Thursday, January 23, 2014

And now it's fire season! The humidity today was extremely low (21% -- the air was so dry that exercising outdoors gave you a sore throat). We've been warned that wildfire danger is high right now. Once again, I have to say that this is not what January is supposed to be like!


Diagnosis and the emotions

"I'm panicking about being diagnosed with type 2 diabetes" reads a search string I found today, in the daily report of searches that yielded a Google reference to my site.

It's a wonderfully ambiguous sentence. Is this a person who has been diagnosed, and is panicking over that? Or someone who is panicking over the fear of being diagnosed soon?

If it's the latter, let us assume that the person who is fretting about a potential diagnosis has some sort of logical basis for thinking that such a diagnosis is imminent. That way, we're not talking about hypochondria, we're talking about an emotional reaction to a situation which is real, or likely to become real very soon.

So, anyway, the "panic" we're talking about here is the panic that people feel when they must come to terms with the reality of having a disease which isn't going to go away after a while, like a headcold. Some diseases, once you're got them, are going to become a permanent part of your life. Being diagnosed with a chronic disease is a life-changing milestone; your life is suddenly divided into the period before and after it happened. You aren't going to stop being diagnosed with diabetes any more than you are going to stop being divorced, or stop being widowed, or stop being an adult.

However, diabetes, like divorce and widowhood and adulthood and other terrifying phenomena, is something you can adapt to, if you put your mind to it. Some people don't adapt to such things, of course; they take up martyrdom as a lifestyle. But you don't have to do that, it's just one of the options. Another option, so long as you're stuck with being diabetic, is to deal with it -- like an adult, which is another thing you're stuck with being.

I try not to think of diabetes as my curse, my existential crisis, or anything of that sort. I try to think of it as my hobby. A boring hobby, some might say, and perhaps not the hobby I would have chosen if I'd thought it through. Nearly 13 years in, I have to admit that diabetes is not a subject of boundless fascination for me. But people have drearier hobbies than diabetes, I can't help noticing. It might not be my first choice, but it wouldn't be in last place, either. At least diabetes has the advantage of being immensely complicated (and, despite intensive research, still pretty mysterious), so there is always something more to learn about it.

I have little sympathy for the "anger" so many people claim to feel upon being diagnosed. The unfairness of it all! How can it be right that they have diabetes and Donald Trump doesn't? (Actually, I don't know that Donald Trump doesn't have diabetes; I was just trying to think of a highly unsympathetic celebrity.) Anyway, I can't imagine why anyone thinks it would be sensible (or even decent) to assume that diseases are suffered only by people who deserve them. If anyone did deserve a chronic disease, it would be people who think of the vagaries of human health as a system of punishment, and are upset because they think others deserved diabetes more than they did.

Most people have much too strong a tendency to read "meaning" into every damned thing that happens. Perhaps the first thing you have to do, when you're dealing with diagnosis panic, is to abandon the idea that the diagnosis "means" something (other than that you now have a chronic disease). Don't start wasting your energy agonizing over what the meaning is. There is no "meaning", so knock it off.

The emotion I invested in my diagnosis, when I got it in early February of 2001, was not anger but embarrassment. My doctor had warned me that I was at risk of becoming diabetic, and I hadn't done anything to change the situation, so the diagnosis seemed like a humiliating failure on my part. I did my best to transform my embarrassment into determination -- I was going to make up for my past mistakes by dealing with the problem well, now that I had missed the opportunity to prevent it.

Whatever negative and useless emotion you may feel about a diabetes diagnosis, try to transform it into a positive and useful emotion. Dwelling on your resentments is not helpful in this situation.

What Color is your Diabetes?

Wednesday, January 22, 2014


California weather insanity continues!

I'm pretty sure January is not supposed to be like this:

I mean it's nice, and all that, especially if you're running outdoors most days, and you're more comfortable in shorts and a sport tee than in multiple layers of rain-gear.

But the fact that there has been very little cold and almost no rain this winter is troubling. Unless we get a very rainy March (it happens sometimes), we're headed into one hell of a drought.


Using colors as a diagnostic tool

Everybody knows one thing that can split white light into a range of distinct colors -- a prism. But other things can have a similar iridescent effect. For example, a thin oil-film on the surface of water...

...or the thin surface of a soap-bubble:

In both of those examples, the thin surface medium (thin enough to be close to the wavelength of a given color of light) produces the color effects. But what causes a similar type of iridescence on the surface of a compact disk?

In that case a slightly different phenomenon is involved -- the disk acts as a diffraction grating:

For reasons I won't go into here (because I don't understand them well enough to explain them clearly), when a reflective surface is marked with grooves or other repeating surface features, and the repeating features are spaced closely enough to be near the wavelength of visible light, then light reflecting off the surface is spread into distinct colors. A compact disk has tiny, repeating bumps on its surface which cause it to act as a diffraction grating:

The bumps are there to mark the disk surface with a laser-readable digital code, which represents the recorded sound. But they also serve as a diffraction grating, so the disk looks iridescent.

As our technology gets better and better at etching microscopic features onto an object, it is becoming easier and easier to create objects which produce spectral diffraction effects -- and researchers are coming up with more and more applications for such things. It isn't all about creating pretty colors -- sometimes those colors can be useful in a practical way. They may be useful, for example, in medical diagnostic testing.

Bear in mind that it's the spacing of the microscopic elements in a diffraction grating which produces the color effects. You can change the colors by changing the spacing. If you can develop a diffraction grating which changes the spacing between its elements in response to exposure to a chemical, you can use the grating as a chemical detector.

One way to create such a detector is to suspend nanoparticles in a hydrogel (the king of absorbent material that a soft contact lens is made of), and use a laser to etch them to just the right size and shape:

The array of nanoparticles functions as a kind of hologram. Depending the configuration of this nanoparticle array, light reflecting off it changes color as the hydrogel is exposed to varying amounts of a chemical which causes expansion of the nanoparticles and alters the spacing between them. The material can therefore be used as a chemical detector.

