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.

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

Let’s first take a look at the reporting.

The lede from MSNBC:

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

The headline from Fox News:

Study: Cholesterol Drug Causes Risk of Heart Attack to Plummet

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

Cholesterol-Fighting Drugs Show Wider Benefit

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

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

Cholesterol Drug Cuts Heart Risk in Healthy Patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

A couple of times per year my friend puts on seminars for people wanting to learn about how the media work. He invited me to one a few years ago in Las Vegas, and I can tell you, it was an eye-opening experience. The program started with my friend asking the attendees to write a few sentences describing what they thought constituted ‘news.’ Before you read on, stop for a moment and come up with your own definition of news. Have you got it? At this meeting virtually everyone (including yours truly and his lovely wife) came up with something on the order of: ‘News is when something happens of sufficient importance to the readers or viewers of a particular media format in a defined local (could be local – could be national) that it requires reporting.’

My friend gathered the papers and started reading them to the group. One after the other was a variation on the theme above. After he had read a dozen or so, he looked at the crowd and said: “Let me define news for you. News is what the media wants you to know.”

In the previous post I wrote the media wanted you to know that the Atkins diet was dangerous, so that’s how they reported it. A reported went in to an oral poster presentation, a tiny sub-meeting of the larger overall meeting, and reported on non-peer reviewed data in such a way as to make a perfectly safe and sensible way of eating, practiced by literally millions of people over the last 30 years, appear to be a danger to health. That’s news because that reporter and his editors said it was.

I’m stressing this because the American Heart Association (AHA) also reports the news, which, in its case, is what it wants people to know. The AHA has an entire publicity arm that sends reports out to doctors all over the world telling them what the AHA wants them to know. And guess what? In none of these reports is the study on the Atkins diet mentioned.

I got these reports by email for every day of the conference. You can click on them by day – Sunday, Monday, Tuesday and Wednesday – to see what the AHA wanted doctors interested in this conference to know. If you burrow down into all the links and follow where they lead, you’ll find that none of them (at least none that I could find) lead to the Atkins diet presentation. Probably because the study wasn’t very important relative to the others, and because any one with a modicum of scientific understanding would see right through it.

But not the public. Members of the public aren’t trained to even find the relevant study much less analyze it critically. So that’s where the reports were sent. To the public. Not to the doctors. I find it interesting to say the least.

One other thing, then we’re through with this travesty of a study. A number of people wrote comments wondering about the inflammatory markers that went up in the folks who went on the pseudo Atkins diet. Here is the full text of a study done by Jeff Volek and his group at the University of Connecticut showing that real low-carb diets bring about a decrease in inflammatory markers. And here is another demonstrating that real low-carb diets bring about improvements in atherogenic lipid profiles in subjects who do not lose weight. So, it’s the diet that does it, not the weight loss that usually accompanies such a diet.

Today I’ve been inundated with comments, emails and even a phone call or two about the ’study’ that hit the news this morning allegedly showing that the Atkins diet causes blood vessel damage, and increase in ‘bad’ cholesterol and increased levels of inflammation. I figured I would take this opportunity to describe how this kind of information gets out there and discuss this ’study’ in particular.

To begin with, this isn’t really a scientific study published in a peer-reviewed journal. It was a brief presentation (about 15 minutes including questions) made at the annual scientific meeting of the American Heart Association in Orlando, Florida a couple of days ago. To better understand where presentations like this one fit in the hierarchy of the scientific world, let’s take a look at how these huge meetings are organized.

The annual Scientific Sessions of the American Heart Association is an enormous meeting with thousands and thousands of attendees. This year’s meeting, which is still going on, is being held at the giant convention center in Orlando, Florida. When the organizers of these kinds of meetings start working on putting them together – which they do years in advance – they begin to contact all the big guns for the major lectures. These lectures are presented during the prime times of the conference when nothing else is going on and they can be attended by all attendees. These lectures held in the huge auditorium are usually by well-known, established researchers who present the data from many years of their work on specific inquiries.

