In my ongoing quest to become a little more technically adept, I started using Google Alerts for a number of things I’m interested in, including my own name.  (Believe me, there are a lot of people out there in the world with the last name Eades, including the Fire Chief of London.)  For those of you who don’t know, you can go to the Google main page and navigate around until you come to ‘Alerts.’  You can then sign up for these ‘Alerts’ to be delivered to you via email.  It’s a free service provided by Google, and it uses the Google system to crawl through cyberspace and find anything (blogs, articles, news reports, etc.) that has whatever word, words or phrases you submitted included and emails the link back to you.  I put a bunch of stuff in and get emails from Google throughout the day.  Most of it is stuff that is totally unrelated to anything I give a flip about, but every now and then it turns up something of interest.  Having my name listed has cost me money because one of the first things I that came back to me was an article about Eades Whisky, which I had no idea existed and which I had to try.  It is expensive, about $75 per bottle, but I ordered some.  It’s very good.  But it hasn’t replaced Jameson, however, by a long shot.

Yesterday I got back a hit about something that I had totally forgotten about:  our rebuttal to the idiotic ’study’ presented by the PCRM (Physician’s Committee for Responsible Medicine – a name straight out of Orwell if there ever was one) a few years ago.  This group, composed mainly of militant vegetarians, came up with an insipid ’study’ during the height of the low-carb frenzy back in 2003.  Neal Barnard, the head of the outfit, appeared on most of the morning talk shows telling how dangerous his study had found low-carb diets to be.  A couple of the national networks called MD and me asking us if we would provide a rebuttal.  We happened to be in Santa Barbara at the time, and we said sure.  Two different networks sent camera crews to interview us late in the afternoon.

As I’ve probably mentioned numerous times, we have an absolute knack for getting pre-empted whenever we get TV time.  This day was no exception.  The news teams were on their way to the little condo we had at the time to set up and shoot our rebuttal when the news came through that Michael Jackson was going to be flying in to the Santa Barbara airport to turn himself in on the child molestation charge that he later beat in court.  Of course, all the news vans and camera crews that were heading for our place were diverted to the Santa Barbara airport, and MD and I never got to rebut the PCRM idiocy on air.

A couple of days later, we flew back to our place in Santa Fe, New Mexico, and as I was walking through the door laden with suitcases the phone was ringing.  It was the guy who ran LowCarbiz.com, the now-defunct online low-carb magazine, calling me asking if we would write a rebuttal that he could publish.  I said sure, and he said he needed it fast.  I left all the unloading to MD and sat down at my computer and pounded the thing out in a couple of hours.  He published it online.  Then a year or so later the low-carb mania died off, and the magazine went down, and I figured all was lost to history.

But, thanks to Google Alerts, I got a ping that someone had dug this thing out and posted it on a forum.

The only link I could find to the original PCRM report was a May 2004 update that pretty much matches the original, which I have a hard copy of to compare.  You can see how scientifically valid this ’study’ is and how worthy it is of a press release and multiple TV appearances by looking at the methods section of the ’study’ to see how the subjects were found.

Methods

In the fall of 2002, the Physicians Committee for Responsible Medicine (PCRM) began a pilot program to test the feasibility of an online registry to identify people who may have suffered health complications related to high-protein, low-carbohydrate diets. A modest Internet advertising campaign was used to notify consumers about the availability of this registry. In November of 2003, PCRM held a news conference to highlight the health problems suffered by some individuals using these diets and to draw attention to the registry.

To report problems with high-protein, high-fat, carbohydrate-restricted diets, individuals voluntarily visited www.AtkinsDietAlert.org and filled out a form available on the site. The registry specifically inquires about the following problems: heart attack, other heart problems, high cholesterol, diabetes, gout, gallbladder, colorectal cancer, other cancers, osteoporosis, reduced kidney function, kidney stones, constipation, difficulty concentrating, bad breath, and loss of energy. In addition, many registrants indicated, in an “other problems” box on the registry, that they had experienced certain other problems while on low-carbohydrate diets. Many registrants reported more than one health concern. Through the online form, most registrants provided their contact information, age, sex, previous health concerns, length of time on the diet, reasons for choosing the diet, and other information.

The registration entries were self-reports and were not subject to verification through medical record reviews or other methods, nor was registration deemed to indicate a cause-and-effect relationship. To help clarify the possible biological mechanisms by which a high-protein, high-fat, carbohydrate-restricted diet might lead to these problems, PCRM dietitians conducted a nutrient analysis of the sample menus for the three stages of the Atkins Diet as described in Dr. Atkins’ New Diet Revolution (M. Evans & Co., 1999; pp. 257–259), using Nutritionist V, Version 2.0, for Windows 98 (First DataBank Inc., Hearst Corporation, San Bruno, Calif.).

Tells you everything you need to know about the scientific standards of PCRM.  At the time CBS, one of the network stations that had Barnard on that morning, actually stated that the ’study’ wasn’t scientifically valid:

The online survey is not a scientific study, so there are no hard facts to say definitively that the Atkins diet is harmful. But the PCRM says there is enough evidence for concern.

But the lack of scientific validity never stops the PCRM’s Barnard from jumping in front of the camera presenting it as such.  Make sure to watch the video to observe the holier-than-thou demeanor.

What follows is our rebuttal to this nonsense.

In The Name of ‘Responsible Medicine’ The Public is Ill-Served
A LowCarbiz Rebuttal to The Physicians Committee for Responsible Medicine Report on Health Concerns Pertaining To Low-Carbohydrate Diets
By Dr. Michael R. Eades and Dr. Mary Dan Eades
© 2003 LowCarbiz/Michael R. Eades, M.D. and Mary Dan Eades, M.D.

Ten Rebuttal Points:
• PCRM uses what is at best anecdotal information and presents it in the guise of a scientific investigation.
• At least a dozen studies have been conducted recently in major medical and scientific research institutions and published in top-notch journals that confirm the lowcarbohydrate diet is superior to the low-fat diet in multiple respects.
• The respondents to the PCRM poll would represent only 0.00001125% or one onethousandth of one percent of individuals following a low-carbohydrate diet.
• Researchers from Harvard recently reported that subjects could eat 300 calories more per day on a low-carbohydrate diet than those following a low-fat diet and still lose the same amount of weight over a 12-week period.
• Dieters would prefer to lose fat rather than lean tissue, which is precisely what happens with low-carbohydrate diets.
• Virtually every study done on low-carbohydrate diets shows that weight loss is accompanied by either an improvement or no change in heart disease risk factors.
• Low carb dieters who consume green leafy and colorful vegetables and low-glycemic fruits are not at risk of osteoporosis (long-term bone loss).
• The whole idea that protein in the amounts eaten in modified low-carbohydrate diets damages kidneys is a vampire myth that refuses to die no matter how many stakes have been driven through its heart by a multitude of medical studies.
• Overall there is no evidence that meat causes colon cancer, or any other cancer, for that matter. Actually many cancer-fighting nutrients are in meat and a reduction in meat intake might be more likely to increase cancer risk.
• As the data continues to accumulate and the studies increase in number, the efficacy of the modified low-carbohydrate diet will finally be established to the satisfaction of all.

On November 20th, the Physicians Committee for Responsible Medicine (PCRM) released a report entitled Analysis of Health Problems Associated with High-Protein, High-Fat, Carbohydrate-Restricted Diets Reported via an Online Registry. The report, which dresses, speaks and behaves like something that might appear in a bona fide medical journal, examines a host of health problems consumers have suffered allegedly as a result of their following a high-protein diet.

We find this report interesting on a number of fronts, not the least of which is in the way PCRM uses what is at best anecdotal information and presents it in the guise of a scientific investigation.

Over the past twenty years when we and other physicians who use low-carbohydrate diets to help our patients lose weight, normalize blood lipids, stabilize blood sugars, reduce their high blood pressure and generally improve their health reported our clinical experience with thousands of such patients we have often been greeted by groups such as PCRM – which view science through a vegetarian or low-fat lens — with cries of “Anecdotal! It’s only anecdotal evidence. If your low-carbohydrate regimen is so good, where are the clinical studies?”

In the last couple of years, however, at least a dozen studies have been conducted in major medical and scientific research institutions throughout the world and published in top-notch medical and scientific journals that confirm what we and others have been saying for years—the low-carbohydrate diet is superior to the low-fat diet not only for weight-loss but for improvement of virtually all of the components of the metabolic syndrome as well.

