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.

Late last night I was transferring some medical papers from my old moribund PC onto my Mac when I came across an article that infuriated me when it came out.   Now it simply made me laugh, although I have to admit to at least a tinge of annoyance still.

As I’ve mentioned before, MD and I often feel like the Rodney Dangerfields of the low-carb diet biz or, worse yet, the Victor Flemings (don’t know who Victor Fleming is?   Look him up and see what he did in 1939.   And you don’t know who he is, right?).   At any rate it seems that whenever low-carb diets are mentioned in a positive way, which, fortunately, that are more and more often these day, we and/or Protein Power never make the list.   It’s always Atkins, South Beach and the Zone.   And of those three, only one is a true low-carb diet.   The other is a quasi, pansy low-carb diet, whose author goes around denying that his diet is a low-carb diet.   The other isn’t a low-carb diet, since a diet in which 40 percent of the calories are made up of carbohydrate hardly qualifies for the modifier ‘low.’   But when it comes to attacking low-carb diets, somehow we always seem to make that list.

Now that I’ve gotten that out of my system (sorry for the whine), I can move on to the paper that attacks low-carb diets and in which we prominently figure. This article, published in the May 2000 issue of the Journal of the American College of Nutrition (free full text here), takes an ‘unbiased’ look at several different diets that were on the market at that time.  The title says it all.

Health Advantages and Disadvantages of Weight-Reducing Diets: A Computer Analysis and Critical Review

Well see just how critical a review this really was soon enough.   The Abstract lays out how the authors went about evaluating the various diets.

Design: Eight popular weight-loss diets were selected (Atkins, Protein Power, Sugar Busters, Zone, ADA Exchange, High-Fiber Fitness, Pritikin and Ornish) to be non-clinically analyzed by means of a computer to predict their relative benefits/potential harm. A summary description, menu plan and recommended snacks were developed for each diet. The nutrient composition of each diet was determined using computer software, and a Food Pyramid Score was calculated to compare diets. The Mensink, Hegsted and other formulae were applied to estimate coronary heart disease risk factors.

So, the authors were going to look at a few hand selected diets, analyze them for nutrient composition, then compare them to the Food Pyramid to rank them in terms of healthfulness. Hmmm. And they were going to use the Mensink, Hegstad and other formulae to estimate coronary heart disease risk factors. Hmmm.

Actually, they ended up using the Mensink and Katan (he of the Katanic verses post) formula to estimate the affect each of these diets would have on the cholesterol levels of anyone following them. To save you the suspense, I can tell you right now that the subtitle of this paper should be: Mensink Katan formula fails miserably at predicting cholesterol levels.

Before we look at what these authors found, let’s look at the lead in to the piece.  Again, the abstract says it all.

Background: Some weight-loss diets are nutritionally sound and consistent with recommendations for healthy eating while others are “fad” diets encouraging irrational and, sometimes, unsafe practices.

Any guesses as to which of their categories Protein Power and Atkins fall into?

At least the description of Protein Power is pretty much on the money, all except the part about closely resembling the Atkins diet in nutrient composition.  Protein Power resembles the Atkins diet more than it resembles the Pritikin diet, but I wouldn’t say Atkins and Protein Power were carbon copies.

Protein Power, written by Michael R. Eades, MD, and Mary Dan Eades, MD, closely resembles the Atkins diet in nutrient composition. They identify insulin as the culprit for obesity. They believe high levels of insulin cause metabolic disturbances in the body leading to elevated blood pressure, cholesterol and triglycerides, diabetes and obesity. They suggest restricting carbohydrate intake will overcome these metabolic disturbances and alleviate medical problems. Guidelines concentrate on the amount of protein rather than fat consumed. Their book outlines methods to determine the amount of protein to consume and gives instructions for planning meals around grams of protein with restriction of carbohydrates to ≤30 grams/day. They emphasize high-fat food choices but permit limited amounts of fruits and vegetables.

Now, as you might expect, when these authors looked at all these different diets and compared them to the Food Pyramid, Protein Power didn’t fare all that well.  A finding of which I am immensely proud.  If you look at the graphic below, you can see that Protein Power was even ‘worse’ than Atkins in terms of the magnitude of its negative direction.  Atkins just won out by a nose in overall bad (as compared to the Food Pyramid) because it had just a little less ‘good’ than did Protein Power.  As far as I’m concerned, having one’s diet be far from the Food Pyramid is good, not bad.  But the authors of this paper don’t see it that way.