Scheduled in around these giant lectures are concurrent meetings, which are held in small conference rooms holding 50-60 or so people. (The photo at the top of this post shows the typical size of one of these sessions) These smaller lectures compete with other lectures taking place at the same time. Usually there are four or five sessions going on at once, which is a major pain if you’re an attendee because invariable two lectures you want to see are going at the same time. (Fortunately, in our case, MD can go to one and I go to the other, so it’s not so bad.) These lesser presentations are often, but not always, made by graduate students or newly minted Ph.Ds or physicians doing postdoctorate work.

At the bottom of the food chain in terms of importance are the poster presentations. These are usually held in a large room and involve a bunch of people with posters describing work that they have done or research in progress.

In between the poster presentations and the concurrent lectures are oral poster presentations. These are lectures about work in progress or small or preliminary studies that have been done but haven’t been published. The ’study’ in question is an oral poster presentation.

When the organizers of these meetings are in the preparation stage they send out a call for abstracts. They get inundated with abstracts and arrange them sort of in terms of significance with the most interesting or scientifically significant ending up being presented as a concurrent lecture. The next down the list are the oral poster presentations, then finally the posters.

The important thing to understand about these presentations is that they are not peer reviewed as they are if and when they show up in a scientific journal. They are sort of peer reviewed on the spot in the sense that other researchers familiar with the specific field ask questions of the presenters or of the people with the posters. But that’s it. There is no scientific review of the data as there is when it is published in a journal. So people can present all kinds of data with no one looking it over other than the folks who ask questions. And sometimes the exchanges at these meetings can become spirited to say the least, which means that those lecturing are often present data much at odds with what other scientists have found doing the same kind of studies. That’s why it’s always good to take anything that comes from a meeting like this one with a huge grain of salt.

If you take a look at the monster program for the 2007 Scientific Sessions of the American Heart Association (click here) you can find the presentation in question on page 407. It is session #3610. You should roam through this program a little just to get a feel for the scope of a meeting of this size and to see just how much is going on at once, which puts perspective on any given oral poster presentation.

These giant meetings are open to the press, members of which get these huge programs just as do the scientific attendees. The folks with press passes go through these programs looking for lectures that they think will give them a headline. They don’t care how insignificant the talk is, who is giving it, whether it’s a poster or an oral poster presentation – they are looking for headlines. And what better headline than that there is a problem with low-carb diets or even better, the Atkins diet itself.

So the stage is set. I would imagine that of the 30 or 40 people (if that many) who attended this talk a large number had press passes. These media types stay after and talk to the speaker to get a few quotes, then head off to the press room, dash off a few hundred words, send it to their service, and head back off for another headline-grabbing talk (or the bar).

Now that you know the genesis of the news report about this oral poster that many of you have read and maybe worried about, let’s take a look at the study itself.

I emailed the publicist for the University of Maryland Medical Center for an abstract of this talk, and he kindly sent it to me within minutes. (I’ve converted it to PDF for you: miller-2007-aha-abstract-diet.pdf.) Remember, this is all there is. Just an abstract, not a real paper. We can tell only a little about what really went on in this study. But let’s take a look.

The people doing this study were obviously tired of hearing about the supremacy of the low-carb diet as a weight-loss tool, and they probably didn’t want to do yet another study comparing the low-carb diet to the low-fat diet for weight loss or lipid improvement or blood sugar normalization or blood pressure lowering because they knew what that outcome would be. Those studies have been done again and again and the low-carb diet always comes out on top. So, these researchers decided to take a different tack.

They wanted to see what happened when subjects stayed on the diet after reaching maintenance, so they took 18 subjects (they started with 26, but only 18 made it through the entire study) and put them on one of three diets: the Atkins diet, the Southbeach diet or the Ornish diet. The subjects stayed on one of these diets for 4 weeks, then followed their normal diets for 4 weeks, then went on another of the three diets for 4 more weeks, then off for 4 weeks, then on to the last of the three diets for 4 more weeks. But the researchers didn’t put the subjects on the weight-loss versions of these diets, they put them on maintenance versions. They did this by weighing the subjects at the end of each week and adjusting their caloric intake so that they neither gained nor lost weight.

