Thursday, March 31, 2011

Another warm sunny day; another sweaty run. I did register for that trail-race in the state park this Sunday, and I even convinced one of my running buddies to register for it too. I'm sure it's not going to be easy, but I'm feeling a little excited about making the commitment. Signing up for these things gives you a new sense of focus, which was most welcome in my case, as I had been feeling a little out of focus lately.

If a disease is purely genetic, then identical twins (who carry identical genes) should both get the disease, if either of them get it. But often that is not the case: having an identical twin with the disease only gives you an increased risk, not a certainty, of developing the disease yourself. In other words, your genes are making you susceptible to the disease, and if the wrong things happen you will fall victim to that susceptibility. But you might not.

Type 2 diabetes is like that: having an identical twin with the disease puts you at a high risk of developing it, but you aren't sure to develop it.

How does that work, exactly? Presumably the genes associated with Type 2 diabetes predispose your body to react in a certain way to a condition which you may or may not experience -- not necessarily obesity, though that seems to be a factor. Perhaps there are many different possible triggers for the development of Type 2 -- exposure to a particular virus, for example, or some kind of severe stress, or some factor which no one has yet imagined.

Greatly complicating the genetic issue in diabetes is the large number of different gene mutations that have been found to be strongly linked to Type 2 diabetes. These are not rare mutations by any means, and different people have different combinations of them. Probably the reason Type 2 seems to be a different problem for different patients is that different patients have a different assortment of the genes involved.

Here's one, for example: the gene known as INSR, on the 19th chromosome:

The code contained in the INSR gene is used by a cell to create insulin receptors on the exterior cell wall, so that the cell can be stimulated by insulin and respond appropriately. A particular defect in the INSR gene causes a particular defect in one little section of the protein for the insulin receptor (that section is shown in green in the picture below).

[Sorry, Doug -- I know I shouldn't have pulled that on a loyal reader with red/green color blindness.]

Obviously, any defect in insulin receptors is a potential cause of problems in blood-sugar regulation. Having this defect increases your risk of developing Type 2 diabetes. But it's just a risk factor; you might have the genetic defect and not develop the disease.

The thing is, the INSR gene is just one of many genes that have a bearing on blood sugar control, and quite a number of these genes have commonplace defects which can increase your risk of developing diabetes. There are genes that relate to production of insulin rather than response to insulin; other genes relate to glucagon receptors, or to fat metabolism, or to signaling within cells. Most people with diabetes are probably carrying a large number of these genes; each one adds only a small risk, but they add up. People who carry few or none of these genes will, presumably, not become diabetic, no matter what happens to them or what habits they adopt. People who carry most or all of these genes are going to have a hard time avoiding diabetes, and perhaps a hard time controlling it, too.

However, based on the evidence of identical-twin studies, your genetic burden does not have to be the absolute arbiter of your fate. Knowing that you are more vulnerable to a problem than other people are means that you need to be more careful about that problem than other people are, not that you need to be more depressed about that problem than other people are.

It's hard to make people understand this, though. People like to think that their future is written in their genes, that the game was over at the moment of conception, and that deck is now stacked so heavily against them that they can't hope to do anything about it. Which is, of course, a textbook example of a self-fulfilling prophecy. When you're trying to settle an uncertain issue once and for all, there's nothing quite like giving up.

We know that, among people carrying the same genes, some develop diabetes and some don't. We also know that, among people who actually develop diabetes, some do well and some don't. So maybe, even after the genetic factors are thoroughly accounted for, it still matters what you do.

To put it another way:
Genes, schmenes! What's the difference so long as you're healthy?

Wednesday, March 30, 2011

Okay, now I'm energized. Not only is it still sunny, now it's downright warm (it got up to about 84 this afternoon). Today was the first time I wore a sleeveless running shirt in a long while. I don't know why, but sweating heavily during a warm-weather run seems to give you a better runner's high afterwards than you can obtain by running in cool weather.

After work, I ate dinner outdoors, sitting in dazzingly sunshine on a balcony overlooking a golf course.

Somehow, the high temperatures today seemed to flip a switch inside me, and all of a sudden I'm feeling invigorated. Lately I have been slipping back into my old feeling of being an impostor in the world of athletic activity -- a weak middle-aged guy forcing himself to perform an unconvincing imitation of running. Now, all of a sudden, I'm feeling as if I legitimately belong to the subculture of running. I felt an urge to do something to nail down that feeling, so after dinner I did what all runners do to prove to themselves that they're real runners: I drove down to the Heart & Sole store and bought some expensive running shoes.

Okay, so now I'm set. I guess the next step is to sign up for some races. 

I used to make a point of signing up for a race or other organized exercise event at least once every month, but I haven't participated in any such event since the 8.5-mile Apple Hill Harvest Run back in November. Of course, that particular event, which took place during a steady downpour, served as an excellent reminder of the reason why most people don't like signing up for such events during the rainy season. Paying a non-refundable registration fee for a run, not knowing what the weather will turn out to be like on race day, takes more faith than a lot of us have.

There are two half-marathons (that is, 13-mile races) coming up in May and July which I'm planning to do, but today I thought I'd look into something coming up a little sooner. I found one possibility: a long trail-run, this coming Sunday, which consists of two laps on a very rough and hilly 7-mile course:

It's a familiar course to me; I run those trails all the time. I'm not sure I'm ready to run that course twice in a row, but the rules for this race allow you to run it as a relay, with a partner taking the second loop. I think I've got one of my running buddies at work interested in doing it with me on a relay basis. I'm sure I'm fine with running one loop, if he's willing to do the other.

You could ask, of course, why there is any point in participating in organized running events, when I'm always running anyway, and sometimes I'm running long distances, and I'm not nearly fast enough to be a serious competitor. Well, there is a particular kind of excitement that comes from participating in a big race, which you can't quite achieve when you're running alone or running with just a few friends. Also, the fact that it's a race forces you to do your best to run faster than you normally do, so the exercise is more intense than usual. Anyway, it's nice to feel part of something, and races give you that feeling. Maybe the reason I've been feeling like a faker lately is that I haven't been in any races lately.

Well, I'll just have to fix that!

Tuesday, March 29, 2011

Another day of beautiful weather, and another hilly run designed to give us nice views of the valley to the west, now that the air is so clear.

The weather was a bit warmer today -- in the mid 60s. And it's forecast to be at least 80 tomorrow, so maybe it's time for me to break out the summer running clothes.

Today I was thinking about unforeseen consequences.

In 1961, Edward Lorenz (the meteorologist, mathematician, and pioneer in the field of "chaos science") was working on a computer model designed to predict weather from a set of initial conditions. He discovered that, if he rounded off one of the data values he plugged in at the start (entering the number as ".506" instead of the more precise ".506127"), that difference of .000127 was all it took to generate a completely different weather outcome.

It turns out that, in a complex, dynamic process such as weather, even the tiniest change in initial conditions can have a dramatic impact on later conditions. And this reminded Lorenz of something: the science fiction story "A Sound of Thunder", which Ray Bradbury had written nine years earlier.

In Bradbury's tale, a time-traveler returns from a brief stay in the age of the dinosaurs, only to find that, owing to his accidental killing of a prehistoric butterfly during his visit, the course of history has been altered; he returns "home" to an unfamiliar society, in which English spelling is different and fascism is taking over. 

Lorenz begin to use the phrase "the butterfly effect" to refer to the way small changes in a dynamical system can have surprising and far-reaching consequences. Although the phrase referred to Bradbury's story, it is often explained by means of the suggestion that a butterfly flapping its wings in Brazil might eventually cause a tornado in Texas (or prevent one, for that matter). The term "butterfly effect" has come to mean any seemingly small change which has larger consequences in the long run.

Although most people who think about such matters are aware that a small change in a complex interactive system can spread out like ripples in a pond, and lead to multiple unforeseen consequences... we nevertheless like to pretend that this is not true in the case of that complex interactive system known as human physiology. In that case, we tell ourselves, the influence of a change can be carefully contained, so that it has no consequences other than the desirable consequence we are hoping to bring about. This is what is known as wishful thinking.

Medication -- any medication -- is created and used in the hope that it will produce a single, desirable result. Or at least in the hope that any undesirable results it produces will be minor, easily tolerated, and clearly outweighed by the desirable result. Unfortunately, it is impossible to predict how well these hopes will be fulfilled, and it may even be difficult to assess how well they are being fulfilled once you start using the medication.

Thalidomide, a drug designed to treat morning-sickness in pregnant women, did its job well, and didn't harm the women. Everything seemed to be fine. Nobody noticed anything wrong, until these women started giving birth, and it turned out that their children had severe deformities. What does morning sickness have to do with fetal development? Certainly nothing obvious; but somehow or other, thalidomide had an impact in both areas. The doctors who prescribed the drug to pregnant women thought they were addressing one issue, but it turned out that they were addressing another one as well, without having the least intention of doing so.

At least, in the case of thalidomide, the undesirable consequences of taking the drug became obvious pretty quickly (the drug was never approved in the US, because the FDA asked for more testing first, and meanwhile the early adoption of the drug in Europe resulted in thousands of cases of deformity). For many medications, it may take years of routine use before undesirable side effects start to become obvious.

In the case of Avandia (a diabetes drug already in trouble because of its role in increasing rather than decreasing the coronary risk that comes with diabetes), we are now starting to see growing evidence that the drug is harmful to, of all things, your bones.

Bone mineral density (and a couple of other markers of bone health) have been found to decline in postmenopausal women taking rosiglitazone (sold under the name Avandia). The researchers are saying that anyone at risk for osteoporosis should not be given Avandia.

I haven't a clue (and I doubt anyone else has a clue) why a drug designed to reduce your blood sugar would also reduce your bone density. What can the connection possibly be? Perhaps we'll never find out, and we'll have to attribute the problem, vaguely, to the butterfly effect. Change one thing, and later you find out that you changed other things along with it.

I am not arguing that medication is always harmful, or that the risk of its being harmful is always unacceptably high. I'm just taking the opportunity to explain that my tendency to see medication as a last resort, not a first resort, is not merely a personal bias -- it does have a rationale.

The dream that we can make drugs which solve one specific problem without affecting anything else -- that we can interfere in the body's complex regulatory systems without producing any unexpected consequences -- is a little unrealistic. One change leads to other changes. "Small" changes can have large consequences. Those consequences might be worth it, if the problem you're solving is big enough, and it can't be solved by other means. But because we aren't sure what all the consequences are, we shouldn't be too hasty about deciding that the consequences are indeed worth it.

If there's a way to solve the problem without taking the drug, and therefore without taking a chance on its consequences, wouldn't it be better to try that first?

Monday, March 28, 2011

It happens once in a while: I get a post-prandial test result which is actually lower than my fasting test result, earlier the same day. If this sounds impossible, let me review some of the factors that could have brought it about.

To begin with, we always need to keep in mind the inevitable fluctuations in accuracy for a hand-held glucose meter. By my calculation, there is a 25% probability that my fasting reading was higher than the actual value and my post-prandial reading was lower than the actual value. The probability that my meter was showing large errors in both directions is lower -- but it ain't zero.

Anyway, my fasting result (90) was a bit higher than average for me, probably because yesterday was my rest day from exercise. So, in order to be lower than my fasting test, today's post-prandial test didn't have to fall quite as far as it might on another day.

Also, I'd done a hilly and challenging 5-mile run just before lunch, so my insulin sensitivity was probably ramped up pretty high. And then I ate a meal which was unusually low in carbohydrates. It's not too surprising that my post-prandial result would be fairly low.

But 80? That's kind of weird. After all, this was hardly the first time that I've had a low-carb lunch right after running; in the past, this scenario has usually produced a post-prandial result in the range of 100 to 115, not 80. 

So, if that result of 80 was genuine, and not an artifact of the meter, it's a little mysterious. However, I have come to understand over the years that not all fluctuations in blood glucose can be predicted before the fact, or explained satisfactorily after the fact. Every once in a while, you're going to go exceptionally high or low, for no reason that you can understand.

Maybe it's just as well, if it keeps us all paying attention.

Maybe the real reason my post-prandial result was so low today was the weather. After a long stretch of wet, dreary days, with rain, and wind, and flooding, and falling trees, and leaden-gray skies... today the clouds vanished, and we had nothing but brilliant sunshine and clear air.

For our lunchtime run we chose a route that goes up the hill to the Paradise Ridge winery, where you can look out over the valley to the west, and appreciate how green and bright the landscape was after all this rain. Today the visibility was so perfect that it seemed as if you could stare at the ridge line 15 miles to the west and distinguish individual pine needles on the trees. And the temperature was great for running: in the high 50s, with no wind.

It's invigorating to run under perfect conditions, especially after you've been running under depressing conditions. Maybe that perked up my insulin sensitivity somehow or other, and that's why my glucose was low after lunch.

Friday, March 25, 2011

That's better -- fasting glucose back below 90 where it belongs. Below 80, actually; all the better. 

It was another stormy day today -- but there was a brief rainless interval, and we managed to fit a lunchtime run into it, finishing it just as the rain was starting up again. Sometimes you hit it lucky!

Yesterday a search engine referred someone to my site because they entered the search string, "are there specific things you can't do if you have type 2 diabetes?".

I wonder who made that search. Someone who has just been diagnosed, and is at the beginning of the self-education process? Someone who has a husband with type 2 diabetes, and is hoping to find that several of the habits which she wishes he'd give up are on the list of "specific things you can't do if you have type 2 diabetes"?

