Tuesday, April 30, 2013

Owing to a sad series of errors, I lost the entirety of what I posted on April 30, and now I can't even remember what was in it. I can only hope that no one who read it was counting on getting a chance to read it again. But since I can't remember the contents of it myself, it's fairly likely that it wasn't earth-shaking in its significance.


Too Nervous, Or
Not Nervous Enough?

Monday, April 29, 2013

Underuse & Overuse

Here's something I found on Exuberant Animal:

No doubt that's all true, but some of the problems outlined in this vicious-cycle illustration can come about not as a result of underuse but as a result of overuse, or of getting older. The definition of "overuse" changes as you get older; you can't get away with as much, and you develop aches and pains more easily as a result of a difficult workout.

On April 21 I did a long trail-run, and felt pretty sore in my left hip and gluteus muscle afterward. It wasn't bad enough that I couldn't keep running the rest of the week, and my pain diminished over the course of last week. By yesterday, I had pretty much forgotten I'd had a problem as the result of a long trail-run the previous Sunday, and I took off on a trail-run with a route that was 8.3 miles long. It wasn't until I was a couple of miles into it that I even felt anything on the left side, and thought, oh, that's right, I screwed myself up the last time I did this! But I finished the run anyway, and hoped for the best.

I was sore in the same place as last time today, and I was pretty slow on my run today. And I really felt it during yoga class tonight -- although, generally speaking, yoga-stretching your sore spots helps more than it hurts, so I didn't go easy on myself.

I am trying to be one of those people who remain active into old age, but I'm becoming more and more aware over time of how tricky that can be. Remaining in the center of that ever-narrowing corridor between "underuse" and "overuse" is not the easiest thing in the world! Today, panting and sweating on the hills in 90-degree heat, I wasn't worrying about whether, by running today, I was doing too much too soon; I was worrying about why I couldn't do it faster.


Panic & Complacency

If the happy medium between underuse and overuse is hard to find, so is the happy medium between worrying too much about your diabetes and not worrying enough.

"Should you panic if you have diabetes type 2?" was the question recently entered by somebody as a Google search string; my instinct is to answer this with an emphatic "No!", because people in a state of panic tend to become confused and make bad decisions. However, I have been unhappily surprised to learn that a lot of people newly diagnosed with Type 2 diabetes err very much in the opposite direction. They do just enough quick research about Type 2 to learn that it's an increasingly common disease which, it is feared, is about to cause an explosion in health-care costs because it promotes serious health problems such as blindness, kidney failure, amputations, and heart attacks... and they think, "okay, no big deal".

How exactly they get from "blindness, kidney failure, amputations, and heart attacks" to "no big deal" is not entirely clear to me, but they manage it somehow.

I started this blog with the intention of not mentioning those awful "complications" any more than I had to, because I figured diabetes patients were getting enough discouragement as it was. I have to pause to reconsider my position sometimes, whenever I am reminded that many diabetes patients live in a dreamworld of denial. Do they need to be frightened out of it?

However much I might be tempted to say yes, they damned well do need to be frightened out of it, I have to consider another possibility: that many diabetes patients flee into a dreamworld of denial because the message they are getting already offers so much fear, and so little hope, that they can't see any way to engage seriously with their diagnosis and not go crazy. So, denial (whatever its potential consequences) is a more attractive option to many patients than taking their disease seriously and finding out what they can do about it. That there is anything they (rather than their pharmacist) can do about it is, for all practical purposes, a secret that is being kept from them. I guess it's my job to bring that secret to their attention. Not that all that many of them are going to find their way to me, but for those that do, I guess I should try to keep my message focused mainly on what they can do, not on what can happen to them if they do nothing.

Sometimes it's a touch choice, though!

Were There's Smoke, Conceivably Their Might Be Fire

Thursday, April 25, 2013

Soft Drinks & Diabetes Risk

A study of thousands of European adults compared soft-drink consumption rates with diabetes rates, and you'll never guess what trend emerged from the data!

It turned out that, the more sweetened drinks you consume, the higher your risk of becoming diabetic. Each 12-oz. sugar-sweetened drink you consume, per average day, increases your diabetes risk by 22%.

I should admit that my use of the verb "increases" in that last sentence was a little reckless. It would be more appropriate to replace "increases" with "is associated with an increase in", because we have wandered right into the middle of the correlation/causation minefield.

As we all learned in school, or should have, correlation does not always indicate causation. That one phenomenon is associated with another does not necessarily tell us there's a causal connection between them. There could be a connection, of course. If the cancer rate is higher in people who live right near the refinery than in people who live in the nicer neighborhood farther away from it, that could mean that the refinery is giving people cancer. But proximity to the refinery might not be the only difference between those populations that is significant to health; if the people who live near the refinery are also older, poorer, and likelier to smoke, you need to consider the cancer risk contributed by those factors before blaming everything on the refinery.

Most people, of course, don't want to be bothered with sorting through all the additional factors that might be involved. They would rather spot a correlation, and jump to whatever conclusion it suggests. That might be considered good enough in the political sphere, but in the scientific sphere it is considered sloppy and dangerously unreliable.

Research about health issues is especially burdened by the difficulty of figuring out whether a particular correlation does or doesn't indicate causation. Health is complicated; the things that can affect it are complicated. And we don't raise people in cages, so health studies of human beings involve test subjects who are free to live their own lives in their own individual ways. Who knows what differences there might be, besides the one we're looking into, between those who developed a disease and those who didn't?

If your study of blueberry consumption finds a lower rate of heart disease in those who ate blueberries often than in those who didn't, you shouldn't announce that blueberries prevent heart disease, until you've at least tried to find out if there was any other difference, besides blueberry consumption, between the people who developed heart disease and the people who didn't. (And even if you can't find any other difference, that doesn't exactly settle the matter forever. Maybe someone else will later find a difference you overlooked.)

In the study sweetened drinks and diabetes, some other correlations showed up as well. Diabetes risk also correlated (not very surprisingly) with obesity -- and (more surprisingly) with consumption of sugar-free sodas. So what do we make of those correlations?

Type 2 diabetes correlates so strongly with obesity that it is now taken pretty much for granted that obesity is capable of causing the disease -- even though we don't yet understand how that works (many causal mechanism have been proposed, but so far as I can determine there isn't a clear winner yet). For today, anyway, let us accept it as proved beyond a reasonable doubt that obesity promotes the development of Type 2 diabetes, somehow or other. (Please note: that doesn't mean obesity is the only thing that promotes diabetes! It can't be, because thin people can develop Type 2 as well.) Okay, having accepted all that, what is going on here with soft drinks and diabetes? Could it be that the people in the study developed diabetes because of obesity, and it just so happens that obese people consume more soft drinks (sweetened or otherwise)?

It could that there are two kinds of correlation going on here. Suppose that sugary soft drinks are associated with obesity because they promote weight gain, while sugar-free soft drinks are associated with obesity because chronic dieters drink diet sodas. If all that is true, then it could be that obesity itself explains all the diabetes cases: the sugary ones play a secondary role, by promoting obesity, but don't promote diabetes directly. The sugar-free ones play no role at all; they are simply a marker of obesity. Is there any way to figure out if this is the correct interpretation?