When these authors looked at saturated fat, evil incarnate in the minds of the lipophobes, they found both Atkins and Protein Power to be full of the stuff.  Especially Atkins.  And we all know that saturated fat increases cholesterol, don’t we?  Well, don’t we?  Maybe the readers of this blog don’t know that.  But the authors of this study along with fellow lipophobes Mensink and Katan know it.  The latter know it so well that they’ve created equations predicting how much dietary saturated fat will raise cholesterol.  And if we look at the graph below, we can see just how high the cholesterol levels are predicted to be in the blood of the followers of the various diets.

Apparently cholesterol will be way up in followers of Protein Power and off the charts in those following Atkins.  But, remember, these are just their predictions.  They aren’t reality.

Before we go on, I want you to take a look at these graphs again.  Remember, these authors are looking at popular diets and diet books.  Along with Atkins and Protein Power, they selected Sugar Busters!, The Zone, Pritikin and Ornish.  And they threw in the American Diabetic Association’s Exchange diet…and something listed on the graph as ‘High Fiber.’  What the heck is the ‘High Fiber’ diet?  All the other diets except for the ADA diet are famous and are described in best-selling books that have each sold over a million copies.  So, where did the ‘High Fiber’ diet come from?  And why is it included?

If we look in the study in the Methods section, we find that the diet is Dr. Anderson’s High-Fiber Fitness Plan.  Huh?  Who the heck is Dr. Anderson and what is his/her high-fiber fitness plan?  If we check the reference citation, we find the following:

Anderson JW, Gustafson NJ: “Dr. Anderson’s High-Fiber Fitness Plan.” Lexington, KY: The University Press of Kentucky, 1994.

Anderson JW?  Who could that be?  Anderson JW?  JW Anderson?  Where have I seen that name before?  Well, the author of this very article were discussing is named James W. Anderson, MD.  Hmm.  Could it be?  Let’s check Amazon.com.  Sure enough.  It’s the same guy.  And he’s weaseling his own diet book in with the lineup of diet books that are all mega bestsellers.  Interesting. And using an article in a mainstream, peer-reviewed journal to substantiate it.  Very interesting, indeed.

And what does Dr. Anderson conclude about all these diets to which he has compared his own book?

The Atkins and Protein Power diets are very high in total and saturated fat compared to current dietary guidelines. Long-term use of these diets for weight maintenance are likely to significantly increase serum cholesterol concentrations and risk for CHD. The Sugar Busters and Zone diets would lower serum cholesterol concentrations and likely reduce risk for CHD. Higher carbohydrate, higher fiber, lower fat diets would have the greatest effect in decreasing serum cholesterol concentrations and, thus, the risk for CHD. While high fat diets may promote short-term weight loss, the potential hazards for worsening risk for progression of atherosclerosis or atherosclerotic events override the short-term benefits.

Jesus wept.

So his diet is in there with the ‘good diets,’ the high-fiber, lower-fat diets that don’t worsen the risk for progression of atherosclerosis or heart disease.  Amazing!

Let’s switch gears for a minute.  Since this paper was published in 2000 there have been numerous scientific papers showing that not only do low-carb diets bring about faster weight loss than do high-fiber, high-carb, low-fat diets, they also improve lipids better.

In 1997 MD and I licensed the Protein Power name and concept along with our own names and likenesses to a company to develop a set of tapes and workbooks to be sold on television.  At the time all this was going on, we were moving our clinic from Little Rock, Arkansas to Boulder, Colorado.  We had boxes upon boxes of patient files from our clinic in Little Rock that we brought with us and kept in storage (the law requires that doctors keep medical records for a prescribed period of time).  The company that licensed our name, etc. wanted to be able to make weight loss claims and lipid improvement claims, which it couldn’t do without substantiation.  They hired a professor of statistics from one of the colleges in Maine (the company was located in Portland, Maine) to evaluate the data from our thousands of patient files.

We told him that we checked blood on patients at the end of their first six weeks on the program and again at 12 weeks.  We also told him that since most patients had a large weight loss in the first week or two, he probably wanted to evaluate patients who stayed around longer than just a couple of weeks.  He decided that since we checked blood at the end of 12 weeks, he would evaluate charts from patients who had stuck with the program for at least that long.  He went through his statistical mumbo jumbo to determine the number of charts he would have to evaluate to get data that would be representative of our entire population of patients (or at least those who were on the program for at least 12 weeks).  Once he arrived at the number of charts needed, he came up with a way to pull these charts randomly. Once he crunched the data, here is the chart he came up with:

As you can see, a Protein Power diet does not raise cholesterol; it lowers it significantly.  And it drops triglycerides and improves the triglyceride to HDL ratio.  He noticed that some patients had substantial blood sugar lowering and asked about it.  I told him that the patients he had noticed were the ones who came in with elevated blood sugars to begin with.  He calculated how many charts he would need to analyze that data point and selected a number of charts of patients who had elevated blood sugars on their initial labs and who were taking no medications.  He then determined the average blood sugar lowering, which was pretty impressive.