The question seems a little naive to me, at least in its apparent assumption that having type 2 diabetes is a simple situation, governed by rules which are universal and absolute. Presumably those "specific things you can't do" cannot be done by any type 2 diabetes patient, ever. Not even a little bit. 

If any such absolute prohibitions exist for people with type 2 diabetes, I am not aware of them. Maybe you can't go into space (I imagine NASA has a list of chronic diseases which disqualify you from joining the astronaut corps, and diabetes is probably one of them), but apart from that, as far as I can tell, people with type 2 can engage in the same professional and leisure activities as anyone else. I have run marathons, and I have eaten pecan pie; I survived both experiences. I don't mean to suggest that eating pecan pie every day (or running a marathon every day, for that matter) is a wise course of action for people with type 2 diabetes; I'm merely making the point that it's not realistic to think in terms of absolute prohibitions.

However, if there are no absolute prohibitions, there are plenty of guidelines, and you need to be following those guidelines most of the time (with the occasional bit of reckless indulgence along the way, if you find that necessary to the preservation of your sanity).

The guidelines you must follow are not easy to state simply, and a lot of them have to be custom-tailored to your personal situation. All of them are ultimately based on a single underlying guideline: adjust your daily habits so as to achieve and maintain a blood sugar level which is either entirely normal or as close to normal as you can get it. Somehow that broad, underlying guideline has to be translated into more specific, practical guidelines for you to follow (about such matters as what to eat, and how much of it to eat, and how much to exercise). The only person who can make that translation is you, because individual characteristics vary too much for any set of rules to apply equally well to everybody.

Guidelines for living have to be nuanced. To me it doesn't seem practical to declare war on, say, potatoes, and make it a rule that you can never eat potatoes at all. Potatoes find their way into a lot of dishes (soups in particular) which you probably don't want to give up. But you need to be aware of the impact which potatoes have had on your blood sugar in the past, and be conscious of how large a serving of potatoes you will be getting in a particular dish.

Today I had a bowl of soup for lunch which had potatoes in it -- but not a lot, and I had just been running before lunch, so I felt that my system was probably ready to handle this particular bowl of soup at this particular time; the post-prandial test result of 122 tells me that I figured that about right. But if I hadn't been running before lunch, or if the potato content of the dish had been higher, or if my recent experience with post-prandial testing had shown a rising trend which had me worried, I might have decided against it.

Life with type 2 diabetes is more about making adjustments and compromises than it is about obeying a set of commandments. The question to ask is not "can I eat bread?". You have to ask a more elaborate question: "how much bread (if any) would it be okay for me to have with this meal right now, considering what exercise I've done in the last 24 hours, and what sort of test results I've been seeing in the last few days, and what else I've eaten today, and what else is included in this meal?". It sounds like a lot to calculate, but at least it's an intuitive calculation (once you're used to doing it). Over time it becomes more a matter of feeling than of analysis. You develop a pretty good sense of what you can get away with, and what you can't get away with it. The trick is to make sure you actually use that sense in deciding what you're going to do. Becoming a saddened spectator to your own behavior, watching yourself do exactly what you know you shouldn't do, is a dangeorus thing, and surprisingly common among diabetes patients. 

It has long been known that diabetes and periodontal disease have some kind of vicious-circle relationship (each condition promotes or worsens the other), and regular dental care is often recommended as helpful in preventing or controlling diabetes. But is there any way to measure how much difference periodontal treatment actually makes for someone with diabetes?

Some researchers at the University of Pennsylvania and the University of New York thought there might be: they looked at 3449 diabetes patients enrolled in CIGNA's medical and dental plans from 2006 to 2008, to see if there was a difference in health-care costs between those who did receive periodontal care and those who didn't.

It turned out that there was a surprisingly large difference: on average, patients who did not receive periodontal care had annual medical costs $2484 higher than patients who did.

The study did not analyze the exact reasons for the difference in costs, however. Nor did it analyze the large discrepancy between the sexes: costs were only $735 higher for women, but $3212 higher for men. The researchers were surprised by the size of this gender gap, and speculated that the reason might be that women were more careful of their health in general, and so were less harmed by lack of periodontal care. (To me that seems an unsatisfactory explanation for so large a discrepancy, but I'm not sure I can think of anything better.)

You might expect that CIGNA would respond to this news by changing their reimbursement structure, so that patients could afford periodontal care and CIGNA's total costs would be reduced, but so far they have not announced plans to do this. When it comes to a choice between an ounce of prevention and a pound of cure, health insurance companies generally prefer the latter. 

Thursday, March 24, 2011

I don't like to see a fasting result above 90 these days, so I have to devote a little thought to why I might have been at 95 this morning.

It could simply be the variability of the meter, of course, or it could also be owing to my oversleeping slightly this morning, and then waking up in a panic about being late -- which usually pushes my fasting test up a little, from the adrenaline or something.

But it could also be that, on the strength of my low post-prandial result at lunch yesterday, I allowed myself to indulge in a little too much carbohydrate at dinner. I did have a serving (a small serving, honest!) of those tiny Yukon Gold potatoes, but maybe it wasn't what my system needed last night.

Well, my post-prandial result after dinner was good, and I hope that tomorrow's fasting result will be back in the 80s where it belongs.

Why is my blood pressure so much lower tonight? Well, I finally decided that the cheap drugstore-brand meter that I bought earlier this month (which has conistently given me higher readings than I'd seen in years) is no good. I hated the thing anyway; just getting its slithery cuff fastened on my arm was enough of a struggle to raise my result a few points, I suspect. Anyway, I bought a more expensive meter tonight (an Omron BP760, which is supposed to be one of the better models available). Result: 112/68.

Of course, it's possible that cheap drugstore-brand meters which disagree with the expensive ones are actually more accurate, not less accurate. Well, a lot of things are possible, but I'm not going to dwell on this particular possibility.

Still worried about radiation drifting over from Japan? Perhaps this will help you put things in perspective. I've adapted the data from Randall Munroe's chart of comparative radiation dosages, with dosage increasing as you proceed down the table. I'm giving the dosages in microSieverts (a measure of absorption of ionizing radiation by the human body). Notice how extreme the differences are between the values given.

25 Examples of Doses of Ionizing Radiation


Source of Exposure

Dosage in microSieverts


Sleeping next to someone (people, like everything else,  are slightly radioctive)



Eating one banana (bananas contain potassium, and 0.012% of that is the radioactive isotope potassium-40)



Living <50 miles from coal power plant for 1 year (coal includes radioactive isotopes)



Arm X-ray



Using computer monitor 1 year



Dental X-ray



1 day in an area with normal background radiation



1 day in an area with above-normal background radiation (e.g., the Colorado plateau)



1 day in an average town near the crippled Fukushima nuclear power plant

13.5 (but highly variable -- see #15 below)


Chest X-ray



Airplane flight, New York to LA (at high altitudes, there is less atmosphere to block radiation from space)



Living in a brick or concrete building 1 year (those materials contain radioactive isotopes)



Average total dose, from Three Mile Island nuclear accident, to someone living within 10 miles






1 day at the most-irradiated sites near the crippled Fukushima nuclear power plant, on March 16 or 17, 2011.



1 year of normal exposure, 85% from natural sources, most of the rest from medical scans



Chest CT scan



1 hour on the grounds of the Chernobyl nuclear power plant in 2010 (24 years after explosion and meltdown)

6,000 (average value, but wildly variable; see also #25 below)


Maximum yearly dose permitted for US radiation workers



Lowest 1-year dose clearly linked to increased cancer risk (no promises that lower doses can't do it)



Dose causing immediate radiation sickness

400,000 (average value, varies)


Dose causing severe radiation sickness, possibly fatal



Dose causing usually-fatal radiation sickness; survival sometimes possible with treatment



Fatal dose regardless of treatment



10 minutes near the Chernobyl nuclear reactor core during explosion and meltdown on April 26, 1986


None of this makes me think of nuclear power as a safe industry, but it does make me relax a little about whatever is drifting over the Pacific from Japan.

And it's nice that nuclear power plants only blow up once in a while. It would be disturbing if it happened more often.


Wednesday, March 23, 2011

If you participate in a large organized running event or cycling event, you will usually be besieged with e-mails for the rest of the year from some sports-photography firm which has taken pictures at the event, and hopes to sell you an enlarged print of yourself participating in it. 

I was more likely to buy those prints back in the day when participating in such an event was not only a new and exciting experience, but was also an experience which I wasn't sure I would live to repeat. Over time, I've become a little less excitable in these matters. I look over the digital proofs they send me pretty carefully, but I usually decided that these photos make me look really fat, really awkward, or both, and I decided against buying enlargements of them.

Today I was sent a reminder form the folks at Facchino Photography, a company which sent its phtographers to the Apple Hill Harvest Run in Camino, California, back in November of last year.  Perhaps that day was even harder on the photographers than it was on the runners, because it rained all morning, and the one thing worse than running in the rain is standing still in the rain while you wait for runners to go by so that you can take pictures of them looking miserable.

To my surprise, the crop of pictures they sent me didn't make me look fat. (They also didn't make it look as if it was raining, which I assure you it was). But, because of my peculiar running form (which I have been trying to correct for years) , they do make me look like I'm walking rather than running.

They also make it clear that I wasn't having as nice a time as I'd hoped to be having, back before I'd realized what the weather was going to be like. (I't s a very pretty area in sunny weather.)

I'm not sure I really need these prints. Some day (I can't help fealing) a race photographer will take a picture of me that I really like, and then I'll order a big expensive copy of it. But this one isn't it.

Right now I'm not signed up for any kind of race before the Napa-to-Sonoma half-marathon on July 17. There are a couple of races in April and May that I'm considering.  But first I want to see this rain come to an end! The reservoirs are full, the drought is over, and it can stop now.

Here are some things that doctors know about type 2 diabetes:

The first two points tell doctors that they need better tools for early detection of diabetes; the third point tells doctors that it ought to be possible to develop such tools (after all, if some kind of dysfunctional metabolic process is going on, there is probably a way to detect that it's going on).

So far, though, doctors have not had much in their toolkit for early detection of type 2 diabetes. If they are going to screen their patient population for potential diabetes cases, what should they look for, and how should they look?

Obesity has long been seen as an early-warning sign of diabetes, but as a practical matter it's really not that helpful. While it's true that most type 2 patients are fat when diagnosed, it does not follow that most fat people become diabetic. A majority of fat people manage to avoid diabetes, no matter how much weight they gain. (Obesity alone won't make you diabetic, if your genes aren't setting you up for that to happen.) And anyway, obesity is now so commonplace in America that "screening" the patient population for potential diabetes patients by excluding thin people wouldn't shorten your list of suspects very much.

Fasting glucose testing, because it is cheap and easily administered, has long been used as a screening tool for type 2 diabetes -- with very limited success. The problem is that, in a patient who is becoming diabetic, post-prandial levels usually go up long before fasting levels do. Far from being an early-warning indicator of what is about to happen, an elevated fasting level often serves merely as the final confirmation of what has happened already. Many patients diagnosed with Type 2 on the basis of other tests continue to see normal fasting results for a year or more.

The hemoglobin A1c test, because its results are influenced by all blood sugar levels at all times of the day and night (fasting levels, peaks after meals, and everything in between) gives doctors a clearer picture of what is going on (at least on average) with a patient's blood sugar. The A1c test is not going to be "fooled" by those patients whose fasting levels remain normal long after their post-prandial levels have started to show dangerous spikes. However, is the A1c test truly an "early" indicator? It's earlier than the fasting glucose test, but that's not saying much. The A1c can indicate a rising trend in your average blood sugar, but it can't detect what is going on during that period when your endocrine system is compensating for insulin resistance by releasing extra insulin, and thus hiding the problem.

Why not test for insulin resistance, then? (Although some type 2 patients supposedly experience a decline in insulin production without developing insulin resistance first, it appears that, in most cases, you could get an early indication of type 2 developing by measuring insulin resistance.) Unfortunately, the test for insulin resistance is no minor procedure. Picture yourself spending a few hours in a hospital bed, with two IV's in your arms (one for insulin and one for glucose), and various test equipment hooked up to you, because the test is somewhat dangerous and your progress has to be monitored constantly throughout it. Obviously this procedure is too invasive, and too expensive, to be used as a general screening tool. The test is used mainly for research purposes; it is seldom used in patient care, unless there is confusion over what kind of diabetes a patient has got. (And in that case, the patient had better have either very good insurance or very deep pockets.)

Another possibility is the OGTT (oral glucose tolerance test), in which the patient's blood glucose is monitored for two hours after the patient swallows (often with difficulty) a disgustingly generous serving of glucose gel. The idea is to give the patient's endocrine system such an overwhelming challenge to its capacity for glycemic control that no weakness can be hidden. (This test is often given to pregnant women as a means of detecting gestational diabetes.) The OGTT isn't as difficult or expensive to administer as an insulin resistance test, but it does take a minimum of two hours, so it's a little cumbersome to be used as  a screening tool for the entire non-pregnant population. Also, it probably can't be called an early warning system, since it only detects the problem after it is already interfering with glycemic control -- ideally, we would want to know what was going on in the background before the more obvious signs of trouble appear.

Another kind of test is needed. And a team of researchers from Harvard and from Massachusetts General Hospital think they have found it. They studied "metabolites", which (in the summary of the research I read) are described as "small molecules", I suppose to distinguish them from those big bulky molecules that have been blocking your driveway of late. (From what I've been able to gather, a protein doesn't count as "small", for present purposes, but the amino acids which are used like building-blocks to costruct proteins do count as small.) Anyway, "metabolism" refers to any of the chemical engineering work which the body has to engage in to accomplish basic life-support tasks such as digestion and growth, and "metabolites" are molecules (such as amino acids) which are left over from the chemical reactions that metabolism requires.