Researchers at Cambridge University are developing such chemical detectors. For purposes of diabetes monitoring, the detectors would be cheaper to manufacture than existing test strips -- and would be reusable!

Because existing glucose test-strip technology is more expensive and is not reusable, insurance companies don't want to cover test-strip expenses and many diabetes patients cannot afford to cover those expenses on their own. Therefore, frequent testing is out of reach for a lot of people.

Of course, a big issue (at least for me) is how accurate this sort of testing technology will be. If it isn't at least as accurate as the current method, and preferably more accurate, I'm not sure I see this as a good thing. I want to see some quantitative results, not "green good, red bad". But it's going to be interesting to watch this develop.


Too Much Information,
or Not Enough?

Tuesday, January 21, 2014


Why my "diet secrets" are still secret

I heard from a reader who wondered what my diet is like, and how much I restrict carbohydrate intake -- and probably also wondered why I haven't been more forthcoming with this information in blog posts, since I am always so explicit about what my exercise regimen is like. Why go on and on about exercise, while keeping mum about diet most of the time?

It's a pretty complicated issue. I'm not sure the time has come for me to reveal more about what I eat, but perhaps the time has come for me to explain more clearly why I'm not revealing more about what I eat.

Actually, there are several reasons why I generally don't give reports on my diet, but an important one is that I don't have any kind of consistent theory about what's the best diet. I try things out. Sometimes I find an approach that seems right for me... but later I change my mind about it, or find that it is impractical for me, or simply get tired of it. I think a lot of different ways of eating can work for people, or can be made to work for people with suitable adaptations. I think a vegetarian diet can work. I think a carnivorous diet can work. I think the "Mediterranean" diet can work. I think the "paleo" diet can work.

For any well-known diet you can name, there are probably people for whom it works. What often happens, once people find a diet that works for them, is that they make it their new religion, and become missionaries for it -- convinced, as most missionaries are, that the diet that works for them is the only one that can work for anybody. They end up devoting a startling amount of energy to denigrating those who have adopted a different diet, and can even become enraged over the issue. (Many meat-eaters talk as if vegetarians were robbing them of their cheeseburgers, and need to be punished for it.) I simply don't have that kind of passionate devotion to any specific diet. I'm not saying there's no such thing as a harmful diet, but I don't accept that there's only one healthful diet and everybody needs to be on it. It may be that there is actually one diet that's the best bet for most people, healthwise, but I don't think the state of human knowledge about nutrition has advanced to anywhere near the point where we could say with confidence what that best diet is.

I do have a few dietary principles that I think are important for people with Type 2 diabetes, but I'll get to that a little later in this post. Anyway, they don't add up to anything that could be called a specific "diet".

Another reason I don't like to report on my diet is that, if I announce what I ate for breakfast, many of readers will assume I'm declaring that this is what they should have for breakfast. I've learned this the hard way. Back in the days when I used to report regularly on what I was eating, I received some pretty savage criticism from people who thought I was "recommending" foods which most Type 2 patients could not eat without spiking their blood sugar. It did me no good to protest that there was a difference between admitting what I ate for breakfast and telling other diabetes patients what to eat for breakfast. Any regular reporting of my diet is inevitably interpreted as a prescription, not a confession. I could argue that it's not my fault that people misinterpret me, but in a way that's not true: it sort of is my fault, if I write something knowing that people will misinterpret it. I now understand that it is literally impossible for me to write "I had toast this morning" without having some people read it and think I wrote "everyone with diabetes should begin the day with toast!".

I think Type 2 diabetes management is a very individual thing, because we all differ in terms of what we can "get away with". The same meal isn't going to have the same impact on my blood sugar as it does on yours. I know I can usually get away with more than a lot of Type 2 patients can. One rather accusatory reader expressed serious doubts that I ever really was diabetic at all, and asked me what my fasting glucose level was at diagnosis. (For the record: 174 mg/dL, which is well over the diabetic threshold of 126.) I think my diabetes diagnosis was perfectly legitimate when I got it, 13 years ago, but I turned the situation around pretty effectively. Probably I was lucky in the timing of my diagnosis, and I got the situation under control earlier than a lot of people get the chance to do. As a result, I am probably less impaired (in terms of insulin production and/or insulin sensitivity) than many people with Type 2, which means that I can usually handle a higher-carb meal than many people with Type 2 can handle. I'm not saying I can eat a big bowl of noodles or a big mound of rice and not expect to spike my blood sugar to >140 afterward. But, at least on a good day, when I've been getting plenty of exercise, I can often have at least a small serving of pasta, rice, or bread. After several years of managing this disease (14 years as of next month), I have a pretty good sense of what my system can handle and what it can't. (But I continue gathering data on the situation, because I know it can change if I take my eye off the ball.)

For example, today at lunch in the company cafeteria I had chicken Parmesan with broccoli. It was also served with some pasta. Not big pile of pasta, and I didn't eat all of it, but I did eat some of it. I just thought I could handle it. I'd had a tough trail-run the afternoon before (9.4 miles, and very hilly), and a low-carb dinner, and my breakfast this morning had been a yogurt with only 16 grams of carbohydrate. Under the circumstances, it didn't seem like a high risk. An hour after lunch my glucose measured only 104, so my estimate of what I could handle was correct in this case. But on another day, if I'd had more carbs and less exercise during the lead-up to lunch, to include pasta in the mix wouldn't have been the right call. And for some people it would never be the right call. So do I really want to announce to the world that my lunch today included pasta, implying that eating pasta for lunch is my idea of a diabetic diet? It wouldn't even be appropriate for me, on some occasions, and I wouldn't want people to think it was recommending it to all people on all occasions.

