H/T to Roy Williams

Product review: Globe Trotter luggage

The photo you see above is of my beloved Globe Trotter Cetenary roll aboard.  I took it with me on this last trip to Hong Kong and London, much to the chagrin of MD, who hates this piece of luggage with a passion.

MD is a packer extraordinaire and is totally practical.  When it comes to packing, ‘cool looking’ isn’t in her vocabulary.  Since we travel so much, we have gone through many pieces of luggage over the years, and she has found the Hartmann bags best for her particular style of packing.  She can cram more into her Hartmann bags than any one believes possible.  And when she pulls her packed stuff out, it all looks great.

She has evaluated other luggage (usually at my insistence), but always defaults to Hartmann whenever she needs a new bag.  She picks the Hartmann bag she thinks looks the best, but would never, ever trade looks for utility.

I, on the other hand, will put up with a little loss in utility for a big load of cool.  And, in my opinion, the Globe Trotter luggage is maximally cool.  I’ve lusted over this stuff since the first time I read about it and saw a picture.  Every time we go to London, I would head for the Burlington Arcade where the main Globe Trotter store is housed and slobber over all the different pieces.  Finally, a few years ago, much to MD’s displeasure, I succumbed and purchased the above roll-aboard or trolley, as they call it.

Every time I try to take it anywhere, MD whines.  It isn’t divided into dual compartments- it’s just one empty box on wheels.  And it doesn’t open completely so that the top lays flat.  She feels it limits the amount that can be packed and easily retrieved, and she’s no doubt correct, but that doesn’t mean it’s worthless.  It has hard sides, so stuff is protected, and it has leather straps so it can’t pop open, and it has a great wheel system, so it’s easy to pull.  But those virtues mean nothing to her, so she always beats me down when I want to take it on one of our trips.

This time, however, I manned up and took it despite her protestations.  It functioned okay at best.  It was a real pain to get into in the overhead of the airplane, what with having to deal with the straps and the locks and the lid.  It’s much easier to simply unzip a bag and reach in.  All the gripes MD had about it turned out to be correct.  I’ve realized that Globe Trotter bags, which have been made since the late 1800s, were designed and built for a time when someone else handled all of your bags when traveling.  They’re made for durability and for unloading once you get to your destination - they’re not worth a flip if you live out of your suitcase as we often do while on the road.

I no doubt looked dashing as I wheeled my trolley across the lobby of the Mandarin Oriental hotel in Hong Kong, but that didn’t make up for the  all the downside.  Globe Trotter luggage does look great, but in this case, at least for my purposes, the looks don’t trump the lack of utility.

The placebo effect and observational studies

I got the following comment (reprinted here in part) on my last post:

Dr Mike, I must say I’m a bit uneasy about your attitude to observational studies. Doesn’t that in effect disparage most “traditional” knowledge, whether architectural (”If we build things in this way, they don’t seem to fall down”), medical (”People seem to recover from their fever when I give them this combination of herbs”), societal (”If we set up this kind of committee, things seem to function more or less peacefully and efficiently”)? I understand that an observational study doesn’t prove anything by itself but it seems that it’s a more formalized kind of traditional observation, one that, crucially, makes itself transparent and therefore open to future reinterpretation. I may be misunderstanding your stance, but I worry that in effect it negates most of humankind’s historical progress, and any kind of inquiry that doesn’t fit your preferred methods.

This commenter sets up the problem in a way that it can be explained easily.  And probably more clearly than I’ve explained it in the past.

As I pointed out in my post on observational studies, these kinds of studies are worthless for proving causality, but useful in defining hypotheses that can be tested.  Let’s take one line from the comment and is it to demonstrate what I mean.

“People seem to recover from their fever when I give them this combination of herbs.”

A perfect example.  Let’s say that some witch doctor sometime in the past came up with an herbal concoction that helped his ‘patients’ recover from a fever.  Over the years this herbal therapy was passed down from witch doctor to witch doctor, and it worked without fail.  A traditional doctor heard of the cure, tried it on a few patients and found that it did indeed seem to work.  Every time the good doctor prescribed this herbal remedy, patients had their fevers break and began to get well.  This doctor told other doctors, many of whom began using the herbs, and their patients, too, recovered from their fevers.  Patients swore by the stuff and rushed to their doctors to get it whenever they got sick.  Traditional doctors and witch doctors alike were in agreement that the potion works like magic.