Because every human body has the same life-support tasks to accomplish, you might suppose that every human body would produce the same metabolites in the same proportions, but apparently not. It is possible to detect metabolites in the bloodstream and measure their abundance, and when you do this, it turns out that different people have different amounts of the various metabolites -- a kind of chemical fingerprint. It also turns out that the abundance of  five of the metabolites (the amino acids known as isoleucine, leucine, valine, tyrosine, and phenylalanine) is elevated in the case of people who will later develop type 2 diabetes! In the study, people with elevated levels of the three most predictive amino acids (not  specifically identified in the summary I read), the risk of becoming diabetic was four to five times higher than in people with low levels of those amino acids. Even among people seemingly at risk for diabetes because of obesity or other fators, the metabolites made it possible to distinguish which of them would actually develop the disease, and which of them wouldn't.

What remains absolutely unclear is why those five amino acids are elevated in people destined for diabetes. Although the article I read claimed that this discovery is giving scientists new insights into how people become diabetic, it doesn't seem to be doing anything of the kind so far. Scientists have something new to make guesses about, that's all -- they can spin fanciful hypotheses about what process might be going on which drives people into diabetes, and leaves behind a telltale clue (elevated levels of five amino acids), but at this point there is no way to know what the process is, or why it produces an overabundance of five amino acids.

This worries me, because it will be very tempting for doctors to assume that elevated levels of certain amino acids are the cause of diabetes. It that happens, the pharmaceutical industry can develop a drug wihcih artificially lowers the levels of those amino acids -- and then claim this as proof that their drug is "effective" (even though it doesn't actually prevent diabetes). If this sounds far-fetched, bear in mind that one of the most profitable drugs in history is Lipitor, which is regarded as "effective" because it reduces cholesterol, even though it doesn't protect you from dying of a heart attack -- which was supposed to be the reason why you cared if you had high cholesterol!

The pharmaceutical industry has always profited from the willingness of doctors and patients to assume a cause-and-effect relationship between lab results and health which has not actually been established. If it has worked for them before, why not go to the well one more time?

I'm glad that researchers have found something which might help us identify diabetes before it starts, so that patients can be warned of the potential problem, and be given advice on how to prevent it from developing. But I hope it doesn't turn into a boondoggle, in which patients spend a fortune on drugs which hide the warning sign without fighting the underlying problem which is producing that warning sign.

Tuesday, March 22, 2011

To celebrate my 15-year anniversary with the company, my boss took me out to lunch today. Restaurants are always challenging in terms of blood sugar management, but fortunately the Thai restaurant he suggested had some dishes that were not total carbohydrate bombs. The fiery seafood soup I ordered didn't include rice or noodles. It did, to be sure, include sweet potatoes, but not in such generous amounts that I thought I would get a bad glucose result afterward.

And I didn't do too badly: 129. That's only a little higher than the average post-prandial spike for a non-diabetic person -- and I hadn't even had my daily workout yet. Anyway, it was a good lunch and I'm glad I was able to "get away with it" in gylcemic terms.

Going out to lunch meant that I couldn't go running at lunchtime today -- which didn't exactly break my heart, as it was raining. But it meant doing a gym workout in the evening. I prefer to exercise outdoors when I can -- and I sometimes prefer that even when it's raining. But it's hard to face running in the rain several days in a row, and that's what the weather forecast is showing me:

Oh well -- I'll do whatever has to be done.

It's time once again for me to look over the search-strings which, according to my internet service provider, directed people to this site in recent weeks -- so that I can try to answer the questions which seem to be implicit in them. I have taken the liberty of correcting the more outrageous spelling errors, but these really are the phrases that real people typed into their search engines...

Chia seeds dissolve rapidly into a gel of soluable fiber, so to some degree they can soften the impact of carbs in a meal -- which presumably means that, to some degree, they can have a moderating effect on hyperinsulinemia (abnormally high insulin secretion, usually triggered by diminished insulin sensitivity).

I wouldn't want to go farther than that in promising what chia seeds will do for hyperinsulinemia, but I don't know of any reason not to eat them, and there are reasons to hope that they may provide health benefits in other areas. Chia seeds don't have any strong flavor, so you can sprinkle them into almost any kind of food.

I'm not sure it can be done. If my own experience is any guide, the night before you go in for a colonoscopy is just not going to be normal evening for you, and maintaining normal blood sugar during that middle-aged rite of passage is just not going to be a practical goal.

Glycation is the unwanted bonding of glucose onto proteins. Hemoglobin is the protein most frequently measured for glycation (glycated hemoglobin is known as hemoglobin A1c, hence the name of the most frequently-administered glycation test).

Glycation is undesirable because it interferes with the normal functioning of proteins, and also because it can promote the formation of unwanted chemical byproducts. In general, glycation has a degrading effect on the health of tissues and organs throughout the body.

Glycation occurs spontaneously whenever proteins are exposed to glucose, and since everyone has some glucose in the bloodstream, some glycation occurs in everyone -- but it normally occurs slowly enough that the body's protein-recycling process can keep up with it, and hold it down to a safe minimum. In non-diabetic people, only about 5% of hemoglobin is glycated, and the percentage doesn't go up over time.

In people with elevated blood glucose, glycation happens faster, and the body's protein recycling process can't keep up with it. In diabetic people, the percentage is higher, and it does tend to go up over time if glycemic control is not maintained, because proteins are being glycated faster than the body can recycle them.

Glycation of hemoglobin is not necessarily more important than glycation of other proteins, but hemoglobin (being present in your red blood cells) is easy to collect for measurement purposes, and gives a good general picture of how much glycation (of any kind of protein) is going on.

That result is too high to be considered normal, but most people (including most doctors) would say that it's pretty good for someone with diabetes. I aim for normal, though, and depending on how your lab defines "normal" for their version of the A1c test, that probably means less than 5.8%.

It is often claimed (falsely, I would argue) that we test for glycated hemoglobin because it is a measure of average blood sugar. In my view, this is getting the thing entirely backwards: glycation itself is the problem, and the main reason we care about average blood sugar is that it affects the glycation rate.

It is true that glycated hemoglobin can be used as a basis for estimating average blood sugar -- with emphasis on the word "estimating". It can't be more than an estimate, because the mathematical relationship between average blood sugar and glycation rate is not the same in everyone (some people are thought to be "high glycators"). If your glycation rate is atypical, your hemoglobin A1c result might yield a misleading estimate of your average blood sugar. But so what? Glycation is what actually affects your health, and that is what the test measures.

Instead of thinking that your high A1c result is "unfair" (because it suggest that your average glucose level is higher than what you have measured) think about how to bring it down. Fairness is not a concept that applies to diabetes anyway.

I have no information to share on this subject, and I'm surprised that the folks at Google thought I might.

Obviously I'm in favor of controlling diabetes without medication, if you can do it.

If you can't get acceptable results without medication, even I would agree that medication might be necessary -- so we have to remain open to the possibility of taking medication later on if we need to.

So long as you can make it work, though, go for it. That approach is what I'm here to encourage.

If you can't achieve good glycemic control without medication, then it is probably time for medication. You and your doctor will have to reach some sort of agreement on what "good glycemic control" means.

I try to get my glucose profile as close as possible to a normal, non-diabetic person's glucose profile -- which means that (based on a study I read recently on the results that non-diabetic people get) I need to aim for fasting results in the low 80s, and 1-hour post-prandial peaks below 125. Those are pretty ambitious targets, though, and I don't always hit them.

My doctor only told me to aim for fasting tests below 110 and post-prandial results below 150. Currently those targets are easy for me to hit. If they later become difficult for me to hit, I will take that as a sign that I need to start thinking about medication.

That sounds dangerous. Maybe it's time to seek other transportation options.

Normal blood sugar isn't defined on a sliding scale based on what you've eaten. Some would say that 140 mg/dl, 2 hours after a meal, is "normal" -- but what I think they mean by "normal" is "pretty good for a diabetes patient".

In healthy non-diabetic people, post-prandial glucose peaks at something like 125 mg/dl about an hour after a meal, and drops from there.

Insulin is supposed to "escort" blood-borne glucose into cells, by stimulating insulin receptors on the exterior cell walls; this is supposed to cause the cell to absorb the glucose.

In type 2 diabetes, the cells are less sensitive to stimulation by insulin than they ought to be -- and the body can't produce enough extra insulin to compensate for the cells' sluggish response to the stuff. 

It's hard to say for sure. Usually, alcohol brings blood sugar down temporarily (because the liver, while it is processing alcohol, concentrates on that and tends to stop releasing stored glucose).

However, this glucose-lowering effect can be overwhelmed, if the alcohol is delivered to you in a high-carb form (beer can be faily high-carb, and some mixed drinks are extremely high-carb -- if there's a tiny bamboo-and-paper umbrella served in it, watch out!). In other words, if an alcoholic drink drives your blood sugar up, the alcohol in it might not be the real cause of the increase.

However, even when significant carbs are not involved, some people do seem to experience an increase rather than a decrease in blood sugar as a response to alcohol. It's hard to say why. Perhaps their blood sugar starts to drop from the alcohol -- and then their endocrine system over-compensates. A "high" is often a reaction to a "low".

Clearly, some people think there is no limit to how long a search string ought to be. 

Anyway, eating food is what usually makes blood glucose rise. Unfortunately, the implied solution ("don't eat food") is a little impractical. But eating less food (while doing more exercise) can be an effective way to limit how much your blood glucose rises.

Sometimes blood glucose rises even if you don't eat a thing, because the liver releases stored glucose to protect you from hypoglycemia -- and it releases too much. In other words, you go high because you were starting to go low, and this produced an over-reaction.

If "after breakfast" means "after I have had an hour to digest breakfast", 112 mg/dl seems like a pretty good number, regardless of whether you are in a stres or not in stres.

I assume this should read "fasting" blood sugar, not "resting". A fasting blood sugar of 6.2 mg/dl is very, very unusual -- at least in a person who is still alive.

But probably you are measuring in mmol/l. In those units, 6.2 is equivalent to 112 mg/dl, which is too high to be called a normal fasting level, but is below the diagnostic threshold for diabetes.  "Pre-diabetes" is the term usually applied to this kind of result. Given the number of people who are in this state, I guess the answer has to be: no, this is not very unusual. But it's not very healthy, either.

The definition of normal blood sugar does not change just because you get old; high blood sugar always has injurious effects on tissues and organs, whether you are young or old.

However, because the harm done by high blood sugar accumulates very slowly, doctors take a more relaxed attitude about glycemic control in an elderly patient, on the assumption that high blood sugar (unless it is extreme) probably won't have time to do any serious harm before the patient is already dying of something else anyway.

70 seems a little early to be taking that attitude, however -- a lot of people live well past 70, and you don't want to be unhealthier during those years than you can help.

If this is a question about how to limit what you eat the night before an A1c test in order to get a better result the following morning, I don't believe it makes any difference. Glycation (which is what the A1c test measures) is a slow, cumulative process. The way to get a good result on it is to limit what you eat during the three months leading up to the test, not during the twelve hours leading up to the test.

It means you're doing better than I have been lately. Even under the new, more stringent recommendations for blood pressure control, 119/74 is considered normal.



Monday, March 21, 2011

There was rain and hail today, but we managed to get our lunchtime run finished before any of that got started. Big dramatic clouds, and a cold wind, but nothing falling on us. Sort of the opposite of what happened to me yesterday. I like it better this way!

Whenever you're thinking of taking some form of medical treatment (particularly on a non-emergency basis), it's a good idea to do a little bit of cost-benefit analysis. It can be surprisingly tricky to figure out whether or not a treatment is "worth it".

Tonight I've been trying to figure out if there is any good reason for me to start taking iodine pills to protect myself from the effects of the radioactive particles which are presumably now drifting my way from the tsunami-damaged nuclear reactors in Fukushima, Japan. The short answer is "no", but it's surprising how much complexity lies concealed behind that one-word answer.

Many residents of America's west coast, having watched as the remnants of the Japanese tsunami damaged our marinas half a day later, became very worried about what would happen when the radiation from Japan's damaged nuclear reactors got here. Drug-stores in my area ran out of iodine pills almost immediately. On-line sources for the pills are either posting "sold out" notices or charging exploitation prices of the cruelest sort.

I was already vaguely aware of the rationale for taking iodine in the aftermath of a nuclear detonation or nuclear-reactor accident: one of the common products of atomic fission is the radioactive isotope iodine-131. Because the thyroid gland absorbs iodine readily (and can't tell the difference between stable iodine-127 and unstable iodine-131), exposure to fission products results in absorption of radioactive iodine by the thyroid gland, and this can cause thyroid cancer.

However, if we can prevent the thyroid gland from absorbing iodine, we can probably prevent it from becoming cancerous. A practical way to achieve this is to take large doses of stable iodine-127. If the thyroid gland becomes so saturated with iodine that it stops absorbing iodine of any kind, it therefore won't absorb the dangerous iodine-131 which has been introduced into the environment.

How are these iodine doses taken? In the form of pills containing the compound potassium iodide, also known as "KI". Immediately I am side-tracked by two questions: why take potassium iodide rather than pure iodine, and why is potassium iodide abbreviated as KI instead of PI? I didn't find an answer to the first question, but a likely guess is that iodine in pure form is either toxic or difficult for the body to process. As for the abbreviation, "K" is used because the element potassium is symbolized by that letter.