Well, you could look specifically at the non-obese people in the study, to see how soda consumption correlated with diabetes in people for whom weight was not a problem. If the correlation with diabetes faded away with weight differences removed, then that would be an indication that obesity was the only factor pertinent to diabetes risk.

Did that happen? Well, yes and no. The correlation between sugar-free sodas and diabetes faded with weight differences removed -- indicating that sugar-free soda consumption was operating as nothing more than an obesity marker. However, the correlation between sugary sodas and diabetes did not fade away with weight differences removed. (It diminished slightly, but it remained.) So, apparently, sugary soda consumption correlates with diabetes risk for some reason other than the connection with obesity.

Not that we would say sugary sodas aren't a public health issue, if they only could make us diabetic by making us fat. That would still be seen as a bit of a problem, I think. Actually, it is seen as a bit of a problem, because most people already think sugar sodas promote diabetes simply by promoting obesity. But it's even worse if they can promote diabetes independently of weight issues.

But, like I said, we're just talking correlation here. We have to keep looking into this, to make sure we've identified all the factors that might be operating.

Things Left Unsaid

Wednesday, April 24, 2013

Truly Comprehensive Diabetes Management!

The AACE (American Association of Clinical Endocrinologists) has released the 2013 "AACE Comprehensive Diabetes Management Algorithm", a suite of colorful charts which guides doctors through the complicated decision-making process involved in looking after a patient with diabetes. When medical guilds of this sort issue their recipes for diabetes management, I always take a look at them to see if thing have changed. That is, are there any signs that lifestyle factors are starting to be seen as significant, or is it still all about meds?

Well, at first glance, it seemed as if lifestyle was getting a new emphasis, if only because the word "lifestyle" was prominently placed in some of the diagrams, as a broad first step in the process. Here it is at the top of one of the charts:

Notice that the "Lifestyle Modification" is without specifics, apart from the parenthetical information that the term includes "medically assisted weight loss" -- in other words, lap-band surgery is the AACE's idea of lifestyle modification. (A separate chart welcomes not only weight-loss surgeries but weight-loss drug treatments into the big "Lifestyle Modification" tent -- and strongly implies that controlling body weight is the only lifestyle issue that has a bearing on diabetes management.)

However, the drug therapies listed below the "Lifestyle Modifications" block are almost fantastically thorough and specific:

I began to notice that something appeared to be missing from these charts. Was I simply overlooking it? To make sure, I used the search engine to see if "exercise" was considered by the AACE to have some potential significance here. This is what my search of the Comprehensive Diabetes Management Algorithm yielded:

So there you have it. When it comes to diabetes management, drugs are terribly important, and exercise is not important enough to mention even once in a "comprehensive" guide to diabetes management.

"The word that describes it is truly comprehensive," says Dr. Alan J. Garber, chair of the AACE task force that produced the new algorithm, perhaps unaware that "truly comprehensive" is two words. "Another reason we call this a comprehensive diabetes management algorithm is that you have to manage the whole patient." Well, he's mastered the lip-service part of the job admirably, I have to give him that.

Perhaps Dr. Garber and the rest of the AACE would defend themselves indignantly by saying that their vague description of "Lifestyle Modification" as "MD/RD counseling; web/remote program; structured multidisciplinary program" was intended to encompass exercise. So there! They covered it, sort of!

Maybe so, but I can't help noticing that they were not content to relegate drugs to a vague allusion of this sort. When they're talking about medications, they've got some very specific things to say about which drugs, when, and in what combination. I find it impossible to believe that the enormous disparity in emphasis between drug treatments and the most useful lifestyle modification one can make does not mean exactly what it appears to mean. The AACE is only interested in pharmaceutical (or surgical) solutions, not behavioral ones.

Who am I to be so sarcastic about all this? Well, I guess I'm the guy who was diagnosed 12 years ago, and would be in a world of hurt by now if my doctor had insisted on following this algorithm. People who are trying to shorten my life must resign themselves to receiving a little bit of sarcasm in response, now and then.


Risk Analysis Time!

Tuesday, April 23, 2013

Yesterday I had a sore muscle and hip joint, as the result of a long trail run on the weekend, and I ran 4+ miles anyway, on the assumption that I was probably promoting rather than derailing the healing process. Well, today I was still a little sore, but less so. I ran 5+ miles, and it was a bit easier. Still feeling okay, still thinking I didn't make a mistake.


Heart Rate & Health

Resting heart rate tends to be inversely related with fitness (meaning one goes down when the other goes up). The fitter you are, the lower your resting heart rate tends to be.

Resting heart rate also tends to be inversely related with mortality. The lower your heart rate is, the less likely you are to die within a given number of years.

But what is causing that relationship? Do people with slower heart rates live longer just because they tend to be more physically fit? Or does having a slower heart rate make you live longer, whether you happen to be physically fit or not?

A Danish medical study known as the Copenhagen Male Study looked at mortality among a 2798 men over a 16-year period, and found that lower heart rates equal reduced mortality, independently of physical fitness. That is, if you manage to maintain a lower heart rate without maintaining your physical fitness (perhaps through meditation, or having a naturally calm personality, or never watching cable TV news), your mortality risk is still reduced. It's very hard to maintain a low resting heart rate without exercising regularly, I hasten to add, but if you can do that, it does help you.

The overall trend was for mortality risk to increase as resting heart rate increased; men with a resting rate over 90 were three times as likely to die within a given time period as men with a heart rate below 50. (As to why this is true, we have lots of speculation and no certainty.)

Well, that's good news for me, because my heart rate decreased a lot after I started my exercise program, and now it's usually below 60 when I'm sitting and below 50 when I'm lying down.

Comparisons between lifespans of different animals tends to show that the slower-heartbeat-equals-longer-life pattern seems to apply across species lines. The faster the pulse, the shorter the life. Mice live a short time, whales a long time. It is sometimes asserted (crudely, I admit, but to a first approximation it's probably fairly true) that animal species, or anyway mammalian species, get just so many heartbeats per lifespan, and you live longer if you don't run through your allotment too soon. Sometimes people try to argue that exercise is therefore counterproductive: it elevates your heart rate the whole time you're doing it. Yes, but regular exercise also reduces your heart rate the whole time you're not doing it. If you run regularly, and your resting heart rate is lower because of that, then at the end of the day you will have used up fewer of your heartbeats than an entirely sedentary person, not more.

Perhaps you're wondering why exercising regularly tends to bring down your resting heart rate. Because exercise is only a behavior (not a chemical substance or a surgical procedure), people find it surprising that exercise can have physical effects that persist after the workout is over. The explanation is that the body tends to adapt to the demands placed on it. Exercising increases energy usage by muscles, and that requires an increased circulation rate, so that the muscles have more fuel and oxygen delivered to them per minute. To meet this demand for more circulation, the body expands its blood vessels (and even grows new ones), and it also strengthens cardiac muscle. The end result is that the heart is able to move a greater volume of blood with each beat. Therefore, when the body is at rest and the demand for circulation is modest, the heart doesn't need to beat so often to get the appropriate amount of blood moving -- so the resting heart rate can be lower. (And is lower, because the body doesn't tend to waste energy.)