By keeping the weight of the subjects stable, any changes wrought by the various diets could be attributed to the diet and not to the lost weight. Many people believe the changes brought about by low-carb diets occur not because of the diet but because of the weight loss the diet induces. And since in most studies subjects on the low-carb arm lose more weight than those following low-cal diets, it seems reasonable to suppose that it is the lower weight and not the diet composition that results in the better lipids, normalized blood sugars and lowered blood pressure commonly seen in the low-carb group.

In this case the weights stayed the same for all the subjects during the various diets, and as you can see from the abstract, the LDL levels went up (although not significantly) in the Atkins group while LDL levels dropped in the other two groups. The abstract says that the researchers drew blood at the end of each 4 week phase on the different diets, and I assume that they also drew blood at the start of each 4 week dietary trial, but the abstract doesn’t say. For all I know, they could have drawn blood for baseline values at the very start of the study and compared the lab values at the end of each 4 weeks to this baseline number, which would make the later numbers suspect. This is one of the problems with ’studies’ like this one. These questions would all have to be answered before such a study could be published in a peer-reviewed journal. But in a conference, pretty much anything goes. It would be left up to an attendee to ask such a question.

Along with the LDL levels, the researchers also looked at a number of fairly arcane measures of inflammation: ICAM2, SELL and SOD1. As far as I know, these are not lab studies that the average doctor can order, but are ones that are done in research facilities for research purposes. In any case these indicators went up on the Atkins diet and stayed the same on the Southbeach and Ornish diets.

Finally, the researchers performed a brachial artery reactivity test (BART), which is a somewhat controversial but nevertheless commonly used test to measure endothelial function. (About halfway this old post is a description of how BART works. If you want a more detailed explanation with a discussion the controversial nature of the test, read this full text article.) As to the outcome of BART, the abstract simply reports the following:

BART testing revealed a significant inverse correlation between flow-mediated vasodilation and intake of total fat, saturated fat and monounsaturated fat.

We’re not told if this correlation holds irrespective of which diet the subjects were following or if these were the numbers while they were following the Atkins diet. From the wording of the abstract one would have to think that these values were reported for all the diets. If so, then the researchers have extrapolated from these numbers that the Atkins diet causes more endothelial dysfunction simply because it contains more fat and certainly more saturated fat than the other two diets.

Based on the abstract we find that

In the absence of weight loss, the high fat Atkins diet is associated with increased LDL-C, reduced endothelial vasoreactivity and increased expression of biomarkers of atherothrombosis. As such, these data suggest that isocaloric conversion to the Atkins diet may negatively impact cardiovascular health as compared to the South Beach or Ornish Diet.

Now, let’s probe a little deeper. And we don’t have to get very deep to see a major flaw in this study.

Before we get to the major flaw, though, let’s look at the LDL changes. As far as I’m concerned, they are a big Ho Hum. I mean, who really cares? How many studies do we have to look at to know that when you cut fat from the diet LDL levels decline? We already have dozens showing us this same finding. Dozens of other studies show us that when fat, particularly saturated fat, is increased in the diet that not only do LDL levels rise a little but HDL levels rise a lot. (I posted about this in the past.) So what little risk we might seem to accrue because of increased LDL levels is more than offset by the greater increase in HDL levels. It even gets better. The majority of studies have shown that when LDL levels increase due to high-saturated-fat, low-carb diets, the LDL particle size increases, making the LDL non-atherogenic. And while LDL levels fall with low-fat, high-carbohydrate diets, the LDL particle size decreases and becomes the small, dense type, which is highly associated with cardiovascular disease.