It is a delicious twist of fate that the tables have turned on PCRM and the group’s fellow travelers who, now, faced with this ever-growing body of credible scientific literature must themselves resort to the worst kind of anecdotal reporting: using a group of respondents to the PCRM website—and an extremely small group, at that—to imply that low-carbohydrate diets are a hazard to the entire population of dieters who follow them.

PCRM reports that “in the fall of 2002, [PCRM] began a pilot program testing the feasibility of an online registry for identifying people who may have suffered health complications related to high-protein, low-carbohydrate diets.” After one year of a “modest internet advertising campaign” by PCRM to “notify consumers of the availability of this registry” a total of “188 individuals reported experiencing problems with high-protein, high-fat, carbohydrate-restricted diets.”

At whom was this “modest internet advertising campaign” directed? How is the PCRM online registry found? The PCRM report doesn’t say, but one supposes the campaign was directed to and the registry found by people who have a predisposition to the PCRM philosophy. So it is reasonable to assume that people finding the PCRM online registry would have an axe to grind with the low-carbohydrate, non-vegetarian diet and lifestyle and would be more prone to report problems.

Even if we make the unlikely assumption that these respondents are all enthusiastic followers of low-carbohydrate lifestyles who have run afoul of their diets, the PCRM numbers are so tiny as to not even approach significance: 188 respondents in one year. The most recent and credible survey we’ve read estimates that there are somewhere in the neighborhood of 32 million people following some version of a low-carbohydrate diet in the United States alone (the PCRM report doesn’t say whether the respondents to their registry were from America only or from throughout the world). Even if that 32 million number is halved, it would mean that the respondents to the PCRM poll would represent only .00001125% or one one-thousandth of one percent of these people following a low-carbohydrate diet, a number easy to not get too excited about. (One wonders what kind of numbers PCRM would have garnered had they put out the request for positive experiences on a low-carbohydrate diet.)

When we look at the problems that the majority of this one one-thousandth of a percent of people report we find that the majority of them suffer from constipation (44%), loss of energy (42%), and bad breath (40%). Not exactly the kind of serious medical problems calling for “the urgent need for monitoring” nor the proposal that our “public health authorities begin tracking the use of high-protein, high-fat, carbohydrate-restricted diets used for weight loss or maintenance and record adverse events” as the PCRM report recommends.

PCRM applied its anecdotal analysis to “health problems associated with high-protein, high-fat, low-fiber, carbohydrate-restricted diets” without really specifically defining the macronutrient composition of these diets. One of the problems in the medical literature is that there is no definition of a “high-protein” diet or a “carbohydrate-restricted” diet. Many studies refer to a diet composed of 40% carbohydrate as a low-carbohydrate diet, which it is when compared to one containing 55-60% of its energy as carbohydrates, but this really isn’t a low-carbohydrate diet as used by the vast majority of followers of low-carbohydrate diet plans.

Other papers report data on diets containing 5-10% of calories as carbohydrate and call them low-carbohydrate diets, which they certainly are, but not the same low-carbohydrate diet as those containing 40% carbohydrate. Another complicating factor is that most researchers use percentages of macronutrient composition to define their study diets whereas we and others who prescribe low-carbohydrate diets along with virtually everyone who follows some form of a lowcarbohydrate diet use absolute grams of usable carbohydrate to set the parameters of the regimen. Anyone following a low-carbohydrate diet knows how precisely many grams of carbohydrate per day he or she is taking in but doesn’t have a clue as to what percentage of caloric energy that represents. Another problem is that these diets are referred to in a number of ways—high protein diets, low-carbohydrate diets, high-fat diets, carbohydrate-restricted diets, etc. Although these terms are used interchangeably they really aren’t. A low-carbohydrate diet doesn’t have to be a high-protein diet; a high-fat diet isn’t necessarily a low-carbohydrate diet; and, nor is a high-protein diet necessarily a high-fat diet. In order to bring clarity to this dietary debate, a definition of just what a low-carb diet is needs to be established.

PCRM and other groups and individuals who are anti-low-carbohydrate diet typically define the low-carbohydrate diet as the Atkins Diet, which in its original form was an extremely low, almost no carbohydrate, very high-fat diet that bears little resemblance to the low-carbohydrate diets recommended by us and others (including the current Atkins plan). Most people on lowcarbohydrate diets focus on limiting their intake of carbohydrates to 30-70 grams per day and let the fat and protein content of their diet fall wherever it may within this carbohydrate restriction.

Compared to the standard American diet, most people following a low-carb diet end up consuming significantly fewer carbohydrates, about the same or marginally higher amounts of protein and fat, and a smaller number of total calories.  (There is little question that the reduction in calories drives the weight-loss engine of the low-carbohydrate diet, a point seized on by PCRM and others as somehow being a slight to the lowcarbohydrate diet. More about this later.)

The vast majority of medical studies published within the past few years have used this modified low-carbohydrate diet as the basis for comparison. Unfortunately, although this modified diet is substantially different from the original Atkins Diet, PCRM and others along with help from the media persist in referring to it as the Atkins Diet. An example: a recent research paper in the New England Journal of Medicine describing the effectiveness of our specific version of the lowcarbohydrate diet, which is substantially different from the Atkins Diet, in reducing weight and improving health was hailed by the media as the “vindication of the Atkins Diet.” Before we move into what the research data shows about the effectiveness of the modified lowcarbohydrate diet, let’s take a look at just how surreal this entire debate has become.

The PCRM report states that “high-protein, high-fat, low-fiber, carbohydrate restricted diets, such as the Atkins Diet, when used for prolonged periods, are expected to increase the risk of multiple chronic diseases and other health problems.” One would assume that according to PCRM that the low-carbohydrate diet would be worse than the standard American diet, but if we look closely is their assumption valid?

A typical American lunch, one eaten by hundreds of thousands, if not millions, of people in this country every day is a hamburger, fries, and a soft drink. To modify this basic lunch to fit the low-carbohydrate regimen dieters would remove the bun from the burger, avoid the fries and have a salad instead, and drink water or some other non-caloric beverage. In the eyes of the PCRM these simple modifications have converted this typical American lunch into a “dangerous” high-protein diet destined to ruin the kidneys, destroy the bones, and permanently damage the hearts of anyone who follows it. In making these modifications, however, lowcarbohydrate dieters get rid of the trans fats and refined carbohydrates in the bun, miss out on the large amount of fat (including trans fat) and high-glycemic carbohydrates in the fries, pass up the quarter of a cup of high-fructose corn syrup in the soft drink, and get a fair amount of carotenoids, flavinoids, lycopenes, fiber, and other anti-oxidants and phytonutrients in the salad. And, significantly reduce the caloric content of the lunch. You will note that the protein content remained unchanged. One would think that the PCRM would applaud these modifications, but instead they decry them. Surreal indeed!

Weight Loss

The caloric restriction that is a by-product of carbohydrate restriction accounts for the majority of the weight loss found with low-carbohydrate diets. Most, but not all. A recent review of lowcarbohydrate diets in the Journal of the American Medical Association stated that virtually all of the weight loss brought about by these diets came as a result of caloric restriction and when compared with low-fat diets there was no difference in efficacy as long as the two diets were equal in calories. A careful review of the individual studies comparing low-fat to low-carbohydrate diets almost always shows that over the course of the diets the people on the low-carbohydrate diets consume slightly more calories than those on the low-fat diet. A couple of recent studies showed a more pronounced and significant difference in the weight loss verses caloric intake between the two diets. One study done at the University of Cincinnati demonstrated greater weight loss in a group of women following a low-carbohydrate diet containing slightly more calories than a low-fat diet. Researchers from Harvard recently reported that subjects could eat 300 calories more per day on a low-carbohydrate diet than those following a low-fat diet and still lose the same amount of weight over a 12-week period. Where does this extra weight loss come from? It is known that dietary fat increases the production of mitochondrial uncoupling proteins, and there is some evidence that carbohydrate restriction might increase the proton leak across the mitochondrial membrane. Either or both of these actions would increase the loss of energy without reducing the caloric intake, but both these mechanisms as well as other theories need more study for clarification.

Clearly, low-carbohydrate diets give more weight loss bang for the calorie buck, but even if they didn’t, even if the weight loss were the same with low-fat and low-carbohydrate diets of equal caloric content, the low-carbohydrate diet would still be the diet of choice for other reasons. As everyone who has ever dieted knows, it’s not just the amount of weight that is lost that is important, but where this weight loss comes from. Everyone would agree that dieters would prefer to lose fat rather than lean tissue, which is precisely what happens with low-carbohydrate diets. Studies done at the University of Illinois, the University of Connecticut and other research institutions have shown that subjects following a low-carbohydrate diet lose more fat and less lean body tissue than those subjects following a calorically equivalent low-fat diet. In fact, in some cases, subjects on low-carbohydrate diets even gain lean body mass while losing fat on lowcarbohydrate diets, a finding virtually never observed in subjects following low-fat diets.