Of course, none of the above gives you any kind of guarantee. Reducing your risk of death from cardiovascular disease is a good idea, but it's not as if nobody ever dies of anything else. For example, The Onion had an article today headlined "Study: Wolf Attacks Still Leading Cause Of Death In The U.S.". It makes grim reading. That's probably what will happen to me, if my exercise program prevents me from having heart attack.

Oh, well. We do our best with what fate gives us!


Expect The Unexpected!

Monday, April 22, 2013

My Rattling Good Time

I had a rather close encounter with a rattlesnake yesterday. I like to be in touch with nature, and when it comes to getting in touch with nature, you really can't do better than coming very close to stomping on a rattlesnake's tail.

Fortunately I saw the thing in time to stop short of stepping on it. I was in the middle of a long trail-run at the state park (I haven't worked out the mileage, but it took over 2 hours to finish the route). It was a beautiful sunny day, and the wildflowers were in bloom, but luckily I wasn't paying too much attention to the scenery around me. I have enough tripping-and-falling experience on those trails to be alive to the danger of stumbling across unnoticed obstacles, so I tend to keep a pretty close eye on the ground immediately before me. So, when I got to the snake (which was right in the middle of the trail, in full sun, and not disguised by irregular tree-shadows) I was quick to spot it, and quick to realize that this was not a stick, this was a serpent!

So I brought myself to a respectful halt, and waited for it to continue crawling off the trail and into the weeds. It had the characteristic diamond-shaped head, and more importantly it had a rattle on the end of its tail (although it was not shaking the thing, because I hadn't sufficiently alarmed it). Okay, Mr. Snake, you take your time and do what you have to do.

I got home and checked to see what the California Department of Fish and Wildlife web site has to say about rattlesnakes. I wondered what advice they had on the subject, for those of us who wander into the off-road part of the world, and wonder what we ought to know about snaky encounters. As expected, their commentary on the subject turned out to be amusingly idealistic and impractical in certain regards. We ought to be more grateful for rattlesnakes, because they "provide humans with a tremendous service; they eat rodents, other reptiles, and insects". When they bite you, 25% of the time they don't actually inject any venom. And even if they do inject venom, you'll probably live. They bite about 800 people a year, and in a typical year only one or two of the victims die. So enough with the whining, already!

The anonymous web authors proceed to list things I can do to minimize my risk of rattlesnake bites, and of course these are things I don't do and don't plan to do. For example, I should wear thick long pants and hiking boots, not running-shorts and running-shoes. Forget that! Also, I shouldn't be alone (forget that too -- I've worn out my running buddies and I'm going to be running those trails alone or not at all). And then there is the mysterious advice to "Step ON logs and rocks, never over them". Huh? Why? What is the thinking there? I'm sure that sounds very practical to someone who is sitting in an office typing up instructions, but have they ever been on an actual trail?

And what do they want me to do if I'm actually bitten? They want me to stay calm (right, got it!), wash the bite gently with soap and water (easily available on the trail), immobilize the affected area (a goal which certainly won't conflict with getting the hell out of that park), and then get myself transported to the nearest medical facility.

Well, at least I know what to do!


Aftermath Of My Trail-Run

This morning I felt sore in the left hip and left gluteus muscle -- which was a bit odd, because I promise you I used the right side of my butt every bit as much as the left side during yesterday's trail run.

In all fairness I should note that my trail-run did have one positive consequence -- my fasting test this morning was under 90, which is where I like it to be (but where it generally hasn't been of late).

But then I was stuck with trying to figure out whether my stiff-and-sore body would be made better or worse by running today. I ended up running, and although the soreness gradually diminished as the run went on (probably due to the endorphins that exercise releases), I never felt great at any point in the run, and I was pretty slow.

I really felt the soreness during my yoga class this evening, but I had the impression that stretching my sore spots was therapeutic and I'll feel better tomorrow. We'll see!

Staying active involves a lot of these kind of dilemmas. When you feel a little stiff and sore, will you be better off if you rest up until you're fully healed, or if you force your stiff-and-sore hardware to get out there and do something? There isn't a right answer, or at least not one that you can know at the time is the right answer. It's always tempting to "rest up" for an unspecified period before exercising again... and the typical outcome is that this unspecified rest period lasts until you get old and die. But that doesn't mean starting exercise up again prematurely can't create additional problems.

My attempt to start up weight-training again last week was too much, too soon; that much seemed clear a few painful days later. But I aim to try again this week, with a lighter workout, and figure out what I can handle before I start ramping up to where I had been before.

You have to strike a balance somewhere between being too cautious and being too reckless. You have to push yourself just enough, but not too much. Unfortunately, we usually find out the hard way what "too much" means.


Easy & Hard Questions

Thursday, April 18, 2013

On Tuesday I did a resistance training workout after a long layoff, to see if my right shoulder was up to it yet.

The answer is "maybe not", because my shoulder, and the triceps muscles in both arms, were pretty sore today, two days later. (Running today, I found it a little painful to swing my arms.) Probably I tried to do too much too soon at the gym; I should have eased into it more. Well, I'll try again next week, with a lighter workout, and see if I can ramp it up slowly without hurting myself this time.

Hear are a few of the questions that people have been asking Google lately -- some with easy answers, some without.

"a diabetic who injects too much insulin can lose consciousness explain why injecting excess insulin could impair brain function"

Clearly this is a pre-med student doing his homework, and hoping there are easier ways to get questions answered than doing the assigned reading.

Insulin injections force the body's cells (especially muscle cells) to absorb sugar from the bloodstream, and this tends to bring blood-sugar levels down. Too much insulin brings the level down too low. Bring it low enough, and you impair brain function -- because the brain burns sugar for energy, and gets into a bad state when blood sugar isn't abundant enough to give the brain the energy it needs.


"is hemoglobin a1c a compensatory process"

I could spend the rest of my life trying to guess what the questioner meant by this.

Hemoglobin A1c is the fraction of your hemoglobin (a protein found in red blood cells) that has sugar bonded to it. The hemoglobin A1c test result is a percentage; if your result is 5, then 5% of your hemoglobin is "glycated" (sugar-frosted). That's all the test really measures; the significance that we attribute to the sugariness of your hemoglobin is another story.

The "glycation" process which causes protein to pick up an unwanted encrustation of sugar is not a compensation for anything; it isn't a purposeful process, any more than rusting of metal tools is a purposeful process. The body isn't doing it to compensate for some other development. The body isn't doing it at all, really; it just happens, like rust happens.

The body can, in a sense, "compensate" for the glycation that occurs, but it can only do this by recycling its proteins (so that the older, more sugar-encrusted ones eventually get replaced). This approach works okay, so long as the proteins aren't becoming glycated faster than the recycling process can replace them. When blood sugar become abnormally high, though, the recycling process does fall behind, hemoglobin gets more sugary, and the A1c rest result goes up.


"can hemoglobin a1c be 0"

No. If you're alive at all, you've got some sugar in your blood, and some of your hemoglobin is glycated. I don't know what the world record low A1c is, but it isn't zero.


"what can influence my a1c"

Almost the only thing that influences it is how high your glycation rate is, and that is influenced mainly by how sugary your blood is. That is why the A1c test is regarded as an indicator of the overall trend in your blood sugar levels.