As you can see, this data (along with the data from a number of other peer-reviewed studies) show that a lot of saturated fat (our patients were encouraged to eat saturated fat) doesn’t raise cholesterol when consumed as a part of a low-carb diet.  Which is why I said that the Anderson study discussed above should have been subtitled: Mensink and Katan equations don’t work worth a flip.

So, eat your fat, watch your carbs, and you’ll do fine.  And thanks for letting me vent.

Yesterday a reader sent me a film clip from ABC news about resistant starch. (Click here to view the video) In this film clip a young woman who is a registered dietitian (RD) spoke about the virtues of a “type of fiber” that she referred to as resistant starch. According to her, this substance can cure a multitude of ills.

There is a type of fiber called resistant starch that’s naturally found in some high carbohydrate foods.

And it’s amazing, the benefits. It ranges from helping us burn fat, helping us boost our immune system, control blood sugar, reduce the risk of type II diabetes and reduce the risk of cancer.

She’s really excited because, as she points out, there are over 160 studies showing the benefit of resistant starch.

Wow! Where do I sign up to get some? It sounds great. Or does it?

There are probably over 1600 studies showing the purported benefits of statin drugs, but we all know what those are. The 160 studies purporting to show benefit for resistant starch are probably in the same mold. Let’s forget about the studies right now and focus more on what we really know about starch and resistant starch to see how well this lady’s claims hold up to scientific scrutiny.

When asked about how resistant starch works, she claims that

it basically gets fermented in the digestive tract, and it creates beneficial fatty acids. One is called butyrate. And what that does is it helps to shut off the burning of carbohydrates. So carbohydrates are the preferred source of fuel, but if they can’t be burned, your body is going to turn to body fat and recently consumed fat instead.

All fiber goes through the digestive tract unabsorbed until it reaches the colon where it is acted upon by colonic bacteria (I suppose you could loosely call it fermented) that convert it to short chain fatty acids, one of which is butyrate (a four-carbon fat). These short chain fatty acids can be absorbed through the colon and used for energy just like any other fat.

So if butyrate “shuts off the burning of carbohydrates,” as our RD says it does, then wouldn’t it make sense to get as much of it as we can? And what happens to all that carbohydrate we don’t burn? Does it just continue to circulate in the blood running our blood sugar sky high? Or does it get stored as glycogen? Does butyrate encourage carbohydrates to head into storage? These are all questions she doesn’t address. Let me help clarify.

The list of foods containing resistant starch she mentions specifically are the following:

• Beans
• Potatoes
• Barley
• Corn
• Brown rice
• Under ripe bananas

She claims that these foods contain about 5 percent of their starch as resistant starch (which prety much agrees with other similar claims I’ve seen in the medical literature). If true, this means that 95 percent of the starch is not resistant starch and breaks down in the GI tract to glucose.

One half cup of any of these foods – so she says – contains all the resistant starch one needs to provide all the above benefits. Let’s take a look.

According to the USDA database if we consume a half cup of cooked potato we’ll end up with 12.9 grams of carbohydrate (almost three teaspoons), of which 10.5 grams are starch. If we go by our RD’s estimate that 5 percent of the total starch is resistant starch, we calculate that our half cup of potato contains about half a gram of resistant starch (0.5265 g to be exact). If we then convert this starch to butyrate we find that we have about 2.3 grams of butyrate (assuming 100 percent conversion to butyrate, which isn’t the case because some is converted to other short chain fatty acids).

So, we eat our half cup of cooked potato, and what do we get? We get almost three teaspoons of sugar and carb that convert almost immediately to glucose and head directly into the bloodstream. The blood volume of a person with a normal blood sugar contains about a teaspoon of sugar, which means that consuming the potato almost quadruples the amount of sugar in the blood. The pancreas then secretes insulin to drive this excess sugar into the cells. This extra insulin then does all the things excess insulin is famous (or infamous) for doing.

But what about the butyrate from the resistant starch? Oh yeah, the 2.3 grams of butyrate. I don’t see how the butyrate is going to do much to stop the insulin spike resulting from the ingestion of the sugars and starch from the non-resistant starch part of the potato. And even if butyrate really does all it is cracked up to do, we wouldn’t really need the potato with all its accessory easily absorbed carb because we can get the equivalent amount of butyrate from a single pat of butter. (Or almost the same – a pat of butter contains 1.45 g butyrate. Two pats of butter contain 3 g or about 1.5 times the amount generated by the resistant starch component of the potato.)