So, this study tells us that when the subjects went on the Atkins diet their lipid profiles actually improved as compared to the other two diets. Why didn’t the researchers just say that? One wonders. One also wonders why – if they went to the trouble and expense to check ICAM2 and the other markers of inflammation – they didn’t bother to check HDL levels or LDL particle size, especially since LDL particle size is lipid parameter that has the strongest correlation to the development of cardiovascular disease.

Back to the major flaw. The abstract doesn’t say how much these subjects weighed. So we can only assume. Let’s assume that they were average weight and required 24oo kcal per day to maintain their average weight. While these subjects were on the Atkins diet part of the study the abstract tells us that they were consuming 50 percent of their calories as fat. Let’s think about this for a minute and do a few back of the envelope calculations. Fifty percent of 2400 calories is 1200 calories. So 1200 calories were fat and 1200 calories were other than fat. Since other than fat means carbs and protein, that means that the other 1200 calories were divided between these two macronutrients. If we assume that 20 percent of calories were protein that calculates out to about 120 grams of protein per day, which is a fair amount and probably more than they actually got. But let’s assume 20 percent. That leaves 30 percent of calories as carbohydrate. Thirty percent of 2400 kcal comes out to 720 calories as carb. And since a gram of carb is 4 calories, dividing it out gives us 720/4 or 180 grams of carb per day. Does that sound like the Atkins diet to you?

Let’s give the researchers the benefit of the doubt and say that they had the subjects on 30 percent protein (180 grams), which I doubt because they would have been scared to death to give someone 180 grams of protein. But let’s assume they bucked up and did it. Running the same calculations on 20 percent of carbs gives us 120 grams of carbs per day – that’s a full 24 teaspoons of sugar’s worth of carbohydrates per day. Or two potatoes and a serving of pasta. Is that the Atkins diet?

See what I mean. It was a flawed study. I already linked to this post above, but it discusses the same issues, i.e., blaming a lab finding on saturated fat when the diet is full of carbs.

What do we care that a low-carb diet showed an increase in inflammation and worsening endothelial function when what was tested wasn’t really a low-carb diet?

In summary: no complete study, no peer review and no Atkins diet. Yet it made the news big time.

Now that you know the story, go back and read the press report of this oral report of a poster. See if your take home message is any different now.

Oh, and one other thing. According to the abstract the study started out with 26 subjects, but only 18 completed it. That’s a dropout rate of over 30 percent. One wonders why these subjects dropped out? And from which dietary protocol? It would be interesting to know, but I can make a pretty good guess.

The April 2007 issue of Annals of Nutrition and Metabolism includes an article on the positive changes in inflammatory markers brought about by the intermittent fasting Muslims undergo during Ramadan.

As the authors put it in the introduction:

Intermittent fasting over a certain period of time is a feature of great religions all over the world and it is well known that nutritional habits, sleeping patterns and meal frequency have profound effects on maintaining human health. One of these fasting ceremonies is Ramadan. Ramadan is a religious month during which over one billion Muslims worldwide refrain from eating and drinking during the daylight hours for 1 month. The duration of restricted food and beverage intake is approximately 12 hr/day for 1 month, which makes Ramadan a model of prolonged intermittent fasting.

The authors are right in that Ramadan is a model of intermittent fasting with a host of subjects to pick from. I’m not sure that 12 hours of food abstinence a real intermittent fast makes, but it is a lot longer without food than the vast majority of us go for a month at a time. There is usually a pre-dawn meal that must be consumed before the sun rises and a post-fast meal that starts after sunset. I’m sure that Muslims don’t eat all night long during Ramadan, so I would venture that every 24 hours is made up of 12 hours without food, a few hours of eating before bedtime, sleep, then a meal in the pre-dawn hours. I would guess that there would be a total of maybe 5 hours during which people eat and 19 hours of each day in which they don’t. And for data gathering purposes, it’s nice that this schedule is maintained for an entire month. Since this fasting is a strong religious tenet for a group of people who take their religion very seriously, the data obtained from Ramadan fasting studies is probably much more valid than that obtained from typical volunteer subjects.

