The first Dietary Goals for the United States (DGUS) were released in 1977 to not a lot of fanfare.  At that time, the great unwashed masses hadn’t really heard much about the word cholesterol, a substance the DGUS recommended that we should limit to 300 mg per day.  Doctors didn’t routinely screen for it, and if they did, they didn’t pay much attention to it.  In fact, at that time – as I recall, anyway – the upper limit of normal for total cholesterol was 240 mg/dl.  I was in medical school back then, and I don’t really remember any emphasis on cholesterol or blood lipids.  I think we had one lecture on it in biochemistry, given by a nebbish little professor we called Mighty Manford (his first name was Manford), who labored away in the obscurity of the biochemistry department. It’s hard to believe in today’s world of lipophobia that as little as 30 years ago, no one much cared about cholesterol.

One of the major players in bringing cholesterol to the public’s awareness was Time magazine. Its piece on cholesterol in the March 26, 1984 issue was a devastating hit piece on both dietary cholesterol and dietary fat.  Both – the article explained – were a main driving force behind the development of heart disease.

Reading this article today, it’s amazing how it drips with misinformation.  At the time, however, most people – physicians included – accepted it as gospel.  Sadly, even today, many physicians who should know better believe in and act in accordance to the bountiful misinformation contained in this piece.

I could write a blog longer than the article (and it’s a long article) describing and dissecting all the many errors, but I’m going to go over just one.  And that one just briefly.  But before I get to that, let me show you just a few of interesting small parts of the article beginning with the very first sentence:

Cholesterol is proved deadly, and our diet may never be the same.

Hmm.  Dietary cholesterol has been proved pretty benign.  But the writers are correct about our diet being changed.

And take a look at this:

For decades, researchers have been trying to prove conclusively that cholesterol is a major villain in this epidemic [heart disease].  It has not been easy.

Have you ever seen a better example of the confirmation bias at work.  We know cholesterol is a problem, and we’re going to prove it no matter what it takes.  So what if the evidence keeps blowing up in our faces, if we work hard enough, we can by God prove what we know to be true.

Although most cholesterol found in the body is produced in the liver, 20% to 30% generally comes from the food we eat.

Actually, the figure is about 15 percent that comes from the food we eat.  Most cholesterol is made in the liver, but not all.  Virtually every cell in the body has the ability to make cholesterol, because it is so important to survival.

The main thrust of the article is about a study demonstrating that lowering cholesterol levels brought about a decrease in cardiac death rate.  Here it is presented in the breathless prose of the Time writers:

That was the reason for the N.H.L.B.I, study. The elaborate, ten-year program recruited 3,806 men between the ages of 35 and 59, all of whom had cholesterol levels above 265 mg per deciliter of blood (the average for U.S. adults is 215 to 220). Half the men were put on daily doses of cholestyramine, an unpleasant, cholesterol-lowering drug that was mixed with orange juice and taken six times a day. One participant likened taking it to swallowing “orange-flavored sand.” Among its side effects: constipation, bloating, nausea and gas. The other half received a similarly gritty placebo. Researchers had decided to use a drug rather than diet to lower cholesterol, because it would have been virtually impossible to control or measure the diet of so many men over so long a period. By the end of the study, the cholestyramine group had achieved an average cholesterol level 8.5% lower than that of the control group and had suffered 19% fewer heart attacks. Their cardiac death rate was a remarkable 24% lower than that of the placebo group.

The lesson is plain, says Dr. Charles Glueck, director of the University of Cincinnati Lipid Research Center, one of twelve centers that participated in the project: “For every 1% reduction in total cholesterol level, there is a 2% reduction of heart-disease risk.” This, says Project Director Basil Rifkind, is the evidence scientists have been waiting for. “It is a turning point in cholesterol-heart-disease research.”

Pretty powerful stuff, you might think.  Which is just what the authors of this article must have wanted you to think.  After all, a failed study doesn’t produce cover stories.

There are more than a few flies in this anti-cholesterol ointment, however.  Let’s take a look at what Gary Taubes writes about this study in Good Calories, Bad Calories:

In January 1984, the results of the trial were published in The Journal of the American Medical Association.  Cholesterol levels dropped by an average of 4 percent in the control group – those men taking a placebo.  The levels dropped by 13 percent in the men taking cholestryramine.  In the control group, 158 men suffered non-fatal heart attacks during the study and 38 men died from heart attacks.  In the treatment group, 130 men suffered non-fatal heart attacks and only 30 died from them.  All in all, 71 men had died in the control group and 68 in the treatment group.  In other words, cholestryramine had improved by less than .2 percent the chance that any one of the men who took it would live through the next decade.  To call these results “conclusive,” as the University of Chicago biostatistician Paul Meier remarked, would constitute “a substantial misuse of the term.”  Nonetheless, these results were taken as sufficient by Rifkind, Steinberg and their colleagues [those who had been searching for ‘proof’ for decades that cholesterol causes heart disease] so they could state unconditionally that [Ancel] Keys had been right and that lowering cholesterol would save lives.

Aside from the lack of any real meaningful data, the authors tried to palm off what they had found from a drug study as being applicable to diet.  Again, from Good Calories, Bad Calories:

Pete Ahrens [a cholesterol researcher at Rockefeller University] called this extrapolation from a drug study to a diet “unwarranted, unscientific and wishful thinking.”  Thomas Chalmers, an expert on clinical trials who would later become president of the Mt. Sinai School of Medicine in New York, described it to Science as an “unconscionable exaggeration of the data.”  In fact, the LRC investigators acknowledged in their JAMA article that their attempt to ascertain a benefit from diet alone had failed.

But that certainly didn’t keep them from trying.

Although there were several people mentioned in the Time article who were examples of the benefits of healthful, low-fat living, the star of the piece had to be Fred Shragai.

