Body Maintenance Reminder!

Thursday, January 31, 2013

My fasting test was lower today than yesterday's was, but my post-prandial test was considerably higher than yesterday's -- after a meal which seemingly was equivalent in terms of carbs! But yesterday's postprandial test was after lunch, and therefore shortly after running, while today's test was after dinner, and therefore several hours after running -- so I wasn't getting the full benefit of the short-term boost in insulin sensitivity that follows an aerobic workout. And I was feeling a bit stressed this evening, which probably contributed. But I think some days I'm just primed to go high, and this may be one of those days. On the other hand, blood pressure is much lower tonight than last night. Sometimes I just can't figure myself out.

 


The Little Yellow Wrench Comes Back

My car (a Honda Civic) has an automated maintenance system which, every once in a while, lights up a little yellow picture of a wrench on the dashboard (indicating it's time to take the car into the shop for a routine maintenance visit), and displays a code indicating what sort of maintenance visit is due.

This happened last week, and the code displayed was "B12". What this is supposed to mean is: "Your car is due for an oil & filter change, inspections of safety/mechanical/emissions systems, tire rotation, and air filter change." But I knew what it really meant: "We know that your car loan was just paid off, and you received the pink slip, and you're thinking that now your bank balance is going to be climbing -- so after you drop off your car for the routine stuff, we're going to call you and say that we've discovered some problems that require costly repairs".

Well, actually, what they called to tell me today to tell me was that I needed new tires and a brake job. (Cost: $1045.24.) In all fairness, I had thought that both of those things were going to be needed soon, and I was already thinking this even before the car loan was paid off. But I also thought, as soon as I had the pink slip in my hand, "this means some expensive work is going to have to be done on this car now, to compensate for the car payments I'm no longer making". I guess the real reason I thought this was that receiving the pink slip reminded me of something: I've had this car (without expensive problems to date) for a while now, so it's due for some spendy repair work.

The same principle applies to the human body, of course: hold onto one of those things long enough, and stuff is going to start going wrong with it, and over time those little problems tend to become more frequent, more serious, and more difficult (that is, costly) to address.

However, there is a complicating factor which makes it much more difficult to predict when a human body is going to break down than to predict when a car is going to do so: the human body has a capacity for self-repair. That capacity isn't limitless (there are problems it can't fix) and it isn't permanent (it tends to decline over time), but to some extent the body is capable of refurbishment and renewal -- and to some extent we can encourage and strengthen that tendency. Most of the things we think of as healthy habits of living serve not to repair what's wrong with us but to strengthen the body's capacity to perform such repairs itself. Because we have no way to measure how good a job we are doing at strengthening the body's self-repair system, we have a very hard time predicting how likely it is for things to go seriously wrong with us.

As I waited for my colonoscopy to be performed earlier this month, I convinced myself that it was going to reveal something terrible. I believed this not because I had any evidence of a problem, but simply because I had a bad feeling that time was catching up with me and surely I was due for a medical disaster. I was as convinced of that as I was convinced, today, that I was going to have to be writing a check for tires and brakes before the day was out. Regarding the tires and brakes, there was independent evidence to back up my pessimism, but regarding the colonoscopy I had nothing more than a dreadful feeling that the result would be much worse this time (instead of better -- zero polyps instead of one).

Maybe all this exercise has protected me against the problems I've been fearing, by giving my body a more robust self-repair system than most people have. But the struggle with time is a difficult one; I'm still exercising, but ever since my Ireland trip last summer I've been having a hard time controlling weight and blood sugar as well as used to be able to do with less effort. This body-maintenance thing doesn't get easier as you get older.

I'm not offering that as an excuse to give up, of course. I still have to do what's necessary. It's just that doing what's necessary seems to get tougher over time.

 


Birthday Aftermath

Wednesday, January 30, 2013


My Morning Comeuppance

Well, that was pretty much inevitable -- a fasting test elevated the morning after a birthday dinner. Especially one that concluded with a dessert that is popular in Ireland (but hitherto unknown to me): Chocolate Biscuit Cake!

Yes, I'm ashamed of myself all right, but it was pretty damned good. But I figured I'd better do an extra-long run today to make up for it. And, lo and behold, after the long run my post-prandial glucose was only 108.

It was a gorgeous day for a run. Sunny and clear and not cold -- just barely cool enough to make running comfortable. It was nice to go up on the ridgeline road and look out over the valley to the west. It suddenly occurred to me that I haven't done an organized running event in a while, and maybe it's time to look for one. There aren't as many of them in the winter, of course, and the examples I found doing a quick internet search were too many miles (or months) away, but I bet I can find something. It's a good motivator.

By the way: the reason my blood pressure is up tonight is that I read something on a news site that made me angry. I guess I'd better stop doing that, and only look at web sites that feature funny pictures of cats.

 


Blood Sugar Control & CVD Risk

A new study says that diabetes patients who keep blood pressure, blood sugar, and LDL cholesterol under control have a 2.5-fold reduction in their chances of being hospitalized for cardiovascular disease -- but also says that controlling blood sugar is the least important of the three. According to the study authors, "It's not as though we're saying glucose control doesn't matter; it does. The point is that we didn't see any additional benefit from getting people down to below 7% [A1c] from, say, 8%". In terms of cardiovascular risk, if the patient's A1c is 7.5%, reducing it to below 7.0% is "probably not what matters... what does matter is LDL-C and blood pressure".

It seems to me that, when you're talking about keeping diabetes patients healthy, it's a little narrow-minded to limit the focus of risk reduction to cardiovascular disease alone. I mean, sure, cardiovascular disease is a major concern for diabetes patients. I get that. But it's not the only concern around. Some people with diabetes don't want to develop kidney disease or go blind, either. Most diabetes "complications" are very definitely tied to blood sugar control, or the loss of it. So, I'm not sure I like to see doctors suggesting that we're paying too much attention to blood sugar control.

I suppose they would argue that they're not saying we need to pay less attention to blood sugar control, they're merely saying that we need to pay more attention to cholesterol control and blood pressure control. However, I'm a little suspicious of this sort of thing. It gets a little creepy when medical specialists start talking not in terms of keeping the patient safe, but rather in terms of keeping the patient safe only from the disease that their specialty is concerned with. What, exactly, is the point of detaching cardiovascular risks from all other risks faced by diabetes patients? Are they expecting to find a cohort of patients who have cardiovascular systems but no other organs?

The study was funded by AstraZeneca and Bristol-Myers Squibb. The former makes a cholesterol drug, and the latter makes a blood pressure drug, but it's probably just a coincidence.

 


The Phoenix Of Snack Cakes

Okay, relax everybody. Reports of the death of the Hostess Twinkie were greatly exaggerated, and the indestructible confection seems poised to rise from its own ashes. The Hostess company thinks it has found a savior for its snack-cake business; C. Dean Metropoulos & Co. and Apollo Global Management LLC have offered Hostess $410 million for the right to be the new makers of the Twinkie.

It doesn't really affect me; I don't eat Twinkies. So long as nobody figures out how to make birthday cakes out of them I'm probably safe.

 


Special Day

Tuesday, January 29, 2013

I got home quite late this evening; I was down in the Bay Area for my dad's 86th birthday dinner. (I hope I inherited his longevity genes.)

I'm afraid my fasting test will be high tomorrow, after the big dinner, but I'll deal with it then. Now: sleep!

 


Mondays Are Strange

Monday, January 28, 2013


My Inconvenient Day

I have become pretty used to the convenience of having a locker room and shower downstairs from my office; at lunchtime I just go down there, change into my exercise clothes, and take off for a run in the neighborhood (and the neighborhood is so hilly that any running route is sure to be a challenging workout). Today, however, this excellent system broke down. We had some kind of sewer crisis, and the bathroom and shower room downstairs were closed all day while heroic plumbing efforts were made. Okay, if that's the way it is -- switch to Plan B!

Plan B was going to the gym after work (and before my evening yoga class). I was planning to do a 4-mile treadmill run, but the treadmills were all in use when I got there; apparently the New Year's Resolution cohort is still hanging in there for the time being. So I did 40 minutes on the stair-climber, telling myself that this was about equivalent to a 4-mile run. It wasn't, and I knew it wasn't, but that was what I settled for today. Afterwards I sat in the hot tub for a little while, as therapy for some muscles that were a little sore from a trail-run on Sunday.

The hot-tub is outdoors, and the skies were clear, so I got to look up at some old friends: the brilliant creamy-yellow planet Jupiter, and the constellation of Orion, with the bright blue star Rigel and the bright red star Betelgeuse... and with the line of Orion's belt pointing down to Sirius and up to Aldebaran. Just points of light, to the naked eye, but I remembered how large a star Aldebaran is -- much larger than our own sun:

And, of course, Aldebaran is small compared to Betelgeuse, a star so gigantic that, if our sun expanded to the size of Betelgeuse, the orbits of four planets (including earth's) would end up inside it.