Then comes a scientist who looks at the data and says, hey, here is a great observational study.  All the observational data indicate this stuff works like a charm, so let’s make that our hypothesis, which, simply stated, is that Herbal Mixture X reduces fever in those who take it.

Now that the hypothesis has been developed, it needs to be tested.  The best way to test it is with a randomized, double-blind, placebo-controlled study.  Our scientist recruits doctors in several clinics across the country who are familiar with the workings of Herbal Mixture X (HMX) and provides them with a study protocol and unlabeled HMX and placebo, both of which look identical.  As per the protocol, any patient who comes into the clinic with a temperature above 101 [degrees] F gets a randomly generated number and either the HMX or the placebo.  Neither the patient nor the doctor knows who is getting the real stuff and who’s getting the placebo, which makes the study double blind.  If the doctor knew who was getting the HMX, then the study would be single-blind, not double-blind, which would not remove the physician bias from the study.  The assumption is that if the doctor doesn’t know which is which, he/she will treat all patients the same and not let some subtle bias slip into the experiment.

When a patient presents to the clinic with a fever, the doctor gives either HMX or placebo and waits to see what happens.  The doctor or staff contact the patients daily and have them report their temperatures.  When temperature has returned to normal, the data point is entered on the patient’s chart.  After a specific number of patients have gone through the protocol, the codes are broken to see which patient got the HMX and which got placebo.  The scientist then crunches the data to see whether the supposed fever-lowering ability of HMX is statistically significantly different from that of placebo.  And, lo and behold, let’s say for argument’s sake there is no difference.

There is a huge outcry from all the docs who have used the treatment.  The study was flawed, they scream.  We know this stuff works.  We’ve used it for years, and we’ve seen it work.  Same goes for the patients who have taken HMX over the years: they swear by it, too.  They say, We don’t care what one stupid study showed - we know it works.

So, another group of scientists takes on the project and repeats the study.  And gets the same results.  HMWX works no better than placebo.  All the same outcries arise, and so the study is repeated a few more times, all with the same result.  Clearly, HMX works no better than placebo when compared in a double-blind, placebo-controlled study, yet thousands of doctors and countless patients firmly believe in its efficacy.  What happened?  The observational data seemed to strongly ‘prove’ that HMX worked, but the actual testing showed it to be worthless.  What’s going on here?

What’s going on and what makes HMX work is the magic of the healer telling the patient that the therapy is potent along with the patient’s belief in both the healer and the strength of the remedy.  In other words, the placebo effect.

Don’t believe me?  With the recent death of Michael Jackson, reported by some as due to an overdose of a potent painkiller, said painkiller, Demerol, is much in the news.  I just read a piece written by a doctor on the placebo effect that describes the strength of this phenomenon.  Most physicians who have been in practice for any length of time have similar stories:

Jane D. was a regular visitor to our ER, usually showing up late at night demanding an injection of the narcotic Demerol, the only thing that worked for her severe headaches. One night the staff psychiatrist had the nurse give her an injection of saline instead. It worked! He told Jane she had responded to a placebo, discussed the implications, and thought he’d helped her understand that her problem was psychological. But as he was leaving the room, Jane asked, “Can I get that new medicine again next time instead of the Demerol? It really worked great!”

A placebo as strong as Demerol?  You bet.  Happens all the time.

I’ve been lambasted by many readers over my comments on the lack of efficacy of HCG treatment for weight loss.  Many have received what they consider to be significant benefit from HCG therapy and can’t possibly believe what they were experiencing is the placebo effect.  However, based on the many studies in which HCG was compared to placebo in double-blind testing, it is no better than placebo.  But that doesn’t deter those who don’t believe.  They know it works because it worked for them.  Which, of course, is how the placebo effect operates.  According to the results of at least 20 double-blind, placebo-controlled studies, these people would have experienced the same weight loss had they been given saline (salt water) injections or drops under their tongues and been told that the therapy they were given would keep hunger at bay and make their excess weight magically disappear as it had worked for thousands of others.  Of course, the 500 kcal/day diet helps, but in the minds of those who have had success with HCG, it is the hormone that does the trick.

Fat cells and adolescence

It has long been thought that fat cell number became fixed at about the time of late adolescence, and now a study using carbon-14 labeling pretty much confirms that hypothesis.

People get fat in childhood and up to late adolescence by increasing the number of their fat cells; people who get fat after adolescence do so not by adding more fat cells, but by increasing the size of the fat cells they already have.