Fred Shragai, 59, of Encino, Calif., is a good example. Fourteen years ago, the prosperous real estate developer had a cholesterol level above 300 mg. At the time, he smoked four packs of cigarettes a day, was overweight (202 lbs. on a 5-ft. 5-in. frame) and routinely put in five or six 14-hour, pressure-packed days a week at the office. Rich sauces and fatty meat were his standard fare for both lunch and dinner, and exercise meant reaching under the bed to grab from his stash of pretzels and potato chips. Shragai was a classic candidate for a heart attack, and at the age of 45, he had one. Nine years later he was hospitalized for an operation to bypass five seriously blocked coronary arteries. In desperation, Shragai enrolled himself in U.C.L.A.’s Center for Health Enhancement. By changing the way he lived, he was told, he could lower his cholesterol level and reduce his risk of another heart attack.

There was much to learn. Cholesterol, as Shragai found out, is packaged by the body in envelopes of protein, and only some of these packages are potentially harmful. The main culprit, LDL (for low-density lipoprotein), is the body’s oil truck, circulating in the blood, delivering fat and cholesterol to the cells. Studies have shown that the higher the level of LDL, the greater the risk of atherosclerosis. Another type of cholesterol package is called HDL (for high-density lipoprotein). It appears to play a salutary role, helping remove cholesterol from circulation and reducing the risk of heart disease. Shragai’s goal was to lower his level of LDL and raise his HDL.

Diet was a first step. To begin with, such cholesterol-rich foods as eggs and organ meats and most cheeses can directly add to the level of potentially harmful LDL. Fat has an even bigger impact, although the reasons are not well understood. Saturated fat tends to raise LDL levels. Butter, bacon, beef, whole milk, virtually any food of animal origin is high in saturated fat; so are two vegetable oils: coconut and palm.

Polyunsaturated fats, which are typically of vegetable origin, have the opposite effect; thus corn, safflower, soybean and sesame oils tend to lower the level of potentially dangerous LDL. Fish oils do the same. In the middle are the mono-unsaturated fats such as olive and peanut oils. These may lower LDL slightly, but tend to be neutral.

The amount of fiber in the diet also seems to influence cholesterol levels. “LDL cholesterol can be reduced 20% in people with high levels just by consuming a cup of oat bran a day,” says Dr. Jon Story of Purdue University. However, Story adds, “that does not mean you can go and eat whatever else you want.”

For reasons that are still under study, cholesterol levels are influenced by a number of life-style factors. For instance, regular exercise can significantly raise the level of protective HDL. Alas, a couple of push-ups a day will not do the trick, says Dr. Josef Patsch of Houston’s Baylor College of Medicine: “You need sustained aerobic exercise for 20 minutes at least four times a week to really benefit.” A less strenuous way to raise HDL levels may be to have a daily shot or two of alcohol. “The evidence is indirect,” reports Epidemiologist Stephen Hulley of the University of California at San Francisco, “but social drinkers have HDL levels as much as 33% higher than those found in teetotalers.” On a more sober note, U.C.S.F.’s Dr. Richard Havel warns: “Anyone who recommends raising HDL by drinking is playing with fire.” Stress too has a detrimental effect. Studies have shown that the cholesterol levels of medical students peak at exam time, while accountants hit their high point around April 15.

By applying these lessons, says Shragai, “my life was totally changed.” Today the man who used to love steak says, “I won’t touch it.” At a restaurant, “if I choose fish, I ask the chef to skip the butter or please to sauté it in wine.” Every morning, regardless of weather, the man who once spurned exercise goes for an eight mile, two-hour hike through the wooded mountain trails near his home. He no longer smokes. His workdays average between eight and ten hours, but he insists, “I can absolutely stay away from the tension now. If I feel the pressure, I take off. Business associates get used to it; I set my own pace.” Shragai no longer lives in fear of a sudden heart attack: his blood pressure and pulse rate are down, and most remarkable, his cholesterol level has dropped to an exemplary 195.

Do a little Googling on Fred Shragai and a few things turn up.  Apparently, Mr. Shragai, a Holocaust survivor, was quite an interesting character.  In addition to being a successful businessman, he donned a Santa suit and entertained children around Christmastime.  As described in a December 1990 article in Orange Coast Magazine,

Shragai, in his late 60s, stands 5 feet 5 inches and weighs 165 pounds, down from his former rotund 200-plus since the doctor put Santa on a diet.  His beard and twinkling blue eyes are his own, he says proudly.

The article describes Mr. Shragai’s joy in his long-term job as Santa to many of his area’s poor residents.  He would visit houses, tell stories and bring presents.

“I’ll do this as long as I possibly can,” Shragai says, his eyes twinkling behind his Santa glasses. “After all, Santa can’t just quit.”

Unfortunately, that wasn’t all that long.  Mr. Shragai died of a heart attack about two months later on Feb 8, 1991 at age 66.

You can read about his life in an article in the Guardian written by his daughter as she came to grips with his death.

Many people who were in Mr. Shragai’s condition – overweight, overworked and overfed – bet their lives that the promise made by the Time article would be fulfilled.  If they quit smoking, cut the fat from their diets, took up exercise and dropped their cholesterol levels, they would avoid an early death from heart disease.  As the Time article said about Mr. Shragai:

[he] no longer lives in fear of a sudden heart attack: his blood pressure and pulse rate are down, and most remarkable, his cholesterol level has dropped to an exemplary 195.

As if these changes undo the risk of heart attack.  We can see from Mr. Shragai’s unfortunate case that they don’t.

Basically, he bet his life – literally – on the recommendations of doctors who were responsible for most of the hype in the Time article.  It’s hard to say whether he won, lost or broke even on the bet, because we don’t know what the outcome would have been had Mr. Shragai continued on his previous path.  Or what would have happened had he gone on a low-carb diet instead.  Based on my years of experience, I would bet that he would have done better on the low-carb approach, but, as I say, there is no way to know for sure.