Aldebaran and Betelgeuse are "red giant" stars; this is a late phase of a star's life cycle. Our sun will go through that transformation, too, once the sun uses up enough of its hydrogen fuel and switches to helium fusion, and at that point the earth will be pretty thoroughly incinerated. Don't panic, though: that won't happen for a few billion years, so no matter how much fiber you eat you're not going to live to see it.

This is what I think about at the gym; you, of course, are free to think about whatever you like.


Diabetes News: Stories For Other People

The trouble with the news stories I read about diabetes is that most of them seem to pertain only to other people, not to me. A lot of what gets published about diabetes relates to drugs I'm not taking and life-stages I'm not going through.

The American Academy of Pediatrics has issued some new clinical guidelines on managing newly diagnosed Type 2 diabetes in children and adolescents. (Unsurprisingly, their recommendation is to go straight for the drugs, rather than giving young people a chance to get things under control with lifestyle changes alone.)

But I'm 55, so my interest in these recommendations is rather academic.

Other news I can't use: the Institut de Recherches Clinques de Montreal (IRCM to its friends) is reporting some success in developing an "artificial pancreas" for Type 1 patients. Essentially it combines a continuous glucose monitor with an insulin pump, but perhaps the real value of the system lies in the sophisticated algorithms it uses to respond appropriately to patterns of rising and falling glucose levels. Apparently the clinical trials are showing that Type 1 patients can achieve better glycemic control, with much less risk of hypoglycemic episodes, with this system than with any approach currently available to them.

No reports so far on how much the "artificial pancreas" costs, but if you can afford to drive a Ferrari I'm sure you can handle it.

Of course, if you don't have Type 1, you'll probably be told you don't need the artificial pancreas anyway. And I don't have Type 1.

So, once again, this is probably big news for some people with diabetes, but it isn't big news for me.

Oh, well, look on the bright side: I've been trying to do everything possible to be unlike the typical diabetes patient. If I succeed at that, then naturally the diabetes news stories that pertain to the typical patient will be irrelevant to me.

Maybe finding most diabetes news irrelevant to you is the best measure of success in managing diabetes.

 


After The Fact

Friday, January 25, 2013


Thoughts On Being Too Late To Prevent Diabetes

The trouble with reading about, much less writing about, diabetes prevention is that in my case it's too late for that. I didn't prevent it when I could have, so any good news I learn about how diabetes can be prevented is good news for somebody else and not for me.

For example, since I'm well past 43 years of age (12 years past it, but who's counting?), it seemingly isn't that helpful to me to know that a new study says sedentary living at 16 is a pretty reliable predictor of metabolic syndrome at 43. Yeah, I guess it is, all right. It was in my case.

And it's not all that helpful for me to know that another new study says daily exercise (even if it's only 20 minutes' worth) protects overweight children from diabetes.

Knowing these things probably isn't that helpful to my readers, either, since I have a feeling most of them are also past the point were "prevention" is an option. My readership does not seem to consist of college students concerned that they might, some day, have diabetes.

I am, and I assume my readers are, well past the ounce-of-prevention phase, and well into the pound-of-cure phase. Can it be anything more than an annoyance to have it pointed to us what we could have done, many years ago, to sharply reduce our risk of becoming diabetic?

Well, I think it's worth being aware of these things, for a simple, practical reason: the things that tend to help prevent diabetes from developing also tend to ameliorate it after it has already developed.

It's too late for us to prevent diabetes; it's not too late to prevent diabetes from killing us.

There you go: your silver lining for the day! You knew you could count on me for it.

 


Worrying About The Wrong Thing

Thursday, January 24, 2013


Diabetes + Kidney Disease = Heart Disease

Here's something interesting and strange: if you are a Type 2 diabetes patient, having or not having kidney disease is the best predictor of whether or not you will have a shortened lifespan... and yet, kidney disease is probably not what will kill you, even if you have it! Sounds a bit paradoxical, doesn't it?

Kidney disease has long been known to be common in diabetes patients. Glycation (the unwanted bonding of glucose to proteins in our tissues) has a tendency to gum up the works, particularly in very tiny structures (such as the nephrons which do the blood-filtering work of the kidneys). This results in a variety of health problems which we think of as "diabetes complications". Kidney disease (specifically, failure of the kidneys to filter the blood properly) is a common diabetes complication: the rate of kidney disease is 42% in people with Type 2 diabetes, 9% in people without it.

However, when people die prematurely and they have Type 2 diabetes, the cause of death is typically heart disease, not kidney disease -- even in patients who also have kidney disease. Superficially, kidney disease is not the biggest issue to worry about.

Or is it?

Researchers at the University of Washington have taken a look at the mortality statistics for people with Type 2 diabetes, and they've noticed that premature death in Type 2 diabetes patients is much, much higher in those who also have kidney disease -- even if the cause of death is heart disease. In fact, in patients with Type 2 diabetes who don't have kidney disease, mortality is not much higher than it is in the general population. Type 2 by itself is apparently not that bad; Type 2 plus kidney disease is very bad, even though the ultimate cause of death will probably not be kidney disease.

The explanation, it seems, is that kidney disease promotes heart disease. When the blood isn't being adequately filtered by the kidneys, cardiovascular trouble ensues. Diabetes patients worry about kidney disease because they don't want to go on dialysis, but apparently they're worrying about the wrong thing. Kidney disease which isn't bad enough to require dialysis can still be bad enough to set you up for a heart attack -- so that you'll die before you ever need dialysis.

Oh, wait a minute. I guess this is the point where I'm supposed to find the silver lining. What's the good news we can take from this?

I guess the good news is that keeping your blood sugar under good enough control to avoid kidney disease is probably enough to avoid premature death as well. Not that keeping your blood sugar under good control is the easiest thing in the world, but maybe knowing this will give us extra motivation to focus on that. So, no, I would not like fries with that.

 


The Search For Truth Continues!

Tuesday, January 23, 2013

Good numbers yesterday in the morning and after lunch, which probably is what encouraged me to overdo the carbs in the evening. Result: fasting result up this morning. I have to keep learning the same lesson over and over, it seems. That's why I have to keep testing...

 


Corrupt Dietitians Unite!

Here's Michele Simon of Eat Drink Politics, writing about the Academy of Nutrition and Dietetics, which turns out to be taking large amounts of money from the food industry. Not that this would lead to any questionable actions, such as recommending Kix cereal in a health education program sponsored by the makers of Kix cereal... but still, you can see how it might create the appearance of impropriety, at least in the mind of a highly suspicious person.

Unfortunately, I don't see a solution to the problem of corrupt health advisors. There is too much money out there, and apparently too little professional pride.

Sorry, but professional dietitians have not regained my respect since I read about this last year, and it's beginning to look as if they're not even trying.

Yeah, who knows if I'm doing any better by you than they are, in the final analysis. But at least no commercial interests are paying me to tell you what they would like to have you hear.

 


Diabetes Denialism

When I look over the Google search terms that led people to this site, I often feel that the people typing these terms are doing web searches on the subject of diabetes mainly for the purpose of convincing themselves that they don't have the disease, despite evidence to the contrary. For example, many of the searches related to the hemoglobin A1c test seem to be from people hoping to establish that the test result is inaccurate in their case, or that the result, even if it's accurate, isn't really as bad as it sounds. Here are some actual examples:

No doubt you think I'm unfairly reading self-delusional intent into innocent questions. Well, maybe I am. But what are the odds?

Today there was a news search phrase which, I thought, really came right out and said what a lot of other people hardly dare to hint at:

"my doctor says i'm a diabetic i don't believe him what do i do?"

What you can do is get a new doctor. If you think your doctor is lying to you, or isn't competent to make a diagnosis, or for some other reason cannot be relied upon to give you accurate information about your health, then clearly you shouldn't be going to this particular doctor. You need to find another doctor whose medical judgment you consider more reliable.

The catch, though, is that it's very hard to know how to shop for a doctor in such a way that you'll be sure to find one who will tell you you're not diabetic. Imagine going to the trouble and expense of finding yourself a new physician, only to discover that this new practitioner is just as dishonest or incompetent as the last one! There you are, stuck with yet another doctor who won't shut up about diabetes!

It's hard to know how to take precautions against such an outcome. If you call doctors' offices hoping to find a new one, you're not likely to get an actual doctor on the phone and have the opportunity to say, "I'm changing doctors because my current doctor says I'm diabetic and I don't believe him, so I need you to promise from the start I'm not going to have any of that sort of nonsense from you". Instead, you'll just have to make an appointment with the receptionist and hope for the best when you go in for your first office visit.

So, before you go to all that trouble, possibly with a very frustrating outcome, ask yourself why you're so sure your doctor is wrong about your being diabetic. Has your doctor falsely diagnosed you before, or told you lies about your health in order to manipulate you? In other words, is there any reasons for your doubts about the diagnosis beyond the mere wish not to have diabetes?