What this difference in method of storing fat means is that it is more difficult to lose weight after a fat childhood than after gaining excess weight as an adult.  Why?  Because obese children have a large number of normal-sized fat cells that they carry on into adulthood.  To lose weight, they must reduce normal-sized fat cells to subnormal-sized ones, a more difficult prospect than reducing the abnormally-enlarged fat cells that are a consequence of adult weight gain back to normal size.  It can be done as evidenced by all the people who were overweight as children who have lost in adulthood, but it’s a tougher row to hoe than for those who got fat as adults.

Exercise and weight loss

Gary Taubes has taken a lot of heat as have I for publishing the idea that exercise doesn’t bring about weight loss.  The body compensates for increased exercise with increased food intake, and it takes surprisingly little food to replace whatever calories were lost by exercise.  Exercise has multiple benefits, and I recommend it to everyone because of those benefits, but, sadly, increased weight loss isn’t one of them.

This concept is one like the placebo effect that many people have difficulty grasping.  I’ve had countless comments from readers who have related their own stories of how they lost weight by a rigorous exercise regimen.  And they may have, but how do they know it was the exercise that did the trick?  How do they know they were losing weight because they were exercising instead of exercising because they were losing weight?  That statement seems ridiculous on the surface because it appears so obvious that the calories expended in exercise are what causes the weight loss.  But how do we know?  Perhaps because of a change in diet the body needs to ditch a bunch of excess calories from fat stores that are being emptied and does so by increasing the desire to exercise or increase fidgeting in an effort to dissipate this energy.  The increased weight loss brought about by this increase in exercise would be perceived as being caused by the exercise whereas in reality the exercise was caused by the need to lose weight.  It’s a difficult concept to grasp, but it has pretty much been shown in controlled studies that simply increasing exercise doesn’t reliably bring about weight loss.

As I wrote above, when people exercise, they generally increase their food intake to compensate.  But it’s not just the exercises itself that increase food intake, it could be simply thinking about exercise.

Researchers from the University of Illinois reported on two studies in which they correlated food intake with advertising encouraging exercise and even with subliminal words that had exercise connotations.  People ate more when simply hearing about exercise or hearing such words as ‘action’ in the context of something else.

Wrote they:

Alarming rates of overweight and obesity in the United States have led to the development of preventive communications and interventions to promote weight loss. As weight loss is contingent on energy expenditure exceeding caloric intake, one popular approach comprises promotion of physical activity. Media and community campaigns often encourage audiences to increase their physical activity by engaging in structured exercise or active routines. The present research was designed to explore potential effects of such campaigns on eating behavior.

Their conclusion:

Overall, the findings from these two experiments are suggestive in demonstrating that exercise messages can exert inadvertent immediate effects on food intake. Such consequences may not be apparent if exercise is the only measured outcome, but could potentially jeopardize weight loss.

The body likes to keep things on an even keel and maintain homeostasis and has all kinds of mechanisms for doing so.  If you walk past a bakery and smell the aroma of freshly baked bread, your pancreas figures there is going to be some carb coming its way soon, so it releases a little insulin in anticipation.  Apparently the same thing happens if you even think about exercise.  You eat just a little bit more to compensate - even before you exercise.

The dark side of fiber

You just about can’t read anything these days without hearing the virtues of fiber extolled.  It seems that fiber is on everyone’s good list.  Even low-carb and Paleo diet advocates go to the trouble of making all aware that their diets contain plenty of fiber.  No one has anything bad to say about it.

Well, I do.  I can’t let one of these odds and ends posts end without linking to one of my own favorite posts from back in the days when I had only three readers.

Take a look here at a post about a pretty good study showing how fiber really exerts its effects.

My slogan has become: Fiber…who needs it?

Video fun
And, finally, I can’t quit without a video.  I saw a guy like the one in the YouTube below on the Johnny Carson Show years ago.  I was stunned back then that someone could do this, and I’m just as stunned now.  It just doesn’t seem possible.  Enjoy.

Click here to view the embedded video.

Instructor teaches Friedewald equation and bad cholesterol

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

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

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

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

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

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

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

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

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

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

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

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

And how did they fare?

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

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

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

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

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

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

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

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

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

The abstract of the study echoes this warning.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

LDL = Total cholesterol - HLD - VLDL

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

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

LDL = Total cholesterol - HDL - TGL/5

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

One more.