In this study 40 healthy, normal weight men and women aged between 20-39 years who underwent Ramadan fasting were compared with a group of 28 similarly aged men and women who did not fast. Data derived from questionnaires indicated that the majority of the fasting subjects ate their last meal between 1-2 AM and their first meal after the fast at around 6:30 PM, which means that most fasted for around 16 hours. (I assume that these subjects did not consume a predawn meal, eating late and preferring to sleep in instead.) The non-fasting subjects ate breakfast, lunch and dinner at regular times. Researchers collected twice-daily blood samples 1 week before Ramadan, during the last week of Ramadan, and 20 days after Ramadan.

Interestingly there was no difference in energy intake and no weight loss difference between the two groups. Apparently the fasters made up for lost time when they chowed down and ate as much as those who ate three squares throughout the day.

…average daily energy and water intake remained comparable in both the fasting and nonfasting group and the working hours of both groups did not change during the whole study. During Ramadan, in the fasting group, meals were taken exclusively at night while in the nonfasting group there was no change in the eating and sleeping habits. …the sleep pattern of the fasting group was delayed by approximately 2-3 h[ours] on average. The energy and the water balance seemed to be constant on a daily basis as the body weight and the 24-hour urinary volumes did not change during Ramadan. Hence there were two major changes in the routine of the fasting subjects: meal times and sleeping patterns.

What did the study show in terms of inflammatory response?

There were significant reductions in interleukin-6 (IL-6), C-reactive protein (CRP) and homocysteine during the fast that, in the case of IL-6 and CRP, lasted for at least 20 days beyond the fasting period.

What does this mean?

In short it means that the Ramadan intermittent fast brought about a significant decrease in inflammation.

IL-6 is a proinflammatory substance released by macrophages and other inflammatory cells that reaches the circulation and ultimately the liver. A number of studies have shown that about 30 percent of IL-6 comes from adipose tissue, especially abdominal or visceral adipose tissue (or more correctly, from the macrophages and other cells of the innate immune system that attack these fat cells). When IL-6 levels are high enough they stimulate the acute phase response in the liver. During the acute phase response the liver releases a number of proteins -including CRP- into the circulation. The job of these acute phase proteins is to prevent ongoing tissue damage, isolate and destroy the infective organism (or, in the case of visceral fat, the invasive organism) and activate the repair processes necessary to restore normal function. CRP is an acute phase protein that binds to certain sites on microbes, probably assists in the helping other parts of the immune system attack foreign and damaged cells, and enhances the consumption of these cells by the macrophages. CRP is an important player in the innate immune response, which is the blind, hardwired early responding part of our immune system.

Both IL-6 and CRP are elevated during inflammation, and both, but particularly CRP, are used as markers for inflammation. There is now a large amount of data showing that elevated CRP levels are a potent risk factor for cardiovascular disease.

The decreased levels of homocsyteine during fasting are an intriguing phenomenon. Homocysteine can react spontaneously with many biologically important molecules, especially proteins. It can react with and cause damage to the folding of important proteins, i.e., enzymes, immune proteins, receptors, growth factors, and structural proteins, leaving them with a configuration that is less than optimally functional. High homocysteine levels cause oxidative damage and are thought to cause inflammation, especially in the endothelium. As a consequence, elevated homocysteine levels are, like CRP, a fairly potent risk factor for cardiovascular disease.

Homocysteine is an intermediary in the metabolic pathway between methionine and cysteine, both important amino acids. Folate and vitamin B12 are essential in making the transition from methionine to cysteine without allowing large amounts of homocysteine to stack up. A deficiency of either folate or vitamin B12 (both B vitamins) allows an increase of homocysteine, which makes it’s way into the circulation and causes problems. What makes this study so interesting is that both folate and vitamin B12 levels increased substantially in the fasting subjects despite their not eating any more food containing these substances than the nonfasting subjects. It’s this increase of the folate and B12 that more than likely decreased the levels of homocysteine in the fasting subjects.

