Wednesday, June 30, 2010  


That's a pretty low post-prandial result (especially considering that there was rice in the bowl of gumbo I had for lunch). But, once again, this low result was for a meal that I ate directly after running. Yesterday's higher result was from a meal that I ate six hours after running. Maybe the message here is that I can handle carbs a lot better immediately after a workout than I can several hours after a workout.

To some extent that would make sense: the downard pressure on glucose levels that is exerted by a good workout fades over time. How fast, though? According to one paper I've read, there are two different "exercise effects" which have an impact on glucose uptake by muscle cells. The first of these two effects (a direct increase in glucose transport, stimulated by muscle contractions and not by insulin) only lasts for 2 to 4 hours. A second effect (an increase in the effectiveness of insulin-stimulated glucose transport) fades much more slowly, over a period that can last up to 48 hours. If there are two distinct mechanisms, one of which lasts longer than the other, that might explain why I seem to do better with the first meal after a workout: at first, both processes are still working, but later I'm only getting the benefit of the second one. Which I guess means that, if I want to include something starchy in a meal, it had better be the first meal after my workout, not a meal taking place several hours later.

But here I am generalizing from a pitifully small number of data points, which is exactly what we're not supposed to do (especially when the data is coming from anything as variable as a glucose meter).


Nice day today...

Sunny and clear, but it didn't get above about 80 degrees. Everybody was outdoors getting some exercise, seemingly.

I finally caved in, and bought a copy of Born To Run, by Christopher McDougall. The book has become a sensation among runners. The author spent time in the Copper Canyons of Mexico, establishing contact with the Tarahumara Indians -- a reclusive tribe legendary for their ability to do long-distance running (well into advanced years) without suffering the injuries that plague most runners who live in modern cultures. The author, who had suffered some painful running injuries himself, wanted to know what their secret was. Whether or not he ever discovers their secret, I'm not sure -- I'm not that far into the book yet. But one minor secret which he has already revealed captured my attention: "Iskiate", also known as "Chia Fresca" -- a drink which the Tarahumara use to fuel their ultramarathon trecks over rough terrain.

The drink consists of chia seeds dissolved in water to form a gel, mixed with lime juice and a bit of sugar (although the sugar seems to be optional).

Chia seeds: that's where the running world and the diabetes world converge. Diabetes patients have become increasingly interested in chia seeds of late, and (thanks to Born To Run) so have runners. Chia seeds have a nutritional profile unlike any other food that I know of: a plant food that provides complete protein, Omega-3 fatty acids, and lots of soluable fiber (in fact, almost all of the carbohydrate in chia seeds consists of fiber). The seeds are also rich in anti-oxidants (which is apparently the reason that they have a much longer shelf life than flax seeds, the most nearly comparable foodstuff).

Soaking chia seeds in water, even for a comparatively short time, causes them to dissolve into a gel; digesting them seems to have a similar effect. This tends to have a moderating impact on the digestion of other carbs consumed at the same time, which is why a lot of diabetes patients like to include chia seeds in a meal (sprinkling them into soups and salads, for example -- which isn't a culinary distraction, because the seeds don't have any kind of strong flavor). Runners are interested in chia seeds for a related reason: consuming something that slows down carbohydrate absorption while providing alternative energy sources (fat and protein) seems like a good way to stay energized throughout a run.

A lot of runners are saying that drinking Iskiate before a run gives them energy, just like the Tarahumara say it does. Anyway, it does seem like a possible solution to a problem I face nearly every day: I'm about to start my lunchtime run, it's been a long time since breakfast, I'm feeling under-fueled -- but I'm afraid to eat anything, because any food I take in now will only upset my stomach during the run. Maybe a drink of Iskiate would be just the thing.

I've seen various recipes for Iskiate, but it seems like the essential thing is to whisk about a tablespoon of chia seeds in a glass of water, give them some minutes to dissolve, add a squeeze of lime or other citrus, and add some sugar if you think that's appropriate (maybe it is, if you're about to run).

If I remember to take the ingredients to work with me tomorrow, I'll try a glass of Iskiate before my lunchtime run, and see how that works for me. But anyway, I'll give it a try soon.


Tuesday, June 29, 2010  


Here's what I hate about post-prandial testing: I got home from work, ate dinner in a hurry, and then had to get in my car to drive to an out-of-town music rehearsal. So, the one-hour point (my preferred test time) came up while I was driving. I ended up doing the test during a lull in the rehearsal, at the two-hour point. 121 would be an okay result for the one-hour point, but I should be lower than that by the two hour point. It was a pretty high-carb dinner. Actually, the whole day was more carb-centric than it should have been -- I'll make an effort to cut the carbs tomorrow.

I think I let all the rushing-around tonight get to me: diastolic blood pressure above 80. Oh well: do some deep breathing, get focused.


The weather was pretty warm for my noon run, and I may have let myself get a little too dehydrated. I didn't carry water, because the run was less than 5 miles, but maybe things have warmed up enough that I should just start carrying a water bottle even on shorter runs. Getting overheated can raise your blood glucose -- maybe I would have handled my high-carb dinner better if I hadn't overheated myself at mid-day.


I've been hearing a lot about ghosts and guests lately. Specifically, ghost-writers and guest-writers. More specifically, the actual and pretended authors of medical research papers.

Johannes Brahms once quipped that one should never be too critical of music composed by royalty, because you never know who might turn out to have written it. Apparently the same caution applies to research papers, at least in the medical field, because the listed authors often had nothing to do with it. Where that is the case, the listed author is known in the trade as the "guest" writer -- a respected academic figure who is paid to sign his name to a paper which was actually written by an employee of the pharmaceutical industry, known as the "ghost" writer.

What is most shocking about this arrangement is not that it goes on, but that it is widely regarded as normal and acceptable. Many universities and journals have no rules against the practice, and no policies demanding that it be disclosed.

Surprise, surprise: guest-writers and ghost-writers have played an important role in promoting drugs which later turned out to be dangerous (such as Merck's painkiller "Vioxx"). One of them (the anethesiologist Scott Reuben) was sentenced to 6 months in prison today, but for fraud rather than guest-writing. He really did write the papers that appeared under his name -- he just didn't do any research on Vioxx or other painkillers; he simply invented the data. That's not considered acceptable. But anything short of that is considered acceptable, including signing your name to a paper that was written for you by Merck. It's only when the survivors of people killed by the drug you promoted start filing lawsuits that this sort of thing comes to light.

Senator Chuck Grassley has been investigating this issue, and has been finding that medical schools, medical journals, and medical societies often have no policy at all regarding the practice of ghost-writing. He issued a staff report on the subject today, and sent it to the director of the National Institutes of Health, suggesting that NIH grants should come with strings attached: institutions receiving such grants must develop and enforce policies governing authorship of articles, and in particular disclosing any involvement by anyone with a significant financial interest in the subject of the research.

What baffles me is how such practices could ever have come to be seen as anything other than criminal fraud. It doesn't matter to me who actually wrote the "autobiography" of some dumb-bell movie star, but if we don't know who really wrote the research papers that claim this or that drug is safe and effective, that's serious.  Why can't people see that?


Monday, June 28, 2010  


I've fallen into the habit of doing fasting tests rather than post-prandial tests; my excuse for this has been that I'd driven my fasting tests low enough that things must be okay with my post-prandial numbers. 

However, I'm often reminded by various commentators on the subject that fasting glucose tests don't always reveal the true state of affairs. If your glucose is going to get out of control, the first sign of it will probably be in your post-prandial numbers, not your fasting numbers. Which is too bad for me, because I find it awfully convenient do a fasting test when I get out of bed in the morning, and then forget about testing for the rest of the day. Post-prandial testing is a pain, because you have to keep track of the clock, and make sure that the time for the test isn't going to come up while you're doing something that demands your uninterrupted attention (such as driving).

Well, much as I dislike post-prandial testing, it's not exactly the heaviest burden that diabetes has placed on me. Today I figured I might as well stop whining about it and start doing post-prandial tests. So I tested myself tonight after dinner.

There are different schools of thought about when post-prandial tests should be done. I've always done them 1 hour after finishing a meal. Some people wait two hours, but I've found by experimentation that my post-prandial glucose peaks at or near the 1-hour point, and I figure it's best to know how high you're going. My doctor's recommended target was <150 after one hour. A truly "normal" (that is, non-diabetic) result is apparently <120, so I figure that's the real target I should aim for, whether it's always achievable or not.

My result after dinner tonight was 104 -- comfortably within the normal range. I didn't "cheat" by eating an extremely low-carb dinner; it was a big bowl of noodle soup. However, dinner was right after I went running, so that might have been a significant factor (perhaps if I'd run in the morning rather than the late afternoon, my after-dinner test result would have been higher, even with no change in the content of the meal). Anyway, I may have just hit it lucky tonight -- I expect other post-prandial tests will probably be significantly higher than this.

So, I'll be concentrating mainly on post-prandial tests rather than fasting tests for a while, and see what happens. I guess it will be my chance to find out if I'm really getting away with everything I think I'm getting away with.


Two more studies questioning (or rather denouncing) the safety of the diabetes drug Avandia came out today; once again, the statistics show that the drug seems to increase the rate of heart attack, stroke, and other cardiovascular problems.

Some are pointing out that the drug doesn't raise the cardiovascular risk all that much -- 60 people would have to take the drug before one of them got a heart attack from it. So why not just take that risk in stride, if the drug is working for them?

This line of thinking reminds me (rather improbably) of a remark I once heard made about Thomas Jefferson. Throughout Jefferson's lifetime, he was often reported to have fathered children with his slave Sally Hemings. For many years, loyal defenders of Jefferson have indignantly rejected these "slanders", but in 1998 they had to find a way to maintain the party line in the face of the DNA evidence, which said that some of the Hemings children were certainly fathered by a member of Jefferson's family, and most likely by Jefferson himself, given that most of his male relatives had little or no opportunity. Jefferson's defenders tried to pin the blame on Jefferson's brother, or at least to insist that, since the question could never be settled definitely, Jefferson should be given the benefit of what little doubt still remained.

While historians and history buffs were arguing about the implications of all this, the documentary film-maker Ken Burns said that most discussions of this whole issue seemed to him to be missing the point. How much difference did it really make whether Jefferson impregnated Hemings? That wasn't the real scandal here. The scandal was that he owned her. He could have done absolutely anything to her that he felt like doing, and there wouldn't have been a thing she could do about it. If we're going to judge him guilty or innocent of anything, surely that's the main issue. Whether any of her children were also his children is almost beside the point, and getting fixated on that one issue can only distract us from a far more important issue.

I think something similar is going on with Avandia. If we get fixated on the question of how much Avandia raises your cardiac risk, and how much added risk is too much, and how many people have to take Avandia before you see the first "extra" heart attack, we lose sight of what ought to be the main issue, and the real scandal of Avandia: it's a diabetes drug that doesn't reduce your cardiac risk!

People seem to forget that cardiovascular disease is the mother of all diabetes "complications" -- the leading cause of death among diabetes patients, and the main reason diabetes is dangerous. Surely the most important measure of whether a diabetes therapy is "effective" or not is how much that therapy reduces your cardiac risk. If it doesn't reduce it at all, what's the point?

To me, a diabetes treatment that does nothing to protect you from heart disease is like an asthma treatment that doesn't help you breathe, or an epilepsy drug that doesn't prevent seizures. Would we accept those hypothetical drugs as "effective" just because they made a number on someone's lab report look better?

Admittedly, Avandia may help to prevent other complications, so maybe there can be a justification for taking Avandia, providing you're doing something else to prevent heart attacks. But is that what's going on? Or are people simply taking Avandia, while doing nothing about the cardiovacular issue hanging over their heads, and thinking that everything must be OK because their lab reports are looking better?

If the end result of all these investigations into Avandia and cardiac risk is that people who are now taking Avandia end up taking some other drug which doesn't reduce their cardiac risk, then I think we will all have missed the point.


Saturday, June 26, 2010  


A bright sunny day; seemingly a nice day to get out of town and up into the hills for a trail-run.

It would have been even nicer if I had done it in the morning, while it was still cool, but I was having a lazy day (not doing anything much more strenuous than making coffee and practicing fiddle tunes), and I had a really hard time convincing myself to get outside and face the world. I didn't manage to drag myself to the state park until 4:30 PM. Well, it was warm by then, but not that warm. And I chose trails that would have me spending more time in the shady woods than in the sunny meadows.

I also had a chance to contemplate some of the mysteries of the woods. For example, there's this one intersection of trails where people keep creating temporary sculptures made by stacking up towers of rocks. Today there was an addition to one of these rockpiles: a stick with panties on it.

I'm not quite sure what the artist had in mind here, but it got my attention, which in some cases is the only thing that the artist has in mind. But this artwork might possibly have had a spiritual significance at which I cannot guess; it may have been there to honor Jurlsufaika, the Forest God of Underclothing, or something of the kind.

Anyway, what with running in the shade much of the time, and stopping to photograph underwear-on-a-stick art installations wherever I encountered them, I can't say I suffered unduly from the heat. I just suffered from not feeling energetic enough for a trail-run. But that wobbly feeling passed, eventually -- I felt much better and stronger during the last mile than I did during the first mile. If I had needed to run a mile or two farther than I did, I could have. But 7 miles was quite sufficient, I felt.