If you're going to doubt a piece of news, you're going to need a reason. Not liking the news isn't a good enough reason.

 


Good Vitamin Bad Vitamin

Tuesday, January 22, 2013


Beta Good, Gamma Bad!

The closer you look at Type 2 diabetes, the more maddeningly complicated it gets. Sometimes I wonder if we will ever entirely understand it.

Although genetics plays a role in raising or lowering your risk of developing the disease, there is no single gene that means you will develop Type 2 diabetes. Instead, there are many gene variants known as SNPs (single-nucleotide polymorphisms -- think of them as one-letter misspellings in the DNA "words"), any of which will modestly increase your risk of Type 2 diabetes. But what is going on with those SNPs? (The acronym is pronounced "snips", by the way.) If any of the SNPs was simple and direct cause of diabetes, everyone who had the SNP would have diabetes as well; at most the SNP is a factor which, in combination with other factors (environmental or lifestyle factors, for example) encourages the development of diabetes. But what might the SNPs be doing, exactly, to encourage the development of Type 2 diabetes?

A Stanford study tried to find out about that by doing a kind of data-mining exercise on 18 different SNPs that are associated with Type 2 diabetes, to see if there was any pattern in the way those SNPs combined with other factors -- patterns which differed between those who did and didn't actually have diabetes.

It turned out that one of those SNPs (it's known as SLC30A4) interacts in a rather peculiar way with two vitamins, to increase or decrease the risk of Type 2 diabetes. SLC30A4 codes for a protein which is abundant in the beta cells of the pancreas (those are the cells that make your insulin supply). The protein that SLC30A4 makes happens to facilitate the transport of zinc into the beta cells, and this happens to facilitate the release of insulin from those cells; obviously any abnormality in that protein is likely to be relevant to diabetes. But the oddity that was discovered about SLC30A4 is that, in those who have it, one vitamin reduces your risk of diabetes and another increases it. Specifically, beta carotene (a vitamin A precursor) reduces the risk of diabetes, while gamma tocopherol (a common dietary form of vitamin E) increases the risk.

Naturally, this study raises a lot more questions than it answers. The beta carotene result is not terribly surprising (beta carotene was already thought to be a reducer of diabetes risk, so this study is just further confirmation of something already reported). The gamma tocopherol result is more surprising. However, we should not be too quick to jump to the conclusion that "vitamin E is bad for you", because a variant of it called alpha tocopherol (which is the variant most often used in vitamin supplements) was not found to increase diabetes risk.

The researchers are now looking to do studies (in rats) to try to confirm that these vitamins are interacting with SLC30A4 to promote diabetes, and also to figure out how exactly that process works.

A question I would like to see answered: if you already have developed Type 2 diabetes, does modifying your intake of beta carotene and gamma tocopherol do anything to make your diabetes less severe?

Stay tuned for further exciting developments on this front! But don't hold your breath: it will probably be years before the picture gets much clearer.

 


Taking That Walk

A study from Japan finds that exercise after a meal -- even rather light exercise, such as a brisk walk -- reduces the postprandial elevation of triglycerides by 72%. (Doing the exercise before the meal is less effective, reducing triglycerides by only 25%). The study involved such a small data set (only ten test subjects!) that I'm not sure it's particularly strong evidence of anything, but I mention it for what it's worth. If you happen to follow the old custom of going for a walk after dinner, I guess there's a reason to continue doing it. (The abandonment of that custom, by Mexican immigrants to the USA, has been cited as a possible contributing factor to the decline in the health of such people after they begin living here.)

Go for that walk!


Sweet Heart

Monday, January 21, 2013

I had the day off work, and the weather was really nice -- sunny and clear and not cold. So I figured I would get in a good long trail-run (a 9-miler) today, even though I did a 7-miler yesterday. I don't usually do two runs in a row that are longer than 5 miles, but today's run didn't bother me at all -- I didn't feel exhausted or sore when I finished. And I managed to get through the yoga class tonight as well, although I was a little crampy. Sometimes I feel as if the main issue I have to manage these days is remaining physically capable of exercising enough to keep my glucose under control. It's a tricky issue to manage when you're over 50, but I'm giving it my full attention and so far I'm doing okay with it.

 


Sucrose & Cardiac Fibrosis

Okay, I'm going to have to introduce some medical terms here that you may not have encountered before. The first is cardiac fibrosis -- which is a proliferation of fibroblasts inside heart-muscle. Fibroblasts are cells which produce a lot of collagen (a protein used in connective tissue); when fibroblasts proliferate within heart muscle, the muscle because thicker and less elastic; this promotes heart failure. I should clarify: the misleadingly-named condition known as heart failure doesn't refer to cessation of heartbeat (that would be called cardiac arrest); heart failure is weakened pumping action which causes the heart to have trouble moving blood volume at the rate that is required. Heart failure happens to be a common health problem among diabetes patients, which is why I'm discussing it here. Diabetes patients need to be aware of heart failure, and of the cardiac fibrosis which causes it.

But what causes cardiac fibrosis? A new report from the Sanford-Burnham Medical Research Institute suggests that dietary sucrose (usually called "table sugar") can cause cardiac fibrosis. For example, in the heart-muscle images below, which show fibrosis-affected tissues in a magenta color and normal tissues in green, the second of the two images shows the effect of a high-sucrose diet:

Okay, the message here is not too hard to interpret: the heart-muscle from the patient on the high-sucrose diet is mostly afflicted with fibrosis, and the heart-muscle from the patient on the normal diet is mostly fibrosis-free. But you might be wondering how old these two patients were. How long had the second patient been on a high-sucrose diet? Probably not very long, I imagine -- fruit flies only live about 30 days.

Yes, that's right: the heart-muscle examined here came not from human beings but from specimens of Drosophila melongaster (fruit flies to you and me).

What is it with researchers and fruit flies, you may be wondering? Why does so much medical research involve studies of a creature not remotely similar to humans?

Well, there are a lot of things about fruit flies which make researchers appreciate them. They're small, fertile (females lay 100 eggs a day), easy and cheap to raise in captivity, and have such short life-cycles that it's easy to follow them through an entire lifespan and even through multiple generations. Also, few animal-rights advocates care what you do to them. Also, it's easy to study fruit fly genes (there are only four chromosome pairs!). Also, there is a surprising amount of genetic overlap between fruit fly DNA and human DNA; about 75% of genes associated with human diseases are found in fruit flies as well. A lot of cellular mechanisms relevant to diabetes in humans operate very similarly in fruit flies.

Admittedly, it's hard to look at a fruit fly and feel much of a bond with it...

...but I guess we'll have to take the geneticists' word for it that we have more in common biologically than we do socially.

Anyway, the research reported here seems to be awfully narrow, as it looked specifically at dietary sucrose, and not at other forms of sugar which might have an impact on heart muscle. The researchers looked specifically at a particular sucrose-processing mechanism known as the hexosamine pathway, which seems to be the specific means by which sucrose promotes cardiac fibrosis. Of course, what they're looking for is the chemical clue that will allow them to invent the next billion-dollar prescription drug. But if, in the process of chasing those dollars, they enable us to understand the role that dietary sucrose plays in causing heart failure in diabetes patients, then the research will end up being useful even to those of us who are trying to stay away from the pharmacy.

 


Frustrating Science News

Friday, January 18, 2013


Researchers Discover...What?

I try my best to keep up with research findings that seem to have a bearing on diabetes, or at least on health, but sometimes the reports that I can get hold of leave a lot to the imagination, and it's hard for me to tell what, if anything, the researchers have found.

Here's a maddeningly terse report from the University of Bern (Switzerland), where something or other has been discovered about the role of benign intestinal bacteria in preventing the development of juvenile diabetes. What was discovered, exactly? That benign intestinal bacteria play some kind of role in preventing the development of juvenile diabetes. There's also an implication that juvenile diabetes may be becoming more prevalent because life is too clean now. In other words, it's possible that we're not getting enough benign intestinal bacteria into children, so the kids are more vulnerable to diabetes-causing immune reactions than they should be. Or not. (The possibility is suggested, not asserted.)

I see this kind of thing all the time, and I don't know what to do with it. I want to find something of value in it, and I can't figure out how to do so, because the information presented is so vague or incomplete. In this case of the example above, the paper seems more like the introduction to a grant proposal, explaining why a particular issue needs to be studied, than a summary of what was learned from such a study.

If bacteria can indeed produce "biochemicals and hormones that stop diabetes developing", I for one would like to know what these chemicals are, and how they prevent diabetes, and why the bacteria are producing these chemicals, and why the human body isn't doing so on its own if the chemicals are so valuable to human health. Is anybody looking into those questions? Just wondering.

 


Now here, by contrast, is a product of research which I can understand: a view of an aurora, as seen from above (specifically from the International Space Station):

It doesn't give me any actionable intelligence about staying healthy, but at least I know what they found. And it's cool, which is sometimes a reasonable substitute for useful.