There are a couple of take-home messages from Mr. Shragai’s case.  The first is that we don’t really know what constitutes true risk for heart disease.  Reduction of blood pressure, weight and cholesterol levels – measures of risk in the estimation of most physicians – didn’t prevent a disastrous outcome.  The second, and, in my view, the most important is that when we make nutritional and lifestyle decisions, we are betting our lives that we’ve made the correct decision.  Even those maintaining their course are making the decision not to change.  Decisions precede actions, and actions definitely have consequences, which means decisions have consequences.

I’m betting my life that saturated fat is good for me and that carbs are bad.  I eat a ton of saturated fat and very few carbs (unless I’m being a very bad boy as I was last night when I indulged in some of my granddaughter’s birthday cake).  So, if Dean Ornish is right and I’m wrong, I could be in deep trouble and maybe live a dramatically shortened life.  But I don’t think so.  Why?  Because the indications that the low-carbohydrate diet is the correct diet for humans comes from so many different sources. (And that’s not even counting my years of hands-on care of many thousands of patients on such diets.)

If you look at the scientific literature, you find that the low-carbohydrate diet is, at worst, the equal of the low-fat, high-carbohydrate diet and at best triumphs over it in spectacular fashion.  If you look at the anthropological evidence, the health of early humans took a turn for the worse when agriculture (read: high-carbohydrate diet) came along.  Pasta, even whole-grain pasta, was the fast food of antiquity.  If you look at the evolutionary evidence, it’s pretty clear that the forces of natural selection molded us to function optimally on a higher-fat, higher-protein diet.  And, finally, if you just look at the human physiology and biochemistry involved, it is clear that a diet high in carbohydrates is not good for us.  Looking at all this graphically from one of my slides below, we can see that all the evidence vectors point to a low-carb diet as being the one most optimal for human health.  Can a low-fat, high-carb diet make this claim?  I don’t think so.  Though many misguided vegans try to make such a claim, their arguments are risible.

You can find a few studies that show a low-fat, high-carb diet performs OK, but where is the anthropological, evolutionary and biochemical data to confirm?  When deciding what diet to follow, remember: you’re betting you’re life.  Consequently, you should view the diet through the various lenses as laid out in the graphic above.  If a new diet looks acceptable through one or two lenses, but not the others, just stick with your low-carb diet and be done with it.

Had Mr. Shragai performed the above analysis, he probably would not have followed the diet he did.  As I wrote earlier, we have no idea as to what his outcome would have been had he gone on a low-carb diet instead of a low-fat one, but I can’t help but believe it would have been better.  Although Mr. Shragai’s case is that of but one individual, since this vapid 1984 Time article came out launching the jihad against fat and cholesterol, the entire country became unwitting subjects in a long-term experiment testing the hypothesis that a low-fat, high-carbohydrate diet is healthful.  And in the intervening 26 years, obesity has skyrocketed and type II diabetes has reached epidemic proportions, leading me and many others to say that the low-fat diet has failed.  At least as applied to large groups of subjects.

Let me sum up the take home message with an unrelated story that oddly illustrates the point.  When I was taking flying lessons years ago, the tower once told me to cross one runway we were stopped short of and proceed to the next one.  I goosed the engine and started across.  My instructor pushed on the brakes and stopped us and asked me what I was doing.  I said, “The tower told me to proceed to runway 15L.”  My instructor said, “Yes, but you didn’t look for traffic coming in on runway 15R (the runway we had to cross) before proceeding.  Here’s what you’ve got to learn.  If the pilot make a mistake, the pilot dies; if the control tower makes a mistake, the pilot dies.  Always check for yourself.”

Sobering words, but ones I remember.  The same applies to diet.  Don’t let Time magazine or anyone else tell you what to do.  It’s your life.  Don’t bet it heedlessly.

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

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

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

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

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

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

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

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

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

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

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

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

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

Give me strength.

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

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

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

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

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

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

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

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

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

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

Here’s what the authors wrote:

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

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

…compliance was assessed with objective biomarkers.

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

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

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

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

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

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

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

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

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

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

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

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.)

Applebee's Quesadilla Burger

One of my readers sent me a link to a segment on ABC News with Charlie Gibson showing just how disgustingly slanted and inaccurate mainstream media reports can be.

Gibson leads into the segment about two reporters who underwent self experimentation on the adverse effects of unhealthy eating.  The reporters, ABC’s Yuji de Nies and Jon Garcia, set out to see what would happen if they consumed a giant meal containing over 6,000 calories.  Here is the result as they reported it.

Click here to view the embedded video.

Pretty brutal, eh?  But let’s shine the piercing light of good sense on what is going on here.  As you might expect, the reality is vastly different from that portrayed by ABC.

First off, let’s look at the actual nutritional content of the food eaten.  As reported in the piece, the total energy content of the meal was 6,190 calories, which included 187 grams of saturated fat.  These were the only parameters reported.  I took the time to go through the links in the article accompanying the video to find exactly where these foods came from.  Here’s what I found.

The burger is an Applebee’s Quesadilla Burger (served with fries, of course); the snack is The Cheesecake Factory Fried Macaroni And Cheese; and the dessert is Uno Chicago Grill Mega-sized Deep Dish Sundae (listed as cookie below).  How do I know these are the exact ones?  These were the ones referenced in the CSPI’s List of Most Unhealthy High-Calorie, Fat and Salty Restaurant Foods That May Clog Your Arteries.  After seeing the photos and comparing to what I saw on the video, these selections are the ones the reporters ate.

I then tracked down the Nutritional Facts for the foods involved (here, here, here and here) and put them into an Excel spreadsheet.  Take a look.