Now, I realize that one could argue that my exercise regimen, about which I am quite explicit, could also be interpreted by readers as my one-size-fits all recommendation for diabetes patients in general. Shouldn't I also keep quiet about my workouts, for fear that readers will think I'm telling them to do exactly what I'm doing in that regard? Shouldn't I be worried that, based on yesterday's blog post, readers will feel obliged to run 9.4 miles on federal holidays? Well, it's a valid point, in principle. But somehow I don't think there's a big risk that people will get hung up on replicating my workout schedule.

I do more exercise than most Type 2 patients feel willing, or even able, to do (that may be why I can get away with eating more carbs than they can). In fact, I probably I do more exercise than I actually need to do, at least in terms of diabetes management. I've simply become comfortable with it (and perhaps dependent on it as a way of combating stress, depression, and suchlike feel-bad conditions). Others who are not comfortable with it are almost certainly not going to do what I'm doing just because I'm doing it. So, I'm not going to worry about being slavishly imitated. However, maybe I should be concerned that some readers will take one look at my exercise schedule and say, "Well, if that's what it takes to manage Type 2 diabetes without meds, then I guess I can't do it". My message is not that people should do the amount of exercise I do, but rather that people do whatever amount of exercise it takes to keep them in control, even if that turns out to be considerably less exercise than I'm doing. I guess I should make that point more emphatically and more often.

Anyway, getting back to diet. What are my general dietary guidelines for people with Type 2 diabetes? I certainly can't come up with anything specific enough to be called "a diet", but I can articulate some principles.

  1. For the most part, diet should be data-driven, not theory-driven. Let your glucose meter, not expert opinion, tell you how a given type of meal affects your blood sugar.
  2. My standard post-prandial glucose test is taken one hour after the end of a meal. A normal, non-diabetic person peaks at around 125 mg/dL at that point. A person with Type 2 diabetes may not be able to achieve a post-prandial level as low as that, but should aim for it anyway, and should especially aim to avoid getting above 140, because that's where blood glucose starts to be a harmful influence.
  3. The impact of a meal on your blood sugar is determined almost entirely by how much carbohydrate (or anyway how much non-fiber carbohydrate) is included in it. Fiber and fat in a meal have a moderating effect on the blood-sugar spike you get after the meal, but don't expect miracles in this area. A high-carb meal is a high-carb meal, and will raise your blood sugar significantly.
  4. A carb is a carb. The difference between starch and simple sugar is much smaller than people imagine. The difference between whole-grain bread and white bread is also much smaller that people imagine. Eating a bowl of rice may not be exactly the same thing as eating a bowl of sugar, but it's pretty close.
  5. The purpose of post-prandial glucose testing is to find out what you can "get away with" in a meal without spiking above 140. If you spike above 140, it means there was more carbohydrate in the meal than your system was ready to cope with, and you need to cut the carbs next time. The more you repeat this experiment, the more you will learn about what you can handle, and the better you will understand how much you need to limit your carbs.
  6. If you had a hard workout earlier today, the amount of carbohydrate you can get away with is going to be a bit higher than if you didn't work out today. Don't rely on this effect, though -- verify it. If you don't gather data, you can't know how big the effect is in your case.
  7. Insulin sensitivity and insulin productivity are both subject to change (not only in terms of day-to-day fluctuations, but also in terms of long-term trends). Therefore, what you can get away with is bound to change over time, so you have to keep on testing to make sure you haven't drifted off course.
  8. As you gather data from your glucose meter over time, keep track of everything that seems to influence your results. All sorts of things can make a difference -- including how much sleep you're getting and how stressed-out you are. Get very familiar with your personal patterns, so that you develop an intuitive sense of what works for you, and what you need to do to get good results and keep them that way.

As you see, that's not a diet. It's more of a procedure to follow. I'm not telling you what to eat -- I'm telling you how to figure out for yourself what you ought to eat. Which, I think, is likely to be a lot more useful to you than any description of what I'm eating.


Website ads I didn't investigate further, Episode 952


Monday Thoughts

Monday, January 20, 2014



Saturday was moving-house day (not for me, but I was assisting in the operation), and I feared that by now I would be crippled up by some kind of pulled muscle, herniated disk, inflamed hip-joint, or other unpleasantness. But no problems so far! Which means, now that 48 hours have elapsed since I carried the last piece of furniture down the stairs, that I'm probably in the clear. I ran 5 miles on Sunday; no problem. And I wasn't afraid to raise the ante today.

As certain other portions of the USA dig out from under heavy snowdrifts, the California weather continues ridiculously warm. It was a beautiful sunny day, and as my office was closed for the holiday, I decided that my exercise today ought to be a nice long trail-run at the state park. It ended up being over nine miles, and aside from the hill-climbing involved it really didn't seem all that challenging. I wasn't exhausted when I finished. I was exhausted five minutes after I started, of course, but that always happens. What matters is how you feel after you get thoroughly warmed up. This time it felt pretty good. As a lot of people had the day off, the trails were pretty busy -- lots of hikers, runners, and mountain-bikers. But only one horse, and that's my idea of a good day on the trails.

I'm not used to having my Monday-evening yoga class a few hours after a tough trail-run, and I found some of the yoga stretches unusually difficult -- particularly the balancing-on-one-foot variations. But my working assumption about any yoga stretch is that, the harder it is for you to do on a given day, the more you need to be doing it.


Magic Food-Chemicals!

At this point, I'm inclined to get suspicious whenever somebody identifies some particular chemical component of certain foods, and declares that this chemical treats or prevents some common human disease.

The next step, of course, is for the vitamin/supplement companies to start selling us capsules containing (or at least claiming to contain) a concentrated dose of the magic molecule in question.

The next step after that, of course, is for researchers to study people who are taking those capsules -- usually finding that the capsules don't seem to be effective at preventing or treating the disease in question.