Sidetracked again! Why is "K" the symbol for potassium? Well, "P" probably was already taken by one of the other elements that begin with P, so chemists needed to use a different letter. Why "K"? Well, it stands for "kalium", which is a neo-Latin name (that is, a modern word contrived to seem Latin) for potassium, derived ultimately from an arabic word related to "alkaline". Meanwhile, "potassium" is named after "potash", a potassium compound obtained by boiling wood-ashes in a pot until it is boiled dry. (Why we don't just call the stuff "kalium", if someone went to the trouble of inventing the word and we use it in abbreviated form, I have been unable to discover.)

Not that any of this information about potassium tells us anything important about iodine. For whatever reason, the compound called potassium iodide is the most useful vehicle for introducing iodine into the human body (it is the magic ingredient in "iodized" salt, for example), and KI is the common abbreviation for that compound. If you're caught in a cloud of atomic fallout, KI is what you need (or at least it's the next best thing to a quick exit from that cloud of atomic fallout, which is what you really need but might not get).

Perhaps surprisingly, there is a natural source for dietary KI: it's in kelp. Boil up a pot of seaweed soup, and who needs KI pills? (However, the kelp that you can buy in grocery stores typically comes from Japan, so let's just forget I made that suggestion.)

Taking KI pills is a good strategy, as far as it goes, but it only goes so far: it protects you from thyroid cancer without protecting you from anything else. (All of the other harmful effects of exposure to fission products are just as much a threat to you as they were before you took the KI pills.)

Also, we need to be aware of certain practical limitations. A dose of KI offers only temporary protection: after 24 hours it wears off. Taking it in advance isn't useful, and unless you've got an endless supply of the stuff, it might be a really bad idea to start taking your pills before the crisis arrives, lest you run out of it just when you finally do have a need for it.

Another, perhaps surprising limitation: some people have a lot more use for KI than others. Not all people are equally vulnerable to the effects of iodine-131. It is mainly children who develop thyroid cancer from exposure to that isotope; the risk is lower in young adults, and in adults over 40 the risk is low enough that, for people in that age group, the pills provide no benefit except in cases of extreme exposure. To quote the CDC, "Adults older than 40 years should not take KI unless public health or emergency management officials say that contamination with a very large dose of radioactive iodine is expected. Adults older than 40 years have the lowest chance of developing thyroid cancer or thyroid injury after contamination with radioactive iodine. They also have a greater chance of having allergic reactions to KI."

What's that? Allergic reactions? Here we come to the little-discussed disadvantages of taking KI.

In some people, KI produces an allergic reaction of the dangerous, suffocating type which can occur in severe shelfish allergies. Most people won't experience a reaction of that type, but there's no way to know in advance whether you will or won't. Now that large numbers of people are being driven by panic to take KI (and probably to take more than the recommended dose, "to be on the safe side"), the nation's poison-control centers are starting to take calls from frightened people who are having a bad reaction to KI pills. As the CDC noted, the risk of an adverse reaction to KI is highest in people over 40 -- the very people who are unlikely to get any benefit from the stuff!

An allergic reaction is not the only potential drawback to taking KI pills. If you have an overactive thyroid, taking in extra iodine may intensify the problem. But taking in extra iodine can also be a problem if you have an underactive thyroid (because, in that case, the thyroid may shut down once it is saturated with iodine).

If iodine-131 has not been introduced into your environment, and you start taking large doses of KI, you are solving a problem which doesn't yet exist, and possibly creating another problem in the process.

The potential disadvantages of KI pills would not necessarily lead us to reject them if there seemed to be a need for them, but they should certainly make us hesitate to use them without need. (And, since the world's supply of KI pills is finite, hoarding them would make them unavailable to the small number of people who actually need them; doing that for the sake of performing what amounts to a voodoo ritual, in order to feel better about an imaginary problem, is a little hard to defend.)

It's probably a moot point, because KI pills have become unobtainable, but it doesn't appear that there is any reason to take them now. Not that I trust information coming from Japan about radiation levels (the Japanese government has always dealt with nuclear accidents, of which they have had several, mainly by lying about them), but the radiation plume from Japan (however strong or weak it may actually be) has a lot of opportunity to thin itself out as it drifts across the Pacific Ocean, and nobody monitoring radiation levels along the west coast has so far found evidence of anything dangerous developing here. Which is not to say that it can't happen, or won't happen. I wish I had some KI pills on hand in case it does happen, but even if I had a bushel of them I wouldn't be inclined to start taking them just yet.

But if you're not satisfied with my own reasoning on this issue, here are some thoughts on KI pills from Richard T. Kloos, MD, Chief Operating Officer of the American Thyroid Association:

"There's no reason that the American public should take these now...

We would like the American public to be knowledgeable and informed, but now is not the time for Americans to panic...

I don't think the American public is at any risk, and I don't think they should be taking any prophylaxis unless a reliable source tells them to do so...

If there's no benefit from KI supplementation, as in the absence of radiation exposure, then even these low-level risks are unacceptable."

But it's funny which risks people worry about and which risks people ignore. A new study from the UK has just found still more data showing that the diabetes drug rosiglitazone (sold as Avandia) heightens the risk of heart failure, heart attack, and death, as compared to the competing drug pioglitazone (sold as Actos). In Europe, the more dangerous drug has been removed from the market, but America's Food and Drug Administration has not done so (the FDA promised to restrict access to rosiglitazone, but then failed to do anything about it). Hardly anyone cares about this problem, which is for real -- but everyone is in a panic over radioactive iodine from Japan, which so far is not real.

Ultimately, the whole Japan/iodine thing seems seriously overblown to me. If the fallout from Japan ever gets bad enough for KI to have any effect on someone my age, it will certainly be bad enough to kill me in a dozen other ways. I might have my deathbed regrets, but they won't be about failing to get in line at the pharmacy before they ran out of KI pills.

I guess I won't have to experience any deathbed regrets about failing to take Avandia, either.

Sunday, March 20, 2011

I don't usually blog on the weekend, but as I took some time off from blogging last week to concentrate on music-making for St. Patrick's Day, I thought I should catch up with you.

Our performance on St. Patrick's day went about as well as you dare hope for on that sort of occasion -- which is to say that the tavern patrons either applauded us or ignored us, and not one of them lurched on stage and tried to grab our instruments to perform a comic pantomime (which, sad to say, is not an entirely unheard-of way for tavern patrons to behave on the Feast of Saint Patrick). This was a new tavern, located slightly away from Sonoma's tiny downtown area, and our audience really consisted of people who were there for dinner and a pint, not people who were there to get staggering drunk. So it all worked out rather nicely. I even remembered to wear green.

The weather here has been very Irish as well -- rain, followed by more rain, and then: rain. There was also some stormy weather of a type that is highly rare in these parts, including a small funnel-cloud which touched down briefly in Santa Rosa and damaged one building (it lifted the roof off a warehouse).

Last night a big rainstorm blew in from the Pacific, and several power lines were being taken down by falling trees. I was without electricity for about 4 hours last night. I made use of the time by practicing fiddle tunes in the candle-light, just like they did it when these tunes were new. It all sounds very charming, but a power failure is harder on me than it is on some people -- because I'm on well-water, delivered to my pipes by an electric pump, so being without electricity also means being without water. I'm glad the power failure didn't last longer than it did!

By late this morning, the rain was stopping, and there was even a little sunshine, so I decided to go for a trail-run in the state park. Of course it started raining again once I was committed to the run, but I half-expected that, and anyway it wasn't a hard rain. However, the storm had had a big impact on the trails -- I had to get around or over quite a few fallen trees. Also, I had to abandon my planned route because Lake Ilsanjo was overflowing and at one point there was a deep and dangerously swift flow of floodwater across the trail. I had to turn around and head back up a very steep hill I'd just come down. I improvised a new route, to get back to where I'd parked my car, but it was about a mile and a half longer than I had wanted to go. (And, of course, once my run was over, the sunshine came back!)

Anyway, it was a pretty hard run -- longer and steeper than what I had bargained for. But a hard workout has its compensations: afterwards I experienced the "good tired" feeling that comes when fatigue is accompanied by a generous release of endorphins into the bloodstream.

Figuring that the run had depleted my carbohydrate reserves considerably, I decided to risk a rather high-carb lunch, in the form of a great big bowl of curried lentil soup. It worked out: 121 isn't a bad post-prandial result, considering the challenge I'd just given my system. I have to admit that one of the reasons I like endurance sports is that a long workout makes it possible for me to indulge in higher-carb meals than I would otherwise be able to get away with. (But I still have to check to make sure I really am getting away with them!)

The weather forecast calls for more rain through Thursdady at least, so I'm not sure the floodwaters are going to be receding anytime soon. Oh, well -- I'll deal with it. Probably I'll use the flooding as yet another metaphor for glycemic control. (Once you get into blogging, everything is a metaphor for something else.)

Thursday, March 17, 2011

This is busy time of year for an Irish fiddler. I'll be taking a few days off to concentrate on musical activities.

Wednesday, March 16, 2011

Type 2 Diabetes Linked to Risk for Major Depressive Disorder With Time reads the Medscape headline. Well, we've certainly heard this one before.

Depression is a difficult subject to discuss clearly, because the popular meaning of the word and the medical meaning are not similar. (It's a little like the word "theory": so long as the public continues to apply the word to speculative ideas, while scientists apply it to confirmed ideas, the widespread confusion over what "theory" means will continue to be a precious gift to creationists.) For most people, depression refers to any kind of unhappy mood, no matter how temporary and no matter how mild. To be "depressed", as we so carelessly define it, might mean no more than that you wanted something and didn't get it. 

Most of us would think nothing of saying that we're "depressed" because of a transitory reaction to some kind of unwelcome news.

It might even be a transitory reaction to a poor posture choice...

...or it might simply be a transitory reaction to being Scandinavian.

We are quick to accuse books, movies, and music of being "depressing"; hearing a song about any sort of real-world problem is enough to make us declare ourselves depressed. But even good news can "depress" us, if it is good news for someone we can't stand.

Almost anything can "depress" us -- anxiety about the future, regret about the past, and envy of those who didn't deserve their lucky break as much as we would have deserved it. Anything that wipes the smile off our faces, even briefly, is enough to convince us that we have entered the state known as depression.

But doctors see depression (or Major Depressive Disorder) rather differently. It is defined as a disabling mental disorder (adversely affecting the patient's family life, professional life, eating habits, and sleeping habits), characterized by persistent and all-encompassing low mood, low self-esteem, and loss of interest or pleasure in activities formerly enjoyed. People with MDD (also known as clincical depression among many other things) have it pretty bad. Some of them barely have the energy to get out of bed in the morning. (In fact, some don't have the energy to get out of bed in the morning.)

Unfortunately, we know very little about what causes MDD. We know that levels of certain neurotransmitters are low in people with severe depression, but that isn't necessarily the cause of the problem -- it may only be a chemical symptom of a problem which is caused by something else. Even in cases where MDD seems to be in reaction to some painful experience, it would probably be too simple to say that the painful experience was the direct cause of the problem -- perhaps the underlying cause of MDD, whatever it is, leads people to react differently to a painful experience than others would. Maybe something we don't yet understand is able to make some people more vulnerable to unhappy events than others are.

Anyway, MDD apparently becomes more likely if you have diabetes. The new study reports that "Patients with type 2 diabetes are 52% more likely to develop ...MDD than the general population". It has been suggested that all diabetes patients should be screened for MDD, but that's a lot of patients to try to screen. The researchers in the new study aimed to narrow the field of potential MDD patients among diabetes patients, by identifying "biologic, behavioral, and psychosocial characteristics at baseline that predict the onset of MDD among primary care patients with diabetes."

In the study, patients were examined three times over an 18-month period. So what did their study find? What characteristics of patients at the start were most associated with MDD later?

"When subpopulations were stratified by moderate negative affect, predictors of MDD were negative life events, elevated body mass index, prior MDD, and poor control of glycated hemoglobin levels (hemoglobin A1c). When subpopulations were stratified by an elevated negative affect, predictors of MDD were negative life events and poor control of hemoglobin A1c levels."

Okay, leaving out the unsurprising news that people who had had MDD before were at risk of having it again, the three things that were associated with MDD risk in Type 2 diabetes patients were:

It would be easy for doctors to pick out diabetes patients who are obese and have high A1c levels, and screen them for depression (although, come to think of it, that might not narrow the field very much). I don't know how doctors would screen for "negative life events", though. ("How likely do you think it is that you're going to lose your job, your home, or your wife before your next appointment? Give me your best estimate of the odds.")

Okay, we'll leave the negative life events out of this (those can happen to anyone), but what exactly does it mean that diabetes patients who are obese and have poor gycemic control are likelier to get MDD?

Do high blood sugar and/or obesity somehow directly cause MDD?

Or do people who are unable to get control of those problems become depressed simply because they are disappointed by their failure to get control of those problems? Or perhaps because they are anxious about what the consequences of their failure might turn out to be?

I don't know (and I don't think anyone else does, either) whether hyperglycemia and obesity among diabetes patients can somehow trigger depression directly. I suspect that a lot of people become severely depressed mainly because they have something to be seriously depressed about (even if certain less-vulnerable people could experience the same problem and not be seriously depressed by it). No doubt there were people who remained chipper all through the Great Depression of the 1930s, no matter how bad the situation became for them -- but the people who were naturally inclined toward depression probably had a pretty miserable time of it.

My own personality does have a tendency in the depressive direction, but I discovered (by accident) that there is a simple remedy which works for me: exercise. When I was diagnosed with diabetes 10 years ago, I started exercising regularly, and have had far less trouble with depression since than than I did before. I'm not Superman, but I usually do okay.