The first thing you might notice is that the total calorie count is 5,708, which is considerable, but is actually 482 calories fewer than the 6,190 reported.  Second, and this is a biggie, the saturated fat content of this meal is only 88 grams, not the 187 grams reported.

The reporters stretched the truth a little in that they reported as if the Mega-sized Deep Dish Sundae were a single treat to be consumed by one person at a sitting.  I’m sure it could be so eaten, but it’s actually designed for four people to share.  The Nutritional Facts list the calories per serving as 690 and the saturated fat as 17 grams.  I’ve used the amounts in all four servings, i.e., one entire four-person dessert, in my spreadsheet.

As you may have noticed, the total carb content of the meal is 745 grams, which converts during digestion to a little over three cups (3.1 cups to be exact) of sugar.  The ABC report, of course, failed to mention the carb content of the meal and ignored any immediate effect this huge intake of carb might cause.  One of the reporters, Jon, claimed that he was ‘sluggish’ and ‘tired’; the implication being that this sluggishness resulted from his huge saturated fat intake.  No mention, naturally, of the enormous amount of carbohydrate and the large increase in insulin release it might cause.  From what I can see from the video, Jon looks to be sporting a little abdominal obesity, which would imply a degree of insulin resistance and hyperinsulinemia.  People with this disorder tend to over secrete insulin in response to carb intake causing an overshoot and reactive hypoglycemia (low blood sugar), which will indeed result in sluggishness.

It’s pretty impressive when the lab tech holds up the tube of blood taken after the meal and compares it to the one taken before the meal.  There is a lot of fat swimming in the serum, that’s for sure.  What the producers of this piece (and, sadly, the doctors commenting although they should know better) want you to take away from all this by the way they set it up is that all that saturated fat went directly into the blood.  And how can you argue with them?  It’s there for all to see.

Problem is, that’s what blood samples look like after almost any meal, especially one that contains carbohydrates.  The fat you see isn’t the fat the two reporters ate; it is the fat the liver has made from the carbohydrate.  It’s the same picture a tube of blood would show after either of the two doctors had eaten a high-carb, low-fat lunch.

The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route.  The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbs.  Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells.  Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature.  Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest.  The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood.  As I say, the fat in the blood you see on the video didn’t come from the saturated fat in the diet, although that was definitely the implication.

But what about the ultrasound showing the blood vessels had changed?  Wasn’t that because of the fat?

I’m afraid not.  The fat from the diet wasn’t in the blood vessels yet, so it couldn’t be the dietary fat causing the change.  So what was it?

How about a little normal physiology.  Let me explain.  The body gets blood where it needs to get it by opening certain blood vessels while closing others.  Let me give you an example.  Have you ever jumped into cold water to go swimming and noticed that not long after jumping in you have to urinate?  What happened?

Your arms and legs have a radiator effect.  Since these appendages have little padding the blood circulating there is exposed to the cold water, and if nothing is done, the cold water cools the blood creating a big problem.  Your body compensates by shutting down the circulation to the skin and areas close to the surface in your arms and legs and shunts that blood to your core.  Your core already has plenty of blood when this happens, so it has to get rid of some.  It does so by sending it through the kidneys where the liquid portion is filtered out and becomes urine.  Suddenly your bladder is full and you have to go.

The body has the ability to direct blood wherever it needs by its manipulation of blood vessel size.  Where do you think blood is needed after an almost 6,000 calorie meal?  That’s right.  The digestive tract.  It takes a lot of work to deal with 6,000 calories, and a lot of work requires a lot of oxygen, which comes from the blood.  So after a heavy meal, the body shunts extra blood to the guts where the works is being done.  It does this by opening or dilating the arteries carrying blood to the intestines and by narrowing the blood vessels in other parts of the body.

Now, think back to the video of the woman whose blood vessel (in her arm) is being examined by ultrasound.  When it’s compared to the previous ultrasound, the one before she ate, notice how much faster the heart is beating.  (The little swishing sounds you hear, each of which represents a heart beat, are spaced much closer together.)  The heart is beating faster because the body is working to digest an enormous amount of food, and this work stresses the heart in the same way that running down the street would stress the heart.  Work is work.

The digestive tract needs extra oxygen to do its work, this extra oxygen can get there only via the blood, so the intestines require more blood than normal.  This extra blood gets shunted there by opening the arteries that feed the gut and narrowing those that go other places where a lot of blood isn’t needed at the moment.  Such places as, say, a relaxed arm.

Anyone with a smattering of knowledge of normal physiology (and apparently an open mind) could predict that the artery in a relaxed arm would narrow after a heavy meal and that that artery would be back to normal six hours later (which it was so reported in this video).

What you’re seeing in this video is normal physiology at work interpreted as being abnormal by a couple of lipophobic doctors who should (and probably do) know better.  It makes for dramatic theater, but their interpretation is nothing but prevarication or ignorance or both.

But had they reported the truth, there would have been no story.  Kind of sad, isn’t it.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Let’s take a look at what they did.

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

Here is a description of the diets:

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

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

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

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

Here is the chart showing the study outcomes:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The news is abuzz with reports of the latest study to come out showing that eating meat, especially red meat, kills us off before our time.  (You can read some of the reporting here, here, here and here.)  Google shows 547 new articles about this study.

Although this study is totally worthless from a causality perspective because it is an observational study, it does serve to confirm the biases of those non-critical thinkers who have already bought into the idea that meat is bad.  To give you an example of such a soft thinker, here is the second comment on the blog post about this study in the New York Times.

I could have told you that 30 years ago. I been a vegetarian for 47 years and I have never seen vegetarians die from heart disease or cancer. They died from basic infectious diseases and malnutrition. Make no mistake it is harder to be a vegetarian than a carnivour but your body does not expel everying [sic] that is in the meat especially red meat.