And now I have Sunday free as a rest day! Which is good, because I have some other, non-athletic things to do, and I want to concentrate on them. I plan to play a lot of music tomorrow if at all possible. I can't devote every day of my life to being a phony diabetes hero.


Suppose you could get a look at your doctor's school records. Would you want him to be an average student? I'm serious, now. Would it be okay with you, if you learned that your doctor was a middling student who managed to graduate but never came anywhere near to being at the top of his class? Or would your prefer that your doctor was an above-average student?

When it comes to health care, do you want excellence? Or is mediocrity plenty good enough for the likes of you?

The reason I ask is that I think people tend to be inconsistent on this point. I think most people want their doctor to be excellent rather than average, because they want to be given excellent health care rather than average health care. However, when it comes to their own management of their own health (which is probably far more significant than anything a doctor can do for them), they seem to want to be average rather than extraordinary. Hence the endless "is-this-normal?" questions posted on diabetes forums which boil down to: "I want someone to reassure me that the results I'm getting are the kind of results that the average person with diabetes is getting". They seem to think that things are okay if they're doing as well as the average patient is doing -- and that there's no need to do better than the average patient is doing.

Unfortunately, doing as well as the average diabetes patient is like doing as well as the average participant in a drug rehab program. Where failure is the norm, don't aim to be normal! You want to set your sights a little higher than that.

It might be okay to be an average driver or an average golfer or even an average parent. It is not okay to be an average diabetes patient. I've seen average patients, late in their careers as average patients, and the spectacle didn't exactly make me want to choose them as role models.

When it comes to diabetes management, you want to be well above average. You want to be at the top of your class. After all, that's what you expect of your doctor, isn't it? If you demand excellence from your doctor, you should certainly demand it from yourself. After all, most of your health care (at least for diabetes) is going to be provided by you. Don't you want above-average health care?


Friday, June 25, 2010  


My 30-day fasting average is now 85. It had been climbing, and I'm glad to see that I've been able to work it down.


You know, I would be lying if I said I was in the mood to go running today. I really didn't feel like it, not one bit. And the running buddy I was with didn't feel like it either. We chatted about this beforehand. While we were doing our preliminary stretches, we got in some prelimary moaning. We talked about how much we didn't want to do this run, and about how hard we were afraid it would be, and about how empty the locker rooms were because even our most sportive coworkers usually don't exercise on a Friday. And having got those preliminaries out of the way, we took off and did the run, and then we felt better.

It's amazing what you can do, once you understand that it doesn't matter that you don't feel like doing it.

Of course, this was also an example of how the exercise-buddy phenomenon works, or should work: two people who don't feel like working out, and admit it freely, nevertheless end up working out, because neither of them wants to look like a quitter to the other.

If you haven't got any exercise buddies, find some. It can make a huge difference.


They're having a problem at work with employees using up internet bandwidth trying to keep track of the World Cup. Well, if they didn't want that problem, they shouldn't have hired so many employees from countries where people care about the World Cup.

I don't care about the World Cup myself, but it has very little to do with nationality. Sports fandom in general is foreign territory to me. When a children's game is being played by a bunch of grown men whom I don't know personally, there is a limit to how much raw emotion I can work up over who wins.

I've even started to have the same problem with fiction. Unless a novelist has done a really superb job of making the characters seem to be both real and interesting to me, my attention wanders. As for some stranger wearing a jersey with a big number on it, he's going to have a pretty hard time snagging my attention in the first place, much less holding it.

I guess what's happened, over the years, is that I've started to get interested in the real world. I'm finding more drama in the problems that scientists are trying to solve than in the problems that football coaches are trying to solve.


These are hard times for the people who want to believe that diabetes and obesity are unconnected. Researchers keep coming out with studies saying that they are, too, connected. What's worse, researchers keep coming out with studies saying that the obesity happens first and the diabetes second (which makes it harder to argue that, if there is a connection between diabetes and obesity, diabetes is a result rather than a cause). Here's one, from Medscape: Later Diabetes Risk Rises With Midlife Weight Gain, Measures of Central Adiposity . (By the way, central adiposity means fat around the midsection, in case you don't have your glossary handy.)

"Weight gain as well as familiar, easily obtained measures of central adiposity in middle-aged and elderly adults can point to increased risk of developing diabetes in later years, both overall and in both women and men specifically, suggests a prospective analysis based on the participants in the Cardiovascular Health Study."

I like that line about the increased risk applying "both overall and in both women and men specifically". Is there a difference between saying that and saying that the risk applies to both sexes? And if not, would it kill them to eliminate some of the redundancies from their prose?

Anyway, the study looked at more than 4000 people (that is to say, men, and women, and also both men and women) over a period of 12 years, and found that body-mass index, weight, fat mass, waist-to-hip ratio, and waist-to-height ratio at age 65 were significant predictors of incident diabetes. "For each measure, there was a graded increase in the risk of diabetes, with increasing quintiles of adiposity". So write the authors, led by Dr Mary L Biggs (University of Washington, Seattle), in the June 23/30, 2010 issue of the Journal of the American Medical Association. Biggs said that the current analysis reaffirms that weight gain during middle age ups the risk of later diabetes. "It didn't really matter which measure we looked at, the people in the highest 20% in the distribution of each of these measures had an increased risk of diabetes compared with those in the lowest."

Of course, it could be argued that the causation implicit in the order of events (obesity first, diabetes second) is misleading. It could be that diabetes is only discovered second -- that the underlying metabolic problem which causes diabetes could be present but unnoticed at an earlier stage, and that this problem could be promoting weight gain. Because the weight gain is far more easily detected than the underlying problem, it's only natural that the weight gain is noticed before the underlying problem is noticed.

I am willing to concede that this objection may be partly correct. However, that can't be the whole story, simply because weight loss (after the diabetes is finally discovered) tends to alleviate diabetes, which should not be the case if obesity is only a consequence of diabetes and is doing nothing to cause it. If gaining weight doesn't push your blood sugar up, then losing weight shouldn't pull it down -- yet it very often does. Therefore, I think the most reasonable conclusion is that weight gain contributes to the risk of developing diabetes later (regardless of whatever else might contribute to that risk).

Of course, none of this is going to convince anyone who has a strong emotional committment to the idea that gaining weight does nothing to promote diabetes. And it's not too surprising that emotions run high on the subject of diabetes, especially when people are fending off real or imagined accusations that it's their own fault they have the disease.

To me, though, it seems that a lot of people are making an exceedingly bad bargain with their emotions. Convincing yourself that you're a helpless victim of fate, who could not have done anything to avoid becoming diabetic, and shouldn't be expected to do anything about it now, might offer some kind of emotional reward. But it's got to be a pretty small reward, compared to the reward you might obtain by accepting responsibility for your situation and seeing what you can do to improve it. It might turn out that you can do a lot -- once you get over the hurdle of accepting responsibility. (I said responsibility, not blame. There's a difference!)


Thursday, June 24, 2010  


Yesterday, writing my blog late at night and sleepy, I garbled some numbers (confusing obesity rates with diabetes rates), and as a result I overstated the incidence of diabetes in the U.S. by a very wide margin. Sorry about the error if you saw it before I had a chance to notice it and correct it.

However, at the rate we're going, I could have just let the error stand, and wait for reality to catch up with my description of it. I might not even have had to wait very long.


This morning I had a light and perhaps inadequate breakfast; at any rate, by the time I was about to go running at noon, I was feeling hungry and weak. While I was getting dressed for the run, I began to fear that I would have a hypoglycemic episode while I was out there. I had a glucose gel in my locker, and I decided to make use of it. Better safe than sorry. It was 25 grams of sugar that I hadn't been planning on consuming today, but it seemed like the sensible thing to do.

I don't have hypoglycemic episodes often -- probably no more often than the average non-diabetic person does (maybe once a year, if that often). It's just that the average non-diabetic person is usually not in the middle of a long run when it happens, so he has the option of reaching for some kind of snack. (And how often are most people out of reach of a snack?) When I'm out there running, a few miles from my starting point, with no food on me or near me, and no money on me even if I happen to pass a taco truck, getting a bit hypoglycemic feels like a crisis -- instead of a minor and momentary discomfort, as it is for most people.

I've never had a serious hypoglycemic episode -- not being on insulin or diabetes meds, I just don't go that low. However, when I go low enough to feel shaky and anxious, I really hate that feeling. If you let me into a bakery under those circumstances, I'd eat their entire inventory. Swallowing a glucose gel as a preventive measure is definitely the lesser vice. Anyway, I felt fine during the run (energetic, even), and after it I was satisfied with having a salad for lunch -- I didn't feel the need to take in a bunch of bread. So I think I solved the problem about as well as it could be solved.

I realize that a lot of people with diabetes, who are on insulin or diabetes meds, are vulnerable to having pretty serious problems with lows. Which is relevant to my next subject.


Researchers have long been fond of doing studies to prove that this or that undesirable thing -- liver cancer, schizophrenia, violence, misuse of the apostrophe -- is more common in people with diabetes. They round up a hundred people who think that the plural of story is story's and then they assemble statistics to show that this patient cohort is twice as likely to have diabetes as people who can spell.

This kind of study shows no sign of dying out (I just read one yesterday claiming that loss of cognitive functioning is more common, more serious, and more rapid in people with diabetes), but it's not exactly on the cutting edge of fashion anymore.

The more fashionable kind of diabetes study these days -- for reasons which I do not find easy to understand -- is one which aims to show that "tight" glycemic control actually does more harm than good to diabetes patients.

The disastrous ACCORD study -- or rather, the disastrous conclusion derived from the ACCORD study, to the effect that controlling your blood sugar causes heart attacks -- has already received a lot of angry comment from people who follow the politics of diabetes, so to speak. (In a nutshell: that rather muddled study certainly did not prove that glycemic control is dangerous in and of itself, although it may possibly have uncovered evidence that being heavily dosed with multiple drugs is not the safest way to achieve glycemic control.)

Today I read a new study which initially struck me as a bit silly, until I started thinking through the implications: Motor Vehicle Crashes in Diabetic Patients with Tight Glycemic Contol: A Population-Based Case Control Analysis. The idea here is not that good glycemic control will give you a heart attack, but that it will send your face through a windshield. The authors conclude, from comparing Hemoglobin A1c results with accident rates, that having "tight" control is nearly three times as dangerous as having "loose" control:

I have to interject here that an A1c result of 6.9 is not my idea of "tight" glycemic control. Some doctors would called it barely acceptable, but I doubt that many would express greater enthusiasm than that. And a result of 9.0 is not just "loose", it's entirely out of control. If research of this kind encourages anyone to think that dwelling in that particular realm would be the "safe" thing to do, then research of this kind is not a public service.

But why would patients with acceptable control (I cannot bring myself to call this sort of thing "tight" control) have a higher risk of accidents? The authors presume it is because diabetes patients with lower numbers are being more heavily medicated, and for that reason are more prone to hypoglycemic episodes. They're probably right (especially as they found that a history of severe hypoglycemic episodes requiring outside assistance correlated even more strongly with accidents than lower A1c results did).

To be fair to the authors, they do include this statement:
"Our findings join a growing and contentious literature correlating low HbA1c values with adverse consequences in adults with diabetes mellitus. For example, three recent randomized trials found that intensive treatment regimens led to both lower HbA1c values and an increased incidence of severe hypoglycemia among diabetic patients. These trials and our study do not prove that striving for a normal HbA1c is harmful; instead, the adverse association might indicate that customary treatments for achieving euglycemia are inexact and potentially hazardous to high level cognitive behavior."

Okay, fine: they're admitting that the problem is not controlled blood sugar, but rather the customary methods used to achieve control of blood sugar. That being the case, why did they not do a study comparing different methods of achieving control of blood sugar, to find out which method was least likely to cause hypoglycemic episodes, possibly leading to a vehicle crash? If they had done that kind of study, we could have learned something useful from it.

Instead, we have a study which finds that lousy-yet-popular methods of controlling blood sugar produce outcomes even more awful than anyone had realized (because the outcomes endanger the general public, not just the patient). If this finding were presented more candidly, the study would at least be instructive. But the highly misleading title of the study, with its reference to "tight glycemic control" causing vehicle crashes, ensures that the study will not even be instructive. Instead of concluding that we need to take another look at the way we control blood sugar, most people who become aware of the report at all will conclude that we need to take another look at allowing people with diabetes to drive.


Wednesday, June 23, 2010  


After work I went downtown to the "Wednesday Night Market", which is a weekly event in my city during the summertime -- they close some streets to put on a farmer's market, and also to gather a crowd for street vendors and a few performing arts groups. I bought some produce, and also saw one of my running buddies leading her dance class in a demonstration of clogging. Once we've completed our lunchtime run, I'm usually through with exercise for the day; she goes off in the evening and dances. Maybe that's one reason why she's a better runner than me. (To see her racing up those hills today, you'd think there was no such thing as gravity.)


Every time I see it stated that the full name of the CDC is "the U.S. Centers for Disease Control and Prevention", I wonder why it's called "Centers" and not "Center". How many "Centers" are there, exactly? It's sort of like seeing a sign outside a civic building that says "Police Departments". If the town has more than one of them, how do you know which one of them to call when you need to report a break-in? I mean, isn't the main idea of a "center" that there's only one of them? Euclid didn't speak of the circle as having "centers", only a center. There isn't a place in the arctic called the North Poles, is there?

