuming.  And the weight started to drop off.  I didn’t understand much about the effects of insulin at the time, but I did understand that cutting back on sugar and starch was making it so I could lose weight without feeling like I was starving.

Q:  On your fast-food diet, you counted calories as well as carbohydrates.  How many calories did you consume, and what did you eat to stay under the limit?

A:  I set a target of 2000 calories per day and kept it pretty close to that.  Unlike Morgan Spurlock, I’m not afraid to show people what I consumed, so my daily menus are posted on our web site, but to answer the question, I basically lived on a diet that’s about midway between The Zone and Protein Power.  Since I wanted to do an honest fast-food diet, I consumed more starch than I would on a true low-carb diet.

So a typical day might be two Egg McMuffins with only half of each muffin and an order of hash browns for breakfast, a double quarter-pounder with cheese for lunch, and another one for dinner, or maybe one of their chicken salads.  I also ate a lot of the chicken strips, which are pretty tasty, but unfortunately that meant I was taking in some trans fats.  I think they’ve finally gotten rid of the trans fats, but they were still using them for frying when I was on the diet.

Q:  And you ate nothing but McDonald’s?

A:  It was all fast food, and it was mostly McDonald’s, but it wasn’t all McDonald’s.  I also ate at Carl’s Jr., KFC, Taco Bell, Burger King and a couple of others.  I ate at least one or two meals at McDonald’s pretty much every day.

Q: Was it difficult, eating nothing but fast food for a month? I don’t think I could do it.  In fact, I’m not sure I could eat nothing but fast food for a week.

A:  It got a little tiresome by the end.  I was bored with eating the same half-dozen meals over and over.  That’s why I thought it was ridiculous when Spurlock played up the idea that McDonald’s food is addicting.  Addictions are progressive.  People consume more and more of the addicting substance, despite the bad effects it’s having on their health.  After eating nothing but fast food for a month, I didn’t touch the stuff for awhile.  Addicting?  Give me a break.

Q:  Are you worried that you’ll be seen as an apologist for the fast-food industry?  After all, they’re not exactly selling health food. As you may recall, that’s one of the reasons I was hesitant to even be interviewed for this movie.

A:  No, they’re not selling health food, and I don’t portray it as health food in this film.  In fact, when I met with some people from McDonald’s to get permission to shoot in their restaurants, I made it clear I wasn’t going to claim their food is good for you.

But it doesn’t have to be bad for you either if you’re smart about the choices you make, and that’s one of the main points I was trying to make in this film.  You can make good choices or bad choices at McDonald’s, just like you can make good choices or bad choices in the grocery store.  People are going to eat fast food in today’s society, like it or not, so they may as well learn to make reasonably smart choices.

Q:  And McDonald’s had nothing to do with this film being made?

A:  Other than giving me permission to shoot in their restaurants, no.  And even that took some doing on my part.  After what Spurlock did to them, they were understandably a bit skittish about allowing some guy with a camera to come in and film himself eating there.

Q:  So you lost weight on a fast-food diet, and you demonstrate pretty convincingly that Morgan Spurlock’s numbers don’t add up.  But there’s a whole lot more to this film than just disputing Super Size Me.

A:  Absolutely.  Once I started working on this film and doing some research into the so-called obesity epidemic and what’s really causing it, and especially once I started looking into the research on fat and cholesterol and heart disease, I was stunned at how much nonsense passes for real science these days.  Most of the dietary advice we’ve been hearing for the past 40 years is just plain wrong.  In fact, it’s worse than wrong; it’s harmful. That’s when it began to sink in with me that this film should be way more than just a reply to Super Size Me.  I changed the focus of the film significantly as I went along.

Q:  You call it the “so-called” obesity epidemic.  Do you really believe there is no obesity epidemic?

A:  You and I have already debated this one back and forth, so let me clarify my position for your readers.  There are definitely more fat people in America now than when I was a kid.  Look around any busy public place, and you’ll see these big, heavy people going by.  So I’m not disputing that we’ve gotten fatter.