So, I'm not going to get too carried away in reporting the latest finding on "flavonoids" -- a family of chemicals which are found in various fruits and vegetables. Apparently some subclasses of flavonoids (especially "anthocyanins" and "flavones") have the ability to prevent or ameliorate Type 2 diabetes by reducing insulin resistance and inflammation.

The flavonoids in general have a molecular shape which looks roughly like this:

So now you know how to spot one when you come across it. The subclass known as the flavones look like this...

...and the anthocyanins look like this:

If your eyesight isn't good enough to recognize compounds by their molecular structure, you can seek out the flavones in cereals and herbs, and the anthocyanins in colorful fruits. Berries and grapes (and wine!) are reported to be a good place to start.

So, okay: is this a bunch of bull? Well, an important thing to keep in mind is that the researchers weren't directly monitoring anybody's flavonoid intake; they were merely keeping track of which foods people said they were eating often, and what the flavonoid content of those foods was. It could well be that they people in the study who showed less evidence of inflammation and insulin resistance were benefiting from something else in those foods besides the flavonoids. In other words, it might be worth your while to eat blueberries more often, but probably not worth you while to take anthocyanin supplement just because blueberries contain anthocyanins and some researcher thinks that's why blueberries are good for you. (If the people in the study who had less insulin resistance also wore cotton more often than other people, would you start taking cotton supplements?)

It's always interesting to hear about these correlations between particular foods and particular health outcomes, but we should try to resist the impulse to jump to conclusions about which capsules from the drug-store's vitamin shelf might be helpful. Start with the blueberries instead. Or the grapes. Or the wine!

What Could Go Wrong?

Friday, January 17, 2014


Be careful what you fish for

Researchers at the University of Pennsylvania have found a way to make transplanted beta cells reproduce inside the pancreas, seemingly paving the way for a future diabetes treatment. Nobody's asking me, but I have some concerns about it. Well, really one concern, but it's a big one.

In the past, researchers have been frustrated by a peculiar difficulty involved with beta-cell transplantation: transplanted juvenile beta cells will reproduce, but won't generate insulin; transplanted mature beta cells will produce insulin but won't reproduce. The researchers have found a way to transplant mature beta cells in such a way that they will reproduce and generate insulin.

The researchers got their inspiration by a rare disorder called hyperinsulinism of infancy. Some babies are born with some mutated beta cells in the pancreas, beta cells which have a tendency to reproduce in abnormal numbers, as a result of which these babies produce too much insulin. Some people think of this condition as anti-diabetes, because the babies have chronically low blood glucose.

It turns out that the mutated beta cells which reproduce excessively lack a protein known as "p57", and the purpose of p57 is to inhibit cells from reproducing. The researchers did some genetic manipulation on human beta cells (to suppress the gene for the p57 protein), and implanted those cells into diabetic mice. The transplanted beta cells not only reproduced in the mice, they also responded to blood glucose by releasing insulin.

It certainly sounds promising, but here's my concern: they are deactivating a protein that inhibits cellular reproduction? To scientists trying to make something useful out of transplanted cells, uninhibited cellular reproduction probably sounds like victory. To me, it sounds like cancer.

The researchers don't seem to address the issue of cancer at all. Maybe they have their reasons for thinking it's not a problem, but I'd like to hear what those reasons are. To me, a protein that inhibits cells from reproducing is not something to be trifled with. I would be surprised if clinical trials of this treatment didn't uncover some evidence of increased cancer risk. And bear in mind that the researchers are provoking this uninhibited cellular reproduction in the pancreas, an organ notoriously inaccessible to surgery and even observation (which is why pancreatic cancer is seldom successfully treated).

For now, I'm planning to leave this treatment to the mice, and see how they get on with it. And the researchers are going to have to find some mice that live as long as I'm planning to, if they want to reassure me that this treatment won't lead to trouble down the road.

Lovely Idea Dies Tragically!

Thursday, January 16, 2014

My schedule at work today was a mess, and I didn't get to do my usual lunchtime run. I'm sure that's why I got a post-prandial result of 141, from a lunch that wasn't especially high-carb. I probably would have got a result of 120 or less if I'd gone running first. The increase in insulin sensitivity that's caused by exercise is an real, immediate, measurable thing. I can almost always see a difference in post-prandial glucose testing if I miss my lunchtime workout.

Oh, well. I did exercise eventually, after work. I usually do manage to fit it in; I just can't always do it when I'd like to.


So Much for the Obesity Paradox

Researchers have been puzzling over something called the "obesity paradox". Here's what it's about: some studies appear to indicate that being somewhat overweight can actually have a protective effect rather than a harmful one on health outcomes -- especially for people with Type 2 diabetes.

Researchers at the Harvard School of Public Health decided to look into this issue, and see if the obesity paradox for Type 2 patients holds up under close examination. (Spoiler alert: it doesn't.)

The Harvard study was larger than previous studies of this issue (there were over 11,000 participants), and the researchers carefully sorted people into categories by more than just weight. The study distinguished between smokers and non-smokers, for example -- and that turned out to be a significant point.

The researchers found no obesity paradox for Type 2 patients. Mortality rates were lowest in people of normal weight, and increased as weight increased. Nothing paradoxical about that.

So why did earlier, simpler studies give results that seemed to show an advantage for overweight people? Apparently because those studies didn't look at other health issues besides obesity, so they overlooked some issues which could be important. For example, smokers tend to be leaner than non-smokers. People with certain other chronic health problems are also leaner. Because earlier studies didn't adjust for such factors, the mortality statistics for normal-weight people included an inappropriately large representation of smokers and people with chronic illnesses, so the people lumped into the "normal weight" category were often unhealthy in some way. If you filter out this effect, so that the "normal weight" category doesn't include an overabundance of people who are unhealthy for other reasons, then the obesity paradox fades away to nothing.

Well, let's try not to be bitter about this.