Red meat is the major culprin [sic] in colon cancer. I actually know people who have colon cancer gene that only eat a no red meat diet and have no issues with their colon. Of course they also do not smoke or drink too much alcohol.

Red meat lobby is very powerful in America – Let them pay for this!

Ah, yes, an enlightened cogitator indeed.

The study published in the Archives of Internal Medicine (free full text here) is a typical epidemiological or observational study.  The reports have it tarted up with a lot of fancy clothes, but it is really nothing but an observational study.  And, as we’ve gone over ad nauseum in these pages, observational studies can’t be used to prove causation.

Even if they could, this study would be questionable at best because the relative risk (RR) is slightly over 1.0.  Because of the nature of the difficulty in doing these kinds of studies with any kind of accuracy it takes a RR of over at least 2.0 to get the serious attention of anyone who doesn’t have a built-in bias.

What I found more interesting than this study (which isn’t interesting or important at all) was the press coverage of it.  And I found especially interesting that which the press didn’t report.

Scientific journals have a couple of ways of getting their articles out there ahead of publication, so that the press can do stories on them.  If it works out right, the reports all hit the media on the same day that the article itself is published.  Doctors who read the journal often find out in their morning newspaper about a new paper before they even get their journal in the mail later that same day.  Many of the larger journals, Archives of Internal Medicine, for example, will issue press releases the week before on those papers coming out that the editors feel are important.  These press releases go to anyone with press credentials (I even get them), and are embargoed until the date of publication of the journal.  Reporters get advanced copies of the papers and get the editor’s (and maybe even the author’s) take on the paper.  Journalists can then write their stories to be timed with publication of the paper.

Another way followed by a number of journals is to publish papers online in advance of their actual publication date.  Reporters troll these advanced online articles looking for material for stories and often write them up for publication before the paper in question makes it into actual publication in the journal.

At the same time that this paper appeared, showing increased red meat consumption to be tied to a slight increased risk of death (and showing that those subjects eating white meat had less risk), a couple of other papers came out in the online pre-publication section of the American Journal of Clinical Nutrition (AJCN), arguably the world’s most prestigious nutritional scientific journal.  These two AJCN papers saw the light of day at around the same time as this highly-publicized study on meat and mortality, but demonstrated the opposite results.  They got no press coverage whatsoever.  Which proves what I’ve been saying all along: the press is biased against meat in general, and especially against red meat.  Knowing this, careful readers should take anything negative thing the media reports about red meat with an enormous grain of salt.

Let’s look at the other two studies published in AJCN.

The first is titled Meta-analysis of animal fat or animal protein intake and colorectal cancer.  One of the constant themes anti meat people like to hammer out is that meat intake, especially red meat intake, causes colon or colorectal cancer.  This is heard so often that most people take it for granted, assuming that there must be a ton of research backing it up.  As this paper points out, there isn’t.

The association between total dietary fat, including fat constituents such as saturated fat, monounsaturated fat, polyunsaturated fat, and cholesterol, and risk of colorectal cancer has been evaluated in numerous epidemiologic [observational] studies.  Results from these analytic investigations have generally been mixed.  Whereas some studies have reported positive associations, several studies have observed null and inverse associations.  In a pooled analysis of data from 13 case-controlled studies, risk of colorectal cancer was found to increase significantly with increasing categories of total daily energy intake.  In the same analysis, and after adjustment for total energy intake, the authors observed no evidence of an energy-independent effect of total dietary fat or specific fat components other than cholesterol.  In fact, many of the associations among men and women were in the inverse direction [i.e., more animal fat equals greater longevity].

Animal foods and meat products contain both saturated and unsaturated fats; however, similar to analyses of total fat intake, several studies have not observed any consistent epidemiologic evidence of an association between saturated fat or polyunsaturated fat intake and risk of colorectal cancer.  Although some studies reported positive associations for consumption of saturated fat, nonsignificant associations at or near the null value [no association] or inverse associations have been observed in numerous cohort studies and case-control studies.

This paper goes on to discuss how the hypothesis that fat and meat intake are a bad thing healthwise got kicked off way back in the 1960s from a presentation at a symposium. In shades of Ancel Keys and his discredited Seven Countries Study, a researcher named Ernst Wynder used the international food and cancer mortality data to demonstrate an increase in colorectal cancer as a correlate of increasing oil and fat consumption.  The hypothesis, although never proven, has been with us since.  The authors of this paper set out to study it once again.

Here is what they did:

To clarify the potential association between animal fat intake and colorectal cancer, we conducted a meta-analysis of prospective cohort studies in which data for animal fat were available.  In addition, we identified case-control studies that reported results for animal fat intake and combined data from these studies with the prospective cohort data in separate analyses.  Because the primary macronutrients in the consumption of animals include protein and fat, we also conducted a separate meta-analysis of prospective cohort studies in which data categorized as animal protein or meat were available.

After sifting through all this data, what did the authors find?  Absolutely nothing.  No correlation between meat and/or fat intake and colorectal cancer.

In this meta-analysis, no consistent evidence of a positive association between  consumption of animal fat and colorectal cancer was observed.  Specifically, we found no association  between the highest animal fat intake category and colorectal cancer.  Furthermore, none of the subgroup analysis (i.e., sex, anatomic tumor site, and study design) indicated positive patterns of associations.

And their conclusion:

On the basis of the results of this quantitative assessment, the available epidemiologic evidence does not appear to support an independent association between animal fat intake or animal protein intake and colorectal cancer.

Like the study above showing the slight correlation between red meat intake and decreased longevity, this study is an observational study, and, as such, doesn’t demonstrate any kind of definitive proof.  But what I find galling is that the meat and mortality study hit all the airwaves and this study – made available to the media at the same time – received zero press.

Yet another study in the advanced online section of AJCN titled Mortality in British vegetarians: results from the European Prospective Investigation in Cancer and Nutrition (EPIC-Oxford) shows that things ain’t always as they seem.  Yet the press refuses to pick up and report this man-bites-dog story.