But when I look around, say, a mall or an airport, most of the people I see don’t look overweight to me, so I don’t buy this notion that two-thirds of us are overweight.  And I certainly don’t think a quarter of all Americans are obese.  The figures have been wildly exaggerated, both by the Centers for Disease Control and by the weight-loss industry, each for their own reasons.

Q:  What are those reasons?  What do they gain by exaggerating the numbers?

A:  The CDC needs epidemics to justify their budget.  They were originally created to wipe out real diseases, things like polio and influenza and malaria.  Well, you’re not going to catch obesity from some virus floating around, you’re not going to get it from the person sitting next to you, so frankly, I don’t think this is even the CDC’s problem to tackle.

The weight-loss industry wants obesity declared a disease so they can get insurance reimbursements for weight-loss treatments and weight-loss drugs.  But to make that happen, they’ve got to create the impression of this looming national health crisis.  So they use stupid measurements like the Body Mass Index to juke up the statistics.  And by focusing on people’s weight or BMI, they’re going after the wrong problem.

Q:  In your film, you say the real epidemic is high blood sugar.  Why do you say that?

On your blog, you frequently write about how researchers often confuse correlation with causation.  That’s what I think has happened with the so-called obesity epidemic; they’ve confused a cause with a symptom.   We know fat people tend to have more health problems, so they decided being fat is the cause of all these health problems.  But being fat isn’t the cause; it’s a symptom.  And it’s also possible to be fat and healthy.

I’m a walking example of that.  A typical checkup for me goes something like this:  “Well let’s see … blood pressure is good, blood sugar is normal, resting heart rate is very good, triglycerides are excellent, HDL is outstanding, stress-test results are excellent, muscle tone is very good.  You’re healthy as a horse, Mr. Naughton.  But you really should go on a low-fat diet and try to lose 20 or 30 pounds.”  And I’m usually hearing this from some doctor who probably couldn’t keep up with me on one of my five-mile hikes.

So again, I don’t think carrying around some extra weight is a health hazard all by itself.  But high blood sugar is unhealthy, no doubt about it.  And we’ve got millions and millions of people these days walking around with high blood sugar.  Just look at the skyrocketing rate of type II diabetes over the past few decades.

We have people in my family who are thin and look good in their clothes, but they have type II diabetes.  So I think it’s misguided to focus so much on being fat or thin.  The focus should be on keeping your blood sugar normal.  Do that and the weight will probably take care of itself over time.

Q:  You blame the blood-sugar problems we have today on poor old George McGovern.

A:  Well, he was certainly part of it.  Going back at least as far as Ancel Keys, we’ve had this misguided attempt to reduce heart disease by telling people to cut back on dietary fat, or to avoid animal fats and switch to vegetable fats.  It didn’t seem to occur to any of them back then that heart disease rates were going up precisely at the same time that people were consuming less animal fat and more of these Frankenstein vegetable fats, like chemically processed corn oil and soybean oil and margarine.

So George McGovern didn’t start the anti-fat campaign, but unfortunately he gave it the official stamp of approval from the federal government, and that’s when a lot of people began to take it seriously.  That’s when you couldn’t walk into a bookstore or open a newspaper without seeing all these books and articles telling us to cut back on fat and eat more whole grains.  So we became a nation of starch-eaters, and the rest is history.

Q:  You make several references to Gary Taubes’ Good Calories, Bad Calories in your film.  How much influence did Gary’s book have on the direction of the film?

A:  I was already finished with my third edit of Fat Head when Good Calories, Bad Calories hit the bookstores, although I had read some of Gary’s articles while researching the film, and those were certainly eye-opening.

When I finally read Good Calories, Bad Calories, it blew me away.  I finally understood, at the cellular and hormonal level, how carbohydrates had made me fat over the years, and why low-fat diets always made me ravenously hungry and depressed.