Tuesday, March 15, 2011

Well, at least my blood pressure is moving down to a healthier level than it's been lately. And my glucose numbers are looking good also. Too bad my weight isn't getting with the program...

It was raining today, and I wasn't particularly looking forward to running in the rain, but one of my running buddies wanted to do it, so I went along with the idea. It's not so bad once you're about as wet as you're going to become. And the hot shower afterwards is better than usual. Oh well: we do what we have to. Or anyway some of us do what we have to. Reading the diabetes forums leads me to suspect that some people just do what they feel like. It doesn't look as if it's working out all that well for them, though.

I find it depressing to read about all the awful things that happen to people who adopt the I'm-just-going-to-do-what-I-feel-like approach to diabetes management, but I suppose that knowing about such things helps me stay on track.

I went through a long phase during which I was only doing fasting tests, not post-prandial tests. I had decided that, since my blood sugar had been consistently normal for years, there was really no need to do anything more than take a fasting test when I got up in the morning. I figured that, if anything started to go wrong with my glycemic control, it would show up in my fasting tests and I would be able to do something about it. Until my fasting tests went up, there would be no need for me to make any course-corrections.

Then I read that, when people are starting to lose glycemic control, the problem usually shows up first in post-prandial tests, not in fasting tests. If you really want to feel confident that you know what's going on with your blood sugar, you need to do both kinds of testing. So, during the summer of last year I started to do post-prandial testing again.

Well, here's a little more information about why that's the right thing to do. I was reading a report today (issued in 2003, but better late than never, I always say) on The Natural History of Progression From Normal Glucose Tolerance to Type 2 Diabetes in the Baltimore Longitudinal Study of Aging. The Baltimore study gathered together 815 test subjects (with an average age of 57 to start with) and tracked them over time to see what sort of health problems they developed. At that point, 488 of them were described as having normal glucose tolerance (which is only 60% -- not a very good showing for people under 60, if you ask me). Okay, what happened to these 488 people during 10 years of follow-up?

Well, to put it simply, the pool of individuals with normal glucose tolerance shrank further:

57% of the individuals with normal glucose tolerance at the start of the study were no longer normal ten years later. (Which means that, by this point, less than 26% of all the people included in the study at the beginning now had normal glucose.)

But the most interesting thing is how this loss of normal glucose tolerance manifested itself:

Of the test subjects who lost normal glucose tolerance during the study, fully 80% of them first experienced high post-prandial glucose without experiencing high fasting results!

The proportions did shift during later follow-up, as more and more of those who initially experienced only elevated post-prandial glucose later experienced elevated fasting results as well. But that particular progression seems to be slow: even after ten years, a majority of the individuals who were having any high readings at all were having them after meals but not first thing in the morning.

It is because of this pattern, in which diabetes first manifests itself in post-prandial testing and escapes detection by means of fasting tests, that there has been a movement to use the Hemoglobin A1c test rather than fasting glucose tests to screen for diabetes.

It is also because of this pattern that we are urged not to rely only on fasting tests to determine how well we're doing at glycemic control. If you don't know what's going on after you eat a meal, you don't really know what's going on.

Monday, March 14, 2011

Hapy Pi Day! (3-14, you see? Well, if you don't see, it wouldn't be worth the trouble of reading an explanation. But if you can figure out why March 3, 2009 was Square Root day, Pi Day shouldn't be too hard to decipher.)

More significantly perhaps, this was the first weekday under Daylight Saving Time, an institution which makes the British monarchy look purposeful and modern. I did remember to set my clocks forward, but an error in programming my over-complicated clock-radio caused me to have a fairly frantic morning. Oh, well; even though I dislike the idea of DST, I try to enjoy whatever advantages it has. Today the advantage was that, after being unable to go running at lunchtime, I was able to do it after work, without carrying a flashlight.

My test result after dinner was a bit higher than I like to see it, but it was a higher-carb dinner than I typically have. I'll aim to do better tomorrow.

Blood pressure continues to be a struggle...

Good heavens, is nothing certain anymore? Researchers are starting to question the medical significance of being apple-shaped!

Despite the illustration, neither condition involves an actual loss of genitalia -- it's about having your body fat concentrated either above the waist (in which case you are an apple) or below the waist (in which case you are a pear.)

Actually, the message from the researchers is a bit mixed, and I shouldn't over-react to it. The Heartwire headline ("Apples" No Worse Than "Pears" in Terms of CV Risk) refers to a study at the University of Cambridge in the UK which took a closer look at the often-heard claim that obesity is more harmful to your health if you are an apple rather than a pear. And people with Type 2 diabetes supposedly tend to be apples rather than pears, so it's of some interest to us whether apples truly have it worse than the pears do, in terms of health outcomes.

This new study was looking specifically at cardiovascular risk, and the goal was to figure out whether body shape truly had an influence on that risk, independent of other factors such as diabetes and high blood pressure. If you filter out such factors, how much does abdominal obesity, all by itself, contribute to your CV risk? For that matter, how much does obesity in general, regardless of where you're storing those extra pounds, contribute to your CV risk?

The new study is thought to be an unusually authoritative one, because it followed a large number of people (220,000) for a long period (10 years), and because it is a "prospective" study rather than a "retrospective" one. In a prospective study you select a group of people, sort them into categories (for example, smokers and non-smokers) and then watch to see what happens to the individuals in each category over time. In a retrospective study, you select people and sort them into categories after whatever was going to happen to them has already happened, and then look back at their personal histories. The trouble with retrospective studies is that the individuals are selected and categorized after it is already known what has happened to them -- which makes it very easy for the personal bias of the researchers to influence their selections, so that they get the results they were expecting to get. In a prospective study, bias is less likely to influence the results, because the researchers make their choices at the start, without the wisdom of hindsight to guide them.

The new study of obesity and the risk of cardiovacular disease was conducted on a prospective basis, so it probably reveals more about what did happen than about what researchers would have expected to happen.

Okay, so what happened? Well, if you adjust for differences in age, sex, and smoking or nonsmoking status, the "hazard ratio" for obesity is about 1.25, with very minor fluctuations above and below that, depending on how you measure obesity:

Measure of Obesity

Hazard Ratio
(corrected for age, sex, smoking)

Body Mass Index 1.23
Waist Circumference 1.27
Waist/Hip Ratio 1.25

In other words, obesity increases your risk of cardiovascular disease by about 25%. But note that it doesn't make much difference what method you use to measure and define obesity -- the hazard ratio is very nearly the same if you define it in terms of waist/hip ratio instead of body mass index! Which means that, at least in terms of CV risk, obesity has the same effect on you regardless of how the fat is distributed on your body.

But what happens if you then correct the results for differences in other risk factors? What happens if you correct for the influence of diabetes, high cholesterol, and high blood pressure? In that case, the hazard ratio drops significantly, to about 1.10, again with very minor fluctuations above and below that, depending on how you measure obesity:

Measure of Obesity

Hazard Ratio
(corrected for diabetes, cholesterol, hypertension)

Body Mass Index 1.07
Waist Circumference 1.10
Waist/Hip Ratio 1.12

In other words, obesity, if you can separate it out from such problems as diabetes, high cholesterol, and high blood pressure, only adds about 10% to your CV risk (regardless of how the fat is distributed on your body), and this increase is regarded as small enough to be of little significance. (Of course, saying that obesity isn't especially harmful once you ignore the chronic diseases associated with obesity is a bit like saying "Apart from that, Mrs. Lincoln, how did you like the play?".)

Back here in the real world, obesity typically is combined with such problems as diabetes, high cholesterol, and high blood pressure; most obese people (whether they are apple-shaped or pear-shaped) cannot claim that they have no trouble with any of those issues. But some obese people can make that claim, and it turns out that they don't have a greatly elevated CV risk. Well, good for them.

I'm not sure I'm as ready as the study's author's are to regard a hazard ratio of 1.10 as insignificant. When a medication increases your risk of a heart attack by 10%, most people see that as a significant concern. And if obesity not only increases your risk by 10%, all by itself, but also promotes other health problems, so that your risk is actually increased by 25% when all is said and doen, than it seems to me that the price we pay for obesity is pretty steep.

However, it is looking as if the cardiovascular risk that comes with obesity is no worse (and no better) if you're concentrating the weight gain above the waist rather than below it.

And now it's time once again for...

Another headline review of cutting-edge health research into issues that you may not have realized were in any doubt!

Friday, March 11, 2011

Although the tsunami unleashed by the huge earthquake in Japan did inflict some damage (mainly to boats in harbor) on the west coast this morning, I didn't need to worry about it, because I'm located too far inland to be affected. However, later in the day, when I heard about the "supermoon" idea that's being promoted as the real cause of the earthquake, that one did bother me -- because you can never go high enough into the hills to escape the rising tide of dumb ideas.

The supermoon theory was put forward by an astrologer who thinks that last night's earthquake was caused by the moon being unusually close to the earth, and that worse is to come on March 19th, when the moon will be even closer to the earth, and on the night of a full moon, ooooooooh!

One tiny flaw in this theory is that the moon was not unusually close to the earth last night (in fact, it was further from the earth than it is on average). The earth-moon distance varies over the course of a month, because the moon's elliptical orbit is slightly more oval-shaped than circular, but that has been going on for rather a long time now, and we seem to be coping with it. (By the way, the amount of variation in earth-moon distance is hardly dramatic -- the shortest possible distance is only about 10% less than the longest possible distance!)

It's true that there will be a full moon on March 19, and that the moon will then be in the part of its orbit that has the lowest earth-moon distance. Sometimes those two things coincide; it's not a rare occurrence, and although it does produce higher tides than we usually get, the historical record does not show that large earthquakes are likelier to occur at such a time.

Even if you know nothing about the moon's orbit or the history of large earthquakes, you could have no excuse for reading about the "supermoon" explanation for the earthquake and not smelling a rat. Honestly, does it make sense that seismologists and astronomers would be uninterested in studying the earthquake/moon connection if evidence for such a connection existed, and that it would be up to the astrologers, of all people, to lead them into the light? The story is obviously suspect from the get-go, but that hasn't stopped some newspapers from running it.

But now I'm wondering if maybe the problem here isn't that people are unable to recognize a bogus story when they hear it -- maybe the problem is that people like bogus stories. Maybe people get a special kind of enjoyment out of accepting a story which they have every reason to doubt. Could it be that the "supermoon" story appeals to people not because they think it's plausible, but because they know it's hogwash, and hogwash is what they like? For a lot of urban legends, the chief selling point is that the story sounds impossible, yet we're told that it really happened. If the story didn't sound impossible we wouldn't enjoy it, now would we? There's a thrill involved in believing something that you know ain't so.

The anti-vaccination movement seems to me to be an example of precisely that sort of thing. At this point the evidence is pretty overwhelming that their claims about vaccines causing autism and other disorders are entirely without merit. But is this leading them to abandon their claims? Not at all. I think they get a kick out of believing something which has been debunked. (Unfortunately, society is going to be paying a high price for the cause they have embraced so whimsically; thanks to their scaremongering, vaccination rates are falling to dangerously low levels, and this is likely to cost lives.)

The anti-vax people are not alone. Similar movements exist to terrorize us about various commonplace and not-measurably-dangerous things, such as aspartame, soybeans, and overhead power transmission lines. Not that excessive exposure to those things is necessarily good for us, but if they were even a tenth as harmful as some would have us believe, the harm would be easy to measure, and it's not.

Often beliefs of this sort are harmless, and there's not much point in arguing about them (if you enjoy thinking that Diet Pepsi will give you leukemia, who am I to spoil your fun?). But I don't think it's a good idea to get into the habit of believing every nightmare scenario or conspiracy theory that comes along.

I sometimes hear some rather reckless views expressed about diabetes, and what causes it, and why more people have it these days. For example: that misguided experts urged Americans to eat a low-fat diet which included a lot of vegetables and fiber and whole grains, and they ran right out and did it, and that's what made so many Americans get fat and become diabetic. Well, maybe, but that part about how we all "ran right out and did it" strikes me as a little fanciful.

Dietary recommendations, no matter how misguided, can only unleash a diabetes epidemic if most people actually follow those recommendations, and so far I'm not absolutely convinced that most Americans really are eating a low-fat diet which includes a lot of vegetables and fiber and whole grains. They might claim that they are doing so, of course. That is always the great downfall fo nutritional studies: they tend to end up measuring the willingness of test subjects to say that they actually are eating the sort of diet which they know they are supposed to say they are eating. (It's like church attendance: America's churches aren't nearly big enough to hold all the Americans who say they are regular churchgoers. Getting an honest answer on a survey is not easy when everyone knows what the "correct" answer is!)

Note that I'm not taking a position here on what sort of diet will or won't cause someone to become diabetic; I'm merely suggesting that, if you're going to blame diabetes on a particular diet, you must first find out if people are really eating that way! Otherwise, it's like blaming an earthquake on our being too close to the moon, without first finding out whether or not the earth actually was close to the moon at the time.

Thursday, March 10, 2011

In his 1906 classic The Devil's Dictionary, Ambrose Bierce gave a wonderful definition of the word "politics": a strife of interests masquerading as a contest of principles.

It's hard to argue that Bierce got it wrong, or that things have changed for the better since his day. Any debate on an issue of public interest is still very likely to involve a lot of posturing by people who want us to think that they only care about what's good for humanity, even though it looks very much as if they care what's good for them. And this is just as true of the politics of science and health as it is of any other sort of politics.