Cardiovascular Disease

It would seem a bad bargain to trade weight loss for a substantially increased risk for heart disease, which is the case that the PCRM makes in its report. While conceding that lowcarbohydrate diets are effective for bringing about weight loss, the PCRM cautions that these diets are “associated with increased risk of…heart disease.” A strange statement since the very studies the PCRM references as showing that the low-carbohydrate diets “facilitate modest short term weight loss” also demonstrate that low-carbohydrate diets improve lipid profiles and enhance insulin sensitivity in their followers, both changes that are known to substantially reduce the risk for heart disease. Virtually every study done on low-carbohydrate diets shows that weight loss is accompanied by either an improvement or no change in heart disease risk factors.

Few, if any, studies of low-carbohydrate diets show a worsening of heart disease risk factors. Most authorities agree that excess body fat is a risk factor for heart disease; so even the studies that show no improvement in other risk factors in subjects on low-carbohydrate diets actually do demonstrate a lowered cardiovascular disease risk implicit in the weight loss they bring about.

Osteoporosis

PCRM is on a little more solid footing when it claims that the Atkins Diet can cause bone loss, but PCRM misses the point entirely when considering the modified low-carbohydrate diet we and others recommend and that most people now follow. Studies going back almost a century describe the bone loss that can occur in people following a predominately meat diet. A diet high in meat alone creates a mild metabolic acidosis in the human body. This metabolic acidosis or excess acid created by the metabolism of meat has to be buffered or neutralized, which the body does by leaching calcium from the body’s storehouse of calcium, the bones. On a day-to-day basis the amount of calcium lost from the bones in this way is insignificant, but over a decades-long period of time can result in osteoporosis. Meat, however, is not the only food that produces such a response. Along with meat, the other two main offenders are grains and cheeses, especially hard cheeses. That’s correct: eating grains causes a metabolic acidosis just as meat does. When you consider the cheeseburger, a staple of the American diet, it’s easy to see why osteoporosis abounds. So, the PCRM correctly points out that the Atkins Diet, which in its original version recommended primarily meat and cheese, could cause osteoporosis if followed for the long term. But what about the modified low-carbohydrate diet? Does it do the same? Most plant foods, other than grains, bring about the opposite metabolic situation; whereas meat consumption causes a metabolic acidosis, green leafy and colorful vegetables and low-glycemic fruits bring about a metabolic alkalosis. The reduction in acid-producing grain consumption along with the alkaline response of the very plant foods recommended on the modified version of the low-carbohydrate diet offsets and neutralizes the acidity from the meat so that there is no net metabolic acidosis and no long term bone loss.

Impaired Renal Function

Fear of kidney damage has long been the bugaboo of people following low-carbohydrate diets. It’s doubtful that anyone pursuing a low-carbohydrate diet for any length of time hasn’t been told at least once that his or her kidneys are in danger. Here again the PCRM doesn’t disappoint; the group is right there leading the chorus. And PCRM doesn’t beat around the bush: “Highprotein diets are associated with reduced kidney function,” so says its report. No equivocation there. But once again PCRM has missed the boat. If we are to believe PCRM, we had better leave the buns on our burgers and eat every fry in the box to protect our kidneys. Studies from around the world have shown that the amount of protein contained in the modified version of the low-carbohydrate diet does not harm the kidneys. Even studies in patients with diabetic kidney disease show they will harm their kidneys more by increasing their carbohydrate intake and running up their blood sugars than they do by increasing their protein intake. In the late 1980s a group did an extensive study in Israel comparing the kidney function of people of all ages who ate a high meat diet with the kidney function of those on a vegetarian diet. The study showed that although both groups suffered a slight reduction in kidney function with age (it’s a sad fact of life—as we age function of just about everything including the kidneys decreases) the degree of loss of function was indistinguishable between the groups. Another recent study of kidney disease in diabetics performed at the University of California in San Francisco demonstrated that caloric reduction was a more potent force in protecting damaged kidneys than restriction of dietary protein. In fact, this study used a low-carbohydrate diet to restrict the calories. The whole idea that protein in the amounts eaten in modified low-carbohydrate diets damages kidneys is a vampire myth that refuses to die no matter how many stakes have been driven through its heart by a multitude of medical studies.

One last point on this subject, an admittedly anecdotal one, but illustrative. The one group of people who eat more protein than any other single group is serious body builders. These people eat anywhere from three times to eight times the amount of protein recommended in any lowcarb diet, and do so for long periods of time. What does this do to their kidneys? It must not do much because it’s never been reported in the medical literature. If the PCRM were correct about protein damaging kidneys there would be lines of body builders queuing up outside of dialysis centers all over the world.

Colorectal Cancer

The idea that meat intake definitively causes colon cancer is another vampire myth that refuses to die. Studies have indeed shown that increased intake of meat might cause colon cancer, but so have an equivalent number of studies shown that refined carbohydrates might cause colon cancer. The studies that the PCRM mustered for its report of course show an increased risk, otherwise PCRM wouldn’t have mustered them. When a situation exists where there are dueling studies it’s always prudent to look at a meta-analysis, which is a study of all the studies. Dr. Michael Hill, a British epidemiologist, performed and published such an analysis. He reported that overall there is no evidence that meat causes colon cancer, or any other cancer, for that matter, and stated that since many cancer-fighting nutrients are in meat, a reduction in meat intake might be more likely to increase cancer risk than reduce it.

By a curious coincidence the day the PCRM chose to release it’s report bashing low-carbohydrate diets was the same day pop star Michael Jackson surrendered to authorities in Santa Barbara County. Upon his release after posting bail the singer was reported by his attorney to have said: “Lies run sprints, but the truth runs marathons.” It remains to be seen how this aphorism applies to Mr. Jackson himself, but there is little doubt that the endurance of the modified lowcarbohydrate diet makes it the major contender for victory in the dietary marathon. As the data continues to accumulate and the studies increase in number, the efficacy of the modified lowcarbohydrate diet will finally be established to the satisfaction of all.

Until then, however, the PCRM and other such groups with a political agenda will continue their feeble attacks on a diet that has helped millions. The weakness of PCRM’s data even it admits publicly. Buried near the end of the PCRM report under the heading “Limitations,” PCRM writes: “The key limitation of this report is that adverse health effects were self-reported and are not likely to have the same prevalence in the general population. Data collection was Web-based and no attempt was made to assure a representative sample.” And yet the PCRM finds these data of a magnitude to require the “urgent need for monitoring” by our “public health authorities.” The PCRM report and the disproportionate amount media attention it garnered are merely a sprint.©2003 LowCarbiz/Michael R. Eades, M.D. and Mary Dan Eades, M.D.

What I find particularly enjoyable about this whole fiasco is that if you Google it, you find our rebuttal much more often than the PCRM idiocy that started it in the first place.  I guess it’s only fitting that it turned out to be a sprint indeed.

Hat tip to Google Alerts and to Cooking TLC

Changes in diabetic nephropathy

I received a short paper from a colleague in Portugal a couple of days ago that demonstrates in just a few pages how science should really work.

The paper from the journal Diabetologia reports on a study done in Pakistan showing that high-dose thiamin (vitamin B1) may be a valuable therapeutic agent in the treatment of diabetic nephropathy.   This small study certainly isn’t the final word, but it does show how medical science should work.

First, the paper starts off in the introductory paragraphs discussing how the idea for high-dose thiamine therapy came about.  Before we get into that, however, let me digress briefly to discuss diabetic nephropathy for those who are unfamiliar with it.

The main job of the kidney is to remove waste products from the blood while keeping the non-waste products, i.e., proteins, sugar, etc. in the blood.  You can think of the kidney as a sieve with tiny holes.  All the waste that needs to be filtered is small enough to fit through the holes while the substances meant to remain unfiltered are large enough to not fit through the holes.  If you were to pour liquid containing both waste and non-waste matter into a long tube with your sieve somewhere in the middle in a place non-visible to you, you could check to see if your sieve were damaged by looking at what comes out at the bottom of the tube.  If you find only waste, then you can be pretty certain that your sieve is functioning.  If, on the other hand, you find material coming out the bottom that should have been caught by the sieve, you can be pretty sure there are holes torn in your sieve.