And here's something else I can understand.

The strange thing is that I never really hated Lance Armstrong, until now. But the problem isn't that I found out about the doping (which is not exactly surprising); it's that I found out a lot more about the harm he's done to others to cover his doping up. And now that I can see how sorry he isn't about what he did to those people, I suddenly want him to do time.

 


Weight Loss Surgery:
The Home Edition!

Thursday, January 17, 2013


DIY Stomach-Pumping

Remember Dean Kamen, the guy who invented these things?

Now he's invented something else, and it's almost as cute. Well, apparently he didn't invent it himself, but he was involved in helping a team of bariatric surgeons (that is, weight-loss surgeons) develop and introduce the thing. I guess the hope is that he will help the new device become as popular and widely-used as the Segway scooter has not become.

Is the new invention something that you will be lining up to purchase? Well, I guess a lot will depend on how you react to this:

Does that make you think "This is horrifying! Humanity has sunk to a new low!"?

Or does it make you think "I gotta get me one o' them things!"?

Either way, you should be aware that the text quoted there is somewhat misleading. Used as directed, the AspireAssist personal stomach pump only removes about 30% of the contents of your stomach; it does not give you carte blanche to eat absolutely any amount of food "without taking in calories". However, in terms of caloric intake, it is roughly the equivalent to eating 30% less than you actually did eat.

Perhaps you're already allowing yourself to think such cynical thoughts as "Couldn't you just eat 30% less, and forget about using the AspireAssist?". Well, in principle, one could do that. But the AspireAssist is intended for people who find eating 30% less very hard to do.

Eating 30% less would have to be very hard to do indeed, before it seemed like a bigger personal challenge than using the AspireAssist. First of all, this stomach pump does not gain access to your stomach by way of the mouth; a tube has to be surgically installed in your stomach, and the access to it is provided by a permanent "skin port":

That phrase "skin port" is brilliant marketing language; I'm sure that a reassuringly breezy phrase such as that is enough to make just about any patient forget that he has a permanent drain-hole in his abdomen which he must unplug and siphon off into the toilet after every meal.

That's from a video demo which you can watch if you dare. Don't worry: it's one of those pleasantly artificial videos in which the gritty details are considerably softened (this patient's most recent meal appears to have consisted of distilled water). Of course, as a musician, my main interest in the video is trying to imagine the circumstances under which the creators of the perky soundtrack music received, and carried out, their assignment. How much were they told about exactly what onscreen activity this score would accompany? Did they write the music first, or did they get to watch the video and then figure out what sort of music would be right for it? Were they thinking the whole time about how this would look on their resumes?

Apparently the AspireAssist is not available in the USA at this point, but clinical trials have shown that people really can lose a lot of weight using it. There are a few concerns, however, about the long-term safety of this particular breakthrough in weight control. Also, there are a few bugs to be worked out, which I have read about, but have decided not to describe to you. (But if you get one of these things, I would advise you to be very conscientious about chewing your food.)

As a blogger it is seemingly my job to tell you what I think about all this; several other health bloggers have offered strong opinions already. Somehow, though, I don't have the strength to face that task tonight. I'm offering no judgments this time -- I report, you decide!


Poor But Sweetened

Wednesday, January 16, 2013


Income and Diabetes

A new study from Canada finds that an important risk factor for diabetes is being poor. Even with screening rates being the same, the poorer you are, the likelier you are to be diagnosed as diabetic (and to do poorly after diagnosis). Of course, the diabetes rate is climbing fast for everyone, but it's the poor who are affected most by the trend.

The study meant to look at diabetes rates, not diabetes causes, but one of the study authors offered some possible explanations for higher diabetes rates among the poor: "higher rates of obesity, poorer diets, a more sedentary lifestyle, affordability of and accessibility to healthy food options and opportunities for physical exercise, as well as health literacy, may all play a role". Another possibility is that a lot of the poorest people included in the study are immigrants from regions where diabetes rates are exceptionally high, owing to local genetic factors -- so, to some degree, the study results may confuse genetic factors with financial ones.

Well, maybe those are the important issues. And maybe the most important issue is one the researchers haven't considered yet. For example: what if depression promotes the development of diabetes... and being poor is really depressing?

 


Our Sugar Overdose

Researchers in New Zealand did a study on the effects of dietary sugar on human health, and you'll never guess what they found. It turns out that sugar promotes obesity! Accompanying editorials point out that dietary sugar (especially in the form of sweetened soft drinks), and refined carbohydrates in general, are bad for our health in a variety of ways; obesity is just the beginning.

Who knew?

Well, pretty much everyone knew, really. But it's information that most people find easy to ignore, especially as the sugar-is-bad message is being put out there by medical researchers with no marketing budget. Coca-Cola, it turns out, does have a marketing budget.

Golly, I wonder which side is going to win this one?

 


Meanwhile, here's a thought from SMBC:


Overcorrection

Tuesday, January 15, 2013


Compensatory Hyperinsulinemia

"What syndrome is caused by overcorrected blood sugars?"

That was a Google search string which someone entered recently, and which yielded a reference to this site. The question is worded a little carelessly, so there is more than one way to interpret it. It could, for example, refer to hypoglycemia (which occurs when the endocrine system tries to bring blood sugar down, and goes too far with it) or to early-morning highs (which occur, presumably, when the endocrine system tries to bring blood sugar up, and goes too far with it). But I'm not sure that I would call either of those temporary situations a "syndrome".

Perhaps what the questioner had in mind was metabolic syndrome. This is chronic hyperinsulinemia, in which the pancreas releases abnormally large quantities of insulin in order to compensate for the body's declining sensitivity to the stuff.

Metabolic syndrome was identified in 1988 by the Stanford cardiologist Gerald Reaven (who initially called it "syndrome X"). He had been trying to figure out why some people have a cardiac-risk profile similar to people with diabetes, even though they don't (yet) have diabetes. Metabolic syndrome makes it possible for the endocrine system to prevent blood sugar from rising to diabetic levels, but the insulin overdose which accomplishes this coverup has an inflammatory effect on the arteries, and promotes coronary heart disease as effectively as diabetes itself would do.

Reaven's rather startling insight was that diabetes (at least the Type 2 variety) can have harmful effects which have nothing to do with elevated blood sugar -- and the trouble can begin before blood sugar ever becomes elevated. Elevated insulin can be enough. Unfortunately, insulin is much harder to measure than glucose (in part because a little insulin goes a long way, and even an overdose of it is still only a trace amount within the blood supply). There are no home test kits for insulin, and even lab tests for insulin are rarely done outside of a research setting, so we are left to guess at what sort of insulin levels our pancreas is generating.

Even though it matters greatly to our health how much insulin our pancreas is producing, we are almost never in a position to find out.

That's one of the challenges of diabetes management: we do our best to maintain day-to-day control of the factors we can measure and keep track of, but we can't measure and track all of the factors that matter. Insulin production is one of the most important factors affecting diabetes management, but we can't measure it and we can't track it. We are left to guess at what is going on in that department.

That might seem like a good excuse for throwing up your hands and saying that the task of diabetes management is impossible. Well, try not to look at it that way. If we can't know anything about, or do anything about, our insulin productivity, that's all the more reason to concentrate as hard as we can about the factors we do know something about, and can do something about.

 


Maintenance

Monday, January 14, 2013


Back to Yoga

My ankles were feeling a bit stiff and sore during today's run, and afterwards it occurred to me that in recent days I had been feeling less flexible than usual pretty much all over my body. And it wasn't until this evening that the likely explanation dawned on me: I had been taking a long break from yoga, and I was starting to pay the price for it.

My yoga teacher shuts down her studio for three weeks during the holiday season, and I extended the break to a fourth week because, when class resumed last Monday, I was resting up after my colonoscopy earlier that day. Obviously, regardless of whether the class was meeting or not, I should have been doing yoga myself, at home, during this month off. And guess what! I didn't! I felt as if I was on vacation from yoga. I don't take a vacation from aerobic exercise, even when I'm quite literally on vacation, but yoga is something I tend to get lazy about.

A peculiar thing about yoga is that, if you do it on regularly scheduled basis, you have no way of knowing whether it's actually doing you any good or not. The only way to find out if it's helping you is to go without it for an extended period, and see if anything goes wrong. I probably would have needed to go without it for more than a month for the problem to become screamingly obvious, but the stiffness I was beginning to experience (just walking around the office at work) should have tipped me off a little sooner than it did.

Naturally the yoga poses were harder to do than usual, after a month off, but I got through it okay, and my muscles and joints are feeling a bit better now.

 


The Checkups-Are-Pointless Meme

A report in JAMA says that "health checks" (which are defined as visits to the doctor "dedicated solely to preventive counseling and screening tests" -- that is, routinely scheduled checkups of healthy people) do not provide a significant benefit in terms of the mortality statistics. On average, people get sick and die at pretty much the same rate whether they go in for routine checkups or not.