Some diabetes patients appear to be "high glycators", meaning that the glycation rate is higher in them, for a given blood sugar level, than it would be in other people. Which is tough luck for them, because it means they have to keep their blood sugar lower, to reduce their risk of diabetes "complications" to an acceptable level, than other diabetes patients do. If your A1c results tend to be higher than you would expect based on your daily glucose testing, this probably means you are a high glycator yourself. If so, rely on the A1c test rather than daily glucose testing as an index of how well you're doing.

A few other situations (such as hemodialysis treatment, or significant blood loss, or blood transfusion) can affect your A1c result, but these are pretty unusual factors and they probably don't apply to you.


"325 mg/dl blood sugar is this high"


It's very high; please start taking this subject seriously.


"is 150 too high for blood sugar for a person without diabetes"

My doctor told me (and please note that he was talking to a person with diabetes) to keep my glucose level under 150 mg/dl an hour after eating. (And under 110 mg/dl before breakfast.) That doesn't mean he was saying anything below 150 after a meal is "normal", just that this was a good target for a diabetic person to aim for.

The average person without diabetes goes up to about 125 an hour after a meal (and then drops down rapidly by down, usually to below 90). It's hard for anyone with diabetes to duplicate that kind of blood-sugar profile -- but keep in mind that it's the normal profile, so if you can't duplicate it despite never having been diagnosed with diabetes, it may indicate that you will be diagnosed before very long.


"is a1c of 6.2 good for a non diabetic"

This is pretty much the previous question dressed up a little differently. 6.2 is considered a slightly elevated A1c result. You won't be diagnosed with diabetes, on the basis of your A1c result, until you hit 6.5. But 6.2 isn't "normal", and you should take it as a warning sign of where you seem to be heading.

Let me put it this way: I was diagnosed with diabetes 12 years ago, and I was very disappointed last October to get a result as high as 5.8 on my A1c test. It seems a little surreal to me for anyone who supposedly isn't diabetic to think that a result of 6.2 might be "good". It's not tragic, but calling it "good" would be going too far.


Soldiering On

Wednesday, April 17, 2013

Can't Stop The Runners

Like most people who run frequently, and sometimes participate in big organized races, I wondered whether the bombing at the Boston Marathon on Monday would mark the downfall of such events. Organized footraces are vulnerable gatherings, after all. They don't take place within a confined and controllable space; they usually take place on city streets, on a course stretching many miles. And they attract big crowds (of runners and of spectators alike). Not only that, it is known when and where the crowds will be thickest: at the start and at the finish. For a terrorist out to kill a bunch of people at once, a footrace is a made-to-order target. Will people be afraid to organize such events now? Will runners be afraid to participate?

Yesterday evening, a Boston running club decided to demonstrate that they weren't going to give up so easily. They put together a 4.8-mile group run along both sides of the Charles River, from East Cambridge to Boston. Despite the last-minute nature of the event (and despite the fact that many of their members had already run a marathon the day before!), they were able to get 270 runners to participate. They also raised at least $3000 in contributions to a fund for those hurt in the bombings.

One of the organizers, P.J. Aspesi, said, "We tried to figure out how we could come together afterward and help, and show everybody that Boston won’t stop running." One of the participants was quoted: "I think about the people who lost their limbs... They woke up today and couldn’t walk. It’s a privilege to be able to run." Other running clubs all over the country are also putting on "solidarity runs" this week. Apparently the running subculture is not going to give up.

My running buddies at work, who have been out of action due to injuries for a long while, aren't giving up either. Both of them tried their hands (or rather their legs) at a lunchtime run today, and managed to do it, but with some cautious walking-breaks when they felt overstrained. Now I'm worried about when they fully recover their former abilities -- and once again I won't be able to keep up with them!

Throwing The Switch

Tuesday, April 16, 2013

I've been on a long layoff from resistance training while I recovered from the rotator-cuff tendonitis in my right shoulder. Tonight I figured it was about time to hit the weights again. Chest-presses still hurt my bad shoulder a bit, but everything else was okay.

To be honest, I dislike weight-lifting rather a lot... but since when is diabetes management about what I like? The research keeps coming in, saying that aerobic exercise alone isn't as good for diabetes management as the combination of aerobic exercise and strength-building exercise. So, if you can lift, lift. And it seems as if I'm physically ready to get back into lifting.

If I wake up with an extremely sore shoulder tomorrow morning, it will mean I went back to lifting too early. But if I don't, I guess I'm good to go.

Ferroelectric Switching & You

A ferroelectric material is made of molecules which are electrically "polar" -- that is, the molecule is positively charged on one end, and negatively charged on the other -- but this polarity can be reversed when an electric field is applied to the material. We usually think of ferroelectric materials as synthetic materials typically used in electronic devices (for displays and memory storage, for example). But researchers at the University of Washington discovered last year that living tissue can be ferroelectric too, and can be switched positive or negative by an electric field.

Now researchers at the same university have found that ferroelectric switching occurs in a lot of flexible, connective tissues which play important roles in circulation and respiration. (Specifically, the switching occurs in a flexible protein known, appropriately enough, as elastin.) And it turns out that, in these tissues, the ferroelectric switching is seriously impaired by exposure to high levels of sugar in the blood. Over the long term, sugar exposure can damage these flexible tissues by allowing them to harden and become rigid. This could be at last part of the reason why diabetes is so strongly associated with cardiovascular disease.

I don't know what this research will lead to. A drug that tries to restore the ferroelectric properties of elastin? Special high-tech clothing which claims to amplify the body's electric fields so that the elastin gets its groove back? We'll see. I'd like to know more about how high blood sugar interferes with ferroelectric switching, but that's just my scientific curiosity talking -- I know it probably won't lead to any profitable remedy in the short term; I just want to know how stuff works.


Burning Off Alcohol

Now we're talking! A new study finds that, in heavy drinkers, the amount of exercise taken seems to determine whether or not the overconsumption of alcohol will result in damage to the white matter in the brain.

How was this discovered? The researchers report that "Analyses examined the relationship of exercise, alcohol, and their interaction to fractional anisotropy in the superior longitudinal fasciculus, external capsule, superior and anterior corona radiata, and fornix." So you see.

And the results? Heavy drinking damages these areas of the brain more in those who aren't getting a lot of exercise. "These results are consistent with the notion that exercise may protect white matter integrity from alcohol-related damage."

So maybe this guy is on the right track after all.


Dreams, Terrorism, & Shrimp

Monday, April 15, 2013

Well, this is a first: I woke up at 5 AM from a nightmare about glucose testing.

When I wake up from a dream about being chased by a giant spider across the surface of Mars, it doesn't take me too long to figure out that this couldn't really have happened. That's why my least favorite bad dreams are the plausible ones: I wake up thinking that they probably did happen, and it takes me a long time (sometimes all day) to convince myself that they definitely didn't.

My dream this morning was about waking up, getting out of my bed, stumbling to the bathroom, taking my fasting glucose test, and getting a result of 122. A very realistic dream, and very much a consequence of the elevated fasting tests I'd been getting the week before.