Maybe the idea is that the CDC consists of two centers, the first of which is assigned to prevent disease, and the second of which is assigned to "contol" whichever diseases the first center fails to prevent. If that's the case, though, it raises the interesting question of why control is listed first, not second, in the name of the agency (or agencies). Putting the emphasis on what has to be done after you fail in your primary mission seems to suggest a lack of confidence. If you were going to give the U.S. Army a new name, you probably wouldn't call it the Departments of Surrender and Victory.

I did some minimal research and found that the CDC has been called many different things since it was founded in 1942 (as the "Office of National Defense Malarial Control Activities"). Soon it branched out to cover more and more diseases. In 1946 it was called the Communicable Disease Center, and they liked the initials of that name so much that they have contrived to retain the "CDC" abbreviation through all subsequent name changes. As of 1970 it was officially called the Center (not Centers!) for Disease Control, and retained that name for 10 years. Then it was (inexplicably) changed to the Centers for Disease Control in 1980. An act of Congress in 1992 changed it again, to the Centers for Disease Control and Prevention.

Well, whatever they're calling it this month, the CDC is still there, and it is just as dedicated as ever. (And no better at basic communication.) 

Anyway, last week the CDC reported the results of its annual health surveys. News agencies reported the gist of it in headlines such as "More Americans exercise, but they are still obese". Here are the specific details that caught my eye:

I don't know how accurate or meaningful the CDC's survey results are, but I report them here for whatever they may be worth.


The difference between butter and margarine can be a matter of life and death. At least, it was for a 21-year-old man in Waterville, Washington earlier this month. His 17-year-old sister was making macaroni and cheese. He asked her if she was using butter; the two siblings then got into a heated dispute about the comparative merits of margarine and butter. The end result was that the brother called the local police to report that the sister had tried to cut his neck with the serrated edge of a spatula. His sister was charged in Douglas County Superior Court with fourth-degree assault. (I'm not sure what "fourth-degree" assault is, but it may be a special category set aside for violence resulting from interfamilial quarrels about oils and fats.)

It used to be thought that jealousy, greed, and religion were the things that drove people to attack one another. These days, nutritional theory seems to be filling that role more and more.
 


Tuesday, June 22, 2010  


Ah, good -- better numbers today. Whenever my test results move in the wrong direction, I'm momentarily afraid that, this time, my efforts at correcting the problem won't work. So it's always a big relief when I make the necessary course-correction and it does work.

Unfortunately, I haven't enough time to say much else today. I went to a house-concert tonight, with the Irish singer Andy Irvine, who was brilliant -- but I got home late from it, and I need to get to bed.


Monday, June 21, 2010  


Oh, no -- everything is up: fasting glucose, weight, and blood pressure! Yesterday was my non-exercise day for the week, and on top of that I attended a big pot-luck dinner. (My rest day is usually on the weekend, and I'm likeliest to be eating party food on the weekend, too -- so those two things do have a tendency to coincide.)

I was on a roll last week (fasting results in the 80s, and mostly in the low 80s), but that winning streak has been rudely interrupted.

Well, time to get back on track. I had a low-carb lunch and dinner, so I hope and expect that I will be able to drive my test results in a downward direction soon. Driving weight and blood pressure down are always much harder.


In recent years I have been hearing many complaints to the effect that saturated fat has been demonized as a specific promoter of coronary heart disease, when in fact the evidence linking saturated fat to heart disease was never strong, and seems to be crumbling entirely.

I have been reluctant to join (or even follow) the debate on this subject, largely because it has seemed far more like a holy war than a discussion. To me there is nothing less informative than a dispute between fanatics. It's like listening to people argue about Israel: when it's over, the only thing that has changed is that you now hold a lower opinion of both sides.

I don't know what got me to the tipping point, but when I saw this article in PLOS Medicine, I thought I should start getting more engaged with the subject. It's called "Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials". The authors (Mozaffarian, et al) report that, despite everything we've been hearing from the nay-sayers, the risk of coronary heart disease really is  reduced when polyunsaturated fats are consumed instead of saturated fats.

But we're in trouble right from the start -- in fact, right from the title of the paper. It's a meta-analysis, and I'm learning to recognize that term as a red flag. (A red flag which we see flapping pretty often, because it is very common for a research paper on a medical subject to consist of a meta-analysis.)

A meta-analysis is a study in which you don't go out and take new data on human or animal subjects -- instead, you look at data that was taken during many other studies, and combine them into a pool.

The argument in favor of doing this is that, when you are researching a subject such as heart-attack prevention, you can't expect to look at a small number of people over a short amount of time and find that enough of them have a heart attack while you're studying them to generate much statistically significant data. For example, if you wanted to test the idea that wearing neckties increases your heart-attack risk, it isn't going to be good enough to report that you studied 94 people for a year, and during that time one of them had a heart attack, and he was wearing a necktie at the time. That isn't a big enough data sample to impress anybody. But if you studied many thousands of people over a long enough period for quite a lot of them to have heart attacks, your data concerning the differences between those who did and those who didn't might be taken more seriously.

The problem is that it would be terribly expensive to study thousands of people over a long period, and you probably couldn't obtain enough funding to do a study that way. What you can do is review the literature to see all the studies that have been done in the past which collected data on people's cardiac health. From all the studies that you can find, you select the most appropriate ones for your purpose, you amass data from all those studies, and suddenly you have a large data base instead of a small one -- so that any conclusions you draw are based on a clear statistical pattern.

But that's exactly the problem: you select the most appropriate ones for your purpose. If your purpose is to support or undermine a particular notion of what's good for people's cardiac health, then your meta-analysis is pretty certain to include the studies which tend to confirm your opinion and not the studies which seem to refute it.

I wouldn't go so far as to assert that a meta-analysis is always a process of cherry-picking data to bolster a hidden agenda, but it's awfully easy for it to become that, and it probably is exactly that in a very large number of cases.

And even in the absence of conscious or unconscious bias on the part of those selecting the data, there is also the problem that the studies that are available for selection have already been selected -- by the publication process. Any survey of published studies is going to be biased because the publication process is biased against reporting of negative results. Studies which don't find the pattern that the researchers were looking for generally don't see the light of day. (This is especially true of studies of drug effectiveness, as the research is funded by drug companies that are not shy about exercising their veto power.)

Because of all this, I see the term meta-analysis and think, "Uh-oh! Who's trying to prove a point here, and how far are they willing to go to win the argument?".

So, the study by Mozaffarian, et al, which supports the idea that saturated fate promotes heart disease, is in the grand tradition. The claimed role of saturated fat in heart disease dates back more than 50 years, to a meta-analysis done by Ancel Keys. His meta-analysis compared heart disease rates to saturated fat intake in 8 countries, and showed that the cardiac risk was highest in countries where saturated fat intake was highest, and lowest where it was lowest.

The only problem with Keys's meta-analysis is what he left out of it. He didn't just have data from 8 countries. He had data from 21 countries. But he included the data from 8 countries, and excluded data from 13 others. Guess how the data he included differed from the data he excluded? Other researchers found that, if they redid the meta-analysis with data included from all 21 countries, the correlation of saturated fat with heart disease faded away. Countries differed in their rate of heart disease, and in their rate of saturated fat consumption, but the two factors did not track each other in a consistent way.

Now, along comes another study which claims to show definitively that there is no association between saturated fat consumption and cardiovascular disease. But here's the title: "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease". That's right: another meta-analysis.

So, how am I to know that this meta-analysis didn't involve just as much artful cherry-picking of data as the meta-analyses which conclude that there is, too, an association between saturated fat consumption and cardiovascular disease? I have been told that it's highly significant that one of the authors of the new study (Ronald M. Krauss) formerly was a supporter of the conventional view of saturated fat as an artery-clogger. Well, fine, but I'm not sure we can assume that people who have changed their mind about something are always progressing from error to enlightenment, and not the other way around. The fact that people are selecting data to build their case remains a problem regardless of what their case is, or what it used to be.

The view that saturated fat is a risk factor for cardiovascular disease is still the orthodox view, but it's an orthodoxy that's increasingly being challenged -- and is not doing a very good job of defending itself. It may well be headed for collapse. I'm not sure that I'm ready to pronounce it dead, but it seems to me that it had a free ride for decades, and needs to make a far stronger case for itself than it has done so far, if it wants continued acceptance.

I guess my view for now is that the role of saturated fat in causing cardiovascular disease is questionable and may prove to be unimportant. At any rate, I'm not seeing it as a high-priority dietary issue -- and I used to accept that it was exactly that.


Saturday, June 19, 2010  


I was in the mood to do something other than running for my weekend workout. It seemed to me that this would be a good day for a hike. I was right.

It was mostly sunny, but the wind was bringing in enough clouds from the coast to keep things cool -- so it was a comfortable hiking temperature, even on the steepest part of the route (where you tend to overheat from the effort).

Actually, the wind was almot too strong for comfort, but once I got into the woods I was sheltered from that.

One of my favorite things about hiking is the way you get so quickly from one kind of environment to another. The mood of the scene is constantly shifting.

There was a lot of climbing involved (1400 feet of elevation gain), but when you do a lot of climbing, you usually get rewarded with good views.

The clouds overhead were moving with startling speed. During the drive home, I was heading the same direction that the clouds were heading, so I checked against the spedometer as I kept pace with the moving edges of the cloud shadows on the road. 42 miles per hour.


As if there weren't already enough controversy and confusion about where to place the diagnostic threshold for diabetes, scientists have now discovered that the most reliable diagnostic tool for diabetes (the hemoglobin A1c test) yields different results for people of different races who have the same blood sugar levels. Naturally, everyone is trying very hard to miss the point of what this means.

It has been noted before that African-American diabetes patients don't do as well as their white counterparts, either in terms of health outcomes or in terms of lab results. Some have blamed this on the presumed racism of white doctors; others have accused black patients of being "non-compliant" with the doctor's orders. Now it turns out that a white patient and a black patient can have the same average blood sugar, but the white patient will score 6.9% on the A1c test (barely acceptable, in the view of most doctors) and the black patient will score 7.1%, or even 7.2% (not at all acceptable). It's totally unfair!

Well, yes. But not in the sense that people seem ready to assume.

The way this finding is being spun, so far, is that the A1c test gives an accurate result if you're white and an inaccurate one if you're black. The test is "unfair" to black patients in that it "accuses" them of not doing as well as they're actually doing.

I say, hold on a minute. What the A1c test actually measures is glycation (the unwanted bonding of sugars to proteins). It is often said, incorrectly, that the test measures average blood sugar. It doesn't measure that, any more than a bathroom scale measures calories.

The A1c result is affected by average blood sugar, and it gives your doctor a basis for estimating what your average blood sugar has been lately. But an estimate is not the same thing as a measurement. If your average blood sugar goes up, your A1c result will go up. But the idea that the A1c result can be translated, by a simple formula, to a reading of average blood sugar was always questionable, and it's doubly questionable now that we know that the glycation rate, for the same sugar level, varies by race.

What people always seem to lose sight of, whenever the A1c test is up for discussion, is that the process which the test actually does measure (glycation) is more important than what most people imagine it measures (average blood sugar). The only reason we should care about whether our average blood sugar is going up or going down is that this affects the rate of glycation. And glycation is the main thing that makes diabetes harmful.

Glycation (not average blood sugar) is what's responsible for most of the damage that diabetes does to people. "Complications" arise, directly or indirectly, from glycation. If glycation didn't happen, it wouldn't matter what your blood sugar level was.

Therefore, if being black means that your A1c reads 7.2% instead of 6.9% for the same average blood sugar level, this is "unfair" not in the sense that it makes you look as if you're doing worse than others -- it's unfair in the sense that you are doing worse than others. Your risk of complications is higher, even though your glycemic control is no worse.

Now, I'm not necessarily ready to concede that glycation really does happen at an accelerated rate, for the same sugar level, just because your ancestors are from Africa. It's hard to see how that would work. Maybe there's been some kind of error in the research that claims to have found this result. But if it's true, then the message which African-American diabetes patients need to take away from it is not that they're doing better than their test results indicate, but rather that they have to do better than the average person just to get an average outcome. Fortunately, they may already be used to that concept.


Friday, June 18, 2010  


"Can peanuts be eaten by a type 2 diabetic person?"

Somebody asked that question on the dLife forum today. I'm sure it must have seemed to them like a reasonable question, and even an important one. Still, you have to wonder what preconceptions they must have been working with, if they were unable to recognize how absurdly broad the question was. You might as well ask if it would be okay for someone with asthma to drive to Boston. Do people really expect there to be absolute rules about such matters, rules which apply equally well in all cases? 

Well, yes -- by and large they do expect that. They think there is a set of commandments written down somewhere -- a list of forbidden foods which must never pass your lips if you have diabetes. The unspoken assumption is that any food which is not on this list can be consumed voraciously. I suspect that, when someone asks if it's okay to eat peanuts, they plan to interpret a "yes" as permission to eat peanuts in any amount they choose.

It certainly would simplify grocery shopping, and ordering in restaurants, if things actually worked that way. I can't eat this, but to make up for it I'll have three helpings of that. There -- my decision is made, and my burdensome task of diabetes management is done for the evening!