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

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

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

HAHAHAHAHAHAhahahahahahaha! Oh man, sometimes I crack myself up.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Let’s take a look at what they did.

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

Here is a description of the diets:

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

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

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

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

Here is the chart showing the study outcomes:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

I apologize for not being more attentive to this blog since leaving Hong Kong a week ago.  But my excuse is that we’ve  been in London.  I’ve always been on the same wave length as Samuel Johnson, who said “When a man is tired of London, he is tired of life; for there is in London all that life can afford.”  I have a great blog post in mind, but I just can’t bring myself to spend the three or four hours it will take me to put it up when London beckons outside my window.

There are so many things to like about London that I don’t know where to begin to describe them to those who haven’t had the opportunity to visit.  For one, it’s probably the only major city in the Western world in which the highest  building is only 46 stories.  Most of London looks much like the photo at the top of this post that I took while crossing the street yesterday - non-skyscraper skylines with old buildings with very old buildings interspersed.  One of the main things I really enjoy about London is the fact that being a pedestrian is almost a full-contact sport requiring full attention, especially for Americans who are used to looking the wrong way when crossing the street.

I loath the American way of being a pedestrian.  In the US pedestrians have the right of way and are usually pretty obnoxious about it.  I can’t stand it when I’m in a car and a pedestrian or a group of pedestrians slowly strolls across the crosswalk, taking their time in an almost passive-aggressive fashion.  The most annoying pedestrians are those who consider it a point of honor not to look at the cars coming to a stop as they saunter across in front of them, as if to look indicates a sign of weakness.  These people know that if the car hits them, it is the driver’s fault and not theirs.  But they don’t stop to consider that they, the pedestrians, will be the ones in the hospital or in the morgue.  They seem not to understand that accidents are called accidents for a reason.  Being kind of an  aggressive person myself, I love to close  on these saunterers at a rate that gets their attention.  I consider it a victory if I make them at least look at my oncoming car and perhaps start to consider if they need to jump or not.

In London there is no doubt.  The roads belong to the cars.  Pedestrians crossing where they shouldn’t be need to be quick on their feet, and even gray-headed duffers jump to when the cars come at them.  And the drivers simply lay on their horns and don’t slow down.  I love it even though I am a pedestrian.  But, I’m no doubt not normal.

We came to London as a part of the big project we’ve been working on.  We had arranged a meeting with Heston Blumenthal and a long lunch at his restaurant The Fat Duck.  Although Heston is probably the best known chef in Europe, he’s not as well known in the United States, but that will change as he has a cooking show that will be coming out there early in 2010.  He is completely self-trained, which is amazing in the world of celebrity chefs, and has only one restaurant, instead of a chain of dozens bearing his name.  But what a restaurant it is.  The Fat Duck has won the title of best restaurant in the world as judged by other chefs for two years running, and can’t run again.  To those of you in the US who want to learn more about Heston and his style of cooking, here is a link to a one hour video special about a Christmas meal he prepared.  Watch it, and you’ll learn why he has the reputation he does. Or Google Heston Blumenthal for many short videos, if you’re not up for watching the longer one.

We met with him for an hour and a half or so and found him to be charming and completely self-effacing.  He comes across in person exactly as he does on TV.  And his restaurant is beyond belief.  We’ve never had such a meal.  In fact, there has never been anything that has even come close.  I took a ton of photos and plan to post about the entire meal, but I haven’t wanted to deny myself London for the several hours it will take me to put up such a post.  We’ll be back in the US tomorrow, and as soon as I go through all the stuff that has stacked up in our absence, I’ll put up the post.  I may even start working on it on the plane.  You will be almost as amazed.  Try to give the video a look if you have the chance, so you can see what a different kind of chef Heston Blumenthal is.

I’ll leave you with a photograph of MD crossing the road on the famous crosswalk at Abbey Road shown on the album cover of the Beatles’ Abbey Road.  Abbey Road Studios where the group recorded for six or seven years is right behind her and to the left.  As many times as MD and I have been to London, we’ve never made the trek over to Abbey Road, but we did early in the evening a couple of days ago.  It was a long hoof, but we made it before dark, and MD, who is a huge Beatles fan, got to fulfill a childhood dream.  And I, of course, selflessly went along to document the occasion.