This in very simplistic terms is what happens in the kidney.  Proteins are large molecules and should never make it through the kidney into the urine.  Protein in the urine in any significant amount tells you the kidney has a problem.  With simple lab tests we can identify microscopic levels of protein in the urine, and anyone having a certain amount is said to have microalbuminuria, which means microscopic levels of albumin (the main protein in blood) in the urine.

In people with diabetes, microalbuminuria means the kidneys are starting to develop nephropathy, or pathology (or disease) of the nephron (the basic unit of the kidney).  To go back to the sieve analogy, they’ve developed bigger holes in their sieve. This condition afflicts about 40 percent of those with diabetes and can (not that it always does, but it can) progress to complete kidney failure, requiring dialysis or kidney transplant.

Diabetic nephropathy is most likely caused by the toxic effects of too much sugar in the blood and is helped, and even reversed, by careful control of blood sugars.  Despite this common knowledge, many unenlightened people continue to treat the condition by limiting dietary protein instead of focusing on the continuing damage caused by elevated blood sugar.  In order to keep caloric intake up, what do people substitute for protein?  You got it.  Carbohydrates.  And since dietary carbohydrates become blood sugar fairly quickly, they end up damaging the kidney more than the protein they are replacing.

Now that you’ve got at least a working notion of what diabetic nephropathy is, let’s look at our paper.

The authors start off with a description of the research on thiamin to date that gives us a nice picture of how the various types of studies all tie together to make real science.

First off, someone noticed that people with diabetes and protein in their urine had low blood levels of thiamine.  This observation prompted researchers to do observational studies of this phenomenon.

In evaluating large numbers of subjects with and without diabetes and protein in their urine, scientists determined that the diabetics typically had lower blood thiamin levels than the non-diabetics.

But, at this step, these studies are simply observational studies and can’t possible prove causation.

The next step in the scientific evolution is to hypothesize that low thiamin levels are somehow involved in the development and/or progression of diabetic nephropathy.  If this hypothesis is valid, then giving thiamin should improve the condition.

Researchers gave thiamin to rodents with diabetes and discovered that increasing blood levels of thiamin reduced or eliminated proteinuria in the animal model.

Here is where the tricky point arrives in the study of drugs – trying them in humans.  As I’ve written many times in these pages, rodents are not just furry little humans.  What often causes no problems for them causes huge problems, including the ultimate problem – death – in humans.  So it is a difficult business to start giving experimental drugs to humans.

In this case, however, it isn’t so bad because thiamin – even in high doses – is non-toxic to humans.  The next step is the randomized, double-blind, placebo-controlled clinical study, which the authors of our paper under discussion performed.

Researchers randomized a group of 40 subjects who had diabetes and microalbunuria into two groups.  Subjects in one group got three 100 mg thiamin capsules per day; subjects in the other group got placebo.  (I couldn’t tell from the paper whether the three capsules were spread out over the day – I would assume they were – or were taken all at once.)  The two groups remained on their supplement regimen for three months followed by a two month washout (a period in which no one either thiamin or placebo).

The results were pretty spectacular.

There was a significant drop in the amount of protein in the urine of subjects taking thiamin as compared to those taking placebo.  Even more exciting was the following:

After [thiamin] therapy for 3 months, regression of microalbuniuria to normal urine albumin had occurred in 35% of the patients.

Over a third of the patients on thiamin had no more evidence of diabetic nephropathy, at least as demonstrated by protein in the urine.  This is a spectacular result, especially for a natural substance with virtually no toxicity.

I appreciate the way the authors of this paper presented their data.  It is much more informative than simply providing the average differences between the study group and the control group.

Take a look at the graphs below.  The upper figure is the overall change in microalbunuria between the groups.  The middle graph is the change in the subjects on placebo; the bottom graph shows the changes in subjects on thiamin.

As you can see, the results of each subject are presented a single line.  You can tell a lot from these kinds of graphs.  For example, you can see that in the thiamin group there was a generalized downward slope to all the lines, which means that all the subjects improved on the regimen, a fact that is most important.  The middle graph, the one showing the results from the placebo is interesting as well.  You can see that the vast majority of subjects had no change while a couple had significant changes.  Why would there be improvement on the placebo?  Who knows?  If I had to guess, I would guess that those subjects taking the placebo who showed the major improvement may have changed their diets on their own.  These were patients at a diabetic clinic who were being treated for their condition, so maybe these subjects were more aggressively treated.  But, it really doesn’t matter because we can see from the flat lines of most of them that there was no change due to the placebo.  This type of graph at least allows us to speculate and to realize why there was a slight drop in the average level of protein in the urine of even those subjects on placebo.

The authors note in their discussion that

this is an encouraging pilot-scale outcome that high-dose thiamin reverses early-stage nephropathy in type 2 diabetes.

They go on – as they should – to recommend larger scale studies to see if their findings hold up.

Based on this study, would I, myself, take thiamin in 300 mg per day doses if I had diabetic nephropathy?  Absolutely.

Although it is only a pilot study, the results are pretty stunning.  But the ‘drug’ is harmless.  So what is the risk?  A few pennies per day for the thiamin?

If this were a study in which, say, statins were used as the agent, I wouldn’t be quite as eager.  I would probably wait until other larger studies had replicated these findings.  Why?  Because statins aren’t harmless.  One can die from them. Or can have miserable generalized muscle aches and weakness.  In other words, there is a lot bigger downside to taking statins than there is to taking thiamin, so I need a much greater level of comfort to make the risk/reward calculation in favor of taking a statin.

The only weakness I can find in this paper is that the authors spent no time discussing the possible mechanism for the benefits of thiamin on diabetic nephropathy.  Perhaps they ran out of time and are saving it for another paper. Alas that is what has happened to me as well.  MD’s group is performing with the symphony today, and I’m being badgered to get ready to leave.  So, I, too shall leave a discussion of the potential mechanism to a future post.

Hat tip to Pedro Bastos for sending me this paper.

First, let me start out by linking to one of my wife’s recent posts.  We’ve had a spate of people writing us through the website asking about cookbooks, of all things.  She did a post a couple of months ago about her favorite cookbooks.  In case you missed it, here it is.

Second, I’m going to start using these link-o-ramas to link to some of my older posts that I think would be of interest to a lot of people now.  One that I thought was pretty good on how to dissect a scientific article didn’t get many readers since I wrote it back when maybe three people read this blog.  The notion that it didn’t get many readers is evidenced by the fact that there are zero comments on it.  So, without further ado, here is Baboon Business.

After all the recent posts about the savagery of the nature, I thought I would throw this item into the mix just to show that nature can be tamed, at least in the short run.  There is a guy who is a fixture in downtown Santa Barbara who has a dog, a cat and a rat as pets.  He is always down on State Street, the main street running through town, with the cat riding on the back of the dog, and the rat riding on the back of the cat.  Here is the YouTube, so you can see for yourselves.

Click here to view the embedded video.

I came across an interesting article titled Is Food the New Sex? in a little journal I get called Policy Review.   The writer of the article posits that our appetites for food and sex have more or less switched positions in our hierarchies of taboos since the 1950s.  She uses a woman who was a housewife in her 30s in the 1950s and her hypothetical granddaughter who is in her 30s today.  The housewife of the 1950s had no taboos on food and all kinds of taboos about sex whereas her granddaughter reads every label and is scared to death of her food, yet expects to live together for a trial run before marriage to her boyfriend and has friends with all sorts of alternative lifestyles.  A fun, but long, article to read.

What follows are a couple of quotes separated by years, but nevertheless related.  So I figured I would post them juxtaposed so that the connection would be obvious.  The first is from Ludwig von Mises (1881-1973), an economist of the Austrian school.

The luxury of today is the necessity of tomorrow. Every advance first comes into being as the luxury of a few rich people, only to become, after a time, an indispensable necessity taken for granted by everyone. Luxury consumption provides industry with the stimulus to discover and introduce new, things. It is one of the dynamic factors in our economy. To it we owe the progressive innovations by which the standard of living of all strata of the population has been gradually raised.

The next quote is from the transcript of a CNBC interview with Warren Buffett last year.  I don’t agree with Mr. Buffett on everything, but I do on this.

…we’ve had a number of recessions in this country; in fact, we had a Great Depression, we had–we’ve got world wars. And throughout, the genius of the American economy, our emphasis on a meritocracy and a market system and a rule of law has enabled generation after generation to live better than their parents did. And, I mean, most of the people in this room, practically all of them last night, lived better than John D. Rockefeller lived. I mean, all kinds of things have happened. And in the 20th century alone, the standard of living of the average American went up seven for one. There’s never been a period like it in history. And that’s not an accident. It’s because we unleash human potential and will continue to do that in the future.