If you ask the man on the street (who has been fed a load of bunkum over the years by the press) if vegetarians or non-vegetarians are healthier and live longer, you will almost assuredly be told that vegetarians are the healthiest.  Most people believe this, but they just don’t want to make the sacrifice to follow the vegetarian lifestyle.  They are willing to give up a couple of years of life to not have to live on a steady diet of beans, tofu, vegetables, fruits and dry bread.  You would think that if a study came out from a prestigious institution (Oxford) published in a top-line scientific journal showing that vegetarians don’t live any longer than non-vegetarians and actually have a higher incidence of some particularly nasty cancers (but slightly lower rates of death from heart disease) it would be newsworthy.  But the press has totally ignored this study just like they did the last one.

This vegetarian study was interesting on a couple of levels.  Not only did it not show a difference in longevity between vegetarians and nonvegetarians, it showed major increases in longevity just from being in the study.  Not long ago I wrote a post about a statin study in which I discussed the adherer verses the non-adherer effect.  A number of studies have shown that subjects who take all their medicines as directed – even the placebos – live longer and/or do better than those who takes their medications irregularly.  There is something about people who go the extra mile that makes them live longer than those who don’t.

In this Oxford University vegetarian study, vegetarian subjects were recruited by all sorts of methods.  Those in the study cast out their nets for other vegetarians and recruitment was done through all kinds of advertising venues.  Those accepted into the study -both vegetarians and non vegetarians – had to jump through a fair number of hoops to get accepted and stay in the study.  And to stay in the study for the ten plus years that it went on.  After the study period, the numbers of deaths in the two groups was tallied, and it was found that vegetarians didn’t live any longer than non-vegetarians.  As a percentage, the number of deaths in each group was the same.

What’s more interesting to me, however, is the difference between the rate of deaths in both the vegetarian and non-vegetarian subjects as compared to their neighbors who weren’t in the study.  The researchers calculated the standard mortality ratios (SMRs) for vegetarians and non-vegetarians from deaths before the age of 90 years old as compared to the mortality rate for non-study subjects living in the same area.

The SMR is the ratio of the observed number of deaths to the number of deaths expected from the national rates, standardized for sex and age, and expressed as a percentage.

In other words, if the observed number of deaths in the study group had been three quarters of that expected in a similar population from the area, the SMR would have been 75 percent.  And would have been a striking finding to boot.  It would have meant that just being in the study reduced one’s risk of death.

When all the data was tallied, the SMR for all causes of death among study subjects was only 52 percent, and was identical in vegetarians and nonvegetarians!  It didn’t matter if you were a vegetarian or a nonvegetarian, as long as you were in this study you were about half as likely to die as your neighbor who wasn’t in the study.  Now that’s an adherer effect in spades.  And I would think pretty newsworthy.  But, like the study above on meat and colorectal cancer, it was completely ignored by the press.

The point of this post is that you shouldn’t get wound up about a study that gets reported throughout the media because there are more than likely other studies that are just as well done and just as important showing exactly the opposite findings that the press chooses to ignore.  You’re not seeing the science as it is, you’re seeing the science as the press wants you to see it, which, typically, is the way that confirms the bias of members of the press.

As a journalist friend of ours once remarked:  what is news?  News is whatever the reporter decides it is.  In my opinion, they decided wrongly in this case.

Detail from Pieter Bruegel's The Triumph of Death

The Dark Ages were an inglorious period of human history bounded on the one side by the Classical Age and by the Renaissance on the other.   These grim times began when a classical empire was savaged by barbarians plunging the world into a long era of darkness ruled by ignorance, superstition and fear, and ended finally by the intellectual stirrings of the Italian Renaissance.

I believe that the latest dietary study published in the New England Journal of Medicine is an early indicator that our own era of dietary darkness may be coming to an end.

Loud have been the cries of all the low-carb bloggers, dieters, and practitioners about this paper, which purports to show that macronutrient consumption doesn’t really matter.  Low-carb, high-protein, low-fat, high-carb, it makes no difference, say the authors, it’s just the calories that count, not the composition of those calories.   As expected, all the major media picked up on the story.

Opined Jennifer Levitz of the Wall Street Journal:

You aren’t what you eat. You’re how much.

That’s the message from a two-year National Institutes of Health-funded study that assigned 811 overweight people to one of four reduced-calorie diets and found that all trimmed pounds just the same. It didn’t matter what foods participants ate, but rather how many calories they consumed.

Tara Parker-Pope of the New York Times writes:

For people who are trying to lose weight, it does not matter if they are counting carbohydrates, protein or fat. All that matters is that they are counting something.

The study has been written about and dissected by so many others that I don’t see any need to go into it in any detail myself.   Everyone with good sense who has read it understands what the deal is.  The researchers, old-school low-fatters one and all, constructed the study in such a way as to ensure the outcome they wanted, which was that all that really counted was the total caloric intake.  They did this by making sure that the diet with the lowest carb content – over 150 g per day – couldn’t possibly be called a low-carb diet by anyone who really understands what a low-carb diet is.   But the authors did call it a low-carb diet and the media perpetuated the myth.

There are a couple of ways this old fudgaroo can be brought off.

First, the way this New England Journal study did it.  If diets of similar but slightly different macronutrients are compared, the likely outcome is that calories, not macronutrient composition, is what correlates with weight loss.  In terms of carbohydrate, it’s only if intake drops significantly that a difference is seen, based on macronutrient composition.  None of the diets tested in this study qualified as a real low-carb diet.