And so, in evaluating any debate about health and health policy, we need to ask the question that lawyers used to ask in ancient Rome: cui bono? ("for whose benefit?"). Who stands to gain from this? In terms of criminal investigation, cui bono is about figuring out who might have had a motive to commit the crime. In terms of debate, it's about figuring out who might have more at stake in the issue than an impartial devotion to Truth. If a particular viewpoint becomes accepted as the conventional wisdom, who benefits from that?

The benefit need not be financial (it might have more to do with advancing a cause, popularizing an ideology, or building an academic career), but it's nevertheless a motive -- it leads people to adopt an idea, and defend it vigorously, perhaps without first making an earnest effort to figure out if it's correct.

We might as well know what sort of personal stake people have in an issue, if we're going to listen to their opinions on that issue. To be sure, knowing who stands to gain doesn't necessarily tell us who's right and who's wrong. You can be pure of heart and still be mistaken, after all. And you can be deeply corrupted by self-interest and still be right sometimes, even if only by accident. Still, knowing who will gain what, if an idea wins the debate, will help us put the arguments for and against that idea in perspective.

Of course, asking the cui bono question would be more useful if it always turned out that one side in the debate was driven entirely by self-interest, while the other side was as pure as the driven snow. It doesn't always work out that way. Often both sides appear to be arguing out of self-interest of one kind or another, and in such cases it is tempting to assume that whichever side we happen to find more sympathetic must be right. Unfortunately, likability is not a reliable basis for distinguishing fact from fiction. Charming people can be wrong, and annoying people can be right (not often, of course, but it happens).

What brings these thoughts to mind is the lawsuit filed today by the Physicians Committee for Responsible Medicine (PCRM) against the US Department of Agriculture (UDSA). The lawsuit relates to the dietary guidelines which the USDA publishes every five years, and in particular to the 2011 edition published in January. The complaint which the PCRM has about the guidelines is more subtle than I was expecting: they say that the guidelines are clear about which foods people should eat more of, but vague and confusing about which foods people eat less of -- and that the USDA's refusal to tell Americans, in so many words, that they should cut down on their consumption of meat, eggs, and dairy products is obviously the result of political pressure applied by agribusiness interests. (For example, compare the explicitness of "Increase vegetable and fruit intake" with  the vagueness of "Replace protein foods that are higher in solid fats with choices that are lower in solid fats and calories and/or are sources of oils.")

Now, just to get this out of the way, it is obviously crazy for the USDA, of all organizations, to be America's advisor on which foods are healthy to consume.  The USDA is concerned with what's good for American agribusiness, not with what's good for American health.  It would be ridiculous to expect the USDA to issue guidelines urging people to stop consuming products which the USDA exists to promote. So, regardless of what the arguments are in favor of (or against) the recommendation "avoid meat and dairy products", I think we can take it for granted that the USDA would never, under any circumstances, convey that message to the American public. I doubt very much that a lawsuit will change that situation.

So, the USDA's bias is hard to overlook. But the PCRM's bias is pretty hard to overlook, too. The PCRM advocates avoidance of all animal foods, and is closely associated with PETA, the radical animal-rights organization. (Also worth noting: there's an organization which exists largely to oppose PCRM and PETA, known as Center for Consumer Freedom. The CCF is, of course, a lobbying group representing the food and beverage industry.)

Okay, so how do we figure out who should win this lawsuit? The USDA and CCF on one side, or the PCRM and PETA on the other? Both sides are clearly biased. One serves the interest of agribusiness, and one serves the interest of animal-rights activists. I think most people will choose sides here based on which group they find easier to hate (the factory-farm barons or the PETA commandoes). However, I'm not sure that choosing sides on that basis will actually tell me whether eating beef has a good, bad, or indifferent impact on my arteries. Maybe I'll just have to figure that out from whatever credible research results I can find.

Unfortunately, the research results on this issue are mighty contradictory! And, of course, any health question that is complicated if you don't have diabetes becomes ten times as complicated if you do have diabetes.

Other than "don't take in more carbohydrate than your glucose meter tells you your system can handle", I'm not sure I have any core beliefs left about what sort of food people with diabetes should eat. I have my preferences and prejudices in this area, but  I don't know what's true; I don't know whom to believe.

I guess that's why I try to focus on exercise instead. I'm pretty sure I can figure out how running affects me. Will I ever know for sure how pastrami affects me? Probably not!

Wednesday, March 9, 2011

I surprised my running buddies today by suggesting we run the Fountaingrove Loop, a long (5.7 miles) and extravagantly steep route which we only do once in a while. I didn't propose this difficult route because I was feeling exceptionally strong today, but because I felt that I was due for an exceptionally hard workout today. Yesterday I hadn't gone running at lunchtime, because of a schedule conflict at noon, and the evening workout at the gym hadn't been tough enough to make up for that. Also, because of schedule and weather problems on Sunday, I didn't fit in a long run on the weekend, as I usually do -- I'd done another middling gym workout instead. I just felt that I owed myself a hard run.

Not that my glucose results have been bad this week -- on the contrary, they've been quite good. But I still have it lodged firmly, in the back of my mind, that I need to do at least one really hard workout a week, and if I don't feel that I've done that, I become uncomfortable. I feel as if I'm storing up trouble, and the consequences will show up soon enough. So, I sometimes push myself, even if there's no evidence that anything is going wrong at the moment. Better safe than sorry!

In yesterday's blog, I talked about America's "diabetes belt", and about some of distinguishing (and possibly relevant) characteristics of the population there (for example, people who live within the diabetes built tend to weigh more and exercise less than people living outside it). But, as I pointed out, there might be other differences between people living inside and outside the diabetes belt, differences which are relevant to diabetes but have not yet been recognized as significant.

Well, it's only 24 hours later, and I've already heard about another apparent difference between people living inside and outside the diabetes belt: in a word, happiness. To the extent that happiness is measurable, there seems to be more of it outside the diabetes belt than inside it.

At least, that is what I conclude from the resuts of the 2010 Gallup-Healthways Well-Being Index. This is an attempt to rate the average local happiness level of people living in a particlar region. Criteria include emotional health (smiling, laughter, etc.), life evaluation (expectation of good times over the next five year period), and physical health (including feeling energetic and well-rested). Overall, America's average score of 66.8 on a scale of 0 to 100 is apparently nothing to brag about, but some states are happier than others.

Hawaii turned out to be the happiest state. No big surprise there, really.

West Virginia was the least happy state. I don't know if I would have picked that state is the unhappiest of all, but I certainly would have assumed that it was in the running. (I don't know a lot about West Virginia, but I know that coal-mining is a big industry there, and that it is more or less legal there for the owners of coal mines to kill their employees; it doesn't sound like a recipe for good times.) Then I noticed that the next four runners-up for last place in the happiness race were Alabama, Arkansas, Mississippi, and Kentucky. Wait a minute -- aren't these unhappy states all located in the vicinity that has been identified as the "diabetes belt"? Why yes, so they are!

Here are the 50 states, ranked from happiest (at the top) to unhappiest (at the bottom), together with my notes on whether each state lies witnin (or partially within) the diabetes belt. Note the trend in the right column as you get further from the top of the table:

Happiness Rankings of States in the USA
Rank State Inside Diabetes Belt?
1 Hawaii no
2 Wyoming no
3 North Dakota no
4 Alaska no
5 Colorado no
6 Minnesota no
7 South Dakota no
8 Utah no
9 Connecticut no
10 Nebraska no
11 Massachusetts no
12 Maryland no
13 Washington no
14 Montana no
15 Kansas no
16 New Hampshire no
17 Vermont no
18 California no
19 Iowa no
20 Idaho no
21 New Mexico no
22 Virginia Partially
23 Wisconsin no
24 New Jersey no
25 Maine no
26 Illinois no
27 Oregon no
28 Texas Partially
29 Arizona no
30 Pennsylvania Partially
31 Georgia YES
32 New York no
33 Rhode Island no
34 Missouri no
35 South Carolina YES
36 North Carolina Partially
37 Florida Partially
38 Oklahoma no
39 Indiana no
40 Tennessee YES
41 Michigan no
42 Louisiana YES
43 Delaware no
44 Nevada no
45 Ohio Partially
46 Alabama YES
47 Arkansas Partially
48 Mississippi YES
49 Kentucky YES
50 West Virginia YES

Hmmmm. It's hard to ignore the trend:

But now that we've spotted the statistical correlation, we are left with the usual unsolvable problem: figuring out what that correlation actually means. It's clear enough that the states with the highest diabetes rates are also the unhappiest states, but why is that the case? Is it because unhappiness causes diabetes, or because being diabetic makes people unhappy, or something else?

As I pointed out yesterday, the diabetes belt has many other characteristics to distinguish it from the rest of the country (notably obesity and lack of exercise); now we must add unhappiness to the list. But how do cause-and-effect relationships really operate among all these variables?

There could be a lot of reasons for people to be unhappy (I mean reasons besides brooding about the fact that you're sedentary, fat, and diabetic). And there could be a lot of ways for unhappiness and health problems to affect one another.

Anyway, it's awfully hard to disentangle all the issues that might be playing into the unhappiness and poor health of people living in the diabetes belt. But if all these issues are inter-related, maybe there is hope that improving one of them might lead to improvements in the others. For example, if people were less sedentary there, they might find that exercise helped them to become less depressed and less diabetic.

You have to start somewhere!

Tuesday, March 8, 2011

Well, that's a lower blood-pressure reading than I've been getting since I bought the new meter. It's still not as good as the results I used to see with the old meter, but I'll keep working on trying to bring it down.

Good results on glucose, though.

I've been hearing lately about America having a "diabetes belt". Wanting to see a picture of it, I did a Google image search, and at first I came up with this:

This is from a web site called, if memory serves, "Products For People So Stupid That They Regard Inhaling As An Intellectual Challenge". Anyway, if you're willing to wear a red and blue yin/yang symbol around your midsection, you can use the fields created by the magnets embedded in the belt to heal your liver problems, your stomach problems, your "naval" problems (I suppose this refers to an unhealthy compulsion to make war on the high seas) and your pancreas problems (that is, diabetes). Why exposure to a magnetic field should cause a diseased organ to heal itself, I'm not sure (human organs aren't constructed of ferromagnetic materials, so a magnet would seemingly have no impact on them). But, looking on the bright side, the product sells for only $4, and as far as I know it hasn't been found to increase your risk of heart attack. Let's face it, diabetes patients are routinely charged a lot more that that, for remedies more dangerous than that.

Anyway, further investigation led me to articles about another kind of "diabetes belt" -- a clustering of counties with high diabetes rates in the American southeast. The counties with diabetes rates over 11% are given a dark red coloring in this map:


Okay, so America has a "diabetes belt". But what does that fact reveal about America, or about diabetes? What does it mean that diabetes rates are exceptionally high in one region?

I guess it means whatever you want it to mean. Depending on which particular axe you have to grind, you can point to any local characteristic of the "belt" and declare it to be the smoking gun. If people living inside the diabetes belt tend to wear flannel shirts more frequently than people elsewhere, then wearing flannel shirts causes diabetes and that's that. Case closed! 

So far, however, I seem to be the only one who has raised the flannel-shirt issue as a possible explanation for the diabetes belt. Most commentators have concentrated on a lifestyle issue of a different sort: in addition to its high diabetes rate, the "belt" also features a high rate of obesity. Most people assume that we need look no farther than that for an explanation.

However, it has also been pointed out that the belt features a high incidence of physical inactivity. People don't exercise very much there -- or rather, people who never exercise at all are more common there. Dark blue in this map indicates areas where more than the 32.6% of the population are physically inactive:

I guess it's not surprising that a population with a high obesity rate would also have a low exercise rate, whether it's because sedentary living encourages weight gain or because being fat discourages exercise.

Neither is it surprising, to most of us, that a population with a high obesity rate and a low exercise rate would also have a high diabetes rate. However, many people like to think of diabetes as a genetic disease, and hate to hear it described as a lifestyle disease. Is there any way they can hope to define the "diabetes belt" as genetically different from the rest of the country, so that lifestyle issues aren't needed to explain why the belt is there?

Well, maybe. African ancestry is said to be more common inside the belt than outside it, and some genes associated with diabetes are more common in Africa than in Europe. But are local differences in the gene pool actually big enough to account for the disparity in diabetes rates? I doubt it, but conceivably the it's-all-in-your-genes crowd have a chance at establishing their case this way.

On the other hand, if you're inclined to blame diabetes on particular foods, as opposed to overeating in general, you might be able to make a case that people living within the diabetes belt eat more of the bad foods, and fewer of the good ones, than people elsewhere. I don't know enough about what people eat within the diabetes belt to know what sort of argument would make sense here, but I've heard that starchy food items, prepared in a deep fat fryer, are staples there.

Clearly there is something very unhealthy going on in the American southeast -- although perhaps it would be more accurate to say that there is something very unhealthy going on in America, and the southeast is leading the way. Rates of diabetes, obesity, and inactivity have been rising all over the country, not just in the southeast. These things just happen to be at their worst in the southeast.

But we should try not to forget that the issue of local variations in diabetes rates is highly complicated, and it might be impacted by factors which we haven't yet considered.

Flannel shirts, I'm telling you! That's what causes diabetes. You heard it here first! (But now I'll probably hear from a reader in the southeast, reporting that nobody wears flannel there, and that diabetes is probably caused by exposure to okra).

Monday, March 7, 2011

I'm still getting higher blood pressure numbers with the new meter, and still wondering if this is real or an artifact. But it's not completely unlikely that I'm letting myself get too stressed about things lately.

At least my glucose numbers were good today. But I want all my numbers to be good, because they all matter. Of course, if I could stop being such a perfectionist about it, maybe my blood pressure would come down a bit! It could well be that one of the causes of elevated blood pressure is frustration at how high your blood pressure is.