Here is a link to a site containing a video of Gary Taubes, Dr. Jay Wortman, Dr. Alan Einstein and me taken last year at a conference in Phoenix.  We’re all expounding on the problems of the low-fat diet.  It’s the first video in the link.  I haven’t watched the other two, so I can’t tell you what’s in those.

For those of you interested in intermittent fasting, here is an article on the subject from the Los Angeles Times.  I’m working on another post on IF that I hope to have up within the next couple of weeks.

Researchers aren’t sure why the body apparently benefits from a state of mini-starvation. One theory is that the process produces just enough stress in cells to be good. “What our evidence suggests is that nerve cells in animals that are on dietary energy restriction are under mild stress,” Mattson says. “It’s a mild stress that stimulates the production of proteins that protect the neurons against more severe stress.”

What they do know is that occasionally going without food or reducing calories daily makes the body more sensitive to insulin, which helps maintain normal blood sugar levels. And animal studies suggest calorie restriction may reduce the risk of cancer by slowing the growth of abnormal cells.

At Fat Head the Movie premiere

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q:  And you ate nothing but McDonald’s?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thanks very much, Tom.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

LOW CARB DIETS PROVE BETTER AT CONTROLLING TYPE 2 DIABETES

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Yet again the low-carb diet emerges the champion.

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

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

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

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

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

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

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

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

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

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

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

Before we launch into this study, which we’re going to just briefly review because I want to spend more time on the commentary, I want to propose to you a thought experiment.  Suppose I ask you to design a study to see what happens when subjects with diabetes eat low-GI carbs as compared to what happens when they eat high-GI carbs.  It seems pretty simple.  If you’ve got half a brain, you would recruit subjects with diabetes, go through all of the randomizing rigmarole to ensure that both groups of subjects were as alike as possible, i.e., subjects in both groups were about the same size, same ratio of sexes, same degree of blood sugar elevation, etc.  Then you would start the subjects in one group on an amount of carbohydrate, let’s say 220 gm per day, that were mainly low-GI carbs and the other group on about the same amount of carbohydrate composed of high-GI carbs.  You would teach each of these groups how to follow their specific GI diets and would have a way of monitoring for compliance.  Then you would set them to it and recheck them in 3 months or 6 months or a year or whatever you decided your study length to be.  Pretty simple stuff, right?

Just for grins, let’s throw in a twist.

Let’s say I’m funding your experiment, and I come to you and tell you that I want you to add another group to your study.  I tell you: Look, I’m tired of Eades, Atkins, Taubes and the rest of these jerks babbling on about how wonderful the low-carb diet is.  We all know – wink, wink – that the low-GI diet is going to kick some tail in this study, so let’s add a group of subjects who will follow a low-carb diet over this same study period.  Then we can show that a low-GI diet is not only better for diabetics than a high-GI diet of the same number of carbs, but is better than the much-vaunted low-carb diet as well.  Or at the very worst, it’s the same as the low-carb diet.  If we can show the low-GI diet to be equal or better than the low-carb diet for the dietary treatment of diabetes, then we can shut those low-carbers up for good.

Sounds reasonable for a study.  But, remember, you are designing this study, and you are a reader of this blog.  You know that a low-carb diet will hammer a 220 gm low-GI diet in terms of weight loss, lipid improvement, blood sugar stabilization, etc.  It’s obvious that the money behind this study doesn’t want the outcome to be what you know it’s going to be.  What to do? What to do?  You wring your hands for a bit, then you hit on a brilliant idea.

You decide to put the subjects in the low-carb group on 200 gm of carbohydrate of their choice.  Hey, now.  200 gm of carbohydrate is lower than 220 gm of carbohydrate, so it’s perfectly legitimate to call the 200 gm of carb per day diet a low-carb diet because it is lower.  Right?

Problem solved.  You’ve set up your study to show just what you want it to show.

Which is pretty much what the folks did who performed the study we’re going to discuss.  Problem is, their study didn’t turn out exactly as they had planned.

Last year a paper with the ungainly title The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic index dietary carbohydrate in type 2 diabtetes: no effect on glycated hemoglobin but reduction in C-reactive protein was published in the American Journal of Clinical Nutrition (AJCN).  This paper describes a study pretty much like the imaginary one I described above.

Three groups of subjects were put on three diets: one group on a low-GI diet, another on a high-GI diet and the third on a low-carb diet.  Those subjects on the low-GI diet consumed an average of 233 gm of low-GI carbs while those on the high-GI diet consumed 220 grams of high-GI carbs and those on the low-carb diet ate 196 gm of all kinds of carbs.  As Dave Barry would write: I AM NOT MAKING THIS UP.

The subjects remained on their respective diets for a year and were then evaluated for differences in outcome.  In almost every condition tested for – body weight, HgbA1c, lipids, blood sugar, blood pressure – ended up not different among the three groups.  The only significant change was that the low-GI group ended up with lower C-reactive protein levels than the high-GI group with the so-called low-carb group right in between.  But, though there was a statistically significant difference between the high- and low-GI groups in terms of C-reactive protein, the measurement was in the normal range for all three groups.  So, the study doesn’t really militate in favor of a low-GI diet in any major way.

But, in my opinion, the study is so flawed that no conclusions should be drawn from it.  Why?  Because the data is so screwed up.  And you know what they say about garbage in, garbage out…

When the initial dietary history was taken on the study subjects to determine their baseline diets in an effort to design the diets for the study period, the researchers determined that these subjects were consuming, on average, about 1900 calories per day.  These were overweight people – both male and female – who were an average age of 60.  All the data needed to make the metabolic rate calculations wasn’t available in the paper, but I was able to extract enough valid data to run the numbers I needed.  And although my calculations aren’t exactly on the button accurate, they are, as they say, close enough for government work. (Which BTW is one of my favorite sayings, one that is positively pregnant with meaning.)

I’ll spare you the brain damage of how I did the calculations, but I applied the Mifflin-St Jeor equations (which are those deemed the most accurate) to the data at hand to determine the actual resting metabolic rates (RMR) of the subjects.  It turns out that the RMR is about 1500-1600 calories per day.  This is the RMR, which is the metabolic rate for lying in a bed barely breathing in a dark room.  To get total metabolic rate, it’s typical to multiply the RMR by a factor depending upon activity level.  For “seated work with no option of moving around and little or no strenuous leisure activity,” it is common to multiply the RMR by a factor of 1.4-1.5.  Let’s assume that these subjects are doing a little more than sitting in chairs all day and go ahead and multiply by the 1.5.  Doing so gives us a total daily energy consumption of from 2250 to 2400 calories, and that doesn’t include the thermic effect of food, which adds about another 10 percent.

Let’s go with 2300 calories, which is almost assuredly low.  If the subjects of this study were claiming to consume only 1900 calories per day (and they weren’t dieting), anyone with good sense would say, ‘hmmm, something isn’t quite right here.’  These subjects could not be weight stable on the regular diets they were on at 1900 calories per day.  They would have to be losing weight.  Over the course of the study – which was a year long – they maintained their weight, they didn’t lose an ounce. In fact, they actually gained a little. If you multiply 400 calories per day (the amount of the deficit between what they claimed to be eating and their total daily energy expenditure) over 365 days, you would find that these subjects had an average caloric deficit of 146,000, which at 3500 calories per pound of fat should mean that they lost about 42 pounds each, but they didn’t lose any weight whatsoever; they gained.  Something strange going on here.

Recall the people in Ancel Keys starvation experiment (which remember lasted only 24 weeks) got an average of almost 1600 calories per day and they became walking skeletons in just a few months.  How could these subjects consume a mere 300 calories per day more for an entire year and not lose anything?  The answer is that the data was incorrect.  And should have been fixed right at the start.

So, basically, the study is worthless. It doesn’t tell us squat other than that people lie about what they eat and some researchers are gullible enough to believe them.  Despite it’s worthlessness, however, this study inspired one of the big-names in mainstream obesity research – Xavier Pi-Sunyer – to use it to demonstrate his own bias or idiocy.  You make the call.

In the same issue of AJCN that the above study appears there was also a commentary by Dr. Pi-Sunyer.  In reading his commentary, I find it almost difficult to believe that so much mis- and disinformation can be accommodated in just a mere page and a half.