After our meeting at the factory we’re working with, the president of said factory treated us all to a feast at our restaurant.  As Chinese tradition dictates, such feasts are accompanied with many, many toasts.  The toast works this way:  the person making the toast picks out a specific person to toast, walks over to that person, raises his/her glass and gives the toast.  The translator translates.  The person receiving the toast answers back.  The translator translates back.  Then both toaster and toastee down drinks in one swallow.  After this, the glasses are immediately refilled by one of the servers.

In our case, the liquor used for toasting purposes was either red wine or bai jiu, a Chinese white wine that is actually more of a distilled liquor.  The Chinese love bai jiu, which has a distinctive flavor.  It’s about 50 percent alcohol and has a front end taste that is kind of like the essence of an infusion of dirty socks in some sort of floral alcohol and a back end like lighter fluid.  It’s an acquired taste, and one that I had sort of acquired after a zillion toasts.

As the meal progressed, the toasting evolved into each toast requiring the downing of both a glass of red wine and a glass of bai jiu.  Thank God we ran out of red wine and baiu jiu before I ran out of consciousness.  The photo above shows me just before downing a glass of each after a toast from the head of operations at the factory.

The meal we had was spectacular. And pretty low-carb.  I kept a photo log of it, which I will lay out below. (We had another good meal earlier in the day that MD posted about moments ago.)

We started with shark fin soup, which I didn’t take a picture of because…I don’t have a good reason.  I just didn’t.  I guess I didn’t think about taking photos until after the shark fin soup.  From there we moved on to a giant prawn and an abalone.  Both were delicious, especially the abalone.  I don’t know what kind of sauce it was cooked in, but it was savory and out of this world.

Then came a weird dish that was served with plastic gloves.  It was a baby dove with head included.  You put the gloves on and tore the little bird to pieces and gnawed the bones.  And, yes, we ate the head.  We didn’t just throw it back and chomp it; we nibbled off the small amount of meat on it .  I watched the Chinese so I could follow suit, and that’s what they all did.  After picking the bones clean, we all removed our gloves and awaited the next course.

What came then was some sort of seafood salad.  And remember, all this food was interspersed by dozens of toasts.

After the seafood salad came the main course, which was a piece of succulent steak that was extremely tender.  It was served with a little pile of fried garlic chips and a stalk of broccoli.

Following the steak, we had a dish of some kind of green vegetable.  I never could figure out what exactly it was, but it was very tasty.  I asked the woman sitting next to me what it was, but she didn’t know the English word for it.  All she could tell me was that it was grown in the area where we were.

Then came a tiny bowl of fried rice.  You can see the size of the bowl by comparing it to the spoon next to it and the little glass the bai jiu is served in.

The we had some sweets, which I admit to eating.  Everyone of them.  By that time, after all the wine and bai jiu, I would have eaten anything.

And finally we were served a small plate of fruit for the end of the meal.

By that time all the wine and bai jiu were gone, thank God.  I thought we had made it through the worst of it, but the factory president, who was the founder of this feast, had brought two kegs of German beer, so nothing would do but that we all traipsed upstairs to a small room and drank glass after glass of mildly chilled beer and ate dried squid, squid jerky, I guess you could call it.  The beer and squid were served along with, believe it or not, french fries.  I ate no fries, but did eat a fair amount of the squid jerky, which was pretty tasteless but did give the jaws a good workout.

It was a memorable evening, and I can even remember all of it.  I even woke up the next morning feeling fine.

I’m rushing to get everything together to catch our flight to London.  I’ll post later on my thoughts on the China and Hong Kong experience. I do want to make one observation, though.  Earlier in the day that this feast took place, we toured the factory.  There were probably at least 400 people working there of all ages.  I didn’t see a single obese person - all were thin.  You may think that they weren’t obese because they were working hard.  You would be wrong.  Almost all of them had fairly sedentary jobs.  They were sitting doing very little strenuous labor.  Mainly just screwing one component on to another as they came down a line.

Your faithful correspondent slaving away

As those who follow me on Twitter know, MD and I made it safely to Hong Kong.  We have in enormously busy schedule while we’re here, so I’ll put up smaller posts as we go along interspersed with some larger ones as I have time.  As you can see from the above photo, I’m hard at it, ensconced in our hotel room overlooking the harbor with the Hong Kong skyline in the background.  Below is another photo from our hotel room window.  Our hotel (for one night) is on Kowloon across from Hong Kong Island, which is the skyline you see.  Actually, it’s only a small part of the skyline.  Hong Kong is New York on steroids.  An amazing place.