I've long thought that diabetes management is, by nature and necessity, a DIY project. If you don't Do It Yourself, no one else can do it for you. Your doctor certainly can't do it for you, because your doctor is not going to be at your side night and day, watching your every move and intervening whenever you seem to be on the verge of making a bad choice.

Of course, if you're rich enough, you can take the Michael Jackson approach, and hire your very own private doctor to be constantly on call to take care of you. But, come to think of it, the Michael Jackson approach didn't work out too well for Michael Jackson, so maybe it's not that good an idea, even for those who can afford it.

At any rate, for those who aren't big-spending pop stars, DIY diabetes management is the only good option available. You don't have a choice between managing your diabetes and having it managed for you; the choice you face is between managing your diabetes and letting it go unmanaged.

To be sure, a lot of the people who go for the latter option like to imagine that their doctor is capable of managing their diabetes, and is actually doing so. Well, maybe, in a sense -- in about the same sense that the Chairman of the Joint Chiefs of Staff in Washington is "managing" the second-shift vehicle maintenance crew at Camp Lester, Okinawa. If you're not on the spot, and you don't have current information, "managing" is too strong a word for your degree of involvement in the situation. When it comes to diabetes management, doctors can advise, but they can't act.

And pretty soon, apparently, they won't be able to advise, either...

A discussion on the dLife forum brought to my attention a study that was done on how well the current generation of medical students, preparing for careers as primary care physicians, are being trained on the subject of diabetes management. In a word, they aren't. Their unfamiliarity with diabetes is almost amazing. (For example, slightly less than 40% of third-year residents could correctly state the goal for fasting plasma glucose.) This seems to be part of a larger, and weirder, pattern of giving primary-care medical students an education which has little to do with the sort of patient care they will actually be involved in (for example, most primary care physicians deal with their patients mainly on an outpatient basis, but their education is focused on in-hospital care; the outpatient care which they will actually perform in is not what they get trained to do).

In a way, you could argue that the medical schools are merely being practical: doctors can't really manage their patients' diabetes, so why pretend that they can? Why not focus on the areas where they can actually do some good?

Well, here's why that breezy attitude is not good enough: millions of people have diabetes already, and millions more are going to, and diabetes causes a lot of serious problems if it's not managed well. Something has to be done about this. Even if doctors can't manage their patients' diabetes for them, they need to be able to do a good job in their advisory role. And it's hard to see how they can advise people on how to control their blood sugar, without at least having a pretty clear idea of what controlled blood sugar would look like.

It seems to me that busy young doctors who have not received much education on the subject of diabetes are unlikely to look beyond the facile half-truths of the conventional wisdom du jour on the subject -- such as the conventional (and very dopey) interpretation of the ACCORD trial results which I complained about in my March 4th blog below. It's the sort of thing that could only be believed by an uninformed person in a hurry, but the medical schools seem to be planning to saddle us with a lot of young doctors who are uninformed and in a hurry.

I'd be the first to admit that a doctor cannot sit down with a patient and explain, in the brief time that a doctor is allowed to talk to a patient these days, what diabetes is and what has to be done to control it. But it does seem as if it would be possible to hand the patient a book which explains these things. It would also be possible to send the patient to a training class on the subject (that's what my doctor did). But what actually seems to happen to a lot of patients, to judge from the anguished messages they post on diabetes forums, is that they're are given a prescription for something and told to eat whole-grain bread and hope for the best.

This isn't good enough.

If doctors have decided that they can't manage their patients' diabetes, shouldn't they just come right out and say so? Patients need to hear this from their doctors in plain English: "I can't manage this for you. I can't keep you safe. I can't ensure that you get a good outcome. I am almost entirely powerless here. How well this turns out will depend on what you do, not what I do. You need to learn as much as possible about this. Here's a book. Here's a class you can take. Here are some web sites you can check out. But you need to take charge of this, because I can't -- and because, if you don't, it's going to be really bad."

Even if doctors were that blunt about it, some patients would still indulge in the fantasy that this is a problem for their doctors to solve. But maybe more patients would realize that this is their problem, not their doctor's problem, and they need to take charge of it. And I think that would be an extremely positive development.

Friday, March 4, 2011

Today was planned to be my rest day from exercise this week, but I decided to run today instead, and shift my rest day to Sunday, when I'll be busy (and when a rainstorm is expected, which is not my favorite kind of running weather). Today the weather was nice -- why not take advantage of the sunshine while you still have it?

The blood pressure reading tonight is not as bad as the one last night, but it's still higher than the kind of reading I've been used to seeing. I wonder if it's possible that my new BP meter is giving me the equivalent of White Coat Syndrome: I worry that it will show me higher readings than my old meter did, and because I'm worrying about that, it does. Well, if that is the case, my readings will probably go down gradually as I become accustomed to the new meter. But if that doesn't happen, I'm stuck with the problem of figuring out whether my new meter is reading high, or my old meter was reading low.

Oh no -- not again! That damned ACCORD trial is back in the news. Exactly why it's back in the news I'm not sure, but every six months or so, somebody warms-over the data from that misbegotten study and publishes another report about it, and the health-news media launch another wave of gross misrepresentations of what that study supposedly found -- with serious negative consequences for diabetes patients.

I don't really want to write about ACCORD, because it makes me angry, but I can't ignore it entirely when it starts receiving press attention once again. I'll try to say what I have to say about it as briefly as possible. 

ACCORD stands for "Action to Control Cardiovascular Risk in Diabetes". The ACCORD study looked at a group of out-of-control diabetes patients considered to be at high risk for cardiovascular disease. The patients were divided into two groups, and one of those groups was given "intensive" drug therapy (insulin combined with multiple oral meds), in order to pursue A1c reduction more aggressively than is usually done. The other group received more moderate, conventional treatment. One of the less expected outcomes of the study was that the rate of death from cardiovascular events was not lower among patients in the "intensive" group -- in fact, it was higher. To many people, this seemed so startling that they couldn't resist over-interpreting it.

In most press reports about ACCORD, the study was described as having shown that "it's dangerous to reduce your A1c". Now, ACCORD did not show that A1c reduction is harmful (such a conclusion would fly in the face of virtually all other evidence ever gathered on the subject). What ACCORD showed was that, within a particular group of very unhealthy patients, one therapy aimed at A1c reduction was less safe than another therapy aimed at A1c reduction. (Which shouldn't come as a big surprise, given that some of the oral medications given to the patients in the "intensive" group are strongly suspected of increasing the risk of heart attack!)

I have heard it claimed (I'm not sure if this is valid) that many patients in the "intensive" group did not actually succeed in bringing down their A1c results, and that these were the patients who died -- there wasn't an increased death rate among the patients whose A1c levels actually did come down. If that's true, the meaning of the ACCORD results is more or less the opposite of what we're usually told it is.

In any case, the fact that one treatment aimed at reducing A1c is riskier than another treatment aimed at reducing A1c tells us absolutely nothing about whether or not reducing your A1c is a good idea. (And we know that is a good idea, unless all other studies of A1c are wrong.)

The ACCORD study asked a very limited question ("will this group of high-risk diabetes patients do better on this particular drug therapy?"), and the answer that came back ("no") has been wildly overinterpreted and overapplied.

When a treatment aimed at a particular therapeutic goal ends up increasing the death rate among patients, we usually blame the treatment rather than the therapeutic goal. If someone published a study which showed that speech therapy for children who stutter does more harm than good, and then it turned out that the "speech therapy" in question consisted of beating the children with sticks, most of us would reckon that the problem here was with the method, not the objective. But, for some reason, we're supposed to see things differently in the case of the ACCORD results. And apparently some doctors are willing to see things differently in the case of the ACCORD results.

These days, many diabetes patients who are nothing like the patients included in the ACCORD study are being led to believe that A1c reduction is dangerous in and of itself -- regardless of how it is achieved. Even patients who aren't taking any drugs at all are, in some cases, being warned of the supposed dangers of having an A1c level much below 7. (One wonders how all those poor non-diabetic people, with A1c levels of 4 to 5, manage to cling bravely to life for as long as many of them do.)

This A1c-reduction-is-dangerous meme is nonsense, and it's dangerous nonsense. Worst of all, it's obvious nonsense -- so why on earth are we still hearing about it?

Thursday, March 3, 2011

Okay, so I broke down and bought a new blood pressure meter, and based on tonight's result it seems to read much higher than the old one did -- alarmingly high, actually. But what's really going on here? Does the new meter read higher than it should? Did the old one read lower than it should? Or is my blood pressure simply high tonight?

The last of these possibilities isn't entirely unlikely. I had a very annoying experience this evening which rather spoiled my mood, and may have driven up my blood pressure. But I'd hate to think that I've been up in this range for a long time without knowing it!

Well, if subsequent history shows that my blood pressure really is higher than I had thought it was, I'll have to deal with it somehow.

Of all my opinions about Type 2 diabetes, perhaps the strongest is that the therapeutic power of exercise is under-emphasized, under-appreciated, and under-utilized. Compared to the feverish attention given to dietary issues (by diabetes patients and their advisors alike), exercise is seriously neglected.

To be sure, the experts usually do mention exercise... in passing... as something which patients ought to be doing. But you'd never guess, from the way they state this dutifully and then drop the subject, that exercise is crucial -- that it provides benefits which are not available from any diet or any combination of medicines.

I'm doing what I can to rectify that situation, but it's not easy. In trying ot persuade people to see exercise as the cornerstone of diabetes management (not as an optional extra which they might want to add to their program, if they have enough time and energy for it), I'm up against two major obstacles:

  1. Most people don't want to exercise.
  2. Most people don't understand how exercise could possibly provide the benefits that it is said to provide (and because they don't understand how it works, they doubt that it does).

These two objections tend to reinforce one another. If you don't want to exercise, you're going to be warmly receptive to the idea that exercising wouldn't make that much difference anyway. And when you don't see why you should exercise, you're not going to try very hard to overcome your reluctance to do it.

Perhaps surprisingly, it is the second of those two objections which seems to me more daunting, for the simple reason that nobody really understands how exercise does what it does for us. Perhaps physiologists would protest here that they have actually learned quite a lot about this, but to me it appears that they have merely catalogued various detectable differences between people who exercise regularly and people who don't, without being able to explain what exercise is doing to people to create those differences.

It is comparatively easy to set up a study in which the effects of exercise are observed and measured, so that we know these effects are real -- but it is very hard to discover the mechanism through which those effects are created.

For example, we know that exercise improves the ability of cells to absorb glucose from the blood. (In fact, this tendency complicates studies of the "glycemic index", because GI is determined by measuring the effect of a given food on blood sugar, and the GI of a given food is considerably higher in people who don't exercise regularly than in people who do.) But if exercise makes your cells absorb glucose more readily, do we know how exercise does that? Yes, say the pysiologists! We understand at least part of the picture: exercise stimulates the cells to product more GLUT-4 transporters (the tiny chemical hooks which poke out through the cell wall and drag glucose molecules inside it). Well, fine, but that sounds to me like a description of what happens, not an explanation of why it happens. How, exactly, does exercise cause the cell to start producing more GLUT-4 transporters? For that matter, how does a cell even know that you're exercising in the first place? I don't think the details of this are especially well understood.

The tendency of exercise to reduce resting heart rate and blood pressure seems to be understood, at least to some degree. If you exercise often enough, and you keep at it long enough, the body starts to refurbish your circulatory system -- enlarging existing blood vessels and adding new ones. With your circulatory capacity expanded, you can pump more blood per heartbeat, and therefore your heart doesn't have to work as hard. But how do these changes come about? How does exercise "tell" the body to do these things?  Nobody really knows. Presumably the body is trying to meet the increased energy demands that come with frequent exercise, but how your body figures all this out and formulates a plan of action is hard to say.

Or, to take another example, exercise tends to bring down levels of LDL cholesterol in the bloodstream. But how? How exactly does it do that? (Don't ask, it just does!)

Exercise effects can be considerably more subtle, and difficult to study, than the effects I've mentioned above. Sometimes it takes the most painstaking scrutiny even to find out what is happening, much less why.

For example, a recent study (conducted in Brazil) looked at sedentary individuals, many of whom had metabolic syndrome (the diabetes precursor), who were put on an exercise program for three months to see how this affected their HDL cholesterol. (HDL is the one commonly called "good cholesterol" because of its role in cleaning out the arteries by dissolving placques that have formed on the arterial walls). People with metabolic syndrome or Type 2 diabetes tend to have abnormally low HDL levels, and raising the level is very hard to accomplish. In this study, three month's worth of exercise did not raise patients' HDL levels. And yet, and yet...

The researchers found that exercise improved the functioning of HDL cholesterol. There wasn't more of the stuff, but it did its job of cleaning out the arteries better. The article expresses this, unfortunately, in jargon clumps: the test subjects had (in addtion to reductions in blood pressure and waist circumference, and a 20% increase in peak oxygen uptake), "increased paraoxonase-1 activity after training -- although not as high as in controls -- and improvements in HDL subfractions' antioxidative capacity. Furthermore, patients' HDL particles more readily accepted free cholesterol and cholesterol esters from lipidic nanoemulsions after exercise training, to a level similar to that in controls."

In other words, as I said, test subjects may not have had more HDL, but whatever HDL they had was working better after they'd been on an exercise program for a while. The researchers concluded: "All these findings indicate that the interference of nonpharmacologic interventions on HDL metabolism goes beyond, and is not accurately reflected by, the plasma HDL levels, highlighting the importance of (also) evaluating the functional aspects of the lipoproteins."