The researchers are quoted in Medscape as follows: "Changing beliefs about the value of general health checks — beliefs that have withstood decades of contrary evidence — will continue to be challenging... New initiatives...should eventually shift patients and physicians away from the non–evidence-based yet firmly entrenched practice of the general health checkup." Take that, silly patients and doctors! Stop wasting precious health-care dollars checkups that don't do any good!

There's a lot of room for doubt about this report, if you ask me. It is a systematic review of other studies on the subject, which means that the authors were able to establish their own criteria for including or excluding individual studies (they excluded "studies that targeted specific diseases", for example). Also, their definition of a health check excluded from the study patients who were managing a chronic condition, such as diabetes.

It occurs to me that patients who are managing a chronic condition first need to find out that they have that chronic condition. There are a lot of chronic conditions which have no alarming symptoms (or no symptoms at all) until they become seriously life-threatening, and patients who develop such conditions are likely to remain unaware of it for a long time, especially if they aren't having routine checkups. In fact, JAMA's review does note that patients who had health checks were likelier to be diagnosed with problems such as diabetes, hypertension, and hyperlipidemia; is that because people who go in for checkups are sicker than other people, or is it because people who go to the doctor are likelier to find out about whatever health issues they have?

Any study which draws broad conclusions about all patients from cherry-picked data on some patients needs to be viewed skeptically. I suspect that this systematic review, like the ones which claim to prove that home glucose testing doesn't do Type 2 patients any good, probably reflects the political economy of the health-care industry better than it reflects the reality of health care as human beings experience it.

Health-care costs have certainly been rising unreasonably fast over time, but unless annual checkups have been turning into monthly checkups lately, I don't think the real problem is that people are being allowed to see the doctor when, so far as they know, there's nothing wrong with them. Given the rising incidence of the chronic health-care problems referenced earlier, it seems to me that it's more important now, not less, for people to be screened now and then for those problems.


Great Weirdos of Science!

Friday, January 11, 2013


Are You A Good Antioxidant Or A Bad Antioxidant?

Okay, here's the man of the hour:

That's the distinguished, and incomparably tactless, biologist James Watson, a Nobel prizewinner (as co-discoverer of the helical structure of the DNA molecule, way back in 1953). Apparently his brilliance as a scientist is genuine -- which it pretty much has to be, if he's going to be as unmannerly and weird as, by most accounts, he is and always has been.

Throughout Watson's long career he has made a specialty of blurting out his opinions about how incompetent his colleagues are, how unattractive women scientists are, and how unintelligent people of African descent are.

He often has occasion to express his bewilderment at how touchy people can be. Every time he says what he thinks, somebody gets mad. Imagine! Can't a scientist think out loud, in a speech at a conference, about how having dark skin causes excessive sexual appetite, without people making a big deal out of it?

He'll always be the co-discoverer of the DNA double helix, they can't take that away from him. What he can't take away from himself, unfortunately, is the disgraceful back-story of that discovery. His work on DNA relied heavily on unpublished experimental data collected by Rosalind Franklin; Watson and his research partner obtained much of that data by stealth, without Franklin's knowledge or permission. In his book "The Double Helix", Watson belittled Franklin (who by then was dead and could not sue him for libel) and he excused his appropriation of her data by arguing that she didn't know what she had -- she didn't understand the implications of her own data, therefore the data ought to belong to whoever knew what to do with it. This excuse has the disadvantage of being clearly untrue (it was Franklin who gave Watson the crucial clue that the sugar-phosphate backbones of DNA were on the outside of the molecule -- not on the inside, as other researchers had been assuming). Nevertheless, Watson has been clinging fiercely to this lame rationalization ever since, despite his eventual admission that many of his putdowns of Franklin were unjust. (I once heard him interviewed on the radio by a woman scientist who tried to explain to him what's wrong with making unauthorized use of another scientist's not-yet-published work, especially when you stole it from her... and Watson wouldn't budge an inch. Franklin didn't understand her data, and he did. Therefore he had a right to help himself to it. That was his story and he was sticking to it!)

So anyway, that's James Watson. He's a scientific genius, and he's also spoiled child (to put it kindly) who likes to get attention and stir things up. He has a mixed reputation among his fellow scientists -- not mixed in the sense that some respect him while others are appalled by him, but in the sense that those who respect him are also appalled by him. Keep all that in mind, while evaluating what follows.

Watson just published an article on antioxidants and cancer -- arguing that, instead of protecting us from cancer (as we've been endlessly told in recent years), antioxidants actually make us more vulnerable to the disease!

The term "antioxidants" refers to any type of chemical which inhibits "oxidation" reactions -- reactions which generate potentially damaging molecules known as free radicals, which can lead to all sorts of harm within living organisms, including cancer. Many different substances act as antioxidants (including vitamins A, C, and E). For years we've been told that we should eat lots of colorful fruits and vegetables (which tend to contain antioxidant compounds), and perhaps should take antioxidant supplements; this would supposedly reduce our risk of cancer, heart disease, and other problems.

The trouble with that excellent-sounding suggestion is that it's testable, and it never seems to pass the test. Studies that looked for a health benefit from antioxidants have failed to find any -- and have even found that antioxidant supplements seem to cause a slight increase in cancer risk, not a reduction.

Watson's idea is that, in terms of fighting cancer, oxidants are not our enemy, and antioxidants are not our friend. Nearly all treatments designed to kill cancer cells (even radiation treatments) do so by producing oxidants within those cancer cells. The cancer cells fight back by producing antioxidants, to undo the effect of the treatment -- and if the patient takes in antioxidant supplements, this will only help the cancer cells win the battle!

There's a complication here: Watson's argument seemingly applies only to someone who already has cancer; wouldn't antioxidants at least be useful in preventing the genesis of cancer in people who are currently cancer-free? Perhaps not: apparently potentially cancerous cells form fairly often in us, and the body destroys them (using oxidants!). If Watson is right, taking antioxidant supplements might interfere with the body's own ability to stop those microscopic proto-cancers from turning into something truly dangerous.

Okay, is Watson right about this? Are we hearing this from Watson the genius or Watson the loon? It's hard to tell. I read one biologist quoted (anonymously, because he didn't want to tangle with Watson) as saying that some of what Watson is saying can be defended based on the data, and some of it can't, and it's probably a good thing that he's stirring up a discussion of this. Okay, but what part of it isn't supported by the data? The anonymous commentator isn't offering specifics.

Given Watson's history of bitter rivalry with other scientists, it is perhaps worth mentioning that the whole idea of antioxidants as a protection against cancer came from Linus Pauling, Watson's chief competitor in the race to discover the structure of DNA. It may seem far-fetched to suggest that Watson would embrace a hypothesis simply because it discredits his old professional rival from 60 years ago. But we're talking about James Watson, folks! If 60 years hasn't been enough time for Watson to put his dealings with Rosalind Franklin in perspective, perhaps he's never made his peace with Linus Pauling either. I'm not saying this is the likeliest explanation for Watson's anti-antioxidant fever, but we can't ignore the possibility.

That's the trouble with assuming that science is about determining who is the biggest name in a given field, and believing that person must be right. Sometimes the biggest name in a given field is crazy. (And sometimes the craziest person in a given field is also right.)

Anyway, if you start to see news articles saying everything has changed, and antioxidants are now bad for you, don't take it too seriously just yet. If Watson is right, non-crazy people will be able to confirm that.


Urination Salvation!

Thursday, January 10, 2013


SGLT2 Inhibitors: Can You Piss Diabetes Away?

Today's news in brief is that, a year after the FDA declined to approve the SGLT2 inhibitor known as Dapagliflozin (on the grounds that the drug appeared to cause a five-fold increase in the risk of certain cancers), an FDA advisory panel voted in favor of approval for another SGLT2 inhibitor known as Canagliflozin (even though it appears to increase the risk of stroke).

If that seems a trifle unfair, I guess I ought to point out that (1) the apparent increase in cancer risk with Dapagliflozin was significantly larger than the apparent increase in stroke risk with Canagliflozin, and (2) "cancer" is a scarier word than "stroke". So you see.

What any kind of SGLT2 inhibitor does is disable a transporter protein (SGLT2) which has the job of latching onto glucose which is passing through the kidneys, seemingly on the way to the bladder, and dragging it back into the bloodstream, so that it isn't excreted in the urine. The kidneys use various transporter proteins as sophisticated filtering agents, to keep desirable compounds in the blood plasma (while undesirable elements are allowed to flow into the bladder). Because of SGLT2, glucose in the blood plasma is almost entirely retained -- practically none of it escapes the body through the urinary tract. However, if blood glucose levels are extremely high, the SGLT2 transporters are unable to keep up with the demand, and glucose starts leaking into the urine. The sweetened, insect-attracting urine of diabetes patients was (in ancient times) the most conspicuous symptom of the disease ("diabetes mellitus" translates crudely as "pissing honey"), and even in comparatively modern times, before the introduction of home glucose monitors, urine test strips were used as a rough indicator of blood glucose levels.