If the obesity paradox made sense, it wouldn't be called a paradox, would it? Obviously something was wrong. Either high body-weight was beneficial in some way that we didn't yet understand... or we were allowing the statistics to be distorted by some complicating factor we had not yet considered. It now looks as if it was the latter. Being of "normal weight" not unhealthy, but some unhealthy people are of "normal weight".

Risks Large & Small

Wednesday, January 15, 2014


How bad is mildly elevated glucose?

You probably don't suffer from glucokinase heterozygosity yourself (in fact, you may not even be able to pronounce it,) but it's worth learning a little bit about the condition, because some recent research on people who do have this problem turns out to be relevant to a lot of people who don't have it.

To be "heterozygous" is to have a mismatch between the two copies of a gene that's located on each of a pair of chromosomes. Heterozygosity often leads to health problems; whatever the job is that those two genes are supposed to do, the job isn't likely to be done well enough if only one of the two genes is working. The typical job of a gene is to produce a specific protein which performs some kind of function within cells. If one of a pair of genes is defective, the cells get only half as much of that protein as they ought to, and that deficiency often makes the cell dysfunctional in a way that has serious consequences for health. Despite what you've heard about people being able to live a normal life with only one kidney, or only one lung, or only one testicle, living a normal life with only one of a pair of genes can be much more difficult.

Some people are born with heterozygosity which limits their ability to produce glucokinase -- an enzyme which acts on glucose molecules, and is used by the human body to detect and measure glucose levels in the bloodstream. (You may not have realized that your body has the equivalent of a glucose meter, but if you think about it, the body obviously must have something like that. Otherwise, the endocrine system would be unable to regulate glucose levels by releasing the right amount of glucose at the right time.) Anyway, some people have only one copy of the gene for glucokinase, and they don't produce enough of that protein. As a result of that, their bodies do a poor job of detecting glucose levels, and they don't produce as much insulin for a given glucose level as they ought to. As a result of that, they develop (early in life) chronically elevated glucose levels -- though not as severely elevated as would be seen in most kinds of diabetes.

The resulting elevation of glucose is a form of MODY (maturity onset diabetes of the young). The term MODY describes a group of similar disorders, usually caused by heterozygosity of one gene or another which results in poor insulin production. There are at least 11 different flavors of MODY; the one that results from heterozygosity of the gene for glucokinase is called MODY 2. This form of MODY is the most common -- and it is also comparatively mild. MODY 2 typically results in a mild elevation of fasting glucose, which persists throughout life.

Some British researchers recently decided that MODY 2 patients represent a kind of "natural experiment". That is, they differ from other kinds of diabetes patients in an interesting way, and this means that studying them might give us some important insights into diabetes in general.

The interesting difference between MODY 2 patients and other kinds of diabetes patients is that MODY 2 patients, even without any treatment, exhibit relatively mild elevation of glucose over very long periods. Therefore, they are equivalent to a patient with a more severe type of diabetes who stays under good control for years. Without trying, MODY 2 patients have hemoglobin A1c levels that are at least a little under 7% (the threshold value at which the risk of diabetic complications starts to make a steep climb). Diabetes patients of all types are urged to keep their A1c levels under 7%. Some of them do; a lot of them don't. But even those who do mange it are always worrying that it might not be good enough. How bad is the risk that they're going to develop diabetes complications anyway?

Researchers at the University of Exeter compared 99 MODY 2 patients with 83 early-onset Type 2 diabetes patients and with 91 controls who had neither condition, to see how they were doing in terms of health problems which are usually seen as diabetes complications. These were people in their late forties or older, so both the MODY 2 patients and the early-onset Type 2 patients had been living with their conditions for a long time.

Trait/Prevalence Type 2 MODY 2 Neither
Average A1c 7.8% 6.9% 5.8%
Microvascular Complications 36% 1% 2%
Retinopathy 63% 30% 14%
Laser Treatment for Retinopathy 28% none none
Proteinuria 10% none none
Microalbuminuria 21% 1% 2%
Neuropathy 29% 2% none
Macrovascular Complications 30% 4% 11%

Here's how I see it: the "Type 2" column represents the outcome of unacceptable diabetic control that goes on for years, and the "MODY 2" column represents the outcome of acceptable diabetic control that goes on for years, and the "Neither" column represents the outcome of superb diabetic control that goes on for years.

The risk of complications is pretty high with unacceptable control; there's no getting around that. But acceptable control yields a mighty low risk, pretty much as low as you get with superb control, for everything except retinopathy.

Retinopathy is apparently a problem which humans are especially prone to, given that the rate is as high as 14% even for the non-diabetic contingent. And the MODY 2 contingent had a 30% rate -- but apparently they didn't have it bad enough to need laser surgery for it (28% of the Type 2 contingent had it bad enough to require treatment).

Anyway, the takeaway message for me is that we shouldn't be as scared of diabetic complications as most of us are, if we have our glucose levels under anything like decent control. The risk isn't as high as most of us are afraid it is.

Farewell to the Thrifty Gene?

Tuesday, January 14, 2014


A Hypothesis in Peril!

The list of gene variants associated with an increase in diabetes risk is long and constantly growing. The last time I looked at a listing of them, the total was less than 30, but now it is apparently over 60. These genes are more common in some parts of the world than others, which explains the uneven geographic distribution of diabetes prevalence. But what explains the presence of so many diabetes-friendly genes in the human genome in the first place? We do we carry gene variants that increase our risk of a disease?

The usual explanation for a disease-promoting gene being in the human gene pool is that the gene provides some kind of benefit. For example, the gene which causes sickle-cell anemia only causes that disease if you inherit a copy of it from each of your parents; if you inherit just one copy of it, that single copy makes you resistant to malaria. The gene is common in parts of the world where malaria is common; in Europe it isn't present in the population, because there it provides no benefit to compensate for the danger it represents. The assumption has always been that genes which increase diabetes risk also provide some kind of benefit as compensation. But what is the benefit?