The authors speculate:

…both folate and vitamin B12 levels were increased in the last week of Ramadan in the fasting subjects and a negative correlation has been detected between these two vitamins and homocysteine levels. None of our subjects used any kind of vitamin supplements and according to the questionnaire, consumption of food containing B vitamins did not change during the whole study period. The changes in the rest-activity cycle and meal schedule during Ramadan may beneficially affect the bioavailability or redistribution of cofactors like B vitamins in the methionine pathway, which in return may lower plasma homocysteine levels. These results are consistent with [a] previous study in which homocysteine levels but not B vitamins were evaluated in the fasting subjects during Ramadan.

This ‘bioavailability’ and/or ‘redistribution’ is similar to that which happens with vitamin C during an all-meat diet. It is well known among arctic explorers that those on diets of nothing but fresh meat don’t get scurvy. The British sailors in the 1700s who were afflicted with scurvy consumed a diet composed primarily of carbohydrates. When British naval surgeon James Lind gave them fresh lime juice their scurvy was cured or prevented. As we all know now, the cure and prevention came about due to the vitamin C in the lime juice. Most researchers and physicians still believe that diets deficient in vitamin C will cause scurvy, but this isn’t the case, especially with fresh meat diets. The glucose molecule competes with the vitamin C molecule for entry into the cells. When glucose molecules are high – as they are in high-carb diets – much more vitamin C is required to compete with the glucose and actually make it into the cells. During all-meat diets, glucose is low, and a much smaller amount of vitamin C can still enter the cells and do its job.

Whatever the case, fasting reduces the levels of homocysteine, which is a very good thing.

Below are the charts showing the reduction of IL-6, CRP and homocysteine in the fasting subjects.

IL-6 Males

IL-6 Females

CRP Males

CRP Females

Homocysteine Males

Homocysteine Females

This study adds to the data showing that intermittent fasting does indeed reduce inflammation. Whether the reduction comes from the long period without food or from the change in sleep patterns the study doesn’t show. But I think it’s reasonable to assume that it is probably the former rather than the latter. Reduction in sleep time all by itself has been shown to be inflammatory, so I would guess that were these subjects to have maintained their regular sleep patterns and fasted fasted, they would have shown an even greater decrease in inflammatory parameters. But that is speculation; we’ll have to wait for the real data.

This paper confirms for me the idea of not eating between meals and not consistently snacking as some would recommend. I like to let things rest totally between meals and not nibble, even on low-carb snacks. Based on the intermittent fasting data that is rapidly accumulating, I think that eating as infrequently as possible is probably the best bet to keep your innate immune system behaving as it should, especially if you follow a higher-carb diet.

On the flight from London to Rome I read an article on the immune system and cancer. It got me to thinking about the immune system and a whole lot of other health problems.

It’s sunrise in The Eternal City right now. I’ve been up early watching the dawn break over St. Peters, which is a couple of miles below the hotel. I figured everyone was getting tired of travel disaster stories, so I thought this would be a good time to sketch out my views on the inflammatory basis of heart disease.

If you read enough in the medical literature you will perceive a change in outlook on the underlying cause of many of the so-called diseases of civilization, especially heart disease. Most authors – mainly, I suspect, out of desire to keep their academic positions and reputation with their peers – throw a bone to the lipid hypothesis before admitting that it probably isn’t the only cause of coronary artery disease. Over the last decade or so the progression has been thus: elevated cholesterol causes heart disease – elevated cholesterol and maybe a little inflammation cause heart disease – elevated cholesterol and inflammation cause heart disease – inflammation along with elevated cholesterol cause heart disease – and now, among the more enlightened – inflammation causes heart disease. In my opinion, it probably is inflammation by itself that is the driving force behind the development and progression of most cardiovascular disease.