So then I spent several minutes lying in bed this morning, trying to think up an explanation for that elevated fasting result, when it seemingly should have been much lower. It gradually dawned on me that this was just a bad dream and I didn't actually get a result like that. Still, I can't tell you how anxious I was about actually getting out of my bed, stumbling to the bathroom, and taking my fasting test. But fortunately the result was only 92, which is acceptable to me.

Tragedy At The Race

It wasn't until after work that I found out what had happened in Boston today: persons unknown set off bombs at the finish line of the Boston Marathon. Scores of people wounded, at least three dead.

My yoga teacher is from Boston, so I figured she would have had a traumatic day, trying to make sure nobody she knew was hurt. As I found out in class tonight, she'd had a more traumatic day than I expected, because she knew her brother (a former star runner, who works for a running-shoe company that was sponsoring some of the athletes in the race) was supposed to be present at the finish line. She eventually learned that he had already left the finish line before the bomb went off, and was safe. She then relayed the good news to her terrified mother (who had just lost her husband, and was now afraid she had lost her son as well), and gave her mother a list of people to call to share the good news. She thought that this task-list would (1) give her mother something to do, and (2) give her mother a chance to hear herself saying to other people that her son was safe, which was bound to have a therapeutic effect on her frazzled nerves.

It must have been a nightmarish day for thousands of of people. Not everyone was able to get the word out that they were safe. Because of fears that the bombs were being triggered by cell-phone calls, cell-phone service was shut down in Boston. Public transportation was shut down as well (with the result that a bunch of people who had just run 26 miles were now obliged to walk long distances to reach their hotels). People already in hotel rooms were not allowed to leave the building.

We are so used to being instantly in touch with everyone, these days, that we are unprepared to deal with emergency situations in which all bets are off, and the safety of people close to us is in doubt for long periods.

Having run a few marathons myself, I couldn't help noticing something revealing in the video of the first explosion: most of the runners didn't even react to it at first, because they were so desperately fixated on making it the rest of the way to the finish line that nothing as trivial as a bomb going off could distract them very much.

Yeah, I know that feeling, all right.


What You Can See, What You Can Do

I specialize in surprising metaphors for diabetes management, but maybe this time I've outdone myself, with a metaphor which is not only unexpected but possibly biazarre.

To get to the point: what can we learn from the mantis shrimp?

Most animals are lucky to have two different kinds of color-sensitive cells in their eyes. Humans are gifted with three: the cells sensitive to red, green, and blue (which, in combination, allow us to see intermediate shades such as orange, yellow, and violet). Butterflies have five types of cells, so they are able to perceive more shades within the spectrum (which, if you make your living hunting down flowers, is probably mighty useful). Notice that the butterflies, who can see more colors than we can, are also more colorful than we are. Coincidence? I suspect not. Perhaps having superior color vision leads to the butterflies becoming more style-conscious.

But even butterflies are practically color-blind compared to the mantis shrimp, which has no less than sixteen types of color-sensitive eye cells.

What happens when an organism is better at sensing shades of color than humans are, and even better at it than butterflies are? Apparently what happens is that they go crazy for color, and dress themselves up in startlingly brilliant hues which most humans would be too embarrased to wear.

In Darwinian terms, of course, it isn't a question of the shrimp consciously dressing up -- rather it is a question of the shrimp choosing the most colorful shrimp around as mates, thus creating "selective pressure" which ensures that successive generations of shrimp tend to become increasingly colorful, as the most colorful shrimp in each generation leave more descendants in the next generation.

But think about it: mantis shrimp become capable of choosing the most colorful mates around because they are extraordinarily sensitive to color. The amount of color data they are taking in is greater, so they are more capable of making color choices.

So there's my metaphor: the more data you take in, the better you are at making choices based on that data.

Some diabetes patients test frequently, and some don't -- but it's the ones who do that have the most options. How much we can know determines how much we can do.


Tricky Questions

Thursday, April 11, 2013

Going Into Detail

A lot of the questions people ask about diabetes and health (implicitly, in the Google search phrases they enter) seem as if they must have perfectly simple, straightforward answers. But, if you think about them for a moment, they turn out to have a little more complexity to them than meets the eye.

Trace Sugar In Urine

For example: "is it normal to have a little bit of sugar in your urine". At first I thought the answer was a simple "no!". Health-related websites often echo comments such as this one from Wikipedia: "Ordinarily, urine contains no glucose because the kidneys are able to reclaim all of the filtered glucose back into the bloodstream". That certainly sounds firm. The phrase "contains no glucose" certainly appears to leave no room for exceptions. Even the smallest amount of glucose in the urine has to indicate diabetes, because when glucose levels aren't above the normal range, the kidneys allow no glucose at all to pass into the urine. It's only when you become diabetic, and your blood glucose level reaches the "renal threshold" of 160-180 mg/dl, that your kidneys start "leaking" glucose.

However, that statement clearly has to be a case of rounding down to zero. Is the claim that the kidneys operate at 100% efficiency? What process, in the history of biology or the history of engineering, has ever operated at 100% efficiency? It seems hard to believe that the kidneys never allow even the tiniest trace of sugar to get through, so long as blood glucose levels aren't elevated. I would expect that the glycosuria test (the lab test that looks for glucose in the urine) would have a normal range which extends at least slightly above zero.

It turns out that that is indeed the case; most labs define the normal range as 0 to 15 mg/dl (that's 0 to 0.8 mmol/l outside the USA).

That is, indeed, a pretty tiny amount of glucose, and I understand why some people would think it was okay to ignore it and just call the amount zero.

I don't agree with them, though. Pretending that a small amount of something isn't there so that you don't have to talk about it is classic dumbing-down. It encourages a falsely simplified view of how things work which, in the long run, encourages people to be dopes. And most people don't need any encouragement in that direction.

But to return to the original question: if "a little bit of sugar in your urine" means less than 15 mg/dl, then yes, that's normal. Anything more than that, though... not good.

Wakeup Call

Now here's an interesting question: "how does a person with pre diabetes feel when they get up in the morning". Like crap, I assume, but that's normal. The early stage of Type 2 which has been labeled "prediabetes" is not severe enough to be associated with any specific symptoms. At that point, you're probably not feeling any worse about getting out of bed in the morning than anyone else is. (Or if you are, it's probably because of something other than prediabetes.)

Murder By Carb

Someone (whom I'm hoping never to meet) asks: "what would happen if i gave a diabetic lots of sugar?". Well, their blood glucose level would go up, that much we can predict with some confidence. But how much it would go up, for a given amount of sugar administered by your wicked self, would depend on such factors as how high it was to start with, how much insulin productivity they have lost, and how much insulin sensitivity they have lost. In other words, there is no predicting how high their blood glucose level would go up, and therefore no knowing whether or not you can trigger a serious medical emergency for them. Certainly it won't do them any good, but if you're planning a homicide I suggest that some other method (almost any other method) would be more reliable.

Wine & The A1c

A clearly worried person asks, "can wine raise a1c test results?".

I would be shocked if wine, a civilized and kind-hearted liquid, were to do anything of the sort. What raises your A1c results is excessive glycation, and what causes excessive glycation is excessive blood glucose. Wine's effect on blood glucose is usually a (temporary) reduction, not an increase. When all is said and done, wine probably has no significant impact on your A1c result, positive or negative.