It has occurred to drug companies that, if diabetes patients develop sugary urine only when the SGLT2 transporters are overwhelmed by extremely high blood glucose levels, then maybe blood glucose levels could be kept from getting that high in the first place -- by inhibiting the action of the SGLT2 transporters, so that a large share of blood glucose flows into the urine even when blood glucose levels are not extremely high.

The catch, of course, is that it's hard to develop a drug which inhibits the action of SGLT2 and does absolutely nothing else. It's only to be expected that a drug which messes with your biochemistry in one area is also going to mess with it in some other area. That's what "side effects" are all about. What if the drug inhibits something other than SGLT2? And what if inhibiting that other thing causes serious problems?

It's hard to know for sure if Dapagliflozin really does increase cancer risk, or if Canagliflozin really does increase stroke risk. These increases could be anomalies that say more about the small sample sizes included in the clinical trials than they say about the actual risks involved in taking these drugs. If you ask me, both drugs are guilty until proved innocent, but "guilty" only of having some degree of risk -- like any other drug. The risk might be worth taking, if an SGLT2 inhibitor works for you, and nothing else does; it would be hard for the reported side effects to be worse than the direct effects of out-of-control blood glucose. I'm not planning to try an SGLT2 inhibitor while exercise is still working for me, but I might try it someday if I need more help than I'm getting from exercise.

By the time that happens, maybe the drug companies will have come up with an SGLT2 inhibitor which doesn't cause cancer or strokes. One of the possible advantages of delaying drug therapy as long as possible is that, by the time you have to take the drugs, they might be better drugs than the ones available now.


Shopping & Binding

Wednesday, January 9, 2013


Medical Consumerism: the Food-Critic Approach!

In principle, crowd-sourced data ought to be a very useful tool for consumers who want to make sure they're spending their dollars in the right place. If I'm trying to choose between two restaurants downtown, why shouldn't I take a look at the scores they are each getting from web sites that summarize consumer reviews?

The trouble is, the scores for those restaurants are probably based on a small number of reviews -- and of that small number, a substantial proportion were probably written by individuals with a personal stake in the matter. How many of the good reviews of Restaurant A, and bad reviews of Restaurant B, were written by the owners and employees of Restaurant A (and their relatives and friends)? Even reviews written by individuals with no personal stake in the fortunes of either restaurant might reflect eccentricities and prejudices which I do not share. How much does it help me to know that one customer claims to be ecstatic about a bread pudding which another customer claims he wouldn't feed to a pig? And isn't it likely that reviews can be skewed negative, in an artificial way, simply because people with a grievance are more motivated to write a review than people without a grievance?

I mention all this because consumer-review scores of this type are not just provided for restaurants and digital cameras; they are also provided for doctors -- and a lot of health-care consumers these days are shopping for an MD by looking up the names of local physicians on "physicians review websites" (PRWs). The two most popular of these are Healthgrades and Vitals; others include RateMDs and Drscore. But are these PRWs actually a reliable guide to the quality of the doctors reviewed there?

The Journal of Urology has published a study of these PRWs, and has concluded that they aren't worth much, mainly because of the extremely small sample sizes involved. The average number of reviewers per doctor in the study turned out to be 2.4, which is a ridiculously small data set. Most doctors get a good rating on these sites, but those who don't can often thank a single disgruntled patient. And who knows if that single disgruntled patient might have an eccentric personal motive? A large sample size would reduce (or at least even out) the impact of eccentric individuals. If each doctor got 500 reviews, I would assume that each doctor would get his or her fair share of unfair bad reviews, so no doctor would be harmed by mere bad luck. But if most doctors are getting scores based on a number of reviews that can be counted on one hand, it's hard to feel that the scores mean much.

I tried testing out the various PRWs by running my doctor's name on them, and I found that (although each site used a different scoring system, making direct comparison difficult), he seemed to get about the same score (around 88%) on each -- just like most doctors do! And the sample sizes were indeed small; one site had a score based on 8 reviews, but 2 was more typical.

I hope most patients aren't naive enough to think that a doctor who scores 90% is necessarily better than one who scores 80%, based on an extremely tiny sampling of consumer opinion. Probably they aren't that naive; I suspect what people are really doing is protecting themselves from some dangerous quack or abuser whose bad reputation they haven't heard about. An extremely low score would be a danger signal, especially if detailed reviews are available which explain what the doctor did that made patients unhappy.

Just for the sake of comparison, I also ran the name of the gastroenterologist who did my colonoscopy on Monday. I wondered if, by the very nature of his specialty, he would be doomed to get a lot of bad reviews. Not so, apparently; he scored he even higher than my regular doctor -- but, again, on a tiny sample size. At least it's nice that people didn't hold his colonoscope against him. Perhaps I didn't express that very well, but you see what I mean.


Insulin Meets Insulin Receptor

Nature is reporting a big breakthrough in our understanding of how the insulin molecule docks with its binding site on a cellular insulin receptor. This is a much more complicated issue than you might suppose, given that the insulin molecule is shaped like this...

...and the insulin receptor that it needs to bond with is shaped like this...

...and the molecules change the shapes that they are folded into, once they make contact. Needless to say, some mighty sophisticated technology had to be used to work out these details. But now that they have finally been worked out, researchers are greatly excited about what this will enable them to accomplish in terms of studying diabetes.

As usual, the excitement relates mainly to the possibility of inventing lucrative new drugs -- such an oral medication that will eliminate the need for injected insulin (the Holy Grail of medical research). But I hope some attention will be paid to improving our understanding of insulin resistance; that would benefit even those of us who are inclined to take the unmedicated approach.


Numbers Games

Tuesday, January 8, 2013


Diabetes and Frozen Shoulder

Adhesive capsulitis of the shoulder, or ACS to its friends (of whom it has but few), also known as frozen shoulder, is an inflammatory disorder in which rotation of the shoulder joint is impeded by "adhesions", meaning sticky bits clogging up the shoulder capsule. It sounds as if it would cause stiff or slow movement; what it usually causes is a nagging ache, which persists at a tolerable level for a long time and then one day, very suddenly, erupts into a volcano of pain that makes almost any movement of the shoulder unbearable.

I've had trouble with ACS over the years, originally in my left shoulder, which is now doing fine. (It took a lot of physical therapy to make it fine, but it's fine.) More recently my right shoulder has been sore, but I've been doing home-brew physical therapy to bring that under control (at the moment, it's feeling pretty good).

Anyway, ACS (like just about everything else that can go wrong with a human body) is said to be more common in people with diabetes. But how much more common is it? When these things are mentioned in a non-quantitative way, it's easy to get the impression that the problem under discussion is much, much more common in people with diabetes. If you have both diabetes and ACS, we might assume that the first problem caused the second. If you have ACS but you don't have diabetes, we might think of you as an unlucky anomaly -- like a non-smoker with lung cancer.

But is this perception accurate? There hasn't been a lot of good data presented on this, so we've been left to guess whether diabetes makes ACS ten times more likely, or twice as likely, or what.

Well, a new study looked at 78,827 people with diabetes and 236,481 without diabetes, and then did a 3-year follow-up to see how many people in each group developed ACS. The result? 1.20% of diabetes patients developed ACS, but only 0.95% of non-diabetes patients developed ACS. When the results were adjusted for age, sex, and dyslipidemia (all of which are factors pertinent to ACS risk), the "hazard" ratio of diabetes ended up being 1.32 (meaning that diabetes increases the ACS risk by 32%).

However, saying that diabetes ups the ACS risk by 32% is a true but slightly misleading. It means almost nothing if you don't know how big the risk is for people who don't have diabetes. Most people, if you told them that diabetes increases their ACS risk by 32%, would never guess in a million years that this means the risk goes up from a little under 1% to a little over 1%. If the condition is that uncommon, I'm not surprised that they had to study tens of thousands of patients before a statistically significant difference in ACS rates began to emerge from the statistical noise.

At least now I feel special! I had thought ACS was a lot more common than that. It turns out that we ACS sufferers are fairly rare; we just stand out, because of the way we keep howling in pain while trying to fit our arms into coat-sleeves.

Anyway, I think there ought to be a rule that no health-news article can report that this or that factor causes an X% increase in the risk of some disease, without saying what the risk is in absolute terms, so that readers can put the issue in perspective. I realize it doesn't sound as dramatic if you say that diabetes "raises your risk of ACS to over 1%!". But that's the truth of the matter, and there shouldn't be anything wrong with telling the truth -- even in articles about health issues.


My Very, Very Special Day!

Monday, January 7, 2013


Colorectal Cancer Screening -- What's In It For You?