When the cholesterol-causes-heart-theory was in its infancy the question became ‘what causes cholesterol levels to go up? Of course this question led to the anti-saturated-fat hysteria that pretty much still has us by the throat. But the same question needs to be asked of anyone who claims inflammation to be the cause of heart disease: What causes inflammation?

Before we address that issue, let me add that in much the same way saturated fat has been demonized as a cause of almost everything, inflammation is thought to be the catalyst for much more than simply heart disease. There has grown up a theory called the ‘common soil’ theory that implicates inflammation as the underlying problem, or the ‘common soil’ from which spring heart disease, diabetes, obesity and the other diseases common to modern man.

No one much talks about the cause of inflammation – most seem to think it is a natural part of the aging process. As we all get older, we become more inflamed. As we become more inflamed, we tend to develop heart disease, diabetes, etc., all of which are diseases that usually strike later in life.

I have a little different opinion.

Before I can argue my theory, I have to make sure we’re all on the same page about what inflammation really is.

Inflammation can’t be understood without at least a rudimentary understanding of the immune system, specifically the innate immune system, so let’s start there.

We humans along with the rest of the animal kingdom have two immune systems: an innate immune system and an adaptive immune system. The adaptive immune system is the more sophisticated of the two, and it’s the one that seems to have inspired the most research interest. The adaptive immune system is the one involved when you have hay fever, an allergic reaction, or get an immunization. It is the immune system that gives you resistance to measles or mumps once you’ve had them. It is the part of the immune system that remembers and can mobilize vast forces quickly when it discovers an invader that it has seen before, say, the measles virus. It is programmable by what it has dealt with before. The TSA would be comparable to the adaptive immune system. After we were inoculated by the events of 9/11, we grew our national immune system to protect against a threat we didn’t know existed until it hit us.

The innate immune system is a different animal. The innate immune system is a primitive, hard-wired immune system that reacts the same way to every threat. Unlike the adaptive immune system that takes a while to activate and get responsive, the innate immune system is always on the prowl and acts immediately. To carry the 9/11 metaphor further, the innate immune system was what acted immediately after 9/11: all flights canceled, all airports patrolled, no cars could stop, etc. It was an immediate, knee-jerk response to an unknown threat.

The innate immune system is pretty much the same. It lays in wait for any invasion and reacts immediately while the adaptive immune system is just getting out of bed.

If you are an animal in the wild or a Paleolithic man (or woman) and you want to survive, you’ve got to worry about two things: infection and trauma. You can get a virus, fungal or bacterial infection or you can get seriously injured. Both can do you in. The innate immune system was evolved to deal with both. (You can also starve, but that’s another matter. Starvation doesn’t happen to you in the same way infection and/or trauma do. Starvation is a prolongation of the typical feast/famine cycle, and is dealt with hormonally in ways we’ve discussed in previous posts. Plus it takes a lot longer to starve to death than it does to be killed by infection and/or trauma. The innate system deals with immediate threats.)

The innate immune system protects you against infection and trauma. It works the same for both. If you get a cut, throngs of immune cells make their way to the cut almost immediately. They begin sending signals putting out the call to other immune cells to head for the injury and join the fray. The blood clotting system is revved up to minimize blood loss. Any bacteria that enter the cut are immediately swarmed on, surrounded, and killed. The area becomes red, swollen, and painful. It is hot. All of which are the cardinal signs of inflammation known since ancient times: rubor, calor, tumor and dolor. Redness, heat, swelling and pain.

If the infection or trauma is serious enough, the cells of the innate immune system signal to the liver for help. The liver springs into action by what is called the acute-phase response, which is the production and release of even more substances to help deal with the threat.

As the injury or infection is dealt with, the innate immune system completes its work and fades into the background, lying in wait for the next exposure.

The innate immune response is something you’ve got to have to survive, but not something you want actively working all the time. You want it when you need it, but you want it to stay in the background when you don’t.

Problem is that the innate immune system can be chronically active, and when it is, you have a set up for heart disease: increased blood clotting, inflammatory cells and their products attacking blood vessel walls, the liver drifting into and out of the acute-phase response, etc. In other words, the lab picture of someone who has heart disease.