I finally understood why there are so many frustrated dieters in the world, trying to lose fat on diets that are basically telling their bodies to store fat.  And I understood why people like my wife and son can’t seem to gain weight no matter what they eat.  They’re not skinny because they’re more disciplined than the rest of us; they just have bodies that reach homeostasis at a very low level of fat accumulation.  If my wife is hungry, she eats.  She doesn’t starve herself into being thin.

So I did some fairly substantial cutting to make room for what I learned from Gary’s book.  And after you put me in touch with him, he generously agreed to proof the script for technical accuracy.  I knew I’d have to simplify the science quite a bit in order to translate it into a film for the general public, but I wanted to avoid simplifying to the point of being incorrect.  Gary helped me keep it simple, but accurate.

Q:  Gary’s work is highlighted in the film, but he doesn’t appear in any interviews.  Were you unable to work out the logistics for an interview?

A:  I would’ve happily flown to New York or wherever to get Gary on film, and he was open to the idea, but his publisher wasn’t crazy about the idea of him appearing in a film that’s billed as a comedy-documentary.  There are a lot of silly moments in this film, all those animated cartoon bits and such, and his publisher was afraid it would detract from Gary’s credibility among the white-coat crowd.

And I think his publisher probably made the right call.  Much as I would’ve loved to have Gary talk about his own work in my film, I understand that his mission right now is to convince the medical and academic types that the prevailing dietary theories are wrong, and I wouldn’t want to be responsible for giving those people any reason to ignore him.  So he can attack their misguided theories with serious science, and I’ll attack them with humor.  Two fronts, same battle.

Q:  Speaking of humor, there’s quite a lot of it in your film.  How much of that was planned, and how much of it just happened?

A:  I’d always planned for this to be a comedy, even back when it was going to be a short piece about how we treat fat people.  I spent a lot of years as a traveling standup comedian, and I like producing funny material.  It comes naturally to me.

But the humor also serves an important, calculated purpose:  it makes people want to watch the film.  Funny documentaries get far more attention on average than serious documentaries.  They get more press coverage, and they sell more copies.

So a lot of the humor was planned, definitely.  The animations, the songs, the scenes where I parody Spurlock, those were all by design.  But some of the funniest moments were a matter of good, old-fashioned luck.  I conducted several hours of person-on-the-street interviews, and some people just happened to be funny.  That’s luck.  On the other hand, some people were funny when I had the lens cap on, or didn’t notice the battery had gone dead.  That’s bad luck.  I had more good luck than bad, so I’ll take it.

Q:  As you explain to the viewers near the end of the film, I encouraged you to try a high-fat, very low-carb diet to see what would happen with your lipids.  You went on what you called a “saturated-fat pigout” for a month, and your total cholesterol went down and your HDL went up, as I predicted.  But you didn’t mention what happened with your weight during that month.  Did you gain or lose?

A:  Yes, after our first interview, you told me off-camera that I could prove to myself that the Lipid Hypothesis was wrong, and I did, to my great relief.  To tell you the truth, I was kind of sweating it out, waiting for the lab results to come back.  I believed what you were telling me, but after a month of eating burgers and steaks and bacon and eggs, there was part of me wondering if I was going to get back a lipid panel that would just say “You’re going to die” across the top.  If my cholesterol numbers had gone all out of whack, it wouldn’t have done very much for the premise of my film.  But as you predicted, the numbers all improved.

To answer your question, I lost two pounds during that month.  That doesn’t sound like much, but I was eating a lot of high-fat, high-calorie food, and I wasn’t exercising much because I was swamped with work, so the fact that I lost any weight at all impressed me.

Q:  So it wasn’t just a matter of counting calories.

A:  It couldn’t be just about the calories.  If you go by the simple calories-in, calories-out equation the so-called experts are always harping on about, I should’ve gained weight during that month.