I'm skeptical that doctors are going to stop being content to measure HDL quantities, and start conducting deeper investigations into how well HDL is functioning. But maybe that will happen.

This article brought back memories of my own attempts to raise my HDL cholesterol, back when I was diagnosed in 2001. Four months after diagnosis (in other words, after four months of exercise), my HDL only went up from a pathetic 32 to a similarly-pathetic 33, and my doctor doubted it would ever go higher than 37, considering how strong the genetic bias towards low HDL is among Type 2 diabetes patients. But in later years, as I continued exercising, my HDL eventually climbed up into the normal range (it's usually above 50; the last time I was tested it was 52). But even in that early test, where four months of exercise had produced no significant increase in HDL, apparently the HDL I had was already working better for me, just because I was exercising.

We don't know why exercise has these effects, or how it manages to achieve them, but it does. So I think we might as well stop arguing and start working out.

Wednesday, March 2, 2011

I'm not exactly drawn to health-news articles which combine the words "diabetes" and "death" in the same headline, even though I have been diagnosed with the former, and as a mortal I'm susceptible to the latter. It's possible that such an article would have some personal relevance for me, but do I really want to read it? If it's only going to depress me, there's no point. But what if I can learn something useful from it -- and even something encouraging from it? Perhaps the headline gives a false impression of the news that appears under it.

When I saw that Medscape article today entitled "Diabetes Linked to Premature Death From Vascular Disease, Other Causes", and once I'd had time to get over my initial reaction (which was, "Well, DUH!!!!"), I decided that reading it might be worth the risk, because it was very unlikely to contain any bad news which wasn't already well known, and it was at least somewhat likely to contain a bit of good news hidden somewhere within it. Which it did, but you'll have to bear with me for a bit while I trudge past the gloomy bits.

The article was actually a summary of another article, newly published in the New England Journal of Medicine (only the abstract is available for free, however). It was a study of risk factors for death from various health problems among diabetes patients. The actual title used by NEJM is "Diabetes Mellitus, Fasting Glucose, and Risk of Cause-Specific Death". Perhaps this title doesn't strike you as significantly more chirpy than the Medscape version quoted earlier, but I have my reasons for seeing it differently.

In changing the title from "Diabetes Mellitus, Fasting Glucose, and Risk of Cause-Specific Death" (which merely identifies the three subjects that are going to be discussed) to "Diabetes Linked to Premature Death From Vascular Disease, Other Causes" (which announces a conclusion about how two of those three subjects relate to each other), the Medscape rewriter (Laurie Barclay, MD) revealed what she thought was the most important or interesting aspect of this report on how various health risk factors vary when diabetes is involved. I don't share her view of this, however.

That diabetes is associated with a heightened risk of death from cardiovascular disease hardly qualifies as a new and startling discovery. Even the size of the added cardiovascular risk factor in diabetes patients (2.3 as reported here) is very much in line with what other researchers have been reporting (usually 2 to 2.5). Yes, cardiovascular risk is at least doubled, and probably more than doubled, in diabetes patients. We knew that. Announcing it is like announcing that moving to Seattle will increase your exposure to rain.

Other diseases, such as various forms of cancer, showed either a moderately higher or slightly lower risk among diabetes patients. The numbers here were not very dramatic; again, this was not where the big news was, so far as I am concerned.

To appreciate what made this study newsworthy, you need to take another glance at the title of the original article: "Diabetes Mellitus, Fasting Glucose, and Risk of Cause-Specific Death". The researchers were not just comparing "diabetes patients" as a whole with the rest of the population, as is usually done (seemingly on the assumption that diabetes patients are all alike, regardless of how well or how badly they manage their condition). In this case, the researchers actually took the trouble to compare the risk factors for diabetes patients who were in control to those who weren't. And... surprise, surprise! It turns out that control matters!

"Fasting glucose levels exceeding 100 mg/dl, but not levels of 70 to 100 mg/dl, were associated with death."

So right there, in what appears (at least in the abstract of the full article) to be a casual throwaway line, we find the hidden gem in this research. This is the big news. The researchers did not find an increased risk of death among those whose fasting glucose was in the 70 to 100 range!

It is hard for me to get inside the mind of someone who could look at this research, and decide that the point worth emphasizing here is that diabetes patients die of heart attacks, rather than that there's a way for diabetes patients not to die of heart attacks.

I can only speculate about the motivations or prejudices that cause medical professionals to filter the available information about diabetes in this discouraging and harmful way -- always burying the good news, and highlighting the bad. My best guess is that medical professionals take it for granted that diabetes patients who maintain excellent glycemic control are so rare as to be statistically insignificant, and there is no point in thinking about those patients at all. When they talk about diabetes patients, they mean the typical kind of diabetes patient, by which they mean the patient who hasn't got control, hasn't got a clue, and hasn't got a chance. What's the point of holding out any hope to such a patient?

The problem is that prophecies of doom tend to become self-fulfilling. If you don't hold out any hope to diabetes patients, they all become the typical patient, because they don't know there is any other option, and because they haven't been shown the evidence that being a non-typical patient can actually work. Why be different, if you don't know that it will make a difference?

Tuesday, March 1, 2011

It's supposed to rain tomorrow -- but then again, it was supposed to snow on Friday night, and that didn't happen. And yet, somehow, I'm readier to believe the meteorologists about the rain tomorrow. If they're right, will I have the willpower to go running at lunchtime tomorrow, even if it's raining hard and my running buddies bail out on the run? We'll see.

But today it was sunny and clear. Cool and breezy, but I was dressed to cope with that. So I went for a run while the sun was still shining.

I'm not much of a traveler, but here's one thing I do like about being very far from home: the local news. I get to watch people I don't know, living in a place where I don't live, getting all worked up about public issues which will never affect me. I find it refreshing to hear all about the great big intractable problem of the day, when I know that I don't have to worry about how that problem is going to get solved. I can enjoy the soap opera of public controversy without being bothered by it, since the outcome won't matter to me either way. 

I sometimes experience a similar sense of blessed detachment when I get tired of gathering information about diabetes, and try reading up on a health problem I don't have. I become a disease tourist, briefly visiting the world of those whose health problems are different from mine, and finding out about the controversies roiling their little corner of the universe. 

Today, for example, I read an article on fibromyalgia, or rather on the comments arising from a debate about fibromyalgia, and I was pleased to note that fibromyalgia is just as big a mess of a subject as diabetes is, and that it has a similar tendency to make people shrill and emotional and unable to listen to what anyone else is saying. In fact, it appears that people misunderstand each other even more deeply about fibromyalgia than they do about diabetes, and it was news to me that such a thing was possible. 

Fibromyalgia and diabetes have a few things in common, it turns out, so perhaps studying one of them has at least a metaphoric relevance to the other. Both "fibromyalgia" and "diabetes" are very broad terms, and each of them probably places too wide a range of health problems under a single label. Both diseases have proved difficult to define satisfactorily, and this has led to problems in establishing firm diagnostic criteria. Both are perceived through a prism of social prejudice, because of the kinds of people who are most typically diagnosed. On each of these points, the problems are bigger in the case of fibromyalgia than in the case of diabetes. It's a mess, all right. 

The biggest reason that fibromyalgia is a mess of a subject is that it's impossible to say exactly what is and isn't included in that subject. Fibromyalgia has been described as "a name in search of a meaning". Fibromyalgia is most frequently described as chronic pain (and hypersensitivity to pressure) in muscles and connective tissues. But that is just for starters. Many, many other symptoms have been idenfitied with fibromyalgia, and each patient seems to have a different selection of these other symptoms. Also, fibromyalgia is typically combined with other diseases (including mood disorders, sleep disorders, and bowel disorders). There is no lab test you can take that will reveal whether you have fibromyalgia or not. Many doctors feel that fibromyalgia is so vaguely defined that it could mean anything, ends up meaning everything, and therefore means nothing. 

A rheumatologist added this comment to the discussion:
"Fibromyalgia is an invention, not a diagnosis. It's a grab bag of puzzling symptoms, not all of which may be related. Calling it a syndrome is premature and unhelpful; symptomatic treatment is offered until we know more."

And an internist:
"Having been practicing primary care internal medicine for 30+ years, I feel like fibromyalgia snuck in the back door while practitioners were looking the other way. I know that sufferers defend their disease vigorously, but it is hard to buy an entity with no diagnostic lab, imaging, pathology, or other objective findings. Physical findings despite attempts to codify them are shaky at best, and a significant number of sufferers improve on antidepressants. What are we treating here? I propose a nationwide poll of practicing primary care physicians, neurologists, rheumatologists, and orthopaedists asking whether they think that this is a real entity. I bet the answer is no. When that is settled, we can get to the business of figuring out what really ails these folks instead of disabling them with an illness and telling them that they will never get better."

Now, it is worth pointing out here (because a great many people miss this point entirely) that, when doctors say that a disease has been so vaguely defined that they don't think it's a "real" disease, they are not necessarily denying that people who report some of the symptoms of that vaguely-defined disease actually have anything wrong with them.

For example, suppose you go to your doctor and say that you think you have this disease you've been hearing about, called SAS (Sore Arm Syndrome). But your doctor rejects the term "Sore Arm Syndrome", on the grounds that it's too vague and covers too many possible causes of a sore arm. Does this mean your doctor is saying your arm isn't sore? No, it does not. Arm soreness is a real symptom, and probably a common one, and I'm sure your doctor believes that your arm is sore. The problem is that inventing the phrase "Sore Arm Syndrome", and applying it to everyone on the planet with a sore arm, contributes nothing to our understanding of the many different reasons why someone's arm might be sore. Arm soreness is a real symptom, but SAS is not a real disease. Note that the internist I quoted above, who said that fibromyalgia isn't a real disease, did not say that people with "fibromyalgia" symptoms have nothing wrong with them -- he said that we need to figure out "what really ails these folks", and that inventing a single name for what ails all of them is not helping us get there.

Other doctors chimed in with reports that a large share of their "fibromyalgia" patients were suffering from something else and improved when that other condition was treated (sleep apnea, depression, inflammatory conditions, and small-fiber neuropathy being the most common examples). Conditions suspected of being able to trigger fibromyalgia symptoms include stress, depression, sleep disorders, food allergies, head trauma, dormant viruses, and vitamin D deficiency (the last of which is currently suspected of being able to trigger anything short of lycanthropy).

One doctor said this:
"I believe that fibromyalgia is, in most cases, a somatic presentation of anxiety or depression. It is real, with pain and inflammation in some cases. But I believe in its essence that it is a form of depression and anxiety in most cases."

This comment infuriated patients who clearly don't know what 'psychsomatic' means: "The time has come for physicians to recognize these illnesses apart from the psychosomatic garbage that has been propagated."

Get a clue, folks: a psychosomatic illness is not an "imaginary" illness which exists only in your head. Psychosomatic means mind-body; a psychosomatic illness is an illness in which the mind-body interaction induces physical symptoms. If stress makes your blood pressure go up, that is a psychosomatic effect, but the blood pressure increase is not imaginary; it is just as real as the stress that triggered it (and far easier to measure). Psychosomatic illnesses are real, they are common, and they are harmful (they are believed to contribute enormously to the incidence of coronary heart disease, for one thing). Psychosomatic illnesses need to be taken seriously, and that won't happen so long as patients continue to flip out every time the word is mentioned. If fibromyalgia is a psychosomatic condition (or if, as seems more likely to me, one of the many diseases that have been herded together under the common heading of "fibromyalgia" is a psychosomatic condition), you are more likely to get relief from that condition if it is properly indentified and understood some day.

Then there is the problem of prejudice: just as most Type 2 diabetes patients are overweight, most fibromyalgia patients are women. Although fibromyalgia patients are not accused of having allowed themselves to become women (in the way that diabetes patients are accused of having allowed themselves to become fat), fibromyalgia patients are nevertheless viewed with suspicion: when a disease is hard to define except in terms of subjective, non-measurable feelings, and the patients are mostly women, people are quick to accuse the patients of self-indulgence of one degree or another: they're either dramatizing a not-very-serious problem, or they're imagining the whole thing. It's either play-acting or hysteria.

Beyond a doubt, there are some people who pretend to have fibromyalgia symptoms -- because there are some people who pretend to have symptoms of everything. And certainly there is a long history of "fashionable" diseases which everyone who is anyone wants to claim to suffer from. But we have to put that sort of thing aside; I think it's likely that a large share of the patients who report "fibromyalgia"  symptoms are suffering from something, even though we don't really know what they're suffering from, and each of them may be suffering from a different thing.

But I don't think they'll get any help until they can stop being so damned defensive and allow doctors to explore all the possible causes of their condition.

Has this long digression about fibromyalgia taught us anything about diabetes? Maybe not much. But what it has taught me, or reinforced for me, is that it's important for us to let go of our anxieties about the assumptions other people will make about our disease, and assign ourselves the task of arriving (as calmly as we can) at a true understanding of what that disease really is.

If I have to choose between (1) a world in which diabetes is thoroughly comprehended by medical researchers, but the broader public misinterprets their conclusions, and (2) a world in which diabetes is not thoroughly comprehended by anybody, I would certainly choose the former. If researchers come to understand diabetes, then before too long I will be able to understand it myself. Whether a majority of the public ever understands it is not an issue I care about. A majority of the public is usually on the wrong side of any scientific issue, including why it gets colder in the winter. That's just the way life is: most people, given a choice, choose ignorance, and we just have to take that in stride. Better to concentrate on keeping ourselves well-informed than to lament that other people aren't making that effort.

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