Much as I like to make fun of this kind of oversimplification, I'm sometimes prone to it myself. The department I work in had an "evening out" tonight, and when it was in the planning stage there had been talk of doing it at at pizza parlor. I cast my vote against that, but no decision was made until this afternoon, and I was fretting about it, because to me that seemed as if it should be a deal-breaker. If they were going to go buy a bunch of pizza, I was going to go somewhere else -- but then I'd be the bad guy. While they were trying to create some team spirit, I'd be going off in a corner to sulk because they weren't eating what I wanted to eat.

As it turned out, we went to a real restaurant, with individual plates of whatever each person wanted to order, and it was pleasant (we ate outside, on a deck overlooking a lake). So I never actually had to face the problem I foresaw. But, in my dread of going to a pizza parlor, was I not oversimplifying the issue as much as the person who wanted a ruling on whether or not a person with diabetes can eat peanuts?

Well, maybe. But my experience of going to pizza parlors with a large group has not been very encouraging. Maybe it's not impossible to eat sensibly under those circumstances -- but it ain't easy. 


Thursday, June 17, 2010  


Yesterday I chose a difficult running route, and I felt pretty strong during the run. Today, I chose an easy route (or at least the easiest one that's available to me from my workplace, which happens to be located half-way up a big hill), and I felt rather weak during the run. I was wheezing a bit; maybe the allergy season isn't as completely over as I had thought. But I still felt better than I had on Monday.

This is a strange aspect of working out on a daily basis: your degree of physical readiness to exercise varies widely from one day to the next, and you usually can't tell, until you're at least a few minutes into the workout, how well you're going to do this time. I used to think that, over time, I would eventually get into such good shape that things would even out, and I would be about equally energetic any day of the week. It hasn't happened that way.

Every day at work, when it comes time to gather up my running buddies (if they're free), head downstairs to the locker room on the ground floor, and get dressed to run, I feel slightly apprehensive. How hard is this going to be? How embarrassing is this going to be, if it turns out that my running buddies are having a good day and I'm having a bad one?

The trick is to go ahead with it, regardless of how apprehensive you feel. I imagine that's where a lot of people drop the ball. They take it for granted that, on a day when you're not feeling energetic, that's all the excuse you need to skip the workout. Then they come to find that, after they've been following that program for a while, they get to a point where they never feel energetic enough to go through with the workout. And then: game over.


My reward for being a good boy and running when I wasn't feeling energetic: a CD I ordered showed up in today's mail. A reissue of an old, lost, favorite LP. Martha Argerich playing Chopin (the Andante Spiannato and Grande Polonaise ). Still as good as I remembered it.

Once I heard a bunch of people at a party talking rather comedically about their old record collections, and how they never listen anymore to anything they bought in the 80s. They'd be too embarrassed to listen to that stuff now. I kept quiet, but I thought they were lame beyond belief. A good record is always a good record. If the music they used to listen to is a joke now, then it was a joke then, too -- only now they're finally in on the joke. You can't buy the musical equivalent of Velveeta and expect it to be a joy forever.

You don't want to lose sight of the long view -- in music, or in anything else. What if you grow up or something? You want to be ready in case it happens.


Diet Characteristics May Influence Diabetes Risk says the headline in Medscape. The EPIC-Norfolk study, originally intended to assess the effect of diet on cancer risk, is now looking at the connection between diet and other diseases. Notably diabetes.

"Residents of Norfolk, England aged 40-79 years were invited to attend a health checkup from 1993 to 1997. They also completed a detailed health and lifestyle survey that included a validated 130-item food frequency questionnaire. From the responses, the energy and weight of food intake was estimated, and dietary energy density (DED) was calculated as the available dietary energy per unit weight of foods."

Patients who already had diabetes, cancer, or cardiovascular disease were excluded. The remainder were followed through the end of 2005 to ascertain clinical incident diabete.

"The investigators used logistic regression to determine whether DED (in quintiles and also continuously) predicted incident diabetes after controlling for other risk factors such as family history of diabetes, body mass index, waist circumference, and physical activity. They also adjusted alternatively for total energy intake and percentage of intake from fat to isolate the impact of DED."

I haven't seen "DED" discussed before. I've certainly heard that energy-dense foods can be a problem, but I thought they were mainly a problem because they made it too easy to take in a lot of calories and gain weight. I hadn't heard that they might be a problem independent of how many calories you consumed or how much weight you gained.

And the result?

"Subjects who developed diabetes consumed a more energy-dense diet than those who did not. The increased risk of diabetes associated with DED was evident in continuous models and when the population was divided into quintiles. For example, each unit of DED increased diabetes risk by 12% after adjustment for age, sex, and body mass index. Further adjustment for occupational status, smoking, physical activity, family history of diabetes, alcohol consumption, and total energy consumption strengthened the association. Compared with the lowest quintile of DED, the risk of diabetes was 58% greater among those at the top quintile in the fully adjusted model."

So what were the differences in the kind of foods these different "quintiles" (a term for the process of separating a population into five segments, each representing 20% of the total, according to the level of some variable) were consuming?

"The authors determined that, compared with the highest DED quintile, participants in the lowest group consumed significantly more fruit, vegetables, and alcohol, and less meat, soft drinks, and a lower percentage of energy from fat."

So there you have it: when you go into the supermarket, spend more of your time at the produce section (and don't forget to stop by the wine rack). Don't spend so much time in the meat department or the soft drink aisle.

Of course, if you're reading this advice at all, you probably have diabetes already, so "prevention" is no longer the issue. But the things that help prevent diabetes also help minimize the harm it can do, so don't assume that preventive measures are a waste of time after you're already diabetic.


Wednesday, June 16, 2010  


Wow, that's got to be the lowest blood pressure reading I've ever taken on myself. I don't know what the explanation is, other than that I had a tough, hilly run today, in beautiful sunny weather (not too hot), and at the moment I'm drinking a glass of Zinfandel, listening to the Beaux Arts Trio playing Haydn, and feeling relaxed.

Today I experienced further recovery from whatever was bothering me on Monday -- running felt easier, and my pace was faster. My running buddy still finished ahead of me, but not by as much this time!


Let me see if I can explain a little more about the research going on concerning "cytokines" (hormone-like chemical signals exchanged by tissues which we don't normally think of as regulatory glands), and the role that cytokines play in inflammation and Type 2 diabetes.

I'm afraid the subject is even more complex than I made it sound yesterday. The cytokines are just the starting point -- each of them triggers a cascade of "phosphorylation events", and these events produce "acute phase reactants". It takes a lot of research to establish what all the reactants in the cascade are, and what effects they have. And then you have to consider what effects these reactants have on one another as well! As I said yesterday, the complexity of these reactions can make it hard to figure out whether a given cytokine is "good" or "bad" in terms of causing inflammation (and, consequently, insulin resistance). The cytokine called IL-6 seems to be inflammatory when it is produced by sepsis (infection), and anti-inflammatory when it is produced by muscle contractions (exercise). What seemingly turns IL-6 "good" or "bad" is the influence of another cytokine known as TNF (and TNF is generated by infection, but not by exercise).

The cascade of reactions launched by TNF has the effect of inhibiting cellular response to insulin. And now it turns out that there's another cytokine which does the same thing, only worse. It's usually called JNK, which doesn't stand for junk, but you can think of it that way if you like. (The longer name for the stuff is "c-Jun N-terminal Kinase".)

Anyway, JNK launches a vigorous cascade of reactants which have the effect of undermining cellular response to insulin. The effects of JNK have been studied in cells "in vitro" (that is, in a test tube), but also in live mice -- including mice which have been genetically modified in various ways, so that the effects of JNK can be compared under different biochemical conditions. All of these studies confirm that JNK promotes insulin resistance. Although no one has tried human experiments involving JNK, in a sense nature has done so, because some people have a genetic mutation which causes them to lack a protein which is supposed to inhibit JNK. And this mutation is known to cause Type 2, presumably because in people who have the mutation, JNK is never inhibited -- it's always at work. (I'm guessing that this mutation accounts for a lot of those cases in which people develop Type 2 even though they're not overweight.)

So, if JNK is a powerful promoter of insulin resistance, what promotes JNK? What would make you have more of it than you ought to (apart form that genetic mutation I mentioned)? Surprise, surprise: obesity. Excessive body fat causes a particular type of chronic inflammation, which in turn causes JNK to be released into the bloodstream.

So, JNK promotes insulin resistance, and two of the things which promote JNK are (1) a form of inflammation triggered by obesity and (2) a genetic mutation which causes some people to be unable to inhibit JNK.

I hasten to add that JNK is only one of the inflammatory pathways that can lead to insulin resistance, and obesity is only one of the things that can cause you to produce too much JNK. But it certainly helps make sense of the the fact that Type 2 is so often associated with obesity.


The American Diabetes Association and the American Cancer Society issued a joint statement today, the purpose of which was to depress diabetes patients in the vaguest possible way.

Their consensus statement essentially says that diabetes and cancer are somehow connected, but nobody knows anything useful about what the connection is. Diabetes, primarily Type 2, is associated with an increased risk of several cancers, including liver, pancreas, endometrium, colorectal, breast, and bladder cancers.

For other cancers, though, there is either no known link to diabetes, or else the evidence for a link is inconclusive. And the really good news, at least for those of us who happen to have a prostate, is that cancer in that organ seems to be less common if you have diabetes. (Not that the advantage is large enough to make diabetes a desirable option for men.) The bad news, if you need any more of it, is that having diabetes not only increases your risk of developing cancer, it also reduces your odds of surviving cancer.

The authors of the statement note that the situation is complex. Cancer and diabetes are complex diseases, with many subtypes. If diabetes increases cancer risk, we don't know why it does. The possibilities include:

In regard to the last point, there are reasons to suspect that one diabetes drug (metformin) actually reduces the risk for certain cancers; this is being investigated. It's way too early to say that metformin should be regarded as preventive medicine for cancer. (Considering how widely it's used, it must not be very powerful preventive medicine, if people with diabetes still face a higher cancer risk overall.)

The authors of the study have expressed the hope that cancer researchers and diabetes researchers, who currently inhabit distinctly separate worlds, will start paying more attention to one another, seeing as the two problems they're working on seem to be related. I guess that's what makes it worth announcing their conclusions in the first place.


Tuesday, June 15, 2010  


Running felt a lot better today, so I chose a hard route (a very hilly one). I still wasn't fast, but at least I wasn't feeling weak and unsteady, which was a great relief. And the weather was nicer today -- a bit cooler.

But tonight was a pub night with friends -- I hope it doesn't set my numbers back too much!


I think part of the difficulty I face, in terms of persuading people to take exercise seriously as a diabetes therapy, is that exercise is not a substance.

Food and medicine are substances, and that's why it's easy for people to accept that a given food or medicine might have an impact on the complicated biochemical problem we call diabetes. But exercise? How could mere movement have anything to do with body chemistry? It's a little like the problem I had, as a child, in accepting the idea that there was vitamin D in sunlight. Sunlight was energy, and vitamin D was a chemical. How could there be a chemical in sunlight? It didn't make sense!

My skepticism about vitamin D in sunlight was entirely justified, by the way. There isn't any vitamin D "in" sunlight, and it was stupid for adults to present the issue to me in that way. The actual situation is not so complicated that they couldn't have just stated it in plain English: skin cells can make vitamin D, but they need to be stimulated by sunlight first. If that was what they'd told me, I would have been able to see how sunlight could have an impact on the amount of vitamin D circulating in my body. But, instead, I was presented with the ridiculous image of vitamin D being formed in the sun, flying through millions of miles of vacuum (riding on a light beam), and then somehow injecting itself through my skin. Can you blame me for not buying that story? The actual story would have been far easier for me to understand, and believe in.

Suppose, however, that scientists had not figured out what the relationship was between vitamin D and sunlight. Suppose they knew that vitamin D deficiency was common among people who got little sun exposure, and that giving such people more sun exposure corrected the problem -- but that they hadn't figured out the mechanism which connected these two seemingly unrelated things. If that were the case, it might be hard to convince people that the connection was valid. The idea of correcting your vitamin D deficiency by going out in the sun might seem like mere wishful thinking (or, even worse, magical thinking).

That's where I think we are today with exercise and diabetes. No matter how much observational evidence there is to suggest that exercise prevents or alleviates type 2 diabetes, people still have a hard time believing it, because they haven't heard a plausible explanation of how it works, and it's hard even to imagine one. I mean, think about it: why should the glucose-regulating part of my endocrine system care whether I spent Sunday afternoon trail-running or sitting in a reclining chair? When I'm digesting my breakfast, why should my ability to process the carbohydrate in the meal depend in any way on whether or not I have been working out lately? So long as that question remains unanswered, it's going to be hard to get people excited about exercise as a tool for diabetes management. Why should people believe that exercising will help, if they can't see how that could be true?

Unfortunately, the relationship between blood glucose levels and exercise is a good deal more complicated and elusive than the relationship between vitamin D levels and sunlight exposure, and it hasn't yet been fully explained. Still, progress is being made on untangling the mysteries of exercise and its effects.

One of the more surprising discoveries related to this subject is that skeletal muscles (that is, the muscles that produce bodily movement, as opposed to the muscles that cause contractions of the heart and intestines) can function very much like an endocrine gland. The former, simpler picture of everything in the body being controlled by hormones released from the endocrine glands has been giving way to a far more complex picture, in which the muscles, the liver, and even fat deposits are capable of generating chemical messengers (known as cytokines) which function like hormones. These cytokines, generated by various organs and interacting in various ways, play important roles in controlling (among other things) the immune system in general, and inflammation in particular.