The most widely accepted solution to the puzzle is the "thrifty gene" hypothesis: genes which predispose the human body to become diabetic also make the human body more efficient in its management of energy from food, so that survival in times of famine is increased. By replacing food shortages with food surpluses, modern humans have created a situation in which the benefit provided by these genes is irrelevant, but the risk they represent is more dangerous than ever. So, the genes aren't helping many people survive food shortages, but they're triggering a lot of diabetes cases among the well-fed.

The thrifty gene hypothesis sounds reasonable, and it hasn't been seriously challenged until now, apparently because there hasn't been an easy way to test the idea and see if it holds up. Until now, anyway.

Apparently genetic testing, and analysis of worldwide gene distribution, has become sophisticated enough for researchers to be able to differentiate between genes adopted early in human history and genes adopted later, and this makes it possible in principle to determine whether particular gene variants have been "selected for" in our species. And a group of European researchers decided to study 65 diabetes-linked genes to see if these had been selected for.

The researchers: "We have investigated the evidence for positive selection in samples of African, European, and East Asian ancestry at 65 loci associated with susceptibility to type 2 diabetes (T2D) previously identified through genome-wide association studies. Selection early in human evolutionary history is predicted to lead to ancestral risk alleles shared between populations, whereas late selection would result in population-specific signals at derived risk alleles. By using a wide variety of tests based on the site frequency spectrum, haplotype structure, and population differentiation, we found no global signal of enrichment for positive selection when we considered all T2D risk loci collectively... Selection favored the protective and risk alleles in similar proportions, rather than the risk alleles specifically as predicted by the thrifty gene hypothesis, and may not be related to influence on diabetes. Overall, we conclude that past positive selection has not been a powerful influence driving the prevalence of T2D risk alleles."

In other words, they looked for evidence that the diabetes-linked genes ("thrifty" or not) were becoming more common due to selective pressure -- and they couldn't see any indication that this had been happening.

I already have my own hypothesis about why the thrifty gene hypothesis is not standing up well to investigation. For whatever it may be worth, here it is...

The thrifty gene hypothesis was developed in an attempt to explain why genes which we (from our modern perspective) see as very harmful have not been weeded out by selective pressure over human history. What we're failing to notice is that, even if the diabetes-linked genes actually aren't "thrifty" enough to provide a benefit to us, neither do they represent much of a danger -- provided we're living in a state of nature.

Over most of human history, getting enough to eat has been a struggle. The diabetes-linked genes may not have provided us with any real benefit, but neither did they do us much harm, because we had not yet created the kind of well-fed human existence in which those genes could get much of a chance to make anyone diabetic. Type 2 diabetes simply wasn't common enough in the ancient world for it to exert much selective pressure against the genes for it. (And those who did develop the condition usually developed it late in life, after they were unlikely to reproduce -- and were therefore irrelevant to gene selection.)

The mere fact that a gene seems undesirable to us today doesn't mean it has done great harm in the past. A gene can persist not because it's providing enough benefits to be selected for, but simply because it isn't causing enough trouble to be selected against. If Type 2 diabetes had been a common condition in the past, and had been affecting people of reproductive age, and had been killing them before they could reproduce... then these genes would be selected against. But we can't expect evolution to eliminate genes which merely make life more difficult for people who have already had all the children they're going to.

That's a fact that people too easily forget about evolution by natural selection: it isn't a program for making the second half of the human lifespan more pleasant. If you would like the second half of your lifespan to be more pleasant, you need to make that your project, not nature's! Nature, like it or not, has lost interest in us by then.

Thoughts on the Frozen Shoulder

Monday, January 13, 2014

Yikes! Monday the 13th: all the horror of Friday the 13th, but without cocktails after work!


Adhesive capsulitis: what's in it for you?

Adhesive capsulitis, also known as rotator-cuff tendinitis, also known as frozen shoulder, also known as 50-year-old shoulder, also known as I-can't-dress-myself syndrome... is a frustrating, mysterious, painful condition that you're more likely to suffer from if you have diabetes than if you don't. However, I don't think of it as a diabetes complication. The statistical association between diabetes and adhesive capsulitis is not that strong. Plenty of non-diabetic people get it. Plenty of other health problems also correlate with it. (It's an inflammatory disorder, and it may correlate with diabetes simply because inflammation in general has a tendency to increase the risk of diabetes.)

Still, if you have Type 2 diabetes, you're a little more likely than other people to develop adhesive capsulitis, and you're also more likely to be in the age bracket in which the problem typically manifests itself. So, perhaps some information on the problem might be useful to you. Also, a reader asked me about my experiences with it. So maybe it's time for an update.

First, let's begin by admitting that the human shoulder-joint is a mighty complicated mechanism. If you look at various anatomical illustrations of it, you will find that no two of them look alike, because each illustrator leaves out different things. (If you don't leave out anything, the image becomes visually unintelligible.) Here's one, selected at random:

The big gray thing in the middle is the shoulder-joint capsule. When you have adhesive capsulitis, this capsule becomes inflamed, and the capsule also become covered with "adhesions" -- needless fibrous tissues that cling to the capsule, thickening it and inhibiting its free movement. Here are some attempts at illustrating this apparently hard-to-illustrate phenomenon:

All sorts of things could potentially trigger the problem. Simply not using the shoulder enough can do it: people recovering from a broken arm, breast cancer surgery, or any other situation which interferes with movement of the shoulder are at risk of developing adhesive capsulitis. (I have begun to feel that my habit of holding my arms too high when I run, thus limiting movement of the shoulders, has contributed to the problem for me, and lately I've been making a conscious effort to hold my arms lower, and swing them more, during my lunchtime runs. It seems to be helping.)