If drinking wine makes it impossible for you to avoid gaining weight, the weight gain could contribute to reduced insulin sensitivity, increased blood glucose, and an increase in A1c results. But that's not a very direct chain of causation; I think it would be pretty far-fetched to attribute any increase in A1c results directly to wine.

Wine in moderation is thought to be protective against arterial disease (people who drink moderately outlive both heavy drinkers and non-drinkers). So long as you don't get too carried away with it, it's probably going to do more good than harm.

Peaks & Valleys

Wednesday, April 10, 2013

Aaarrrgh!!! Another fasting test over 100! Nobody can say I haven't been exercising, so clearly I need to cut carbs more than I have done so far this week.

Thin Air, Thin Thighs

the International Journal of Obesity has noticed something odd about the way the obesity rate varies from one region to another. If you look at a map of obesity prevalence in the US...

...and compare it to an elevation map of the US...

...you find that the it's the highest-altitude regions which tend to have the lowest rates of obesity. (The Rocky Mountain states, and especially Colorado, have long been known for their lower obesity rates. And I don't need to tell you what Mississippi and Louisiana have long been known for, at least in terms of public health stats.)

There are exceptions to this pattern, and the exceptions are interesting. Some low-lying regions have pockets in which the obesity rates are low. These pockets, it turns out, tend to be in the more heavily urbanized areas:

In other words, low obesity rates are strongly associated with two unrelated things: high altitude and high urbanization.

Any difference in health statistics between urban and rural areas is pretty likely to reflect differences in the way people live. The trouble is, there are a lot of differences between urban and rural life, and it's hard to know which of those differences has the strongest impact on obesity rates. (Some people think obesity rates are lower in an urban setting simply because urbanites are under more social pressure to conform to expectation about how people should look.)

But how on earth would altitude have an impact on obesity rates? Apparently this is not as strange a finding as I would have expected. Reduced oxygen intake (which inevitably happens at higher altitude) is known to interfere with hormone signaling in such a way as to decrease appetite and promote weight loss. Also, ordinary functioning at higher altitude can place greater demands on the body, leading to accelerated burning of calories.

I don't know that moving to Colorado is actually going to cause anyone to shed pounds. But, if this study gets enough publicity, I look forward to seeing the next best-seller: The Denver Diet!


Poverty As Therapy

If living in the mountains isn't the solution for you, you might try poverty. (Especially these days, when poverty is pretty likely to try you.)

A new study examines the health effect of an economic crisis in Cuba during the 1990s, and found that a lot of people were in bad enough shape financially that they had to cut their food intake. The resulting weight loss was followed by an improvement in the nation's health, in terms of heart disease and diabetes! (And, of course, the improvement evaporated once the crisis was over.)

"Rapid declines in diabetes and heart disease accompanied an average population-wide loss of 5.5 kg in weight, driven by an economic crisis in the mid-1990s. A rebound in population weight followed in 1995 (33.5% prevalence of overweight and obesity) and exceeded pre-crisis levels by 2010 (52.9% prevalence). The population-wide increase in weight was immediately followed by a 116% increase in diabetes prevalence and 140% increase in diabetes incidence. Six years into the weight rebound phase, diabetes mortality increased by 49% (from 9.3 deaths per 10 000 people in 2002 to 13.9 deaths per 10 000 people in 2010). A deceleration in the rate of decline in mortality from coronary heart disease was also observed."

I'm not sure there's going to be a best-seller called The Poverty Diet, though. (Unless they sell it really cheap.)



Tuesday, April 9, 2013

100 is a better fasting result than 106 (which is what I got yesterday), but it's still higher than I'm comfortable with. Let's see if I can work it down to below 95 tomorrow.


Plugging In The Numbers

It's always comforting to think that we can reduce something complicated and confusing to a simple formula.

That's only a joke, by the way -- but a lot of people would like phenomena in the real world to be reducible to a simple formula. Certainly a lot of people feel that way about the various kinds of data we collect about our diabetes. We want to be able to plug it all into an equation which reduces everything to a simple numerical answer which means "you're doing fine, quite worrying!" (or else, maybe, "you're dying, give up!", but we hope that's not the answer equation spits out).

For example, we have the formula "28.7 X A1c – 46.7 = eAG", which supposedly translates the result of a hemoglobin A1c test to estimated average glucose in mg/dl. How this helps anyone is a little unclear to me, because you still have to decide how high a figure for "estimated average glucose" is acceptable. Wouldn't it be simpler to just take the A1c result, and ask how high a figure for that is acceptable? The formula seemingly just takes you farther away from what the test actually measures (the percentage of your hemoglobin that is sugar-coated). But people like formulas, especially if somebody is telling them whether the result of the formula is good or bad. Not that the promoters of "estimated average glucose" have done an especially good job of clarifying what kind of eAG figure is good or bad; my prediction is that we'll eventually stop hearing about it, and just go back to hearing about A1c results. (In fact, it looks to me as if things are moving in that direction already.)

I could be wrong about that, though. Formulas can take on a life of their own. Most of us have heard that you can find your maximum heart rate during exercise by subtracting your age from 220; it turns out that this formula was literally worked out on the back of an envelope by two cardiologists while they were on a plane on the way to a medical conference. They had no idea that this rough estimate of theirs would eventually be treated as if it were a Law Of Nature, and were a little alarmed at how religiously it was later adopted.

Formulas can do a pretty good job of describing simple interactions in nature (the orbital movement of a planet around the sun, for example). But even then, the formula must assume an artificially simplified situation (perfectly spherical objects of uniform density, moving through perfect vacuum, with no other planets around). If you want to take those other factors into account, you must greatly complicate the formula (or else tolerate a bit of imprecision in the results).

Biological systems are vastly more complex than planetary systems. You can't take all factors into account (because we don't know enough about them), so we have no choice but to tolerate imprecision in the results -- and not a little imprecision, a great deal of it. For example, the formula for converting hemoglobin A1c results into estimated average glucose assumes (among other things) that the glycation rate (the rate at which sugar bonds to proteins), for a given blood glucose level, is the same in all individuals. But we don't know that this assumption is true. (Actually, we know it isn't true.) So, the eAG formula has the advantage of providing a simple answer which seems understandable, and the disadvantage of providing an answer of unknown accuracy.

When it comes to health, we need to be willing to accept "guidelines" rather than rules, and think in terms of relative risk rather than absolute categories of "don't worry!" versus "you're doomed!".

We can't expect a formula to tell us exactly what we should expect. The formula doesn't know what's going to happen to us. It might be able to give us a rough estimate of our risk, and that can be useful information. But it's only useful information if we act on it -- and we won't act on it if we decide to round the answer down to "don't worry!".


What Doesn't Kill Us

Monday, April 8, 2013

Yikes, 106 fasting! And it's my fault, all right. I had too much to eat yesterday, and especially too many carbs. (Social eating: always a problem for me.) And, on top of that, the long run I'd had planned got crowded out of my schedule, and I had only a 4-miler, which is pretty much my minimum even on a day when I'm eating more cautiously.