As type 2 diabetes seems to be triggered or worsened by various forms of inflammation, it seems clear that cytokines are important to understanding diabetes. However, it isn't easy to determine the effect of a particular cytokine. Some of the cytokines seem to produce different effects under different circumstances. An especially puzzling example is the cytokine known as Interleukin-6 (usually referred to as IL-6), which seems to achieve the impossible by both promoting inflammation (which leads to insulin resistance) at some times, and reducing insulin resistance at other times. During exercise, the skeletal muscles release a great deal of IL-6, which would have been expected to cause insulin sensitivity to decline -- and yet insulin sensitivity goes up rather than down after a workout. How is this paradoxical result possible?

It's hard to say for sure, but some researchers in Copenhagen have found an interesting difference between the set of cytokines released as a result of exercise and the set of cytokines released as a result of sepsis (infection):

In either case, IL-6 shows a big increase, and some other cytokines are released as well. But the cytokine known as TNF (tumor necrosis factor) is released only as a result of infection, not exercise. Apparently IL-6 has a harmful, inflammatory effect (with a resulting reduction in insulin sensitivity) when it is released together with TNF. But when IL-6 is released without TNF, as in the case of exercise, its effect is helpful rather than harmful, and insulin sensitivity is improved rather than degraded.

I'll talk about more aspects of this later in the week, as time permits.


Monday, June 14, 2010  


Well, this is odd: even though the weather wasn't as hot today as it was yesterday, and even though my run today was only half as long as the one I did yesterday, today's run was harder on me. I felt wobbly and weak from the start, and I was definitely slower than usual. I don't know what was wrong. I wasn't dehydrated (I had taken in enough fluids after yesterday's run to regain the weight I'd lost during it). I don't think I was hypoglycemic, either, despite the feeling of unsteadiness, because the other symptoms I get from a low were missing -- most notably the hunger. I didn't even have an appetite after I'd finished the run and taken a shower, and I'm usually very hungry then.

Maybe running in the heat yesterday did something to me that wasn't apparent at the time. Maybe I depleted my energy reserves a bit yesterday, and hadn't recovered yet.

Yoga tonight wasn't especially easy either, but I didn't fall over, and didn't feel like I was in any more danger of it than usual. Maybe it will help speed my recovery from whatever is amiss.

Maybe to you it seems perfectly obvious what was wrong: that I was trying to run again, the day after running an 8-miler, when I should have been resting up from it. Once upon a time that would have been true for me, but by now I've got myself into a state of training where I should be able to run 8 miles and still be up for running again the next day. Usually it's not an issue.

But a possible issue is that I didn't get enough sleep last night -- so in order to avoid that problem tonight, I'll retire early, and cut this short. I've been reading up on some interesting research that I'd like to discuss, but it will be a complicated discussion and I think I'll have to leave it till some time later this week.


Sunday, June 13, 2010  


The weather is finally warming up -- close to 90 degrees this afternoon. Circumstances obliged me to do my trail run when it was warmest, in the early afternoon. I wouldn't say it was easy, exactly, but it wasn't that hard. I was in the shade a lot of the time. I carried water with me, of course -- I'm not crazy.

I carried glucose, too, though as usual I didn't need it. Generally speaking I can do long runs (up to about 13 miles) without taking in any sugar, but there's always a remote possibility that I'll have a hypoglycemic episode. If that happens, and I'm in the middle of the woods, miles from anywhere, I don't want to be without an emergency supply of sugar.


I have taken the opportunity before to poke fun at the "anger" so many people claim to feel about being diabetic. I mean, what are they thinking, exactly? At whom are they "angry"? It's not as if some mean person deliberately gave them diabetes. Allowing yourself to get furious at no one in particular seems to me like a mighty undignified way to waste time.

When you get angry over a hard-to-use PC application or a hard-to-understand tax form, you at least know that somebody actually designed these things, with a callous disregard for those who would later have to use them. You don't know who the culprits are (which I'm sure is fortunate for them), but you know that such people exist, because PC applications and government forms don't just occur spontaneously in nature. Furthermore, you know that these people could have made things a lot easier for you, but they chose not to. So, your anger at least has some rational basis. It's theoretically possible that you could locate the perpetrators and strangle them some day.

But there isn't even a theoretical possibility that you can some day track down the person who gave you diabetes. Because nobody did. Diabetes really does occur spontaneously in nature, after all. No evildoer required.

But the people who say they are angry about having diabetes often mention an additional detail about why they are angry: it's not fair! They don't necessarily mean that it's not fair for other people to have diabetes, but it's certainly not fair for them to have diabetes -- on that point they are clear.

I'm surprised anyone wastes time on this "fairness" concept, either, but since they do, I guess it's a subject worth exploring.

Even though it's a familiar cliche that "life isn't fair" -- we point it out whenever undeserved bad luck comes to our attention -- large numbers of people seem to bring to life a false expectation that it is fair, that we should be able to count on good things happening to good people and bad things happening to bad people. Why anyone expects this is a little hard for me to understand. Does no one watch the news? Has nobody noticed, over the past few years, that the Wall Street rogues who have thrown millions of people out of their jobs and homes are being repayed with bonuses rather than prison terms? It's perfectly possible for vile people to have splendid things happen to them, and for good people to have their lives torn to pieces.

I'm not saying life is set up to reward bad people and punish good people. I'm just saying that life is not set up to reward or punish anyone. Life is not set up. Life is not even trying to be fair. Life doesn't care about who's been naughty and who's been nice.

But sometimes the people who complain about the unfairness of their having diabetes are a little more pointed about it: they think it's unfair for them to have diabetes because they don't fit the profile of the stereotypical diabetes patient. They're not fat! They were never fat! (Or, at least, they're a lot less fat than certain diabetes-free people they could name!)

I think these people are a little unclear on the risk-factor concept. Obesity increases your risk of becoming diabetic, but that doesn't mean your risk is 100% if you're fat and 0% if you're not.

If you want to minimize your risk of being injured in a car accident, there are a lot of things you can do to bring the risk down. You can wear your seat belt. You can stay within the speed limit. You can make sure that your brakes are working. You can avoid driving while drunk. You can avoid driving while sleepy. You can put down that damned cell phone.

Doing all these things will bring your risk down -- but not all the way to zero! There is always some possibility that you will follow all these rules and still get hurt (while someone else breaks each of them and gets away with it). If that happens, will you complain that it's not fair? Well, yeah, it's not fair, but so what? Nothing bad that happens to us is fair. Nothing good that happens to us is fair. Fairness doesn't enter into it. We know that -- so why do we talk as if we didn't?

There are people who, noticing that they've been luckier than other people they know, decide that there must be a reason for that: they deserve better luck than other people they know. And sometimes they have the appalling bad taste to announce this conclusion publicly. Someone I used to work with (until he lost his job in a round of layoffs) had an encounter downtown with someone who is still employed at my company. The still-employed one was handing out religious pamphlets, and explained to the unemployed one that "I think Jesus is the reason I still have a job". The unemployed one told me about it, saying "I guess Jesus likes him better than me". The insensitivity of saying, to an unemployed person, that you didn't suffer his sad fate because you're in solid with Jesus is simply unclassifiable. Surely it merits a lightning-bolt between the eyes. But I know that's not going to happen to him -- not because he really is enjoying divine favor, of course, but because life is not fair.

Ultimately, the logical weakness that I see in this complaint about unfairness is pretty much the same logical weakness I see in all the vague talk about "anger". If you think the situation is unfair, to what authority are you going to send your petition to have this unfair situation rectified? Who allowed this unfair thing to happen to you in the first place? What government agency do you think it is that determines the fairness of medical problems, and ensures that only people who deserve diabetes actually get it?

Managing diabetes is such a demanding business that I hate to see people with diabetes wasting their time on ideas that are both unhelpful and embarassingly dumb. Everyone with diabetes has, by definition, more important things to think about than whether or not it is "fair" for them to have diabetes.

What sets diabetes apart from other diseases which people might "unfairly" suffer is that, if you have diabetes, there's a lot you can do about it. If you had cancer or Lou Gehrig's disease, there might be very little that you could do about it, so sitting around brooding about the unfairness of the situation might make a kind of sense. But in the case of diabetes, there's plenty you can do. And you're probably not doing it, if you're too busy sitting around brooding about the unfairness of the situation, and wondering what it all means.

Here's what it means: nothing. Here's what wondering what it means is worth: nothing. So please, just say to yourself that life is not fair, and then get on with making the best of it! 


Friday, June 11, 2010  


I need to tell you about an interesting study on stress and exercise. But before I tell you about that, I need to tell you about telomeres. But before I tell you about telomeres, I need to tell you about aglets.

I can already see that it's going to take me a long time to work my way back to the subject of stress and exercise, but if you stay with me on this, the journey might prove interesting.


I'll say one thing for aglets -- they're pretty easy to explain. Aglets are those little cylindrical tips on the ends of your shoelaces. Why do shoelaces have aglets? Because, without them, shoelaces tend to fray at the ends. Aglets are there to prevent your shoelaces from doing that, and gradually unraveling on you. Aglets won't make a shoelace last forever, but a shoelace with aglets will last a lot longer than a shoelace without them.

Chromosomes, it turns out, also have a tendency to fray at the ends, and need some kind of protective device there to keep them from unraveling.

When a cell divides, the chromosomes (long strands of DNA) have to replicate themselves, and as part of this process the DNA strand has to unzip itself, starting from the middle. During this unzipping, the last few DNA "letters" (that is, the base pairs) at the end of the strand are torn off and lost. Obviously it wouldn't be acceptable for a little more genetic information to be lost each time a cell divides (who knows what you'd end up with if that kept happening?), so the chromosomes are equipped with aglets on the ends -- except that, in this case, the aglets are called "telomeres".

Actually, telomeres don't function in quite the same way that aglets do. They aren't rigid structures which prevent the DNA strand from fraying at the end. Rather, they are chains of the same sequence (TTAGGG), repeated over and over and over. The number of repetitions can be in the range of 1500 to 2000. This "TTAGGG" sequence isn't meaningful genetic code -- it's just padding, tacked onto the end of the chromosome, so that it can be sacrificed each time a cell division occurs. In other words, the chromosome does  fray at the end during a cell division, but no actual genetic code gets lost in the process; the only thing that happens is that the telomere has to sacrifice some more base pairs.

But notice what this means: every time a cell divides, and the chromosomes in it are replicated, the telomeres get shorter. This process can't continue forever. It takes a lot of cell divisions before the telomeres finally run out of base pairs, since they start out with a lot of them to begin with. But, over the course of a lifetime, a lot of cell divisions need to take place. Not that you're still growing, of course -- but cell divisions also take place as part of the body's basic maintenance processes. Tissues get worn out, or damaged by trauma, or injured by disease, and the healing process that restores these tissues involves cell division. So, over the years, your telomeres do tend to get whittled down.

What happens when the telomeres get short enough that they can no longer provide adequate protection to the actual genetic content of the chromosome? Well, the cell is programmed to enter a "senescent" state when that happens. The cell stops dividing. And eventually the cell dies.

This is assumed to be one of the reasons that we have a limited lifespan; as telomeres are whittled away, and more and more cells enter the senescent state, the body's healing processes go into decline. Diseased or injured tissues can no longer be repaired. Damage builds up; things fall apart.

You might think that this is a problem which medical science should be trying to solve: why not find a way to lengthen our telomeres, so that our cells can go on dividing forever, and we'll stop aging and become immortal? Well, there actually are some researchers looking into that possibility, but don't get too excited just yet. There are some pretty serious problems with the idea of lenthening the telomeres. It seems that there's a good reason why most cells have telomeres of a fixed length.

I should point out that some types of cells, which need to reproduce frequently (such as sperm cells), do have the capacity to add to the length of the telomeres, so that the cells can continue dividing. Cells in this category produce an enzyme called telomerase, which lengthens the telomeres by tacking new base pairs onto the end of the DNA strand. Most of the body's cells, however, don't produce telomerase, so the telomeres in most cells can only get shorter over time, not longer.

It sounds as if telomerase must be a potential fountain of youth. If we could only get ordinary cells to produce telomerase, than the telomeres in ordinary cells would lengthen, and cells would continue dividing without limit, instead of shutting down and dying. The good news is that this phenomeonon sometimes occurs spontaneously; the bad news is that, when this occurs, it means you have cancer.

Apparently cancer is a two-stage process. What happens first is that a mutation causes a cell to start dividing rapidly, creating many copies of itself. However, this clump of fast-dividing cells usually reaches a limit of growth when its telomeres get too short: the cells stop dividing, and the result is a microscopic tumor which can't grow any further or do us any harm (most of us probably have several such undetected tumors somewhere inside us). But if, while those cells are still dividing, one of them undergoes a mutation which causes it to start producing telomerase, that cell is (to use the actual medical jargon) "immortalized" -- its telomeres get longer instead of shorter, so it can keep on dividing without limit. If this happens in a tumor cell, the tumor grows and spreads. To minimize the risk that this scenario will play out somewhere within the body, the gene that produces telomerase is turned off in most of the body's cells. And it stays off, unless an unlucky mutation turns it on.