Adhesive capsulitis typically develops gradually, as a comparatively mild but annoying ache in the shoulder-joint itself, and also in the upper arm (as a result of inflammation of the tendon which leads down from the shoulder to the biceps). Often the pain is situational: you feel it only when you use your arm in a certain position, and you unconsciously develop strategies for not using your arm in that position. (Making that kind of adjustment without thinking about it is surprisingly easy to do -- and I ought to know, because I've done it.) Also, the pain is (for unknown reasons) typically worse at night, and can make it difficult to find a comfortable sleeping position.

I had that kind of low-grade ache in my left shoulder for a year or two before anything serious came of it. But here's the creepy thing about adhesive capsulitis: it can suddenly flare up, literally overnight, into quite severe pain and immobility of the arm. Apparently the inflammation (or swelling triggered by inflammation) gets bad enough that there just isn't enough room in that shoulder joint for tendons and muscles to move freely without causing very serious pain.

My mildly sore left shoulder finally made the transition to disabling pain at a very inconvenient time -- less than a week before I was due to run the Napa Marathon. I had gone through three months of arduous training for the race, and now I had to cancel it, because my doctor assured me I would regret it if I tried to run that far in that condition.

It was hard to argue with him. Attempting to lift my left arm was impossibly painful. I would get into the car and use my right hand to grab my left and hoist it onto the steering wheel. At work, I had my left arm in a sling to elevate it above the computer keyboard. Sleeping in bed was impossible, but I found that I could sleep in a reclining chair propped at just the right angle. Getting my arm into the sleeve of a shirt or jacket was a prolonged project which I needed to allow extra time for in the morning. Running a marathon was clearly not the best plan for me that week. (But perhaps you would have to go through three months of marathon training to understand how frustrating it was to drop out just before race day.)

My doctor wanted to give me a cortisone shot right in the middle of my unbearably painful shoulder joint, but he couldn't catch me. His Plan B was to send me to a physical therapist. On my first visit, the therapist did get a little cortisone into my shoulder without injecting me (he used an electrically charged pad that drove the stuff through my skin without causing pain), but everything else we did involved him forcing my arm to move farther and farther in terribly painful directions. I had a lot of exercises to do at home, too. Over the course of a few weeks I made a "textbook recovery", as he put it, and was no longer disabled at all, but to get entirely rid of the soreness I had to continue doing exercises at home for months.

My left shoulder is now symptom free. But a couple of years ago my right shoulder started doing the same thing! I figured that I would simply start doing the exercises again, on the right shoulder instead of the left, and because I was taking action before there was any serious flareup, the recovery would be much faster. That turned out not to be the case, and last year (just when I thought the problem was virtually gone) I had a painful flareup and had to redouble my efforts to get it under control. At the moment, my right shoulder is feeling better than it has in two years, but I can never be sure it won't flare up again.

Adhesive capsulitis is a frustrating disorder because, even with fairly aggressive physical therapy, it can take a long time to go away (typically a year or two).

If you have symptoms of adhesive capsulitis in the initial, mild form, my advice is not to wait for agonizing pain and disability before doing anything about it. You may need to see a physical therapist to figure out which particular exercises are right for you (the problem affects mobility differently in different people), but the internet is full of suggested exercises which you might want to try out to see if they help you.

One of the more useful exercises I've seen for the condition (using a towel as a prop) was demonstrated on, of all things, the David Letterman show. The comedian Ricky Gervais complained about having a bad flareup of the condition, and Letterman showed him the exercise that helped him recover from it. It's a video worth watching, not only because it demonstrates a useful exercise, but also because it gives you a pretty vivid picture of what the problem is like. And by the way, Gervais is able to left his arm considerably higher than I was able to at my worst. This a really nasty problem we're talking about. If I ever get it in both shoulders at once, I'll have to be hospitalized.

Anyway, that is what adhesive capsulitis is like. Be on the lookout for it. If you start to get a persistent ache in your shoulder, which you think you can live with so long as you find a different way to reach into the laundry dryer, do take it seriously, and talk to your doctor about addressing the problem before it blows up into something agonizing. I didn't take it seriously enough during its mild phase, and I regretted that when I woke up crippled by it one morning. This is not a problem to take lightly!


It's Back!

Thursday, January 9, 2014


The Return of Dapagliflozin

Dapagliflozin, the Type 2 diabetes drug which the Food and Drug Administration declined to approve 2 years ago this month (owing to concerns about its safety) has now been approved by the same agency.

Two years ago, when the FDA rejected dapagliflozin, I wrote that the makers of the drug (Bristol-Myers Squibb and AstraZeneca) should find a new name for it, one that is easier to spell and pronounce. They more than met my expectations: the drug will be marketed as "Farxiga", which is shorter, easier to spell, easier to pronounce, yet just as funny. (The drug is already approved in Europe, but for some reason it is called Forxiga rather than Farxiga there.)

The FDA's decision to approve the drug was not based merely on the new name, however. They also appreciated that the drug makers provided some reassuring clinical data on the safety of the stuff. Some of the earlier data showed that Farxiga increased the risk of bladder cancer and breast cancer; more recent data alleviates this concern (although more studies will have to be done to settle the issue). There are also still some concerns about possible cardiovascular risks.

But what is Farxiga exactly, and how does it work?

The drug is an SGLT2 inhibitor -- which means, to put it simply, that it allows the glucose in your bloodstream to leak into your urine, so that every time you take a bladder break, you piss your diabetes away.

You may have heard that glucose leaks into your urine anyway, drug or no drug. Not quite true: that doesn't happen if your blood sugar is normal -- or anywhere near normal. As your blood gets filtered by your kidneys, the substances in your blood are selectively filtered. Some are allowed to flow into your bladder, to be excreted as urine, but others are latched onto by specialized transporter molecules and dragged back into your bloodstream. The transporter molecule known as SGLT2 is the one that is tasked with latching onto glucose and returning that to your bloodstream. It works quite efficiently, and almost all of the glucose in your bloodstream is retained rather than excreted. It's only when you have poorly-controlled diabetes that the blood glucose level gets so high that the SGLT2 transporters are overwhelmed, and glucose starts leaking into your urine.