I had a colonoscopy today, and... hey, wait a minute! Where's everybody going? You all come right back here this instant, and listen to me! This is an important subject. It's probably not your favorite subject, but don't run for the exit just yet.

My casual field research (which consists to mentioning the subject to my friends, and noticing how much their faces contort in pain and disgust) leads me to conclude that many people dread having a colonoscopy, and are resisting the efforts of their primary care physicians to schedule one for them. One friend told me that she flat-out refused to have the procedure done. Another told me that he has been "putting it off" -- for two years now. A lot of people really, really dislike the idea of having a colonoscopy.

Doctors are unhappy about this state of affairs. Some types of cancer screening are of uncertain value (prostate cancer screening, in particular, has been accused of doing more harm than good), but colonoscopic screening for colorectal cancer (beginning at age 50) is pretty clearly established as a procedure which actually saves a significant number of lives. It is thought to be especially important for anyone with Type 2 diabetes, a disease which has been identified as a risk factor for colorectal cancer. (The reason for the connection is uncertain, but it may be that hyperinsulinemia, and other hormonal imbalances associated with Type 2, encourage tumor growth.) Some have argued that anyone with Type 2 diabetes should probably start colonoscopic screening at age 40, rather than the standard 50, as the impact of Type 2 on colorectal cancer risk is about equivalent to being 10 years older than your actual age.

Anyway, I assume that most of my readers are being rather forcefully encouraged to have a colonoscopy soon -- but are reluctant to go through with it. Without taking it on as my duty to convince anyone to have a colonoscopy done, I might as well give my readers who haven't had it done, and are feeling anxious about it, a clearer understanding of what is actually involved.


There have been various publicity campaigns created to overcome public resistance to the idea of having a screening colonoscopy. I don't know if any of them have been especially successful. One approach is to mock the public for its fear of the procedure:

Another approach is to try to keep it light-hearted, with lots of wordplay. There is something about this subject which almost forces us to make puns, even if we're trying not to. And if we are trying to, we have almost unlimited opportunity. It's good to get it behind you! In hindsight you'll be glad you did! All's well that ends well!

And then there's the Science Fair approach, in which the public is invited to see Our Friend The Colon as a much more fascinating organ than they had hitherto suspected:

However, I don't think the public can be faulted too much for feeling nervous about the prospect of having a doctor do this...

...with equipment that looks like this:

(And by the way, gastroenterologists: you might want to arrange it so that, when the patient is wheeled into the procedure room, the first thing he sees is not you holding that apparatus, and gesturing expressively with it, as if you had just hooked a marlin.)

To be clear, the scariest-looking parts of the apparatus do not go inside the patient. All those knobby, spiky, metallic elements are there simply for the doctor to use in controlling the much narrower part which actually does make the journey.

But I'm getting ahead of myself, because the procedure itself is a comparatively minor part of the entire colonoscopy experience. (I had to rewrite that sentence; originally I said it only came at the end of the whole experience -- you see what I mean about the difficulty of avoiding inadvertent wordplay.) In a sense, having a colonoscopy is like running a marathon: the event itself is less of an ordeal than all the preparation that leads up to it. (The problem continues: I originally wrote that it takes less out of you.)

The fun begins a few days before the colonoscopy itself. You will receive some detailed instructions on how to prepare your GI tract for the big day, so that your colon is truly ready for its closeup. In my case, I was told that four days before the procedure I should stop eating "nuts, seeds, popcorn, tomatoes, peanuts, corn, berries, and breads or crackers with visible seeds". That's quite a list of exclusions, if you think about it: some of those ingredients are pretty widely used in commonplace foods.

Then, the day before the procedure, the going really gets tough: you're not allowed to consume anything but clear liquids all day. (And liquids don't count as "clear" if they have a red or otherwise dark coloring (which looks too much like blood to the colonoscope's wee camera). My diet for the day consisted of white grape juice and chicken broth.

Following the instructions carefully, I took four laxative tablets at 2 PM. But that was little more than a preliminary gesture; later in the afternoon, things got really serious. I had mixed a rather massive amount of another laxative, in powder form, into two quarts of Gatorade. At 5 PM I started drinking the stuff. I have to admit that it didn't taste too bad (especially compared to the mixture I'd used for my first colonoscopy 15 years ago -- which was like gulping seawater and trying desperately to keep it down). But two quarts of Gatorade is a lot of Gatorade, especially for someone like me who normally doesn't drink Gatorade, and worries about the sugar in it. (I figured I'd better let go of the whole issue of glycemic control for this occasion.)

I had been warned of various symptoms (besides the intended one) which drinking this stuff might cause, but the only one I actually suffered from was chills -- which was easily dealt with by wearing a down jacket indoors. Anyway, about 75 minutes later the brew began to do its real work. That's when you know you're really committed to the adventure; you're going to be visiting the bathroom at frequent intervals for the next several hours, and eventually there's going to be nothing but water coming out of you. I can't speak for anyone else, but I think this is the most difficult part of the colonoscopy experience (in part because, at that point, nobody's giving you any drugs to help you feel better about the situation).

In the morning, I checked my fasting glucose, fearing it would be very high because of all that Gatorade (it was 100, which I figured wasn't bad under the circumstances). I called a taxi to get to the endoscopy center. They won't let you drive home from the appointment, because the IV sedation they give you during the procedure takes too long to wear off. At the front desk, I not only had to assure them that I had arranged for a friend to drive me home (one of my running buddies from the office), I even had to give them his name and phone number.

Then the gradual stripping of clothing and dignity began, along with the repeated medical histories. By the time all was said and done, I was asked the same set of questions by four different people who apparently aren't on speaking terms. Or maybe they were all playing Good Nurse Bad Nurse, to see if I would change my story. They were a bit worried about me being an unmedicated diabetes patient, so I let them measure my glucose (it was 104 at that point -- which wasn't bad because I'd taken in more sugar since my fasting test). They hooked me up to heart monitors and blood pressure monitors, started an IV, wheeled me into the spookily darkened room where the procedure takes place, and added to the IV some of those "drowsy syrups" that Mr. Shakespeare wrote about. During the procedure they look at a video display to see whatever the colonoscope is discovering, and presumably keeping the room dark gives them a clearer view of the image. It looks sort of like this (but this is a picture of somebody else's colon, not mine -- mine's prettier):

To my own surprise, this time I was watching along with them. In the past, I was knocked pretty much unconscious by the IV sedation, and never saw the monitor at all. This time, for whatever reason, I was awake enough to watch the monitor, and although I had originally thought that I didn't want to look, even if I were awake enough to do so, something about watching the screen in a darkened room gave the whole thing a theatricality which made it seem more like a movie-going experience than a medical one. It was all very atmospheric, this journey through a long dark tunnel lit up by a point-source illuminator.

I half expected a "Directed by Peter Jackson" title card to show up on the screen at the end of this journey through the Mines of Moria.

Not being a gastroenterologist, I wasn't really in a position to judge what I was seeing, but it looked normal to me. Or maybe my brain was responding to auditory cues -- my doctor and his two assistants were talking among themselves, very casually, about something else the whole time, and they never said anything troubling (such as "Whoa! What the hell is that?") which would signal me to think something was wrong. Nothing unexpected turned up.

End result: a normal colonoscopy. They didn't find any polyps (which was a relief to me, because they'd found a small one last time, and I was worried that things would be worse rather than better, simply because I'm older this time). I didn't get an absolutely perfect score -- there were some minor indicators that I should be a little more conscientious about getting fiber into my diet -- but in terms of anything that could be a cancer precursor, I got a clean bill of health.

I was still slightly groggy from the sedation after I got dressed, so it was a good thing that my friend gave me a ride home -- especially as I don't remember much about that ride home, and I'll have to check tomorrow to see if I thanked him for the ride.

What else should I make you aware of about the test? Well, it didn't hurt, which might be something you've been worrying about. The first time I had this done, there was some pain when the device went around the first left turn, but when I complained (or rather when I tried to crawl away to safety, dragging the hospital behind me), they gave me a few more drops of medication and I instantly went to sleep. This time, oddly enough, I had just enough sensation to feel the colonoscope move inside me, but not enough sensation for it to hurt. It probably sounds to you as if this would be profoundly disturbing feeling even if it didn't hurt -- but the sedative they were giving me took care of that; I really didn't care.

Another point worth mentioning: because you have so thoroughly emptied your colon before the procedure starts, it tends to collapse in on itself; in order for the scope to get through it, and get a clear view of the walls, the colon has to be inflated with air during the procedure. You don't feel that, unlikely as that seems, but a lot of the air stays in there after the scope is removed, so you do spend the rest of the day farting it out.

I got home and took a long nap to get rid of the lingering effects of the sedation. I had a dinner of actual food (with a post-prandial glucose reading of 93 -- excellent). Then I spent the evening writing up the experience, for the benefit of my readers -- most of whom probably deserted me after the first paragraph, but you can't say I didn't try! Not that I have an intention of being an evangelist for colonoscopy; I just want to give people who are afraid of the procedure a realistic account of what it's like.