We flew over on Cathay Pacific business class, which, if you’ve got to make a 15 hour flight, is the only way to go.  Great seats that make into beds, great service and spectacular food.  The only wierd thing about the whole experience is the realization of how seriously the Chinese and the Honk Kong-ese take the swine flu.  All the cabin attendants on the plane wore masks.  We had to fill out a health declaration to enter Hong Kong and another when we got to our hotel.  I would estimate that about a fifth of the people walking around are wearing masks.

But, masked or not, the folks at Cathay Pacific put out some good food.  Good low-carb food, at that.  Below is a photo of my breakfast on the plane.  Lightly scrambled eggs with salmon, terrific wobbly bacon, sausage, broiled tomato and some hash browns (that went uneaten).

Cathay Pacific breakfast

Last night we ate in a restaurant not too far from our hotel.  We asked our guide (the guy we’re working with who is a Brit, but lives here about half the time) for a traditional restaurant, not a tourist restaurant.  The restaurant he chose was capacious; I would bet there were at least 200 people dining there.  And we were the only non-Asians.

We sat at a large round table with a lazy susan in the middle.  The waiters kept bringing food and putting on the lazy susan; we rotated the dishes and served ourselves from them with chopsticks.  Our host apologized because he said the restaurant wouldn’t be serving rice like we were used to in Chinese restaurants in the US.  He said the notion that people ate a lot of rice over here is not true - at least not in Hong Kong and the parts of China to which he travels often. (Our host doesn’t know what MD and I do - we are here on a totally different matter that has nothing directly to do with low-carbing.)

We had numerous dishes, all of which were some kind of meat.  The favorite of the table was crispy beef, which is shown below.  Absolutely delicious.

We ate mountains of various kinds of meat and fish and ended up with a giant plate of Peking duck, which we were almost (but not quite) too full  to eat.  During this entire feast, the servers brought only one vegetable dish to the table.  It’s pictured at the right.  Sauteed, not steamed, broccoli. Delicious. Not a single grain of rice did we see.  A few noodles, but not even many of them.  And no bread. And, sadly, no napkins.  There was a box of what we would call facial tissues on the table that we used as napkins.  But that was it. Oh, in looking at the picture above of the crispy beef, I noticed one other vegetable dish that I had forgotten about because I hadn’t photographed it specifically.  It is the Chinese cole slaw to the upper right of the beef.  All cabbage that is tangy, crisp, spicy and delicious.  They must have brought us a dozen of these little dishes of it.

I looked around at as many of the other 200 patrons as I could see from our table and as we walked in and out.  All were eating the same things we were.  Meat, meat, meat. Of the 200 patrons and dozens of servers I saw, there wasn’t a single obese person.  My observation of Hong Kong as a whole is that there aren’t really any obese people here, at least by US standards.  There is some chubby, but not much obese.  At least not that I’ve seen.

We are heading via ferry and car to mainland China today to go to an industrial city with a population of 60 million.  You read that correctly.  60 million.  The factory we are working with is there, and I’m keen to see it.  We will stay there tonight, then be back to Hong Kong tomorrow.

I figure it’s about time for another grab bag of a post updating everyone on what’s going on at Casa Eades and throwing up a few interesting articles and websites.

The Verdi Requiem

The Santa Barbara Choral Society’s Verdi Requiem was a triumph last weekend.  As you can see from the photo above, MD was pretty whipped when it was over.  Apparently, it’s pretty demanding on soloists, orchestra and chorus.  And, as you can see from the photo above, the listeners don’t have the same burden.  Other photos here.  A recent review of the concert here.

The concert was pretty well attended, although not as well attended as it would have been had the entire city not been consumed with worry about the fire from the week before.  Santa Barbara is just now returning to normalcy.  The receipts from the door covered a little over 40 percent of what it cost to put on the production.  When I heard that figure, I thought the whole thing was a financial disaster, but I learned that that figure is typical for non-profit arts productions.  Around 40 percent of the cost comes from the people who buy tickets – the other 60 percent comes from patrons who sponsor the event.  In other words, the ticket prices are subsidized by the nobless oblige of the wealthy, a large number of whom consider it their obligation to support the arts.  So, next time you go to a great performance that costs you $25 to see, thank a rich person that you didn’t have to pay $60.

Twitter adventures

As anyone who has followed me on Twitter knows, I spend a lot of time reading and posting to Twitter since I first posted about it.  It’s a great way to do mini posts because users of Twitter are limited to 140 characters, so it’s tough to get too verbose.