If, in out quest for the fountain of youth, we try to turn on telomerase production in body cells which normally have it turned off, we might end up halting the aging process, but only at the cost of hugely increasing our cancer risk. In other words, we probably wouldn't be around long enough to enjoy very much of the "eternal youth" we were theoretically achieving for ourselves.

Very likely, the maximum length of human telomeres is what it is, and the maximum length of the human lifespan is what it is, simply because this is the best compromise nature has been able to make between degenerative aging (if a limit is placed on cell divisions) and cancer (if no limit is placed on cell divisions). Decreasing either of those risks would probably increase the other. Maybe we just have to accept the telomeres we have, and not try to lengthen them artificially.

However! That only means that we probably can't extend the theoretical maximum for the human lifespan. It doesn't mean that we can't do anything to try to live out a fuller share of that maximum lifespan than most people do. To put it another way, we can't lengthen our telomeres -- but we can slow down the rate at which our telomeres are shrinking.

It might seem, from my preceding description of telomeres, that the only reason they get shorter over time is that another chunk gets torn off the end of them every time a cell divides. Actually, there's more to it than that.

Telomeres erode over time, for reasons unrelated to cell division. Anything that puts stress on the cells -- inflammation, oxidation, whatever -- tends to erode the telomeres. The clinical evidence says that most of the undesirable conditions which we associate with degenerative illness have the effect of eroding the telomeres. High blood pressure tends to erode the telomeres. Emotional stress, with its attendant release of inflammatory hormones (adrenaline and cortisol) tends to erode the telomeres. Obesity tends to erode the telomeres. And, of course, elevated blood glucose tends to erode the telomeres (don't tell me you didn't see that one coming!).

The consequence of all these factors is that some people are "aging" faster than others are. If aging consists of diminishing telomere length (and apparently it does, to a large degree), then some of us are getting old faster than necessary. It seems that we could age more slowly if we could eliminate, or at least reduce, such problems as obesity, hypertension, inflammation, and stress.

A recent Medscape article entitled "Exercise May Buffer Effects of Stress" looked at telomere length in a group of women who were under stress. At least, the women said they were under stress, and considering that many of them were caregivers to a parent or spouse with dementia, I'm inclined to take their word for it. The women may all have been under stress, but they were unalike in one interesting way: some of these stressed-out women were exercising, and some were not. It turned out that the women who were not exercising had abnormally short telomere lengths for their age; the women who were exercising had telomeres of normal length for their age, despite the stress they were living with.

Okay, so this was a small study, and perhaps not so rigorous in its methods (or so specific in its reported data) that we can say it proves very much.

It's just one more piece in an accumulating mountain of evidence that we have to do something about the accelerated aging process that goes on in people with diabetes, and that exercise is one of the more effective things we can do about it.


That's all for now -- may the force be with you, and may the aglets on the ends of your shoelaces and chromosomes remain bright and shiny!


Thursday, June 10, 2010  


I think my allergy season is drawing to a close -- over the last few days, outdoor running doesn't seem to have caused me any significant allergy symptoms. During May, I was slightly ashmatic (my lungs seemed inefficient, and running felt terribly effortful, as if I were running at a high altitude) -- and after I got back indoors my eyes would often be itchy and swollen. I think that's over now. Good riddance!

I must admit that my allergy seasons have been getting milder in general, ever since I took up outdoor exercise in 2001. I guess the frequent exposure to whatever was blowing around outside has desensitized me a little. Being around cats, at certain times of year, is still a big problem for me, but I haven't been exercising with cats, so maybe that's why I've made no progress on that front.


When I was originally diagnosed with Type 2 diabetes, I was sent to a class on the subject, and I was told that the human body can derive glucose from any of the three macronutrients, but that the three are very different in terms of how much glucose can be obtained from them, and how quickly:

The bottom line was that carbohydrate was the macronutrient you had to watch. I produced a "spike" -- lots of glucose hitting the bloodstream in a hurry -- which was what you needed to worry about. For protein and fat, the total yield of glucose was much smaller, and was produced so slowly that it wasn't likely to lead to any kind of dramatic overflow. (For most people, protein makes up a rather small percentage of total calories anyway.)

Because I was taught all that, in a class that my doctor sent me to, I assumed for a long time that it was uncontroversial -- that it was common knowledge. I thought just about everyone knew and accepted that half of the protein you eat turns into glucose. However, I eventually noticed that this fact (if fact it was) never seemed to be mentioned in any literature or discussion about diabetes. What was going on?

I've been researching the question a bit tonight, and it turns out that the issue is more complicated and confusing than I had been led to believe.

It has been known, at least since 1915, that a certain amount of ingested protein can be converted to glucose. The maximum possible glucose yield depends upon the amino acid mix that's in a particular protein; it can be anywhere from 50% to 80%. For beef protein, the yield is about 56%. But that's the theoretical maximum yield, not the actual yield. Just how much of the protein gets converted to glucose after you eat it is apparently something which the body is able to decide for itself. At any rate, some studies have found that digesting protein often contributes much less glucose to the bloodstream than would be expected.

This study on the "Effect of Protein Ingestion on Glucose Appearance Rate in People with Type 2 Diabetes" found that ingestion of protein (specifically in the form of beef) results in "little or no increase in circulating glucose concentration in nondiabetic people or in people with type 2 diabetes mellitus". This outcome was considered surprising and rather puzzling; the apparent explanation for it is that ingesting protein stimulates a release of insulin that is out of proportion to the glucose-making potential of the protein itself. Perhaps that is why another study found that, when Type 2 diabetes patients ate a combination of carbohydrate and protein, their blood glucose afterwards was 34% lower than it was when they ate the carbohydrate by itself!

Well, the reasons for all this are not fully understood, but the bottom line seems to be that, as a practical matter, eating protein by iself does not have a significant glycemic impact, and it even seems to have a moderating effect on the glycemic impact of any carbohydrate that is consumed along with the protein.

I'm not claiming that this is a game-changing discovery -- the overall message that I had been given in that class was that only carbohydrate made a major contribution to glucose spikes after meals. But I'm glad that I found out a little more about the matter.

It's always worth knowing more about this diabetes thing.


Wednesday, June 9, 2010  


Elections have consequences, as they say. And here's the election consequence that captured my attention today: the much-hated former CEO of a company I used to work for is going to be the Republican nominee for Senator of my state. Just when I thought she was out of my life for good, and no longer in a position to hurt anybody!

But that's the way the world works. We shouldn't be surprised that unpleasant people always seem to end up running things. Pleasant people generally do not start from the assumption that they ought to be running things; in effect, they cede the field to the unpleasant, the minute they decide against being unpleasant themselves.

My election-night dinner, on the other hand (the high-carb meal that was brought to me because the waiter misunderstood my order) doesn't seem to have had any consequences, and that's good. Fasting test of 81 -- that'll do fine!

My blood pressure's quite low this evening, and I can think of three reasons for that:


I didn't even realize that there were official photos being taken at the race on Sunday. But one picture was taken of me, just as I was approaching the finish line, and they're offering to sell me a print of it.

Well, it doesn't make me look fat -- that's a plus. But I had just shaved off a beard the night before, and the resulting paleness of my face seems to contribute to the general impression of an old man struggling to draw his last breath. I probably don't need a framed enlargement of this.


A lot of people with diabetes are furious about the widespread tendency to speak of diabetes as a simple consequence of obesity. The message they are hearing (or believe they are hearing) could be summarized thus:

These people point out angrily that diabetes is genetic, that it runs in their family, that it's not their fault -- and they also point out (they clearly think this is the clincher) that some people with diabetes aren't fat, and lots of fat people aren't diabetic! Therefore, diabetes can't have anything to do with obesity -- all this talk about obesity and diabetes is simply mythology, and everyone should shut up about it henceforth.

It's the kind of logic that people turn to when they're feeling defensive and angry. In another situation, they might use the same kind of logic, and point out that sober drivers get into accidents sometimes, and drunk drivers often make it home safely! Therefore drunk driving can't have anything to do with road safety -- all this talk about drunk drivers causing accidents is simply mythology, and everyone should stop making such a big fuss about it.

I don't think anyone who has seriously examined the subject of Type 2 diabetes would assert that it is caused simply and solely by obesity, or that the disease has no genetic basis. Several specific genes have been implicated in the genesis of the disease. However, the mere fact that genes play a role in diabetes (as they do in all health issues) is not quite the game-changer that angry diabetes patients often try to make it appear.

Conceding that genes play some role in determining your risk of developing Type 2 diabetes is not at all the same thing as conceding that the disease is of purely genetic origin.

Conceding that obesity is not the only risk factor for Type 2 diabetes is not at all the same thing as conceding that it isn't a risk factor at all.

Several genetic mutations have been linked to an increased risk of Type 2 diabetes, but no genetic mutation has been found which causes the risk to be 100%. If the disease were purely genetic (as in the case of Huntington's disease), then a genetic test at birth could reliably tell us who was going to become diabetic and who wasn't. But the reality is that having the wrong genes only increases your risk of becoming diabetic, without turning the risk into a certainty. Therefore, other risk factors must be involved -- risk factors which combine with the genetic bias towards diabetes, and turn the diabetes potential into a reality. Those risk factors include, but are not limited to, obesity -- particularly abdominal obesity (although why it should matter whether the fat is centered at the waist or the hips is obviously a puzzling issue). 

It is sometimes asserted (with more confidence than I think the evidence warrants) that obesity is a result, not a cause, of Type 2 diabetes. The idea is that the underlying metabolic problem which makes you diabetic also makes you fat -- and it makes you fat first, thus creating the false impression that fat is causing the problem.

The trouble with the theory that fat is only a result, never a cause, of Type 2 diabetes is that significant weight loss following diagnosis often brings about a dramatic reduction in blood sugar. If the extra weight wasn't pushing blood sugar upward, getting rid of the extra weight shouldn't pull blood sugar downward, should it? Yet it often does.

At least one of the genes that is strongly associated with Type 2 diabetes seems to interfere with the way the body burns fat, and thus increases your risk of obesity. Perhaps that's the only reason it is associated with diabetes: it sets you up to be biased towards weight gain. But not everyone who carries that gene gets fat -- and among people who do carry that gene, it's the fattest ones that have the highest prevalence of Type 2 diabetes. Perhaps they also carry another gene which increases the odds that obesity, if they develop it, will push their blood sugar up.

My main point is that obesity remains relevant to Type 2 diabetes regardless of what other factors may or may not be interacting with it. It would be irresponsbile -- criminally so -- to pretend that obesity is not relevant, simply for the sake of placating those who become defensive and irritable whenever the subject comes up.

On the other hand, I admit that it's very crude and inconsiderate to insist upon recommending weight loss to people with diabetes who are not overweight, or to talk as if diabetes were purely a body-weight issue, unrelated to any other issue -- when we know that that is not the case.

I think people need to know about all the things that can put you at risk for becoming diabetic. It's stupid to talk as if obesity is the only issue. It's even more stupid to talk as if obesity is not an issue at all.


Tuesday, June  8, 2010  


Oh, how nice -- a mid-term election! My opportunity to act as if I know something about the people who want to be district attorney. I hadn't filled out my sample ballot yet, and after work I decided to have dinner on the balcony at the country club across the street from where I work, and make my solemn decisions over dinner.

I placed my order with the waiter (whose first language was definitely not English, but I thought he understood me), and went to work on the ballot. I live in California, where there are always sure to be several ballot initiatives, and the trickiest part of voting here is to figure out what kind of fraudulence is involved in each ballot measure, and which pack of scoundrels is backing it.

The task was slightly easier than usual this time: there were only five initiatives on the ballot, and two of them were quite brazenly the handiwork of a pair of corporations aiming to get the law changed so that it favored their intersts at the expense of the public interest. No need to waste a lot of time thinking about voting for those. Of the remaining three, one was an obvious and uncontroversial "yes" (nobody seems to be against it, so why didn't the legislature just pass the thing and save us the trouble?), one was a possible "yes" but too doubtful in its impact for me to take a chance on it, and one was a likely "yes" which I ultimately decided to take a chance on because the people who are against it are the sort of people you want to be against. But what if that one turns out, after I vote for it, to be something very different from what I thought I was voting for? Just as I was entertaining that anxious thought, the waiter showed up with my dinner -- and it wasn't what I had ordered. The waiter was sure I had said something else.

I'm not the sort of person who makes scenes in restaurants and sends things back to the kitchen, but I came close to making an exception this time. The waiter had substituted a high-carb dinner for the low-carb one I'd wanted. I thought it over. Well, my fasting result was only 83 today, and I had a pretty solid workout, and I a light lunch. I figured I could probably handle this. Treat it as a "vacation day"...

So I ate my high-carb dinner, trying my best to enjoy it. In a way I did, and in a way I didn't. And then I went back to working on my ballot, holding the thought in mind that what you think you're asking for is not always the same thing as what your'e going to get.

So then I went and voted, and did a few other errands downtown, and by the time I got home, it was already nearly 2 hours and 30 minutes after I'd eaten my high-carb dinner. Was there any point in testing that late? I decided that there was. The result turned out to be 103. Strictly speaking, that proves nothing about how high I went at 1 hour, or even at 2 hours, but at the same time I feel somewhat reassured. If I had been very far out of bounds earlier, I probably wouldn't be quite as far down as 103 by the time I finally tested.