There is a second way the effects of macronutrient composition can be minimized, leading the unwary or the unintelligent (or those who have an agenda) to misunderstand.  If you keep subjects on very-low-calorie diets, you find that the weight lost is virtually all a function of the caloric intake.  Why? Because if subjects don’t get enough calories to meet even the most basic caloric needs, all calories go to keep the body alive.  The hormonal influences of these calories don’t matter.  So, if you want to have weight loss be strictly a function of how many calories are consumed, put subjects in metabolic units to they can be observed closely, keep them on 500 calories per day of any mixture you want, and watch the weight come off about the same no matter what the macronutrient composition.    This is the trap that Anthony Colpo fell into when he decided that macronutrient composition didn’t matter and wrote a book listing a bunch of metabolic studies proving his point.   Virtually all of the studies fell into this extremely-low-calorie category, and would be expected to show weight loss strictly as a function of calories and not macronutrient composition.  But, as we all know, this idea doesn’t hold up in the real world of more normal calorie consumption.  (I suspect that Anthony has even figured this out by now since he’s pretty much vanished from the face of the earth.)

These researchers – Stark, Bray, et al – from the low-fat, it’s-only-calories-that-count school set up a low-carb straw man, then knocked it down with this study.  And a lot of people got the message.  In fact, while we were in Seattle over the past few days, I heard no fewer than three people mention that a new study had shown that only calories really counted.  So how can I write that this is the last gasp of the dark ages of nutrition?

Easy.    Think about where we’ve been and what has happened.

Petrarch (1304-1374), the Italian genius and man of letters, who started the process of dragging the world from the recesses of the Dark Ages wrote:

Each famous author of antiquity whom I recover places a new offence and another cause of dishonour to the charge of earlier generations, who, not satisfied with their own disgraceful barrenness, permitted the fruit of other minds, and the writings that their ancestors had produced by toil and application, to perish through insufferable neglect. Although they had nothing of their own to hand down to those who were to come after, they robbed posterity of its ancestral heritage.

Now, consider the history of the low-carb movement.    Gary Taubes laid it all out in Good Calories, Bad Calories.  Up until the late 1950s/early 1960s scientists the world over were homing in on the fact that excessive carbohydrate intake makes people fat.  There were international conferences, symposia and numerous papers published tying carbohydrate intake to fat accumulation.   The metabolic pathways involved were worked out in detail.   Physicians were prescribing reduced carb diet to their patients for weight loss.  It was the classical age of low-carb. Then the barbarians struck.

Ancel Keys published his Seven Countries study and began to demonize fat. The nutritional dark ages began.  For the past forty years we’ve languished in this wilderness of idiocy.  Just as there were a handful of great works of art produced during the Dark Ages, there have been a few prophets crying out during this time of low-fat, high-carb error, but the mainstream has ignored them or ridiculed them and forged ahead advocating whole grains and complex carbs while besmirching fat, especially saturated fat. During these times, obesity, diabetes, GERD and other disorders of excess carb intake have skyrocketed to epidemic proportions, a fact the main stream appears oblivious to. More carbs and less fat – that’s how you solve the problem, we’re told.  And the people get fatter and more diabetic. These mainstream pushers of carbs have forgotten the “writings that their ancestors had produced by toil and application” and have allowed it “to perish through insufferable neglect.”

“Although they had nothing of their own to hand down to posterity,” they instead filled the medical and scientific journals of their time with insipid studies designed to prove their own ill-derived hypotheses.  These are studies that will be laughed at in generations to come.

But it has all been changing.  Think about it.  When I first went out on the stump in 1989 promoting a low-carb diet, I was attacked almost everywhere I went.  Robert Atkins was, too, when he went out 15 years earlier.  We both described our clinical experiences with low-carb diets and were met with derision. “All anecdotal,” they said. “Where are the studies?  Show us the studies.”  We couldn’t really show them the studies because recent studies hadn’t been done. I countered by asking, “Where are the studies showing low-fat diets prevent anything?”  But that question was usually shrugged off with a condescending smirk.

Look at the progression over just the past five years.  Thanks to a ton of research comparing low-fat diets to low-carb diets, the mainstream thinking has first gone from the low-fat, high-carb diet is the best for weight loss, lipids, reducing cardiovascular risk, and good health in general to Okay, maybe the low-carb diet does bring about more weight loss, but at the price of clogging your arteries.   Then to Well, the low-carb diet may bring about quicker weight loss and at least an equal reduction in cardiac risk as low-fat diets do in the short term, but where are the studies showing safety over the long term?  (One could of course counter with Where are the studies showing the low-fat diet is safe over the long run?  And one often does.)  As the long term data has started to trickle in showing no problems with low-carb diets for the long haul, the mainstream has been left with pretty much no place to hide.  So, now, as a last ditch effort, they are resorting to the calorie defense.  It’s all calories.  It has nothing to do with macronutrient composition.

If you think about it, this is a pretty amazing admission for them.  Could you imagine any one of these clowns making such a statement during the height of the low-fat frenzy? They are basically saying, Low-fat, low-carb, high-protein, high-fat: it doesn’t really matter.  They all work. It’s simply a function of calories. This is a huge admission for them.  It’s the last step before actually admitting that the low-carb diet is superior across the board.

And this admission will come.  But probably not for a few more years because it won’t come from any of these guys.  This is as close as it gets.  But these are the guys who were training when Keys and his idiocy held sway. That’s what they learned and that’s what they built their careers on.  But they are old and ready to move on.  When they do, the younger people with a different outlook will come to the fore.

As the great physicist Max Planck said

A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it.

The old generation is waning and this study is one of its last gasps.   Granted, they had to fiddle with the experimental design yet again to get the results that they wanted, but this study puts low-carb on par with any other diet, including the low-fat diet beloved by them all.  No longer can they cast aspersions on the low-carb diet.

I think a nutritional renaissance is on the way.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

It’s pitiful that they are so desperate.