I kind of repeated that experiment again later.  I was booked on a cruise ship for five weeks as a comedian, and of course cruises are notorious for being diet-busters.  So during those five weeks, I ate burgers, steaks, bacon, sausage, eggs, seafood and salads with bleu cheese dressing.  I didn’t touch bread or potatoes or rice.   I limited my alcohol consumption to a little red wine here and there.  Since the performers work at night, on a lot of days I had a fourth meal after midnight.  There’s no way this was a low-calorie diet in disguise, as some of the low-carb critics like to claim.  At the end of the five weeks, I weighed exactly the same.  Calories in versus calories out can’t explain that result.

Q:  How did working on this film change your own dietary habits?

A:  I used to more or less limit my carbs, but I also granted myself a lot of “special occasion” days where I had the bagel, or the lasagna, or the chicken-fried steak.  After all the books and articles I read for this film, and especially after reading Good Calories, Bad Calories, I’m a lot stricter, and frankly, it’s easier to pass up those foods.  If I look at a baked potato, I see a big glob of sugar sitting there.

I also don’t worry about saturated fats and cholesterol at all.  In fact, I believe they’re good for me.   I’ve noticed that when the flu goes around, or when practically everybody I know has a cold, I pretty much never come down with anything.  Maybe it’s just a placebo effect, but I truly believe the butter and the coconut oil and the egg yolks and the beef fat I consume keep my immune system strong.

Q:  What kind of reactions are you getting from people who’ve seen the film?

A:  That’s what is really gratifying, seeing how this film affects other people.  My composer swore off sugar and starch after working on the film, and he lost 15 pounds.  Same thing happened with my sound engineer.  He realized his morning bowl of whole-grain cereal wasn’t actually good for him, and he switched back to eating meat and eggs for the first time in decades.  He lost 15 pounds, which is great, but even more importantly, he was able to stop taking Prilosec.  He’d been taking that stuff every day for years.  All of his digestive disorders are gone, and he feels healthy.  At our premiere party, he told me this film had literally changed his life.

Q:  So what’s happening with the film now?  What’s next?

A:  Now it’s up to the distributors.  The U.S. distributor is getting the film into the big video stores and department stores, and it’s already selling on Amazon.  The international distributor is selling to the DVD and TV markets in a couple dozen countries.  It turned out the world-wide premiere was on a satellite network in Israel back in December.  I started getting all these emails from people in Israel, asking me questions about the film, or just wanting to know when they could buy it on DVD.

Q:  Any plans for a follow-up film, or a film on a different topic?

A:  I have some ideas for future projects, but no concrete plans yet.  I bankrolled Fat Head myself, so first I have to wait and see if it generates a healthy profit.  If it does, I’ll definitely make another film.  This project took an incredible amount of work, way more work than I thought it would be when I started it, but at the same time, it was a blast.  Other than being on stage doing standup comedy, this is about as much fun as I’ve ever had while working.

Thanks very much, Tom.

Tom has generously agreed to answer any questions any of you might have about his film, so fire away in the comments section, and I’ll get them to Tom.

There is an old joke that goes something like this:

Question: What is Mozart doing in his grave right now?
Answer: De-composing.

The same question could be asked of the living right now who are working hard on their diets and seeming to go nowhere body weight-wise.

Question: What’s happening right now? Why am I not losing weight?
Answer: You’re Re-composing.

As you can see from the picture above, body composition matters a lot.  It’s not the particularly the weight you carry as much as how it is distributed that counts.  As I’m forever asking my female patients, What difference does it make if you weigh 200 pounds if you’re wearing a size 4?  Although that situation is unlikely, they get the point.

A soon-to-be-published study by Donald Layman and his team at the University of Illinois demonstrates this phenomenon nicely.  And shows that by increasing protein intake – even while keeping carb intake much higher than I would recommend – increases fat loss while increasing muscle and lean tissue mass.

Here is how the study was set up.