I was pretty clueless about Twitter until I started using it, so I assume others are clueless as well.  If you are not in the know about this social networking tool and would like to keep up with these mini posts, there are a couple of ways you can do it.  You can sign up for Twitter and follow me (and anyone else you would like to follow).  It takes maybe one minute to sign up for Twitter.  All you need is a working email address and a username and you’re in.  Once you are a Twitteree (or whatever they’re called), and sign up to follow me, you can read these mini posts as I put them up.  If you want to sign up, click here and get started.  If you do start, you will probably find that a bunch of your own friends are using Twitter, so you can keep up with them as well.

The other way you can access these mini posts is by clicking on the little blue bird logo that says FOLLOW ME ON TWITTER.  If you click there, you will go to a page that gives you all the latest mini posts, but you’ll have to keep going back to get the updates as they come in.  Here is a link to the page you will find.

I occasionally Tweet (a Twitter mini post is called a Tweet, a loathsome word if there ever was one, at least when applied to activities of grown humans) on personal stuff, but mainly the Tweets are mini posts on medical articles or other news articles that I think are of interest along with anything else I find that strikes my fancy.

For those of you who do follow me on Twitter, I apologize for any Twitter faux paux I may have committed.  One of the things that most appealed to me about Twitter was the notion that I could put up these mini posts without anyone responding.  But, alas, I was wrong.  I discovered a few days ago that people can respond and several hundred have.  I was taking time from feverishly mini posting by looking around my Twitter home page when I found a highlighted link that said: @DrEades.  When I clicked there, I was appalled to find several hundred responses to Tweets I had made.  I learned that when people respond to Tweets, it ends up in that section.  So, I wasn’t off the hook.  But I couldn’t possibly respond to several hundred people – even at 140 characters a response.  So, if you replied to something I wrote and I didn’t respond, you now know what happened.

I did have a couple of interesting experiences in responding however.  When I discovered the @DrEades section and found the zillion responses to my Tweets waiting there, the most recent one was from a lady who took me to task for one (or several) of my political Tweets.  She wrote that she had always liked my nutritional writing but that my political postings had alienated her.  I decided to reply to her just to see how the whole reply thing worked.  I sent her one of my favorite Thomas Jefferson quotes:

I never considered a difference of opinion in politics, in religion, in philosophy, as cause for withdrawing from a friend.

Then I watched her site and found that she had deleted the Tweet to me, which is how I learned that one could delete these things once they are up.  They can’t be changed, so if you make a grammatical error (which, sadly, I have done a few times) it can’t be fixed, only deleted.  Then she deleted me from her list of people she follows.  I guess the Thomas Jefferson quote alienated her even more.

People are really strange.  I posted a Tweet about an email that I had received a dozen times about how George Bush has a state of the art, energy-efficient ranch house in Crawford, TX while Al Gore has a giant, energy-gobbling house in Nashville.  I always ignored the email because I thought it probably was an urban legend kind of thing.  Then someone sent me a link to the Snopes report on it, which said that the email was true.  I posted the Snopes report on Twitter.  Then I started to wonder what makes Snopes the last word authority on everything, so I started looking into that.  I discovered that Snopes is a husband – wife team, who live in a double-wide house trailer on the outskirts of Los Angeles.  They do all the checking themselves.  I was stunned.  I always figured that Snopes was some kind of outfit with a staff of hundreds that checked out all these things.  The notion that the ultimate authority on everything was just a mom and pop operation who make their living by ads on their snopes.com website.  Now that I know the situation, I’ll be more careful when I accept snopes as the last word on everything.

I put up a Tweet that said basically Who would’ve thought Snopes was a mom and pop operation?  Some guy signed up to follow me on Twitter, and immediately sent a nastygram to @DrEades that said If Snopes is a mom and pop outfit, what does that make the Protein Power blog? A ‘Pop’ outfit?  I replied that the Protein Power blog is a ‘Pop’ operation, but isn’t considered by anyone to be the last word on everything.  He then deleted me from his list of people he followed. As I say, a lot of bizarre people in the weeds out there.

The whole experience has been very strange indeed.  But I’m still working my way through it, probably alienating people right and left.  So join up, follow me, and watch the fun.

Upcoming travel plans

MD and I are leaving late Sunday night for Hong Kong, then to Guangzhou, back to Hong Kong, then to London.  Sadly, the entire trip will be a working trip.  We’re hard at it in our efforts to change the world, and this trip is all about that.  By the time we get back, I should be able to write about what we’ve been working on.