I was tempted to write a little essay tonight, all about how, in my twelfth year of managing diabetes without medications, glycemic control is starting to get harder for me. But it would be a little dishonest, because I think the main issue isn't that my physiology is working harder against me lately than it used to -- the main issue is that I've been trying to get away with too much lately. Maybe I'm getting a little tired of setting a good example. On the other hand, I don't really want to set a bad example, either. The world has enough of those as it is.

Okay, then. Heave a sigh and get back to work...


"Can a A1c level 10 kill u?"

That terse question was a phrase that somebody typed into their Google search window. As Google apparently referred them to me, I should perhaps try to address the question, which seems to come from a planet of absolutes, where whatever doesn't kill you doesn't need to be worried about.

A hemoglobin A1c test result of 10 means that 10% of your hemoglobin is sugar-coated. Since the normal proportion is 5%, having 10% of your hemoglobin sugar-frosted indicates that your blood sugar has been abnormally high in the past few months, so a great deal of extra "glycation" (unwanted bonding of sugar to proteins) has been going on within your body.

Yeah, it's abnormal -- but can it kill you?

It worries me when people talk in these absolute terms. Hitting 10% on the A1c test won't kill you -- today -- but it's not where you want to be. Stay at 10% long enough, and it will kill you eventually, by undermining your health in all sorts of ways.

One way in which a persistent A1c level of 10 can undermine your health is to increase your risk of diabetes "complications". For example, retinopathy (an eye disease which is common in people with poorly-controlled diabetes) becomes likelier over time if your A1c result is elevated. But how much elevation of A1c causes how much elevation of risk?

Well, let's say your A1c result holds steady at 7 over a long period. By the time fourteen years have gone by, you will still have about a 90% chance of being free of retinopathy.

By contrast, let's say your A1c result holds steady at 10 over a long period. By the time fourteen years have gone by, you will have a 0% chance of being free of neuropathy. By then it is also highly likely that you will have also have other diabetes complications, including peripheral neuropathy (painful nerve-damage in the extremities), kidney disease, and heart disease.

So, no: getting a 10 on one A1c test won't kill you. But it's a very bad sign, and it indicates you're in a situation which cannot be allowed to continue, because it is the kind of situation which tends to get steadily worse, and steadily more dangerous, as time goes by. (It is also a situation which tends to become more difficult to change as time goes by, so you might as well start changing it now, while it's still comparatively easy to accomplish.)


No Fooling

Thursday, April 4, 2013

Not my best day. Owing to a power failure, my clock radio did not wake me at the appropriate hour. I overslept a bit, and then woke up in a high-adrenaline panic. That scenario usually leads to an elevated fasting test, and that's what I got this time. At least my post-prandial result after lunch was low.

I wasn't feeling up to running in the rain today, so I went the gym after work and did my time on the stair-climber. Not the ideal workout, but at least I did something.

Believing Your Own Eyes

Would you say that this is a "healthy" food?

You wouldn't?

Well, how about this one?

Yes, I thought you would conclude that the second one was a little better for you.

The second one is the same as the first, of course, and the information in the calorie label is the same. But the second one is green, and we all know that means it's good for you.

These images were from a study on the effects of the visual design of food labels on the perceived healthfulness of foods. People given the same nutritional information, and the same photos of the food involved, reached more optimistic conclusions about whether the food was good for them, if the calorie label was green. A bit of red in the picture raised their anxiety level, but green reduced it.

It's amazing to think that we're that easily manipulated, but evidently we are.


It's The Diet, Stupid!

Bariatric surgery (weight-loss surgery which minimizes the volume of the stomach) has been shown to improve glycemic control dramatically in people with Type 2 diabetes. Some people even call the procedure a "cure" for diabetes. There has been some controversy over how the surgery does what it does for diabetes, however. Is it simply that the surgery limits the ability of the patient to take in food? Or does it change something else about the patient's physiology which greatly mitigates diabetes?

Well, a study looked into this question, and found that patients who adhere to the same severely restricted diet which post-surgery patients are pretty much forced to follow are just as likely as actual surgery patients to get the reductions in blood sugar which have made bariatric surgery seem like a miracle cure.

The catch, of course, is that staying on such a restrictive diet over the long term is extremely difficult. People can do it for a while, purely through an effort of will, when they are taking part in a study. But over the long haul, they have a very hard time with it. The "miracle" involved in the surgery is that it doesn't give you much choice about sticking to the diet, as you know you will experience a lot of pain and nausea if you don't. And most of us are already so much in the habit of avoiding pain and nausea whenever possible, we just automatically know what to do whenever pain and nausea enter the picture. A more abstract commitment to doing what's good for us is a little less motivating, it seems!

Editing Note: I typed "nausea" as "nauses" above, and my spell-checker asked me if "anuses" was what I meant to write. No, actually; I did not intend to comment on what happens when "pain and anuses enter the picture", if only because this blog isn't about politics.

"Enough" Insulin

Wednesday, April 3, 2013

Last night I succeeded in getting to sleep an hour earlier than usual. And then, as dawn was approaching, I woke up an hour earlier than usual, and couldn't back to sleep. When it comes to sleep, I absolutely cannot win.

The Big Question

The other day somebody entered this Google search string: "what would happen if body couldn't produce sufficient levels of insulin". This caught me by surprise; it's seemingly a very basic and obvious question -- perhaps the basic diabetes question -- and yet it's not often asked. And it turns out to be a more complicated question than it appears!

After all, how much insulin is "sufficient"? How do we define that? For most of the critical substances which we have circulating in our blood, we are told in a straightforward lab report how much of it we ought to have, and how much we actually do. Sodium should be in the range of 136-145 mmol/L, and you're at 142 -- splendid! Calcium should be in the range of 8.2-10.2 mg/dL, and you're at 8.7 -- keep up the good work!

But we don't get this kind of feedback about insulin. Usually they don't even measure it clinical tests -- it's hard to measure, and the amount of it in the blood fluctuates so much under different circumstances that it's hard to define a normal range for it. So you're not likely to get a report from your doctor that says the normal range for insulin is 46-52 nanoSomethings, and you've only got 34.

The impression diabetes patients get generally is that they don't produce "enough" insulin -- but they have no idea what "enough" insulin would be, or by how much they are falling short of that.

As a practical matter, we could define "enough" insulin as "enough insulin to normalize your blood glucose level". There is something a little misleading about that, however. Look at it this way: how much bandage on your finger is enough? That sort of depends upon whether or not there is a bleeding wound on your finger. For an unwounded finger, no bandage at all is required. A small wound would call for a small bandage. A large wound, or multiple wounds, would increase the bandage requirement (or raise the stakes enough that sutures, rather than bandages, would be needed).

How much insulin is "enough" depends upon such fluctuating variables as how insulin-sensitive you are, and how much glucose you are dumping into your bloodstream by consuming carbohydrates.

People with Type 1 diabetes produce little or no insulin, because an auto-immune reaction has knocked out the pancreatic beta cells which manufacture the stuff. They don't produce "enough" insulin in the sense that they produce no insulin, or almost no insulin.