One-hundred thirty overweight men (58) and women (72) between the ages of 40 and 56 were recruited into the study.  None of the subjects smoked, took cholesterol-lowering drugs or had any medical condition that might affect the outcome of the study.  In other words, the study subjects were relatively healthy overweight middle aged people.

These subjects were randomized into two groups.  One group was started on a diet (PRO) containing 1.6 gm protein per kg body weight per day and under 170 g carbohydrate per day.  The other group went on a diet (CHO) composed of 0.8 g protein per kg per day (the minimum Recommended Daily Allowance (RDA) for protein) and over 220 g carbohydrate per day.

The diets for both groups were formulated to be equal in energy with  1900 kcal/day provided for males and 1700 kcal/day for females.  Total fat content was the same in both the PRO and CHO diets.

Diet differences between groups were designed to reflect direct substitution of foods in the protein groups (meat, dairy, eggs, and nuts) for foods with high-carbohydrate content (breads, rice, cereals, pasta, and potatoes).  The education guidelines for the CHO group followed the USDA Food Guide Pyramid and emphasized restricting dietary fat and cholesterol with use of whole-grain breads, rice, cereals, and pasta.  For the PRO group, the education guidelines emphasized use of high-quality, low-fat proteins including lean meats, reduced-fat dairly, and eggs or egg substitutes.  Both diets included 5 vegetable servings/d and 2-3 fruit servings/d.

This study is unusual in that it provided a comprehensive nutritional education program along with an intense degree of nutritional monitoring throughout the 12 months of the study.  Most nutritional studies give the subjects a lead in lecture or series of lectures, then pretty much leave them alone.  To help ensure compliance, these researchers met with the subjects weekly throughout the study.

Subjects were evaluated at the start, after a 4 month period of active weight loss and finally after an 8 month maintenance period.  The entire length of the study was 12 months.

At the end of the 4 month weight-loss period, subjects on the PRO diet fared substantially better than those on the CHO diet.  Fewer people in the PRO group had dropped out of the study, and those who remained experienced an increase in HDL-cholesterol and a substantial reduction in triglycerides as compared to those on the CHO diet.  Those subjects on the CHO diet had greater reduction in LDL-cholesterol than did those following the PRO diet, but those changes didn’t old over the full 12 months.

Most interesting was the finding that although both groups lost equivalent amounts of weight over the first 4 months (actually, the PRO group lost a little more, but not a statistically significant amount), those in the PRO group lost 22 percent more fat than the subjects in the CHO group.  Since weight was essentially the same in both groups, those in the PRO group maintained or lost less lean mass while losing fat.  Which means that, despite the weight being the same, those in the PRO group ended up smaller than those in the CHO group.

As I’m sure everyone knows, fat is lighter than muscle.  If you trade a pound of muscle for a pound of fat, the scales don’t change.  But size does change because a given weight of fat occupies much more volume than the same weight of muscle.  You can see from the photo to the right how much less space 5 pounds of muscle take up than does 5 pounds of fat.  Plus, muscle is more metabolically active in that it burns more calories, and it actually does something for you.  Muscle makes you stronger; fat just weighs you down.

I know that many female readers will not want to gain extra muscle.  They shouldn’t worry, however, because in the absence of exogenous anabolic steroids women won’t become ‘muscle bound’ or non-feminine appearing.  What generally happens is that the muscle replaces fat within the muscle.  We’ve all seen marbling in beef, which is fat within the muscle tissue.  With the extra protein, new muscle replaces this fat, and the muscle may even become a little smaller in females while at the same time becoming more dense and stronger.

Let’s take a look at a couple of graphs that demonstrate nicely the difference in fat loss with greater protein intake, even in the face of what I consider way too many carbs.

The graph on the top shows the difference in fat loss between those PRO and CHO subjects who completed the entire 12 months of the study irrespective of how much weight they lost.

The bottom graph shows the difference in fat loss in those who were able to maintain a weight loss of at least 10 percent of their starting weights.