I will take a lot of photos and continue to blog during the trip.  And Tweet.

Comments on the blog

I continue to be mired in comment woes.  I just checked, and I have 78 comments in moderation, some of which have been there for weeks.  It has kind of become a comments graveyard.

I’ve whined about the comment situation for that last two years. I’ve said that I wasn’t going to continue to answer questions and was just going to post the comments as they came in.  My resolve would last for about two days, then I was right back answering all the questions.  Now, I’ve gone into a funk over the whole thing, and have devolved into just ignoring the comments that require answering and letting them stack up, which I hate doing.  But, I’ve been so busy lately that there isn’t much else I can do.

I was reading a book titled Economic Sophisms by one of my heroes, Frederic Bastiat, when I came across the following paragraph that, in a way, applies to the comment situation.

We must admit that our opponents in this argument have a marked advantage over us.  They need only a few words to set forth a half-truth; whereas, in order to show that it is a half-truth, we have to resort to long and arid dissertations.

It’s easy to pen a comment that says, Hi Doc, what are your thoughts on this article? and attach a link.  I have to read the article, pull the actual study, read it, think about it, then write an answer that is considerably longer than the original comment.  What takes a commenter 20 seconds to write ends up costing me an hour or two to come up with an intelligent answer or even an ‘arid dissertation.’

I’m also getting a lot of comments asking for my ideas and recommendations on personal health issues.  People send me lab results and want to know what I think.  Without treating a given individual as a patient, medico-legal restrictions prevent me from answering these kinds of questions.

I never read the comments on blogs that I read, so I must assume that many people don’t read the comments on this blog.  But I end up spending way more time dealing with the comments than I do writing posts.  If I didn’t have to deal with the comments, I would write more posts.

I noticed that Mark Sisson, whom MD and I had lunch with yesterday, has started making posts out of some of his comments in a Dear Readers section of his blog.  He takes several comments that he thinks may be of interest to all his readers, posts them, and throws them out for the combined wisdom of all his readers to deal with. I may start doing this myself and weighing in along with the readers.  If anyone out there has any advice for me on this issue, I’m all ears.

Soda tax in New York

I just read this article this morning.  Was going to make a mini post out of it, but thought it would be better here.

A New York state senator (I’ll leave it to you guess from which party) says that by adding a measly one cent tax to each can of non-diet soda sold, the state of New York can add $100 million per year to its coffers.  If this is true, it means that citizens of and visitors to the state consume 10 billion cans of non-diet soda annually!  The population of New York state is a little over 19 million.  Dividing 10 billion by 19 million calculates out to about 525 cans of non-diet soda per man, woman and child in the state.  That’s almost 90 six-packs per person per year.  Wow!  There have got to be some low-carbers who live there who drink zero six-packs per year, which means that some other poor slob is drinking 180 six-packs per year.  That’s a lot of high-fructose corn syrup.

To my way of thinking, this is an onerous tax.  It moves $100 million from the pockets of the citizenry and puts it in the coffers of the bureaucrats to spend.  And, despite the fact that it sucks off 100 million bucks, the tax isn’t high enough to discourage consumption, so it really has no societal advantage except for transferring funds from the citizens to the government.

Where does your beef come from?

I don’t mean what part of the country.  I mean what part of the cow.  Here is a great site created by the University of Nebraska and the University of Florida showing way more than I (and probably you) need or want to know about beef anatomy.  But if you really do wonder where a flank steak or some other piece of beef comes from on the cow, click here to find out.  A lot of work went into this site.

Gradient gel electrophoresis

For those who hate to pay big bucks to have a lab tell you how much small, dense LDL you have, here’s how you can do it yourself.  That’s right.  With a drinking straw and a few other simple ingredients, you can make your own electrophoresis equipment and test your blood anytime you want for minimal expense.  Warning.  This is a real geek site.  I doubt that many will want to put together their own equipment, but at least it shows what’s involved in making a primitive version and how complex the testing process is.  May make you not feel so bad dropping the money to get the test done professionally.

Feel better immediately

And, finally, here is your feel-good YouTube of the day.  Watch this huge prank (if that’s what you would call it) played on the people in the train station at Antwerp one morning.  Really delightful.  Watch the faces of those watching.

Remember, don’t forget to help me out on this comment issue.  All suggestions will be appreciated.

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