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

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

Despite the title of this post, it isn’t really about why low-carb is harder the second time around per se. It’s more about attitude toward dieting and why diets in general are difficult, sometimes even the first time.  What with it being a new year and all, I figured I would go ahead and get things stirred up early with my thoughts on the psychology of dieting.

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

A typical conversations goes something like this:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

And all the above happens in just a few seconds.

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

But, this can all the dealt with.

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

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

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

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

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

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

All of you commenters have done your job.  You’ve brought up several issues that I neglected to address in my last post.  Let me address them now.

First and foremost is the question about peri- and post-menopausal hormonal balance.  From long experience I can tell you that it is difficult for many women to lose weight in the peri- and post-menopausal years, especially the peri-menopausal years, without some hormonal balancing. It can be done, but it is more difficult.  MD keeps promising to post on the subject in detail, but right now she’s up to her eyes in another couple of projects that are consuming most of her time.  That time not consumed by her projects is consumed by little ole me, who needs his fair share.

There is a book on balancing hormones that I feel is the best one of the bunch out there right now.  It is by an acquaintance of mine, whom I run into at medical meetings all over the place.  His name is Uzzi Reiss, M.D, and he is the gyn doc to the stars.  I’m not kidding.  He probably takes care of half the peri- and post-menopausal Hollywood crowd.  He has an enormously busy practice.  I pushed him to write a book early on, but he deferred saying that he couldn’t afford the time away from his practice.  But he finally did come out with one.  It was published about 7 or 8 years ago, and so isn’t completely up to date, but, as I said, I think it’s the best of the bunch out there, written by someone who certainly knows what he’s doing.

At the time he wrote this book, he was using Tri-Est, which is a blend of all three forms of estrogen found in the normal female.  MD prefers more estradiol than found in Tri-Est for weight loss purposes; in fact, she, herself, uses only estradiol.  At the time Dr. Reiss’s book was written compounding pharmacies weren’t as common as they are today, so it wasn’t as easy to get estrogen compounded so specifically.  I think for those of you interested, Dr. Reiss’s book will give you a lot of information to get you started on your own quest.  Many women – MD included – started out on Tri-Est and starting fiddling from there.  The most important thing is to work with a physician who knows what he/she is doing to get your hormones working for you instead of against you.

Another subject I left off is sleep.  Numerous studies have shown that more good quality sleep will help with weight loss.  As we age, it becomes more and more difficult to get good quality sleep.  Often regaining the formerly lost weight brings on acid reflux and GERD, which tend to cause awakening in the middle of the night.  And once we get going again on a low-carb diet, we usually get into a little ketosis, which makes falling asleep a little more difficult yet.  There are a few things to be done.  First, the low-carb diet – even the second time around – typically gets rid of the reflux and GERD pretty quickly.  (I’ve got another post that I’ll probably put up next week about a supplement that will knock reflux on its head quickly.)  You can help with falling asleep, which is what most people are troubled with, by doing a couple of things.  First, get some low-dose sublingual melatonin tabs.  These you can dissolve under your tongue as you turn in.  It’s important that you take the melatonin right before you turn out all the lights – don’t take it and stay up and watch TV or read.  You want the room to be dark.  The pineal gland releases melatonin as a response to darkness, and its function is to help you get to sleep.  It has antioxidant properties, along with many other functions, but you will be taking it to sleep.  There is a fall off in melatonin release by the pituitary with aging, which is one of the reasons people have more difficulty sleeping as they get older.  So, try the melatonin if you’re having trouble.   The other thing you can do is to have a cup of herbal tea right before bedtime.  And sweeten the tea with either sugar or honey.  That’s right.  Real sugar.  A teaspoon of sugar is about 5 grams of carb, which won’t do a lot to hinder your weight loss, but it will be enough to shut down ketone production long enough to get you to sleep.  And if you think a teaspoon of sugar isn’t all that much, remember, it’s the total amount circulating in your blood if you have a normal blood sugar.

Another reason people have difficulty losing as they get older is that their livers don’t function as well.  As we get older we tend to have more aches and pains, and we take more Tylenol and Advil and similar OTC medications for them.  These drugs are metabolized in the liver, and, consequently, they consume some of the liver’s capacity.  Same goes for coffee.  No one likes coffee more than I.  But when I want to pick up my weight loss after I’ve gone off the wagon for a while, I cut back on my coffee.  Why?  Because caffeine is metabolized in the liver just like the above drugs.  It also consumes some of the liver’s capacity.  I switch to decaf for a few days whenever I’m getting back on the straight and narrow.  If you can’t stomach the thought of decaf coffee (and I don’t like it, myself) drink decaf Cafe Americano.  (Here is a YouTube on how to make an Americano starring yours truly.)  There is not as much difference (at least to my palate) between decaf and regular espresso than there is between decaf and regular coffee.  Finally, as we age, we tend to drink more.  Most people drink like fish during college, then slack off.  They start to pick it back up (never to college levels, though, thank God) as they drift into middle age.  Alcohol is detoxified in the liver just like caffeine and OTC pain relievers.  All these things add up to put quite a load on the liver.  And if you’ve regainded weight, you’ve probably got some fatty accumulation in your liver and it’s not working at peak levels anyway.  All these added substances that compromise the liver even more don’t help.

Insulin stays in the circulation because it is put there by the pancreas and because it isn’t metabolized in the liver.  A liver that isn’t functioning up to snuff won’t break down insulin as rapidly as it should.  Consequently, higher levels of insulin mean more difficulty in losing weight.  Plus, since the liver is the major organ involved in the entire metabolic process, it works a whole lot better to stabilize everything when it is unhindered by having to detoxify a lot of unnecessary stuff.  Which is why you need to baby your liver when you restart your low-carb diet.

I’m sure I’ve still forgotten some other factors, and I’m sure you all will remind me.  I think I’ve got some of the smartest readers in the blogosphere.  Thanks for chiming in.