I had read the paper before I read Dr. Pi-Sunyer’s commentary, so I was pleased that right up front he got to the heart of the issue, which is the lousy data.  If you’re going to have a study looking at the differences between diets, it seems pretty obvious that food intake is your most important data.  This issue was not lost on Dr. Pi-Sunyer.  After starting off with the obligatory summary of the paper under review, Dr. Pi-Sunyer cuts to the chase:

[The paper] shows the difficulty of accurately measuring food intake in overweight persons. The average body mass index (BMI; in kg/m2) of the group was 31, and the range was 24–40. The average caloric intake reported with the 3 diets at baseline ranged from 1810 to 1930 with an average weight of [approx] 84 kg and at the end of the study ranged from 1800 to 2020 with a slightly higher average weight. Patients did not lose weight; they actually gained. But, even if he or she is very sedentary, a person weighing 84 kg requires more calories than are reported in the study to maintain weight. Thus, the reporting of caloric intake by diaries is shown clearly to be inaccurate, and there is significant underestimation of energy intake. Such underestimation has been reported previously from this laboratory [Pi-Sunyer's] and by many others. The tools for measuring food intake in humans are very imprecise, as documented here. Yet investigators (and journals) persist in publishing such data as if they were accurate and persist in presenting percentages of macronutrients to one decimal place (see Table 3 in reference 1) as if there were any confidence in such decimals.

Dr. Pi-Sunyer clearly grasps the notion that the data is totally flawed.  And I was heartened.  But then he goes on as if a) the data were valid and b) that the tiny differences in carbohydrate intake are meaningful.

After noting that there was no difference found in the levels of HgbA1c between any of the study groups, he writes:

…compared with baseline data, these mildly diabetic type 2 patients actually did worse with regard to HbA1c and weight while following each of the 3 experimental diets. This finding suggests that we must be careful about disrupting subjects’ or patients’ diets with radical, doctrinaire changes that may actually be counterproductive. Furthermore, the diets had carbohydrate contents that varied from 39% to 52% of energy intake, and yet this variability had no effect on the subjects’ HbA1c. This finding confirms previous reports that the proportion of carbohydrate in the diet is not very important in determining the concentration of fasting blood glucose and that variations of 10% to 15% of total calories make little difference to overall control in patients with early type 2 diabetes

Here we have our first two pieces of dis- or mis-information.  He says these data (that he has already deemed as useless) suggest “that we must be careful about disrupting subjects’ or patients’ diets with radical” changes that could make them worse.  Say what?  What’s radial about a diet that goes up a few calories and doesn’t do much of anything and obviously wasn’t followed anyway?  This is subtle anti-low-carb talk.  Then he comes out with the much less subtle anti-low-carb propaganda that this study (the one filled with meaningless data) “confirms previous reports that the proportion of carbohydrates in the diet is not very important…”

Indeed.  Readers of this blog know what would have happened had the third group gone on a real low-carb diet instead of the 196 gm “low-carb” diet the study subjects actually (supposedly) followed.  “Confirms previous reports that the proportion of carbohydrates in the diet is not very important..”  Are these the same reports that have appeared in most of the major scientific journals showing the low-carb diet to be superior for weight loss, blood sugar stabilization, reducing blood pressure and normalizing lipids?  Are these the reports he’s talking about?

Then writes he:

This report is unique in having followed subjects for 1 y and in using careful monitoring of the subjects’ diet and providing continued professional nutritional advice. It is interesting that the long-term results show that the 3 diets had little ultimate effect on either triacylglycerol or HDL-cholesterol concentrations. Thus, the arguments of the champions of a low-GI or a low-carbohydrate diet—that these 2 types of diets will result in lower triacylglycerol and higher HDL concentrations—have not been upheld in this careful, year-long dietary study.

Huh? “Careful, year-long dietary study.”  Dr. Pi-Sunyer, are you talking about the crappy year-long dietary study that you just trashed for having lousy data?  Or will lousy data do to promote your anti-low-carb bias.

He goes on and on dissecting out various tidbits of this finding and that, all of which are, of course, meaningless, but that doesn’t stop our friend from trying nevertheless.

At last Dr. Pi-Sunyer ends on a hopeless note:

Finally, for the proponents of a low-GI diet, the fact that these investigators, who are well known for their nutritional expertise, were able to provide a sustained difference in GI of only 8 units over 1 y attests to the difficulty of maintaining a low-GI diet over the long term. A realistic lower-GI diet that could be sustained in these patients with mild type 2 diabetes had no significant effect. Given the data from Wolever et al and the previous equivocal data with respect to this issue, it seems unwise at this point to burden type 2 diabetes patients with trying to pick and choose among different high- and low-GI foods.

“…these investigators, who are well known for their nutritional expertise…”  They are so adept at doing nutritional research that Dr. Pi-Sunyer spends the entire fist third of his commentary trashing their work.  Unbelievable.

Methinks Dr. Pi-Sunyer could almost be a contender for the Blackburn award.

But, sadly, such is the state of much published nutritional research these days.

Oh, and did I mention that Dr. Pi-Sunyer is on the scientific committee to determine the 2010 nutritional guidelines?

The point of the cartoon above by Eric Allie holds true for the recently released Jupiter study: the reporting of the data by the media often overshadows the actual data.

Let’s first take a look at the reporting.

The lede from MSNBC:

People with low cholesterol and no big risk for heart disease dramatically lowered their chances of dying or having a heart attack if they took the cholesterol pill Crestor, a large study found.

The headline from Fox News:

Study: Cholesterol Drug Causes Risk of Heart Attack to Plummet

The New York Times headline and lede (on the front page, no less):

Cholesterol-Fighting Drugs Show Wider Benefit

A large new study suggests that millions more people could benefit from taking the cholesterol-lowering drugs known as statins, even if they have low cholesterol, because the drugs can significantly lower their risk of heart attacks, strokes and death.

The Wall Street Journal, usually a more measured source, effuses:

Cholesterol Drug Cuts Heart Risk in Healthy Patients

AstraZeneca PLC’s cholesterol drug Crestor sharply lowered risk of heart attacks among apparently healthy patients in a major study that challenges longstanding heart-disease prevention strategies. The findings could substantially broaden the market for statins, the world’s best-selling class of medicines.

I could go on, but you get the picture.  I’m sure you’ve read all this in your own papers.  But it’s not just the papers and media that are harping on this study – it s even the statinators themselves.

Here is the commentary from Steven Nissen, M.D., a Master Statinator if there ever was one:

The extent of reduction in death, heart attacks, and stroke is larger than we’ve seen in any trial I can remember. I don’t know how you get much bigger than that.

Says Dr. W. Douglas Weaver, president of the American College of Cardiology:

[The findings] really change what we are going to do in the future. This targets a patient group that normally would not be screened or treated to prevent cardiovascular disease.

And in a statement that I’m sure will prove true, Dr. Weaver follows up with:

This will become an important part of the armamentarium of the primary care doctor. I see this as being part of that panel of preventions that they will be applying in men over 50 and women over 60.

Dr. TIm Garder, president of the American Heart Association, opines without any evidence whatsoever that

This is likely to be a class effect, not a specific drug effect.  This is a win for all statins, I would say.

The above is a sampling of the reporting and the blathering so far about the Jupiter study.  The general impression that most people (and, sadly, most physicians) will take away is that statins will prevent heart disease even in those people who don’t have risk factors for heart disease. Any one of any sex at any age should queue up for a dose of statins to prevent heart disease.

That’s the reporting.  Now for the data. What does the study actually show?

If you believe the data from this study (we’ll get to that later), it indicates that men over 50 and women over 60 with normal LDL-cholesterol levels AND elevated C-reactive protein levels who took the very expensive ($3.50 per day) statin drug rosuvastatin (Crestor) minimally reduced their risk of developing heart disease or dying of any cause as compared to those who took placebo.

That’s it, folks. And that’s only if you believe the data.

The study says nothing about men under 50 or women under 60.  The study says nothing about other types of statin drugs reducing risk.  And the study applies ONLY to those men over 50 and women over 60 who have fairly markedly elevated C-reactive protein levels.  The study says nothing about anyone of an sex or any age who doesn’t have a markedly elevated C-reactive protein level.

So, what’s the big deal?  Well, the big deal is that there is finally a study that shows some benefit to statin drugs in terms of decreasing all-cause mortality. And, as I’ve posted before, those studies are few and far between.

There is so much excitement on the part of the statinators of renown because their coffers will soon be filled to overflowing with fees from AstroZeneca (and other statin manufacturers that want to piggyback onto this study) for speaking gigs promoting Crestor. (Here is a post on the payola to doctors promoting anti-depressant drugs. Drug company income from anti-depressant drugs is a drop in the bucket compared to the income from statins, so you can only imagine how lucrative it is to be a speaking statinator.) There is considerable excitement at AstroZeneca and the other statin makers because the physicians who are non-critical thinkers and non-study readers (sadly, the vast majority) will commence giving statins to just about everyone who walks through their office doors.