These days we like to talk about "activity" rather than "exercise". Apparently the thinking behind this is that the E word is too scary, and you need to ease people into the idea of getting off the couch. Therefore, we need to encourage the idea that doing just about anything more lively than playing chess is roughly equivalent to exercise, or at least has pretty much the same benefits. Why go jogging when taking a walk is just as good?

I'm sure that taking a walk is a big improvement on not taking a walk, so if the promoters of "activity" are succeeding in getting people to go for a walk who would otherwise never crawl out of their reclining chairs, I guess that's a step in the right direction. What worries me is that I'm afraid people are starting to see "activity" not as a transitional stage on the journey to "exercise" but as a satisfactory destination in itself.

But is "activity" really enough? Specifically, is it enough for people who have been diagnosed with Type 2 diabetes, and who therefore need to do something about (1) the loss of insulin sensitivity typically associated with that disease, and (2) the decline in cardiovascular health typically associated with that disease?

It's fairly easy to find out, from direct experimentation, whether or not "activity" is getting the job done for you in terms of glucose control. If going for a two-mile walk every other day is all it takes to hold your blood sugar within the normal range, then that's all it takes. I seem to need more than that, myself.

It's a little harder to figure out is whether "activity" is getting the job done for you in terms of cardiovascular health. There really is no way to be absolutely sure how well you're doing in that department, aparting from waiting around for years to see if you have a heart attack or not. However, there is one superficial indication that's fairly easy to track: what's going on with your blood pressure?

My own blood pressure was high at the time of diagnosis, and I was taking an ACE Inhibitor (monopril, specifically) to manage it. After I lost a lot of weight, and my doctor could see that I was sticking to my exercise program over the long haul, he decided that it was okay for me to stop taking the monopril, and since then my blood pressure has gone down rather than up. I'm almost always under 130/80, and often under 120/80. My resting pulse is usually well under 60.

Anyway, I've found that intense exercise such as running (typically on hilly terrain, because that's what we have in these parts) seems to do for my blood pressure today what light exercise (such as walking a mile or two) failed to do for me in the past. My view of the matter is that, in terms of dealing with the cardiovascular issue, "activity" doesn't cut it.

And now I have some support for my view of this matter. A Medscape article today reports the following:

"A new analysis of the longitudinal Coronary Artery Risk Development in Young Adults (CARDIA) study, published online June 1, 2010 in Hypertension, shows that both physical fitness and physical activity are inversely associated with the development of hypertension over a period of 20 years. But importantly, the researchers illustrate that activity was significantly associated with nonhypertensive blood-pressure readings only when fitness levels were the highest."

The study, at least as reported in Medscape, is frustratingly imprecise about how the fitness categories were defined. But the fact that the main benefit went to those in the highest fitness category suggests pretty strongly to me that going for a walk is just not good enough.

On the other hand, if going for a walk is all you can do -- at least go for a walk! 


Monday, June  7, 2010  


Sunday morning (make that early Sunday morning) I drove to the town of Sonoma for the Hit The Road Jack race. It's a popular event. There were 1429 runners, which is a lot of people to bring into a town as small as Sonoma. I left my place driving in dense fog, but it was sunny and warm when I arrived.

There was a shorter race of 2.2 miles, but I was in the longer one, the 10-kilometer distance (a very standard distance for footraces -- it's equal to 6.2 miles). It took me slightly under an hour to finish (59:07), which I'm sorry to say is 8 seconds longer than I needed to run the same race last year.

I'd like to be able to claim that the only reason I was slower this year was that the higher temperature this year made running more difficult -- but probably the more pertinent fact is that I weighed three pounds less when I ran it last year, and three pounds is enough to make a difference.

Trying to see if I could find any dignity for myself by poking around in the statistics, I figured out that only 41% of all runners in the race finished ahead of me. So, I was among the first half of runners crossing the finish line, not the second half! However, that's including both male and female runners in the comparison, which isn't how these things are usually done. If I look only at the men, almost 65% of them beat me.

Ah, but that includes all age groups! What if I only include men in my own age group (50-59)? I'll look a lot better if I only compare myself to them, and leave out all the younger guys, won't I? Actually, no. There are a lot of good runners in their 50s, and in fact I came out a tiny bit worse when I compared myself to that group than when I compared myself to male runners of all ages.

So it looks like there's no escaping the conclusion: I'm not a fast runner. Why, then, do I keep participating in races?

Let me explain that in the most roundaout way conceivable.


When I see a movie set in some historical period or mythical world, I pay a lot of attention to the little details that the movie's production designers have put in place -- the touches that tell you somebody's really thought about what kind of equipment would be in the kitchen of an English country house in 1924, or even about what kind of patio furniture elves would build.

These things matter. It's the incidental details, in movies and stories, that give you a persuasive sense of entering into a different world. We're in Paris in 1780, and an aristocrat steps out of his carriage; the fact that his black shoes have red heels tells you instantly that somebody has done his homework. You know this even though you are wholly unfamiliar with 18th-century fashions in men's shoes. A telling detail proclaims itself instantly, no matter what you know or don't know going in, and it establishes credibility. (This helps you get through the moment when you suddenly realize that the French aristocrat with the red-heeled shoes is Keanu Reeves.)

I love these details. I like the atmosphere they create in a story. For that matter, I like the atmosphere that incidental details create in real life.

The accessories associated with a particular trade or hobby carry a kind of magic for me. One of the reasons I find it interesting to watch a demonstration of, say, blacksmithing is that I get to watch someone working with tools and materials that I perhaps didn't know existed (and would not know how to buy, if I ever needed them myself). When I took up the fiddle, I brought all sorts of new objects into my life -- the instrument, the case, the rosin, the strings, tuning forks, metronomes, and many other items that most people will never deal with.

Not to mention old books on Irish music, complete with the odd combination of titles in Irish Gaelic and instructions in conservatory Italian:

For whatever reason, I just love the artifacts of specialized activity; I find a kind of romance in it. This makes it hard for me to throw things away.

When I got home yesterday morning from the footrace in Sonoma and removed the bib number that was safety-pinned to my running shirt, I didn't toss it in the garbage. I don't preserve these things in a systematic way (I am not a keeper of scrapbooks); I just added it to a pile of other bib numbers, on a shelf in my bathroom.

But after I'd had a shower (and a nap, which I'd promised myself to take after the race), I started going through the little pile of bib numbers. They brought back memories -- in some cases, memories of races that I'd forgotten I'd run. I was surprised how vividly I was reminded of what those races had been like -- the weather, the terrain, how many other people were running, who else was there that I knew. I guess that's what souvenirs are for.

I layed out a bunch of these things on my kitchen floor to make a little collage and photograph it.

That's only a sampling of the events I've done in recent years. You may well ask what is the point of participating in so many of these things. Certainly it isn't because I think I'm eventually going to win one of these races if I keep on trying. (As in the case of yesterday's race, I'm usually beaten by a solid majority of the male runners.) And if you're not running with a realistic expectation of winning -- if you're just running 6.2 miles because you want to run 6.2 miles -- then you can do it more conveniently by yourself, at a time and place of your choosing, without having to pay a registration fee and pin a bib number to your shirt.

But I like the incidental details that go with a race. I like the whole cumbersome business of clearing a date on my calendar, and registering for the event, and worrying about what the weather will be like, and setting the alarm for an early wake-up, and trying to figure out how much of a breakfast is enough without being too much, and getting to the race location, and waiting in line at the port-a-potties, and then waiting nervously for the race to start. 

And, when the race finally gets under way, I like the excitement of running with a big crowd of other people, the constant mental struggle against the urge to take it easy and slow down, the odd bits of conversation you overhear between other runners, the surprising meet-ups with people you know who turn out to be participating in the race along with you. And then, of course, the great relief when you cross the finish line, and you get to hang around watching the runners behind you come in. And the post-race conversations with other runners you know. And the post-race hot shower that seems luxurious out of all proportion to what you have a right to expect.

The race, as special occasion, seems to cause a heightening of every sensation. And there are a hundred incidental details involved in it that seem striking and meaningful. And it creates a record which you can look up later. And there are nearly always souvenirs (the race T-shirt, the bib number) that you can hold onto, and remind yourself of the race long afterwards.

Well, I've tried my best to describe the feeling I have about these events. It's elusive, and not easily explained to those who have never participated in such things. But once you have participated, you're likely to keep doing so.


Friday, June 4, 2010  


It's sometimes shocking to discover that other people don't see things the way you do.

I remember vividly the first time I saw Skrik, the most famous work of the Norwegian expressionist painter Evard Munch. Skrik is usually translated as "The Scream" or "The Cry", although the Norwegain word really means "Shriek". Anyway, I thought I knew the whole story that the painting was telling -- it was so obvious.

The woman in the foreground is terrified. Two men are following her in a public place in the evening, and she feels sure that they are going to attack her, but she can't do anything about it, because there's no way for her to prove that her suspicions are valid. There's nobody around who knows her or will believe her. She's on her own, and entirely helpless. She's afraid to turn around and look at them, but she knows they're there, and she knows that there's no way she can get away from them. She feels paralyzed, unable to act. And I don't think she actually shrieks -- she wants to, but doesn't dare. The cry of terror here is an internal convulsion, so powerful that it seems to roil the landscape around her.

I have since learned that the rest of the population is not necessarily on board with my interpretation of this picture. For starters, a lot of people see the figure in the foreground as a man, not a woman. Or as "a sexless figure".

Some claim that the figure in the foreground was inspired by Munch's viewing of a mummy in a French museum, crouching with its hands on either side of its head. Two paintings by Munch's friend Paul Gaugin are known to have been inspired by that same mummy:

And recently I read Munch's own acount of his inspiration for the image, which doesn't seem to match mine very well: "I was walking along a path with two friends -- the sun was setting -- suddenly the sky turned blood red -- I paused, feeling exhausted, and leaned on the fence -- there was blood and tongues of fire above the blue-black fjord and the city -- my friends walked on, and I stood there trembling with anxiety -- and I sensed an infinite scream passing through nature."

So, in the painter's own description, the two figures in the background are friends walking away, not enemies approaching. And the shriek, far from being internal, is coming from all of nature. Seemingly I'm wrong on every count.

However, the location of the scene in the picture is very precisely known: the water in the background is Oslofjord, as viewed from the hill of Ekeberg, in Oslo, Norway. And we also know exactly what Munch was doing there: at the foot of that hill, facing the fjord, was a mental hospital. He was visiting his sister Laura, who was interned there.

I've thought it over, and I stand by my story.

 


Art can be interpreted any way we want to interpret it, but science is different, right? Isn't it?

Not necessarily. Scientists never have all the data they want. In some sciences, and above all in medical science, they sometimes have only the most fragmentary evidence to work with, and must fill in the gaps with reasonable assumptions. At least, we hope the assumptions are reasonable. But when the amount of assumption gets out of proportion to the amount of evidence, we begin to share Mark Twain's unease about museum dinosaurs that consist of a little bit of bone and a great deal of plaster. Sometimes a scientific conclusion seems to consist more of interpretation than of fact.

I'm sure it would be possible to do a study showing that the incidence of coronary heart disease correlates with the progressive loss of hair color. You could lay out the statistics so that they told the story in stark and unmistakable terms.

Could it be any plainer? The figures don't lie! The pattern is clear! White hair causes heart disease!

Therefore, if you don't want to have a heart attack, you need to dye your hair. You don't want to let your hair go white, or even gray, because we all know what happens to people like that, don't we?

Now, so far as I know, there isn't anybody out there selling hair dye as a means of preventing heart disease. But why isn't anybody doing that? The evidence is as good for that idea as it is for a lot of other ideas that have won general acceptance.

I guess the main reason that people aren't using hair dye as a means of preventing heart disease is that we all know about an obvious alternative explanation for the correlation between loss of hair color and increased cardiac risk. People with white hair may have more heart attacks than people with dark hair, but it's because people with white hair tend to be older than people with dark hair, and heart-attack risk tends to increase with age.

Hair color and heart attacks have no direct connection with one another; the only reason they correlate is that both happen to be connected to a third variable, namely age. Imagine what it would be like if we didn't know about that third variable! If nobody had ever noticed that hair tends to whiten with age, the connection between white hair and heart disease might seem a lot more meaningful to us than it actually does.

All sorts of things correlate with heart disease besides hair color, or rather age, and the science (such as it is) of heart disease prevention is focused on eliminating those things, so that they don't get a chance to cause a cardiovascular problem. But what if these things don't play a direct role in causing heart disease? What if, like hair color, they simply happen to be associated with some other variable which is itself the true cause? If, for example, low HDL cholesterol is not a cause of heart disease, but a consequence of some unidentified factor that is a cause heart disease, then raising your HDL cholesterol won't solve the problem, any more than dying your hair will solve the problem.

Or: even if low HDL does play a direct role in causing heart disease, we still can't take it for granted that raising it will solve the problem no matter how we accomplish that. It might make a difference how we raise it. Raising it by means of some chemical intervention might create more problems than it solves, for all we know.

At any rate, because heart disease is so complicated and so incompletely understood, it's not good enough to come up with a remedy that reduces one of the factors that correlate with heart disease. The remedy also needs to reduce heart disease. Otherwise, we're just talking about the hair-dye approach in a more expensive form.