As you can see, the fat loss in those in the PRO group were substantially greater than those in the CHO group even though both groups were on an equivalent number of calories.

The series of graphs to the right show what happened to lipid values in the subjects in both groups.  HDL-cholesterol went up more and stayed up in the PRO subjects.  Triglycerides went down more and stayed down in the PRO subjects.  Subjects following the CHO protocol tended to have a reduction in LDL-cholesterol as compared to those in the PRO group, but as the study continued, the LDL-cholesterol began to return to pre-study levels.  This finding has been replicated in many other studies.  A high-carb, low-fat diet reduces LDL in the short term, but the changes don’t last.

The authors of this study made some interesting points in the discussion part of the paper.

Across all 3 analyses [the data was analyzed in three different ways], the PRO group averaged ~21% greater weight loss and 27% greater fat loss than the CHO group.  Further, irrespective of the amount of weight lost, participants in the PRO group obtained greater improvements in body composition as reflected by greater FM [fat mass] loss and attenuated relative lean mass loss.

In addition to the beneficial effects of the PRO diet for changes in body composition, more participants in the PRO group completed the study (64%) than in the CHO group (45%) and attained ≥ 10% weight loss (31 vs 21%, respectively).  These findings demonstrate greater compliance with a moderate PRO diet designed within the DRI [Daily Recommended Intake] guidelines for macronutrients for long-term weight management than the CHO diets often advocated for weight loss.

This is information you can use with friends and family who are, for whatever reason, adverse to going on a real low-carb diet.  The beauty of this particular study is that all the protein, carb and fat recommendations are within the government-approved RDAs.  The PRO group had a protein intake that was at the upper end of the RDA for protein and carb at an amount that was far from the lower end of the RDA for carbs.  (Of course those of us in the know realize that there is no lower end requirement for carbs  – many people get by with zero or close to zero carbs.  But we’re talking the government here. So, nuff said.)  What this means is that you can encourage friends and family to go ahead and eat a government-approved diet yet still get some of the benefits of a semi-sort-of low-carb diet.  A real win win.

Multiple mechanisms have been reported to explain increased loss of body weight and body fat with higher protein diets.  Higher protein diets appear to increase satiety, increase energy expenditure, and/or maintain lean tissue with higher metabolic activity.

Improvements in body composition, including reducing body fat and maintenance of lean tissue, are critical for prevention of weight regain and long-term health status.  Evidence is accumulating that the RDA for protein is inadequate to maintain muscle mass in adults during aging, with a physically inactive lifestyle, or during energy restriction for weight loss.  The current RDA for protein represents the minimum protein needs for healthy young adults with adequate energy intakes.  During weight loss, energy restriction increases the protein needed to maintain muscle mass and protein needs expressed as percentage of the reduced energy intake nearly double.

Just to give you an idea of the amount of protein we’re talking about here, let’s take the so-called average person who weighs 70 kg (154 lbs) and calculate daily protein requirements based on the protocol of this study.  70 kg  X 1.6 g/kg/day = 112 gm protein per day.

If you want to use pounds instead of kilograms, use 0.73 gm protein per pound per day.  If you weigh 200 lbs, then the calculation would be 200 lbs X 0.73 gm/lb/day = 146 gm protein per day.  Since meat contains about 7 gm protein per ounce, this 146 gm could be gotten in about 21 ounces of meat per day.  So we’re not talking about a small amount.

I’ll leave you with the conclusions of the authors of this study, with which I mostly concur.

The findings of the current study demonstrate that although energy deficit is the major factor for body weight loss, the macronutrient composition affects body composition, blood lipids, and long term compliance.  Specifically, a PRO diet with protein at the upper end and carbohydrates at the lower end of the AMDR [Acceptable Macronutrient Intake Range] is more effective for reducing % Fat and improving dyslipidemia.

I can only add that were the protein kept high (along with the fat) and the carbs slashed to around 30-50 gm per day, the results would have been even more impressive.

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.