But why does the innate immune system become chronically active instead of just springing into action when needed?

What follows is my opinion and is purely speculative. But I think it makes sense.

We know the innate immune system is primitive and primed for action against infection and/or trauma. It’s the only immune system we have with first-strike capability and is primed for any immediate threat.

We now have a threat we didn’t have during our Paleolithic days. Now we have the threat of overnutrition. We are eating types of foods we didn’t eat in the past and in amounts we didn’t eat in the past. This overnutrition is a threat to our survival and it stimulates an innate immune response because that’s the only response we have. The innate immune system senses danger, reacts, but unlike the cut that heals or the bacteria that gets destroyed, the overnutrition continues. So the innate immune system remains chronically active.

Let me give you one example before I end this already overlong post. (You’ll be begging for more travelogues and tales of airline snafus after this)

When we overeat, the body has to dispose of the excess calories. (I’m talking about the typical high-carb overeating here.) The logical place to stuff them is into the fat cells, which is the first place they go. They go into the subcutaneous fat, the fat under the skin, but outside the body cavity. This is the place nature intended excess fat to go. Subcutaneous fat isn’t particularly aesthetically pleasing, but it’s also not particularly unhealthful. It’s fat where fat is supposed to be.

When the subcutaneous places to store fat are filled (or, for example, when fructose is a large component of the diet) the excess calories go looking for other storage places. The next place these calories go is into fat inside the body cavity – around and within the organs themselves. This is not a good place for fat to be.

The innate immune system regards this fat – called visceral fat – as a foreign invader and attacks. Multiple studies have shown that visceral fat is crawling with macrophages, one of the foot soldiers of the innate immune system, whereas subcutaneous fat isn’t. Once these macrophages invade the visceral fat, they begin signaling – as is their wont being on the front lines of the innate immune system – to other macrophages to join the battle. They also release toxic substances to damage and kill the foreign invaders. These substances reach the blood and are carried throughout the circulation.

Normally these macrophages and other cells of the innate immune system do their jobs, getting rid of the invaders, and mopping up. In the case of visceral fat, the fat just keeps on coming. And the innate immune system keeps on working. And the heart and blood vessels keep on getting damaged.

But it’s not just overnutrition in terms of overeating; it’s also overnutrition in terms of constants eating.

Overeating leads to the fat accumulation that stimulates the chronic inflammation, but simply eating does it as well. Eating is an inflammatory process. A number of scientific studies have shown that eating a meal, regardless of the macronutrient composition, causes acute inflammation, which makes sense when you think about it. Food coming into the body is a foreign substance that fires up the innate immune system – but it does so briefly until the food is digested and the various fats, proteins and carbohydrates are broken down into their basic units and absorbed into the blood stream. (Although it might seem strange that food that we absolutely need to live could cause inflammatory problems, it makes sense when you realize that the very oxygen we breathe and that we would be dead in about four minutes without is slowly killing us also.) When the average American noshes along throughout the day snacking on first this then that the inflammatory response becomes chronic.

Over the past couple of decades just two of dietary changes – eating more and eating more often—have led to a state of chronic inflammation. The changes in diet composition have had an additive effect as well. Numerous studies have shown that while carbohydrates in general cause more of an inflammatory response than other macronutrients, fructose specifically causes the most rapid and intense inflammatory response of all. Polyunsaturated vegetable oils of the omega-6 variety (the majority) are inflammatory, trans fats (all of which start out as vegetable oils) are the worst, and most of the fat of animal, fish and dairy origin are actually anti-inflammatory. Sadly, we’ve been busy replacing the latter with the former. We find ourselves as a nation in the situation where most of our population is overfed the wrong kinds of food all too often with resulting high rates of obesity and chronic inflammation.

This post will probably raise more questions than it answers, which is good. I’ll expand on these themes in later posts and flesh out my ideas a little more.