The much-criticized ACCORD lipid study (criticized more for overinterpretation of data than for collecting bad data) looked at diabetes patients who were being treated for cholesterol problems with fenofibrate, a drug which is claimed to reduce LDL and triglycerides while raising HDL -- thus correcting not one but three lipids problems commonly seen in Type 2 diabetes patients. And the study found that, indeed, fenofribrate did all those things for the diabetes patients. The only thing it didn't do was give them a reduced rate of "adverse cardiovascular events". Also, it caused kidney problems in some patients, who had to drop out of the study for that reason.

So, once again (sorry if you've heard this before, but it keeps on happening, and it's not my fault) we have an expensive medication which "works" in the sense that it causes a striking improvement in certain factors which correlate with heart disease, but doesn't make heart disease itself any less likely.

It's hair dye, in other words. But that's just my interpretation, of course. Other museum-goers are free to read the picture differently.


Thursday, June 3, 2010  


Hmmmm -- they're backing down a bit on this stuff...

The medication known as 2-acetyloxybenzoic acid, or acetylsalicylic acid, has been around for a long time. The German company Bayer started selling it as a pain-reliever in 1899, under the trademark name "Aspirin". However, "Aspirin" (capitalized) became mere "aspirin" in 1919, when the name lost its trademark status as part of the terms of the Treaty of Versailles which ended World War I. After that anybody could make it and sell it as "aspirin".

I've never read the Treaty of Versailles, I confess, but it must have been a very comprehensive peace treaty indeed, if it not only ended a world war but also settled the trademark status of a headache remedy. (And "Aspirin" was not the only trademark that bit the dust as the result of that treaty! Apparently "Heroin" became a generic at the same time. It was a tough year for the patent-medicine industry.)

The thing about aspirin is that it has been "grandfathered-in". We don't remember a time when people weren't taking it. Aspirin didn't have to win FDA approval, any more than beer did. We have simply been assuming all our lives that aspirin is the mildest and safest remedy in the world. And any time someone thinks of another use for it, we take it for granted that there's no downside to using it in that way.

Because aspirin has anti-clotting properties, it has in recent years been recommended as a means of preventing heart attacks, and millions of people (including me) have been taking a small dose of aspirin daily. But now the experts are starting to back down, at least a little bit, from the daily-aspirin idea.

Today there was a joint statement issued by the American Diabetes Association, the American Heart Association, and the American College of Cardiology, to the effect that daily low-dose aspirin is being recommended to too many people.

Current recommendations are for pretty much everyone over 40 with diabetes to take a daily aspirin, as a means of preventing cardiovascular disease. It's becoming doubtful, however, that the benefits of daily aspirin (in the form of reduced cardiovascular risk) always outweigh the disadvantages of daily aspirin (in the form of heightened risk of bleeding).

Apparently aspirin has only a modest impact on cardiac risk, so your cardiac risk has to be fairly high in order for aspirin to be "worth it". Also, other things that patients can do (such as getting their cholesterol under control) reduce cardiac risk far more than aspirin does. If the use of aspirin weakens people's motivation to take more effective action, on the assumption that the aspirin is taking care of the problem, then it's a net loss.

The new recommendation for diabetes patients is to take daily aspirin only if (1) you're a man over 50 or a woman over 60, and (2) you have at least one additional major risk factor for cardiovascular disaease. These "major" risk factors would be things such as smoking, hypertension, dyslipidemia (problems with blood fats), and a family history of cardiovascular disease.

I've been taking low-dose aspirin on my doctor's recommendation. However, that recommendation was made a long time ago, and when I saw him last year he seemed to be backing away from it. He didn't tell me to stop, but he implied that it might not be important to continue, because I had eliminated the things that had seemed to put me in the cardiac-risk category earlier. I guess I'll have to ask him, the next time I see him, where he stands on all this now. I think I'll keep on taking the aspirin until I get a chance to ask him, though. Or maybe compromise on taking it every other day.

Wait a minute. Suddenly I'm reminded that my dad had a gastric-bleeding problem once as a result of taking aspirin daily. If that sort of reaction to aspirin can be hereditary, maybe I'm at risk for it. I think I'll definitely have to revisit this issue with my doctor!
 


The day began cool and cloudy, and ended that way too, but when I went running at lunchtime it was sunny and warm and even rather muggy (at least by local standards -- Californians generally have to leave their state before they achieve a full grasp of the humidity concept). I found that 4.4 miles was plenty.

My new running shoes are working out well. I was concerned at first that they might be a little too wide, but if I lace them up firmly they're snug. And, being new, they have a bit of extra bounce to them. I'm not going to tell you what brand they are, because that would make it sound as if I'm recommending them -- which would be pointless, because running shoes that are great for one person can be awful for someone else. I once bought a pair of shoes from a leading maker, and they chafed my heels so umercifully that they were completely unusable. And yet, I'm sure there are people for whom those shoes would be perfectly fine.

I don't think there's anything harder to shop for than running shoes. Individual needs vary so much that product reviews don't help, and recommendations from your friends usually don't help either. Sometimes it's not even a sure thing to buy shoes that have worked well for you in the past, because the design or materials of the shoe may have changed over time -- and if the shoes haven't changed, maybe you have!

But I think these are good. Which is fortunate, because I think I'm going to do the 10K race in Sonoma on Sunday.


Wednesday, June 2, 2010  


Today the dLife people sent me a kind invitation to take part in an on-line survey, with the offer of a $20 gift certificate (which I would receive if I was among the first 1,000 dLife members to participate). I followed the link they sent me, not primarily because I was craving the gift certificate but because I was curious about what questions the survey would ask, and what those questions might reveal about the thinking of the people who crafted the survey. It turned out that they revealed too bloody much, as you will see shortly.

So, I clicked on the link, and a window opened that said "BGM Concept Test", and greeted me in the following terms:

Thanks for taking the time to take this survey.  Your answers will help determine the design of some important new products.

Many of the questions in this survey will refer to a blood glucose meter as a "BGM."

After completing this survey you will be able to claim your specific prize. We will email it to you in a few days once the quota of surveys has been filled.

If you don't have time to finish the survey right now, you can always come back by clicking the "save and continue survey later" link in the top right corner of the survey window.

On to Question 1:

Which of the following do you currently have? (Select all that apply.)

I chose "A traditional hand held blood glucose meter", which I would imagine is a pretty common choice in this survey.

And now -- Question 2:

Which of the following do you currently take to help manage diabetes? (Select all that apply.)

I chose "None of the above", which I imagine is a pretty uncommon choice in this survey. Apparently it's an even more uncommon than I thought. As soon as I made it, the following message appeared on my screen:

Sorry, you do not qualify to take this survey.


I don't know what they are hoping to learn about diabetes patients from this survey, but whatever it is, they're pretty sure that they can't learn it from someone who isn't on drugs.

This is not the first time that something like this has happened to me. The people who do surveys and studies of diabetes patients emphatically do not want to hear from those of us who are managing the condition without meds -- or who "aren't taking our meds", as they would put it. I once participated in beta test of a software tool designed to evaluate cardiac risk; despite all the excellent lab results I reported, the tool still rated me as having a high risk of heart attack because I "wasn't taking my diabetes medication". In my feedback, I pointed out the tool had simply assumed that medication had been prescribed for me and I wasn't taking it, when the reality was that no medication had been prescribed for me because I didn't need it. I got a reply explaining that, well, the test wasn't designed with someone like me in mind. They obviously thought they were being perfectly civil to me, but there's a limit to how politely you can say "You don't matter".

And I don't matter to these people -- heaven knows they've told me so clearly enough. Collecting data from someone like me can only screw up the statistical model they're constructing of the "typical" (that is, sterotypical) diabetes patient.

A lot of research (whether it's "pure" research, or marketing research -- which I imagine is what dLife is actually involved in here) is about separating the signal from the noise. You look at the bewildering variety of the real world, and try to find a pattern in it. Unfortunately, it's sometimes hard to tell whether you are "finding" that pattern or creating it. If the way to make a statue of a horse is to start with a block of marble and chip away everything that doesn't look like a horse, very often the way to find a pattern in data is to collect a bunch of data and then throw out whatever part of it doesn't fit your preconception of what the pattern ought to be.

The corrosive assumption that diabetes can be controlled only with meds has eaten its way into nearly all commentary about the disease. For example, Medscape published today a report (reprinted from Diabetes Care) under the headline "Thiazolidinediones and Sulfonylureas Most Effective in Lowering HbA1C ". But it turned out that they didn't mean these drugs were the most effective method of lowering HbA1c -- they were only the most effective method of lowering HbA1c by means of oral diabetes medications. No comparison was made to lowering HbA1c by means of lifestyle adjustments, and the part of the report called "Study Limitations" didn't mention that omission as having any possible relevance. "Overall, OADs lowered A1C levels by 0.5% 1.25%, whereas thiazolidinediones and sulfonylureas lowered A1C levels, to a slightly greater extent, by approximately 1.0% to 1.25%." It's okay to compare pills with pills, but it's not okay to compare pills to something that might turn out to work better.

Not many studies ever compare the effectiveness of diabetes drugs to lifestyle-based diabetes management -- but I've seen at least one study that did make that comparison, and the drugs turned out to run a distant second. I'm not surprised that such comparisons were not made in the case of the report I've been describing, as its authors have financial ties to various pharmaceutical companies.

I am perfectly willing to accept that my approach to diabetes management is not typical. What I'm completely unwilling to accept is the assumption that whatever is not typical is therefore irrelevant, and should be ignored. Not so long ago, it was not typical to refrain from smoking; should it have been assumed that people would never give up smoking in large numbers, and it was pointless even to discuss the possibility?


Tuesday, June 1, 2010  


Today I had a Senior Moment in regard to bringing all my exercise stuff with me to work. I remembered to take my gym bag, and I even remembered to add to the bag the new running shoes that I bought on Saturday. What I did not remember to add to the bag was a towel.

I don't know if you've ever taken a shower after a run and then attempted to dry yourself off with paper towels. I've done so, and it doesn't exactly help you cut a dashing figure in the locker room -- or even back in the office, where the basic futility of the whole enterprise is symbolized vividly by the damp patches darkening your clothes. I don't want to go through that any more. When I forget my towel, I just change my workout plans; that's the new rule. So, when I discovered today that I had no towel, I resigned myself to running in the evening instead. I guess it didn't matter that much: my running buddies were both stuck in meetings at lunchtime, so I would have been running by myself anyway. What really bothers me is that I can't remember simple things like that. I was hoping that exercise would prevent Alzheimer's, but at this rate it's looking more like Alzheimer's is preventing exercise.

Of course, I did have a nice evening run, so all's well that ends well. But I've just placed a towel by my front door. I'm hoping that stumbling over it in the morning will remind me to take it with me when I leave for work.


I like reading biographies, even though they tend not to have happy endings, and even though quite a lot of biographies are sad all the way through.

I thought the biography of the French composer Maurice Ravel (1875 - 1937) would not be particulaly sad, as the composer enjoyed worldly success, and seemed to have lived life on his own terms and to his own satisfaction. But I had always been puzzled about why Ravel stopped writing music about five years before he died, and when I finally got around to reading his biography recently, I found it very sad indeed to discover the reason for that.

The precise reason for Ravel's problems in his last five years of life is to some degree disputed. The apparent explanation is that he had a blocked artery in the brain, although some think that an auto accident (which was thought at the time to have left him shocked but uninjured) might have given him a concussion which caused or worsened the problem. The trouble with this alternative explanation is that the composer was already exhibiting neurological symptoms (including aphasia, the language-impairment commonly seen among stroke victims) before the accident. 

At any rate, Ravel became increasingly unable to communicate around this time. Speech was difficult, writing worse. At first he could still write a letter, if he took enough time over it -- his last effort was a condolence letter to a friend whose mother had died, and the composer had to write it over a period of days by looking up each word in the dictionary to make sure he could spell it correctly. Writing music was impossible. His friends found that taking him to concerts of his own music was a decidedly bittersweet pleasure for him. He complained that there was so much music still inside him, and now there was no way for it to come out!

It's painful to imagine enduring five years of that kind of frustration, especially when you hear a performance like this one (of the piano piece "Jeux d'eau", Ravel's impressionistic depiction of water splashing in fountains), and think about what it would be like have music like that coming into your head, and be completely unable to share it with the world. Perhaps that was why Ravel finally consented to have an experimental brain operation (his doctor thought that the problem might be a tumor). No tumor was found, only the arterial blockage, which surgeons were not at that time particularly adept at repairing. And the composer was unable to recover from the surgery. That he thought the risk was worth taking speaks volumes about how miserable his condition must have been making him.

I'm not sure that most of us need, or at least ought to need, any special motivation to want to avoid having a blocked artery in the brain, but maybe it's useful to be reminded of how cruel the consequences of a health problem can be. To me, at least, Ravel's predicament during the last 5 years of his life (unable to spell, barely able to speak, constantly composing music in his head which nobody would ever be able to hear) sounds unbearable. I'm a musician, of course, so I'm primed to see more tragedy in a musical loss than some people might. But anyone should be able to understand how heartbreaking it would be to lose the ability to do the main thing that your identity is built on.

The world will not mourn if I develop an arterial blockage in the brain which makes it impossible for me to go down to San Francisco's Irish pubs and play music on the weekends. But it will be a pretty big loss to me. So I guess I'd better keep on running.


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