If the benefits of the resistant starch come from its conversion to butyrate as our RD avers, and if it requires the amount per day found in only one half cup of potato (or of the other foods she lists) as she also avers, then why not provide ourselves with one and a half times as much by eating a couple of pats of butter per day, which come without the extra three teaspoons of sugar? We get the butyrate without having to convert and we don’t get the extra carbs. Makes perfect sense to me.

Amazingly, our RD recommends adding the half cup of one of the resistant-fat-containing foods to the rest of whatever you’re eating that day. So, if you’re already on a ‘normal’ diet, i.e., one pretty high in carbs already, she is recommending that you add, say, a half cup of cooked potato to the mix so that you will ‘lose fat, reduce blood sugar, and lower insulin levels.’ Hmmm. Sounds a little snake oily. Sounds like she’s telling porkies.

While I’m at it, I have to mention one other little porky she tells during the interview. Says she

…and because resistant starch doesn’t get digested or absorbed it fills you up but you don’t get any calories from it.

Okay. Let me get this straight. First, she tells us that it converts to butyrate, a fat, which is absorbed and works miracles once it is absorbed. Second, she tells us that we don’t get any calories from it. Have I got that right?

She is correct in saying that resistant starch (as well as any other type of fiber) gets converted to short-chain fatty acids. And she is correct in saying that the short-chain fatty acids get absorbed. But when they do get absorbed, they contain 9 kcal per gram, just the same as any other fat. So they are not free of calories. That’s why fiber is counted in the total calorie count on nutritional labels. Fiber does make it’s way through the upper digestive tract without being absorbed, but it does get converted to fat and absorbed in the lower GI tract, i.e., the colon. So, I guess we could say she’s a fibber when it comes to fiber. At least in terms of its calorie content.

This brief discourse should put you off of resistant starch even without knowing what anti-nutrients are (resistant starch is an anti-nutrient), why they’re there and what they do. We’ll save that for a later post.

Now that you know the real story behind resistant starch, go back and watch the video to see how filled with misinformation it really is. Which also goes to show why you should never believe anything like this you see in a short spot on a news program without checking it out first.

Hat tip to Terry for sending me the video clip

Let’s engage in a sort of thought experiment. Let’s assume that way back in the early days of medicine doctors always wanted to see us cough up mucus from our lungs. Since mucus is a kind of breeding ground for all kinds of nasty bacteria, it would make sense in the olden, pre-antibiotic days to want patients to hack up as much of this stuff as possible to get it out of the body where the bacteria could no longer wreak their havoc.

Let’s assume that doctors of old–who didn’t realize that the excess mucus was the body’s way of ridding itself of something foreign, i.e., the bacteria or viruses causing the infection–started equating coughing up ‘healthy’ amounts of mucus with good health. It’s not too far a leap to imagine these doctors supposing that if they could get their patients to cough up stuff all the time, the respiratory system would stay clear of the mucus that harbors all the pathogens that cause lung problems. Druggists might come up with concoctions that would cause people to cough, even if they didn’t need to.

Now let’s imagine that the idea that coughing up large amounts of mucus-laden sputum reaches the point of a national obsession. People, especially the elderly for whom respiratory infections are much more dangerous, discuss with one another how much sputum they produce and how often. If they don’t cough as much or as productively as they perceive those around them are doing, they go to their doctors who prescribe a sputum inducing medicine for them. People everywhere are obsessed with keeping their respiratory systems clean.

Now, someone comes along and says, Hey, world, I’ve got the perfect product to keep everyone coughing productively. Use my product and before you know it you’ll be coughing your head off and ridding your lungs of all kinds of nasty junk. Here, try one of these. It’s called a cigarette.

In today’s modern world we all know what cigarettes do. The irritation of the smoke damages the lining of the tubes that carry air into and out of the lungs. As the damage continues, goblet cells (so called because they resemble little goblets), the cells that produce mucus, increase in size and number, producing more mucus to coat and protect the cells lining the airways. As the smoking continues, so does the damage, and so does the double duty of the goblet cells. Ultimately, in far too many people, the production of the protective mucus from the goblet cells isn’t able to keep up with the damaging effects of the smoke and cell injury occurs. As these cells are damaged, they cease to function properly, and ultimately die. They are then replaced by new cells, which themselves go through the same cycle. Somewhere along the way one of these cells, due to the damaging effects from the smoke, undergoes a malignant transformation and starts to reproduce itself. When this happens lung cancer is born.