The situation with Type 2 diabetes patients is less straightforward. If they've had the disease a long time, they may produce less insulin than a non-diabetic person would, but they're not completely shut down in the way that Type 1 patients are. And a lot of them do produce as much insulin as a non-diabetic person would -- or even more! Their problem is that they suffer from "insulin resistance": a diminished sensitivity to insulin. Their endocrine system tries to compensate by releasing an overdose of insulin. But this strategy has a couple of drawbacks. First of all, the pancreas might not be able to generate above-normal levels of insulin forever; as insulin-production diminishes over time, the necessary overdose can no longer be provided. Second, there are negative health consequences to having a chronic insulin overdose. Excess insulin is thought to have an inflammatory effect on arterial walls; it promotes heart disease, and may be the main reason for increased cardiac risk in Type 2 patients.

And so, there is an inherent problem in defining "enough" insulin as "enough insulin to normalize your blood glucose level". If you have a serious problem with insulin resistance, the amount of insulin it takes to do that could be harmful in other ways. Taking insulin, or taking drugs which increase your production of insulin, may solve one problem by creating another.

That is why some patients (by which I mean myself) try to solve the problem not by increasing the amount of insulin we have (so that we have "enough") but by increasing our sensitivity to insulin (so that a smaller amount of it, which perhaps we can produce without pharmaceutical help, becomes "enough").

Exercise, not insulin, in other words.

But to return to the original question: what would happen if the body couldn't produce sufficient levels of insulin is that cells, especially muscle cells, wouldn't absorb enough glucose out of the bloodstream, so that the glucose level in the blood rose to toxic levels, resulting (admittedly after a long time) in sickness, disability, and death. So we definitely want to have "enough" insulin. But that is a problem we can solve not by obtaining more insulin, but by reducing the amount of insulin that qualifies as "enough".


Melatonin & Diabetes

Tuesday, April 2, 2013

How's Your Pineal Gland Doing?

If you have no idea where your pineal gland is, that's not too surprising: this is not the sort of gland that adolescent curiosity is likely to have put you in touch with. The pineal gland is tucked away pretty inconspicuously, in the middle of your brain, and the thing is about the size of rice-grain anyway.

Ever since anatomists discovered that the pineal gland is there (and it's found in all vertebrate species, not just in humans), they've been trying to figure out what the thing is for. The clues were mighty confusing. Pineal cells closely resemble the retinal cells in the eye, and the activities of the gland (such as they are) are keyed to light levels, even though the gland is not itself exposed to light. Seemingly the pineal gland communicates somehow with the eyes. It was suspected that the pineal gland was some kind of vestigial eye which vertebrates no longer possessed, and indeed the gland is sometimes called "the third eye", among other terms -- it is also the "conarium" and the "epiphysis celebri" (the less scientists understand a thing, the more names they make up for it). And, just to complicate the picture, some evidence seemed to link the pineal gland to skin color.

I should clarify that the pineal gland wasn't linked to the skin color of the animal possessing a pineal gland. What happened was that scientists isolated a substance produced by the pineal gland (in cows, specifically), and found that injecting this substance into juvenile frogs caused the color of the frog's skin to change. (Why it occurred to anyone to try that, I am unable to explain.) It was assumed (incorrectly, it seems) that the substance regulated production of melanin in the skin, and for this reason the substance was called melatonin. (As so often happens, the name stuck, even though the reason for it didn't.)

Well, if the pineal gland's secretion of melatonin didn't regulate skin color, what did it regulate? It turned out that it regulates the sleeping/waking cycle, and other daily cycles for biological processes ("circadian rhythm" is the catch-all term for such cycles).

Circulating levels of melatonin in the blood rise and fall according to a 24 hour cycle. Specifically, production of melatonin by the pineal gland is inhibited by high levels of light (specifically blue light wavelengths, which we tend to get from daylight but not from most artificial light sources). In the evening, as your eyes cease to take in blue light wavelengths, the retinal cells in your eyes stop sending whatever message has been telling the pineal gland to inhibit melatonin production. So, your circulating melatonin levels climb, and eventually you get sleepy. At least that's how it works for normal people; my pineal gland seems to do the opposite, and release melatonin only in the daytime. (I'm desperately sleepy at 1 PM, and alert 12 hours later. I've always had this problem, but it seems to get worse and worse over time.)

My apparent melatonin problem may be relevant to my diabetes. After all, diabetes is strongly associated with sleep disorders. Nobody knows why, but not getting enough sleep tends to reduce insulin sensitivity and trigger diabetes. A recent study looked at melatonin secretion levels in women, and found that low melatonin secretion is an independent risk factor for diabetes.

I hasten to add that this doesn't mean low melatonin secretion directly causes diabetes; more likely it causes people to get less sleep. All the indications are that lack of sleep (no matter what the reason for it happens to be) is itself a cause of diabetes. Insufficient melatonin is probably just one of the many reasons why some people don't get enough sleep. Sleep apnea, insomnia, and insane personal schedules can do it too.

Melatonin supplements are easy to get at the drugstore, without a prescription, if you think you might need them. My own experiments with them have not demonstrated a dramatic effect; it could be that my real problem isn't that I don't produce melatonin, but that I don't respond to it properly. It could also be that I should take the melatonin earlier in the evening than I have been doing, so I am going to start experimenting with that.



Monday, April 1, 2013

April Fool's Day

I considered doing an April Fool's Day prank blog-post, announcing some imaginary diabetes research finding. What convinced me not to do it is that almost nobody is going to see this post until April 2, so it will be too late then, really. And anyway, I'm not sure that media pranks of this sort are a good idea. It's hard enough to tell real news and fake news apart as it is.

I usually think I'm pretty good at telling the difference. Nobody needed to explain to me that this one was faked up by the people at The Onion:

But then I come across this lady:

That would be Sue Everhart, Republican Party chairman for the state of Georgia, who recently warned that legalization of same-sex marriage would lead to straight people pretending to be gay in order to marry their friends for the sake of getting health insurance.

This happened. At least, so far as I can determine it happened. So, perhaps the real difficulty involved in crafting a good April Fool's Day prank news story is to come up with something weirder than public life as we actually experience it these days. (I'm waiting for the second installment of this story, when it dawns on Everhart that, by her logic, we have to outlaw opposite-sex marriage, too.)

Well, anyway, the real world is out there, and I'm probably not going to succeed in out-weirding it. So I'll just comment on what's actually going on.


Potheads & Diabetes

Sometimes research reports are more interesting when the researchers don't find what they were looking for than when they do.

A recent study attempted to show that chronic marijuana-smoking is a cause of diabetes. There were some grounds for suspecting that it might be, after all, and the researchers set out to verify this. It turns out not to be true. Or, if that is going too far, the study couldn't find any evidence that it's true.

To be sure, the study did find that chronic cannabis use was associated with "visceral adiposity" (abdominal fat), perhaps because of the evil weed's notorious tendency to stimulate appetite. Not only that, the added abdominal fat tends to show diminished sensitivity to insulin. However, that's as bad as it got. The study did not uncover an association with any of the other problems cannabis was suspected of causing, such as fatty liver, impaired insulin production, overall insulin resistance, or glucose intolerance.

No doubt the researchers were bitterly disappointed by this outcome, but the abstract doesn't reveal what they did afterward to unwind and forget about their frustrations.

Red wine does the trick for me; maybe they should try that. (But cautiously: too much of that can cause problems that cannabis doesn't.)


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