It appears to be another modern medical triumph – everyone profits but the patients.  Looks like Erasmus was way ahead of his time when he wrote about Jupiter way back in the 14th century.

Jupiter, not wanting man’s life to be wholly gloomy and grim, has bestowed far more passion than reason /you could reckon the ration as twenty-four to one.

Passion to reason in the ratio of 24 to 1.  That equation certainly applies to the media covering this study and the statinators feeding them their info.

Let’s take a look at what the study really shows.  But before we do, let’s psychoanalyze the people putting the study together.  What do you think they wanted out of this study.

Typically a study starts with an hypothesis, say, zinc cures the common cold.  The study then involves giving people suffering from colds zinc or a placebo to see what happens.  The researchers then say that the data confirms the hypothesis or refutes it.  It’s not good to go into a study with a predetermined idea of what you want.  You just need an hypothesis.  Your hypothesis could be that zinc has no effect on the common cold.  You wouldn’t go into a study with the idea that we’re by God going to prove zinc cures the common cold.  It just doesn’t work that way.

But what about the Jupiter study? Know what Jupiter stands for?  It stands for Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin.  Which translates to by God we’re going to prove that statins prevent something.  We certainly know the mindsets of the people running this study.

After a couple of critical reads of this paper (full text here), I can’t see a real problem with the data.  But there are a few sort of fishy things going on with this study and three really fishy things.  Before you read on, give a quick read through to a post I wrote a while back about relative risk so that you will be familiar with the kinds of statistics we’ll be talking about.

Although the relative risk numbers in this study appear to be correct, you’ve got to realize that these are small numbers we’re talking about.  Out of almost 18,000 subjects there is a difference of not quite 50 deaths between the two groups during the years over which the study took place.  Which means, of course, that neither subjects in the placebo group nor subjects in the Crestor group were at great risk of dying.  There is a difference, but in these small numbers (as explained in the post linked above) it is almost meaningless.

You can really see the difference when you look at this graph taken from the study.

Notice the bottom two curves.  Those are the all-cause deaths from the placebo and Crestor groups.  As you can see, the two curves are pretty much superimposed upon one another.  That’s what it looks like when very small numbers are involved.  The authors had to use a different scale to make it look like there was a major difference as they did in the two divergent curves at the top of this chart.

Let’s look at the sort of fishy aspects of this study.  First, the patient population is most unusual.  How many subjects are there out there who have both normal LDL-cholesterol levels (defined as 130 mg/dl or below) AND elevated C-reactive protein levels.  Not very many.  Especially if you eliminate anyone with any history of inflammatory disorders, which the researchers did.  Most people who have an inflammation arising from the metabolic syndrome, obesity or other common inflammatory disorders will have both elevated lipids AND elevated C-reactive protein levels.  They are typically found together.  The authors of this study had to use 1315 sites in 26 different countries to get the 17,802 subjects involved.  Simple division tells us that there were an average of about 13 subjects per center.  Not many.  To paraphrase F. Scott Fitzgerald who said “the rich are different from you and me.”  Well, these subjects are different from you and me.  And what may work for them may not necessarily work for you and me.

Second, when you look at Table 1 showing the baseline characteristics of the participants, you can see that in virtually all respects the two groups of subjects look identical, which is as it should be in a randomized study.  But closer evaluation indicates that there not identical in a couple of parameters.  In the category Family history of premature CHD (coronary heart disease) we see that there are 51 more subjects with a family history of premature CHD in the placebo group than in the Crestor group.  Since a family history of premature CHD is probably the strongest risk factor for developing premature CHD, do you think a few more of the subjects in the placebo group may have developed it?  And maybe died as a result?

Third, looking at this same table and checking the very next category, Metabolic syndrome, we find that 71 more patients in the placebo group with metabolic syndrome than we do in the Crestor group.  Since the metabolic syndrome is another strong risk factor for development of CHD, do you think some of that difference in deaths could have come from this disparity in the groups?  As I say, not conclusive, but fishy.

The three real fishy things are more problematic. First, according to the paper

At the time the study was terminated, 75% of the participants were taking their study pills.

Which means, of course, that 25% weren’t taking their study pills.  And we don’t really know how many of the deaths in the study group came from the 75% taking their meds or the 25% who weren’t because the data was evaluated using an intention-to-treat analysis.

The second fishy deal on this study is that both the placebo group and the Crestor group reported the same number of side effects.  Say what?  Crestor is a potent statin, known for causing side effects, and the group taking this drug reported no more side effects than those taking the placebo.  That’s real fishy.  When you look at the most common side effect of statin drugs – muscle pains – only 19 people out of 18,000 reported this symptom: 10 in the Crestor group and 9 in the placebo group.  Something totally fishy is going on here.

Finally, the fishiest thing of all.  They stopped the study right in the middle of it.  When studies are done that might put people at risk by giving them potentially dangerous drugs, it is typical for an outside group to take a peek at the data at certain milestones to make sure the study medication isn’t killing people.  When this data is evaluated, and it is found that subjects on the experimental medicine are dying at unacceptably high rates, the study is often halted.  I’ve never seen a study halted because the placebo group was dying at higher rates. That really makes me wonder.

One of the negative findings in this study was that the group on Crestor developed diabetes during the trial at a significantly higher rate than did those on placebo.  I suspect that the outside group checked the progress of the study, found that the subjects on Crestor were at the time of the evaluation showing better results than those on placebo, so the decision was made to stop the study while it was looking good.  Had it gone on for the full term, the deaths could have evened out, way more people could have developed diabetes, or who knows what might have occurred had the study continued.  So, the powers that be decided to quit while ahead.

But, let’s assume I’m taking this study at its absolute worst.  Let’s look at it in the best light possible.  If we do, we find that a small group of unusual patients – those with low LDL-cholesterol AND high C-reactive protein – may slightly decrease their risk for all-cause mortality by taking a drug that costs them almost $1,300 per year and slightly increases their risk for developing diabetes.  That’s the best spin possible given the data from this study.  Compare that to the spin the media is giving it.

Think again.

A story appeared in the online version of Time Magazine last year that I read when it came out, put aside to blog about later, then got sidetracked.  A reader sent me a link to it a few days ago, which brought it back to the front of my mind.

The article discusses a study being done in Germany using a carb-restricted diet to fight cancer.  In pre-WWII days, a German scientist, Otto Warburg, received a Nobel Prize for his work in sussing out the fact that cancer cells don’t generate energy the same way that normal cells do.  Cancer cells get their energy, not like normal cells, from the mitochondrial oxidation of fat, but from glycolysis, the breakdown of glucose withing the cytoplasm (the liquid part of the cell).  This different metabolism of cancer cells that sets them apart from normal cells is called the Warburg effect.  Warburg thought until his dying day that this difference is what causes cancer, and although it is true that people with elevated levels of insulin and glucose do develop more cancers, most scientists in the field don’t believe that the Warburg effect is the driving force behind the development of cancer.

But it stands to reason that it can be used to treat cancer that is already growing.  Since cancers can’t really get nourishment from anything but glucose, it stands to reason that cutting off this supply would, at the very least, slow down tumor growth, especially in aggressive, fast-growing cancers requiring a lot of glucose to fuel their rapid growth.

Thomas Seyfried (the same Thomas Seyfried mentioned in the article) has shown that ketogenic diets in animals and humans can stop malignant brain tumors.  There is no reason to believe they wouldn’t work in humans as well.

A group in Germany is looking at such diets in a small pilot study.  Patients are only admitted to the study when all standard therapies – chemotherapy, radiation, surgery, etc. – have failed and they have basically been sent home to die.  In fact, a few were so far gone that they died within the first week of starting the study. You couldn’t ask for a study group more destined for failure, but, according to the Times article

The good news is that for five patients who were able to endure three months of carb-free eating, the results were positive: the patients stayed alive, their physical condition stabilized or improved and their tumors slowed or stopped growing, or shrunk.

If you understand the Warburg effect and the metabolism of cancer cells, it’s easy to see why this therapy works, even in patients who at at death’s door.  Since the cancers can use only glucose, and since glucose is made in the cancer cells slowly and inefficiently, the cancer cells have to rely on outside glucose to provide nourishment for their rapid growth and replication.  People on very-low-carb diets produce ketones, which take the place of glucose in other cells that can use these ketones for fuel.  But cancer cells can’t use the ketones since ketones have to be burned in the mitochondria, which are dysfunctional in cancer cells.  If you can keep blood sugar low, then growth of the cancer cells may be held in check long enough for the body’s own previously overwhelmed immune system to rally and beat the vulnerable cancer back.