We know what happens to the lungs with smoking. We know that all the coughing and mucus production isn’t a good thing–it isn’t protecting us from disease; it is the result of disease. But if we lived in a society that worshipped bringing up mucus every day, how long would it take us to figure out that smoking wasn’t particularly good for us?

Into this society of mucus lovers a researcher comes along and writes a paper showing how cigarettes cause an increase in mucus. He talks to the press and tells them about his research, saying, ‘I’ve now figured out how these wonderful cigarettes work to improve our mucus production. They damage the cells, which then make and release more mucus to protect themselves. It’s really wonderful how the body responds thusly. Now that we know how it all works, let’s go out and smoke even more.’

Preposterous, you’re probably thinking. Only if you live in a society that doesn’t worship regular mucus production.

We live in a society that worships regular bowel movements. Doctors for the last few hundred years have focused much of their effort in ensuring the regularity of their patients. Many people, the elderly especially, are obsessed with moving their bowels daily. Most people, if asked, would probably reckon that it’s not good to have fecal matter just sitting around in the colon. Get it out of there, they would say. It can’t be healthy. Just as it escaped the notice of our doctors in the scenario I imagined above that animals in the wild don’t bring up copious amounts of mucus daily, it has escaped the notice of doctors today that animals in the wild, especially carnivorous animals, don’t always have daily bowel movements, and that when they do, such BMs aren’t always huge and loose.

Into our bowel-regularity-worshipping society there has come a substance that ensures regularity. It’s called fiber. It is sold everywhere in diverse forms. All manner of ‘experts’ from our doctors to our grandparents encourage us to consume plenty of fiber. If we can’t get enough from the foods we eat to achieve regularity, we are encouraged to buy supplements. Everyone is on the regularity bandwagon and, by extension, the fiber bandwagon. The much despised Jane Brody has written countless times on the virtues of fiber, WebMD encourages us to get our share, even C. Everett Coop exhorts us to keep the fiber coming. And, despite numerous studies showing that fiber doesn’t really do squat for us healthwise, everyone continues to recommend it.

To paraphrase John Huston: Evidence? We ain’t got no evidence. We don’t need no evidence. We don’t have to show you any stinking evidence.

Into this society of bowel movement lovers a researcher comes along and writes a paper showing how fiber causes an increase in regularity. Our intrepid researcher’s name is Dr. Paul L. McNeil; he is a cell biologist at the Medical College of Georgia. I’ll let him tell how it all works.

When you eat high-fiber foods, they bang up against the cells lining the gastrointestinal tract, rupturing their outer covering. What we are saying is this banging and tearing increases the level of lubricating mucus. It’s a good thing.

Indeed?

He goes on:

It’s a bit of a paradox, but what we are saying is an injury at the cell level can promote health of the GI tract as a whole.

Really?

He goes on to explain that even though epithelial cells usually live less than a week, they are regularly bombarded, in most of us at least three times a day, as food passes by.

These cells are a biological boundary that separates the inside world, if you will, from this nasty outside world. On the cellular scale, roughage, such as grains and fibers that can’t be completely digested, are a mechanical challenge for these cells.

But in what he and colleague Dr. Katsuya Miyake view as an adaptive response, most of these cells rapidly repair damage and, in the process, excrete even more mucus, which provides a bit of cell protection as it eases food down the GI tract.

As reported in ScienceDaily

In research published in 2003 in Proceedings of the National Academy of Sciences, Dr. McNeil showed proof of his then decade-old hypothesis that cells with internal membranes use those membranes to repair potentially lethal outer-membrane injuries. A recent paper published in Nature in collaboration with Dr. Kevin Campbell’s laboratory at the University of Iowa showed how human disease, including certain forms of muscular dystrophy, can result from a failure of this mechanism.

An outer membrane tear is like an open door through which calcium just outside the cell rushes in. Too much calcium is lethal but that first taste signals the vulnerable cell it better do something quick. With epithelial cells, several of the internal mucus-filled compartments fuse together within about three seconds, forming a patch to fix the tear. In the process the compartments expel their contents so, almost like a bonus, extra mucus becomes available to lubricate the GI tract.

And a final telling paragraph.

The scientists aren’t certain how many times cells can take a hit, but they suspect turnover is so high because of the constant injury. Potentially caustic substances, such as alcohol and aspirin, can produce so much damage that natural recovery mechanisms can’t keep up. But they doubt a roughage overdose is possible.

(You can click here to read this study in its entirety in PLoS Biology)

So, we have a situation where a product causes damage to the cells lining a tube, causing them to produce a lot of mucus in an attempt to protect themselves. In the process many of these cells die and are replaced by new cells. And this is perceived as a good thing.

My question is: is it really a good thing?