Non-Genetic Stuff

Friday, January 4, 2013


Better Numbers

I did manage to get a lot more sleep last night than I had the night before, and I got better glucose numbers as a result. Or at least I think the better numbers resulted from the improvement in sleep, since everything else was pretty much the same. When it comes to diabetes management, you have to make your best guess -- knowing that the metabolic variables which really matter are hidden from you.

Oh, well. We do what we can, with the information we can get hold of. If we didn't like groping around in the dark, relying on very inadequate clues about what we're dealing with, we should have chosen a different disease.


DNA is Not the Whole Story!

One of the surprises that came out of the first successful efforts to clone mammals is that clones can differ from one another. Cloned sheep, which most people assumed would be absolutely identical in every way (after all, how individual are non-cloned sheep, let alone cloned ones?) turn out to have differences. They may not even be the same color!

The reason this counts as a surprise is that we have been trained to think that DNA controls absolutely everything about a living organism; therefore, clones (which have the same DNA) must be indistinguishable from one another.

The reason this isn't true is that, of the four types of large molecules which make up the cells of a living organism, two are "template-dependent" and two are not.

A template, by the way, is a reusable tool for replicating a pattern -- the classic examples of templates are cookie-cutters and dress patterns. In biology, the template is the sequence of coded base-pairs along a strand of nucleic acid (DNA or RNA), which is used for (1) making more nucleic acid molecules of the same type, and (2) making proteins. No doubt about it, these things are important, and especially important to the embryonic development of an individual organism. The matching DNA of clones does indeed result in them looking alike in most respects; and these similarities can be described as "innate", meaning that they are destined to be there from the start, and nothing which happens to the organism is going to change them.

However, the other two large molecules which make up the cells of a living organism are not template-dependent. These are the "lipids" (fat-based compounds) and "glycans" (sugar-based compounds). As these molecules are not defined or controlled by what is in the genes, they are "acquired" or "metabolic" rather than "genetic". Lifestyle rather than genetics determines what sort of lipids and glycans are in your cells.

Scientists hoping to figure out what causes people to develop Type 2 diabetes need to be looking at what is going on with lipids and glycans, not just what is going on with DNA and proteins. DNA plays some kind of role in Type 2 diabetes (diabetes does run in families, and some ethnic populations have higher diabetes prevalence than others), but DNA is clearly not the whole story. Diabetes prevalence varies more dramatically from country to country, and from decade to decade, than DNA does; lifestyle is necessarily a factor, and probably a bigger factor than genetics is.

Scientists at the University of California at Santa Barbara are pursuing that lead, investigating the role of the lipids and glycans in the development of Type 2 diabetes.

I was hoping to report to you tonight on the results of their research to date (which is specifically focused on the tendency of the beta cells in the pancreas to fail to detect elevated blood sugar, and respond to it by releasing appropriate levels of insulin, apparently as a result of changes caused by lipids). However, their results seem to be a lot more complicated than I am ready to try to summarize tonight, at least if this diagram is any indication:

I guess what I can say tonight is that there's a lot more going on than genes in the development of Type 2 diabetes, and researchers at UCSB are taking a close look at the matter.

I do hope to be able to say something more useful about this in the future, but that's the bulletin for tonight!


Sleepy, Cold, Isolated Running

Thursday, January 3, 2013


Sleepless in Santa Rosa

I had a bad case of insomnia last night, and that seems to be the likeliest explanation for my elevated fasting result this morning, which (based on other considerations) I had hoped would be lower than yesterday's, not higher. Being short of sleep tends to degrade insulin sensitivity about as effectively as exercise improves it, so it doesn't take much more than a sleepless night to undo the effect of a good run.

Oh well -- I'll try to do better tomorrow morning, by doing better at sleeping tonight. Of course, that's easy to say, isn't? I intended to sleep better last night than I ended up doing. Sometimes it's out of our hands. I'll take some melatonin and hope for the best!


The Lonely Runner

My running buddies are out of town this week, so my lunchtime runs are necessarily solo acts. I've got no one to complain to about the cold.

Not that it is cold, by the standards of most non-tropical locations. It seldom gets truly cold in this part of California, and it wasn't today, so I was running with shorts on, not full-length pants. Still, it was in the 40s, which is about as cold as you want it to get when you're wearing shorts. (My inventory of long running pants is pretty limited, so I only use those when absolutely necessary. Shorts I have in abundance.)

Still, I needed to go out there, with nobody else to keep my spirits up. I often recommend to beginners at exercise that they ought to be working out with other people (making exercise a social activity makes it a lot easier to do it, and to keep doing it). But even if you've found other people to exercise with, they're not going to be there for you every day. You have to find a way to get something out of running (or whatever kind of exercise you do) whether you're alone or in company.

Today I chose a longer route which goes up to a ridge line road, giving dramatic views of the town from above. As it was a clear day, I knew I'd be able to see a long way, and I'd certainly get a good view of my workplace, a couple of miles to the east. There's something oddly comforting about looking down on the office from that distance, and from that altitude, and knowing that I got this far away from the place under my own power. Anyway, that was a pleasurable ingredient that I chose to include in my workout today, to make it a satisfying experience rather than just an item to be checked off my to-do list.

You have to find something to savor in the experience of working out. If there is nothing more to savor in it than the relief of being done with it for the day, then you probably haven't yet found a way of working out that's ideal for you.


A New Year Dawns

Wednesday, January 2, 2013


Wanting What We Can't Have

I had a pretty high-carb lunch (potatoes played a role in it), so I figured I'd better test afterwards to see if I got away with it. Well, I sort of got away with it. My post-prandial level of 132 mg/dl is within my doctor's guidance of <150. However, a truly normal post-prandial level would be more like 125, so I prefer to hold it down to that if I can. My dinner was much lower in carbs (chicken and vegetables, no starch), and the result after that was only 97. Like it or not, it matters what we eat.

It's too bad I'm so fond of starchy foods. When I was Ireland, and I was served a salmon lunch that included potatoes prepared three different ways, the cornucopia of spuds didn't seem over-the-top to me. It seemed just about ideal, actually. I could easily handle being a strict vegetarian if there was no limit on the amount of cereal, bread, pasta, and potatoes I could eat. Unfortunately, it doesn't work that way -- at least if you have diabetes.


Does Weight Matter?

Most of us have been warned against assuming that "if some is good, more is better". An overdose is not necessarily better than a dose, and in fact it's probably a great deal worse.

However, we are seldom warned against the opposite tendency: assuming that "if a lot is dangerous, a little is bad". Once we have established that a huge excess of something can kill you, we tend to assume that even a small amount of it is harmful. Whenever it turns out that things aren't that simple -- that something we assumed to be toxic can actually be benign -- we think we have discovered an oddity; often we call it a "paradox".

The "French paradox", for example, was the discovery that people in France (and in some other Mediterranean countries) had a comparatively low incidence of those cardiovascular diseases which, in America, were being blamed on fat consumption -- even though the French were eating a comparatively high-fat diet. Even more paradoxical was the discovery that, although very high consumption of alcohol was associated with elevated risk of heart disease, so was avoidance of alcohol -- moderate drinkers were at less risk than heavy drinkers, but also at less risk than non-drinkers.

Apparently there is an "obesity" paradox as well. A huge meta-analysis recently reported in JAMA says that, although severe obesity is definitely linked to higher mortality, being somewhat overweight is not. In fact, mortality is a little lower for overweight people than for "normal" weight people.

The study is open to attack from any number of angles; for one thing, the weight categories were defined by Body Mass Index, a notoriously problematic measure in that it characterizes muscular people as overweight. It could turn out that the reported lower mortality for overweight people came about because that's the category that athletic people were placed in.

Still, I thought it might be nice to begin the new year with some encouraging news on the subject of body weight. With most of us trying to recover from holiday weight gains, it is nice to hear that being overweight might not be as bad as we thought, so long was we don't carry it too far. However, for anyone with Type 2 diabetes, excess body fat tends not to be helpful in terms of glycemic control. So, I shouldn't leave you with the impression that scientists have now proved body weight to be irrelevant for everyone. If you can't maintain glycemic control at your present body weight, losing weight may be necessary, regardless of what the JAMA article says.

 


Does Fructose Matter?

Another study finds that, because of the way the body responds to fructose versus glucose, foods containing fructose promote overeating. The satiety signals which are supposed to kill your appetite after you've had enough to eat are generated within the body following ingestion of glucose, but not following ingestion of fructose. The presence of sucrose (which is half fructose) and HFCS (which is slightly more than half fructose) in so many processed foods is probably causing people to eat more of those foods than they would if the foods contained glucose instead.

I don't know what we do about this, but that's what the researchers are saying.


Uh-oh! I'm being replaced!



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