Now, given all this, if you had a big cancer eating you alive and you were offered a chance for salvation by doing nothing more than following a low-carb diet, would you take it?  I certainly would.  But, not everyone does. I was stunned to read the comments of Dr. Melanie Schmidt, one of the researchers, about people dropping out of the study.

[Some] dropped out because they found it hard to stick to the no-sweets diet: “We didn’t expect this to be such a big problem, but a considerable number of patients left the study because they were unable or unwilling to renounce soft drinks, chocolate and so on.”

Let me see if I’ve got this right.  A lifesaving therapy is offered to patients who have undergone the misery of radiation therapy, chemotherapy, and surgery, and who are beyond hope, and this therapy requires nothing more than eating a lot of butter, meat, cream, cheese, etc. while avoiding most carbohydrates.  And a considerable number” drop out because they can’t give up carbs?

I say it again.  And you don’t think carbs are addictive?

As a coda to this post, I’ve got to tell you that MD at this very moment is rolling out a fondant that she made a couple of days ago.  She was dragooned into making the birthday cake for our granddaughter whose party is tomorrow.  The kid doesn’t want a store-bought birthday cake, she wants a custom-made cake by her Nanny, which has become a tradition.  She wants a Razor (a Swat Kat) cake, so MD is having to free-hand it.  Although she’s never made a fondant before, she figured that would be the easiest way to frost and decorate the cake she has in mind.  I wandered over to get a cup of coffee and pulled off a tiny piece of the stuff and popped in my mouth just to see what it tasted like.  Her fondant is made with powdered sugar, corn syrup, and lard (not the vegetable shortening called for in the recipe), and it is good beyond belief.  I’m sitting here writing this post, and after a tiny, tiny piece (maybe 3/4 inch by 1/2 inch by 1/8 inch) of fondant, I am obsessing over how easy it would be to walk the 10 feet to where it is and start throwing it down by the handfuls.  So, yes, carbs are addictive.  Especially the carb-fat combo.

Lest you get the wrong idea, our granddaughter’s parents keep her on a kid’s version of the low-carb diet most of the time.  The cake is a once a year deal.  Thank God.

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

Another common variant:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Researchers presented data from a long-term study (almost 30 years long) showing that subjects who lowered their blood sugar levels with drugs for a period of 10 years reaped large rewards in terms of reduced incidence of heart attack and reduced incidence of all-cause mortality long after the end of the study.

Here is how the study was done:

From 1977 through 1991 patients were enrolled in a study to determine the benefits (or lack thereof) of intensive glucose lowering with medications (insulin or sulfonylurea) compared to conventional glucose control achieved through diet (more about which later).  Researchers randomized the subjects into the drug-treated, intensive-glucose-control arm or the diet arm of the study and waited and watched for ten years.  At the end of the ten years, the subjects on the intensive-glucose-control arm demonstrated a reduced risk of microvascular complications, a nonsignificant reduction in incidence of heart attack and no improvement in all-cause mortality.  (There was a subset of obese patients in this study who were treated with metformin who showed significant reductions in incidence of heart attack and all-cause mortality by the end of ten years.)

Other than the improvement shown in the obese diabetic patients on metformin and the decrease in microvascular complications, there was no real advantage to the strict glucose control within the ten year study period.  After the study was completed, the subjects were no longer followed regularly for their disease and were returned to the care (or lack thereof) of their own physicians.

Researchers then performed a 10-year post study monitoring just to see what had happen, and were surprised to learn that those patients who had undergone the strict glucose control experienced fewer heart attacks, fewer diabetic symptoms, and lower all-cause mortality.  The reductions in risk were, in my opinion, extraordinary.   There was a 15 percent reduction in heart attacks and a 13 percent reduction in the most important statistic of all: all-cause mortality.

Said one of the directors of the study in a comment that beggars belief and is worthy of the Reckless Award for a stupid statin statement as reported on HeartWire:

UKPDS [United Kingdom Prospective Diabetes Study] has definitively shown today that early glucose-lowering in the longer term really does impact on cardiovascular disease in people with type 2 diabetes. We’re talking about a 13% reduction in all-cause mortality and a 15% reduction in MI. Now, that may not be as big as what we see with a statin or something, but given the millions of people with diabetes, this is a very substantial change, and it is over and above the other treatments that patients are getting.

“Now, that may not be as big as what we see with a statin…”  Are you kidding me?  This guy must be another one who has drunk way too much of the statin-laced cool aid.  If the companies that make statins could get even half… half, hell, if they could get even a third or a fourth of these results, there would be dancing in the streets in statin land.

I’m putting the following in bold so that it will stand out.

As I’ve written countless times in this blog, randomized, placebo-controlled studies (the only kind that matter) have shown that statins provide no decrease in all-cause mortality (the only statistic that really counts) in women of any age whether they’ve ever had a heart attack or not.  These same studies have shown that statins provide no decrease in all cause-mortality in men over the age of 65 regardless of whether or not they have ever had a heart attack.  The only group of people for whom statins have shown any benefit in terms of a decrease in all-cause mortality is men under the age of 65 who have already had a heart attack.  And even in these men, the decrease in all-cause mortality is minuscule.  So minuscule in fact, that some authorities don’t even think the expense of statins is worth the tiny risk reduction.

A 13 percent reduction in all-cause mortality is pretty huge, and seems to be a ‘legacy effect’ of the strict blood sugar control these subjects experienced during the ten years they were on the study.  To be completely accurate, it could be said that the drugs these subjects took are what is bringing about their decreased risk of death, but given the side effects of these drugs, I kind of think that is doubtful.

Chronically elevated blood sugar, even when elevated just a little, is toxic to the blood vessels.  Knowing this, it makes sense that if blood sugar is kept tightly regulated for ten years, less damage should accrue to the vascular systems over this period.  And, since heart disease is the major killer of people worldwide, and since heart disease is a manifestation of vascular damage, it also makes sense that if you minimize vascular damage for ten years, you will have less risk of heart disease and earlier death.  At least that’s the way I see it.

From the hindsight of today, it’s really easy to see why those with tightly controlled blood sugars would have fared better than those on the conventional diet, when you realize what the conventional diet was at the time of this study.  From the original paper in The Lancet (1998) 352(9131) 837-853:

The patients were advised to follow diets that were low saturated fat, moderately high fibre and had about 50% of calories from carbohydrates…

That pretty much tells us all we need to know.  Ten years of a high-carb diet verses ten years of tightly-controlled blood sugar.  Which do you think caused the most vascular damage?

Almost three years ago I wrote another post on the subject of the sugar hypothesis, but that was at a time that this blog had about 12 readers.  Those of you who weren’t readers way back then might want to give this one a look now.  It shows that variations even within the normal range of blood sugars are correlated in a dose-response fashion with mortality.

The take home lesson of these studies is that blood sugar is much more closely correlated to health and longevity than are cholesterol levels.  Yet everyone is focused on cholesterol.  Why?  Because the drug companies want us to be focused on cholesterol.  The pharmaceutical industry has brainwashed the public and, even worse, has brainwashed most of the doctors out there (as evidence, see the quotation above by the director of the UKPDS, who is an academician and should know better).

The nice thing is that it’s pretty easy to tightly control your blood sugar levels without drugs.  How?  By taking blood sugar control out of the hands of your pancreas and turning it over to the liver.  You can do this by keeping your carbohydrate intake low enough to ensure that your liver has to produce glucose.  When the liver gets into the glucose production business, it turns it out in a slow, steady fashion, making just the amount necessary.  Blood sugars stay low, and glucose-induced damage to the vascular system is minimized.  If you follow a good-quality, whole-food, low-carbohydrate diet, your blood sugar will stabilize.  If you’ve already got type II diabetes, following such a diet might not completely solve your problem, but it will make it a lot better.  I have never seen any kind of therapy that works better than a low-carb diet to lower and stabilize blood sugar levels.  It truly is amazing.  If you do have type II diabetes, you must work with your physician to regulate your medications because you will need to reduce your dosages or eliminate the medications very quickly or your blood sugar will fall too low too fast.  As one of my colleagues says when telling other physicians about this therapy: nothing in your medical experience heretofore will have prepared you for how quickly this will work.  And, unlike some other therapies it works everytime