This leakage of glucose into the urine isn't sufficient to normalize blood sugar (for one thing, the leakage doesn't even start to happen until your blood glucose is pretty far above normal). However, researchers wondered if they could exaggerate the effect, by using a drug to suppress the activity of the SGLT2 transporters. In that case, some glucose would leak into the urine all the time, and this might prevent glucose from getting very far above normal. So, researchers started developing SGLT2 inhibitors; Farxiga is an example of this new class of diabetes drugs.

Advertising for Farxiga tends to use imagery suggesting that the drug adds a spigot to your body for draining sugar out of you.

The clinical evidence supports the claim that Farxiga reduces hemoglobin A1c results, and also can cause weight loss (if you don't take in any extra food to make up for the unburned calories you're excreting). I assume that's why the FDA approved the drug, despite lingering concerns about cancer and cardiovascular risks.

But what are the more run-of-the-mill side effects which patients taking Farxiga can expect?

Well, one issue to watch out for is dehydration. You're going to be urinating more; make sure you're taking in enough extra water to make up for that.

Another concern: having sugar constantly flowing through your urinary tract tends to promote the growth of micro-organisms, especially yeast. Both men and women will have to watch out for infections of their genitalia.

Pissing away your diabetes suddenly doesn't sound so cool, does it?

I guess my reaction to this new drug is: you first, guys!

Exercise and Geography

Wednesday, January 8, 2014


Exercise as a regional trait

If you display American exercise statistics from the Center for Disease Control on a map, you find that exercise rates aren't all that high anywhere, but they're notably higher in some states than others. The variations in exercise rates are not the same for aerobic and muscle-strengthening exercise (or for the combination), but in general, exercise rates are highest in the western states and the northeast, lowest in the midwest and deep south. The maps below show the exercise-intense states as darker.

Why there is so much regional variation in exercise rates is not entirely clear. It isn't just a case of warm local weather encouraging outdoor activity; some of the warm-weather states (such as California) have high exercise rates, but it's probably not snowstorms that prevent Alabamans from working out. Is exercise simply a cultural/geographic phenomenon, popular in some places and unpopular in others?

Maybe it isn't exactly geography. The statistics show that exercise rates correlate with all sorts of other things which also vary regionally. Exercise rates tend to be notably higher among more educated people, and among people with higher incomes. Professionals and creative workers tend to exercise; blue-collar workers tend not to. Politics, religion... apparently for anything people can differ in, their exercise rates differ along with it. Perhaps exercise rates differ regionally because the sort of people who exercise more happen to be concentrated in certain parts of the country.

I work in a company that is full of the sort of people who exercise, and the company encourages that tendency by providing locker rooms, showers, a weight room, and various other facilities. The lunchtime workout is, if not exactly a universal practice, certainly an accepted part of the corporate culture. Lots of people do it, including lots of people in management positions. That people see me doing it every day seems to have won me more respect than I would have thought likely, especially as I have continued to do it over the past twelve years. People notice it, and surprise me by commenting on it in an admiring way.

In short, I'm surrounded by people who support me in what I'm doing. What would it be like for me if I lived in a place where doing what I'm doing is regarded as self-indulgent or downright weird?

Doctors and public-health spokesmen often advise us to do things which might be easy to do or hard to do, depending on where we live. Maybe exercise rates are low in Alabama not because it doesn't occur to anyone who lives there to do it, but because anyone who lives there and tries to do it is going to get a lot more discouragement than encouragement. Maybe that will change; there are organized footraces in Alabama (including a marathon in Mobile this coming Sunday!), and if enough people get involved in such events, social support for exercise will be reinforced more and more over time.

But I strongly suspect that exercise rates are low in regions where social support for it is low, and that is an issue which public health organizations need to look at.


The Health Gamble

Tuesday, January 7, 2014


Life is risky. Sue somebody if it doesn't work out!

I had always thought that obstetricians were the doctors who were most frequently sued for malpractice. I had heard that a jury is always willing to assume that the doctor who delivered a baby is somehow responsible for the baby's having two heads.

But it turns out that I was wrong; cardiologists are the most-sued doctors, according to the New England Journal of Medicine, with the typical cardiologist having about a 20% risk of being sued during any given year. A cardiologists who completes a career without being sued at least once is considered a rare bird.

I guess it makes sense in a way: cardiologists treat people with heart disease, which is the leading cause of death in the USA. If you're a cardiologist, a lot of your patients are going to die. And then their families are going to say it was your fault.

An interesting Medscape article on the subject recounted the tale of William Martinez, a Georgia man who visited a cardiologist's office in 2009, complaining of chest pain that radiated to the arm. Martinez was only 31 years old -- rather young for coronary heart disease -- but based on the symptoms, the cardiologist said that Martinez was at high risk of having coronary heart disease, and ordered a follow-up test to confirm it. The test was scheduled for 8 days later. The cardiologist's version of the story is that Martinez was warned to avoid exertion while waiting to take the test; Martinez's family says no, he was not warned.

Warned or not, Martinez did not avoid exertion during the waiting period. The day before the scheduled test he engaged in a threesome, with a woman who was not his wife and a male friend, and died. His family sued the cardiologist, and in June of 2012 a jury awarded them $3 million.

Call me unsympathetic, but if you have symptoms of heart disease, and you go to a cardiologist to get these symptoms checked out, and the cardiologist says you're at high risk of heart disease, and you're scheduled to go in for a medical test tomorrow to confirm you have heart disease... this may not be the ideal night for you to be living out your hottest fantasy. Even if the doctor didn't say you shouldn't do this, don't you realize pretty clearly that it's risky?

But maybe that's what's exciting about it -- it's risky. It's risky in other ways besides the cardiac risk, but the cardiac risk was part of the picture in this case. Probably that made the thing more appealing to Martinez.

Life is full of risks. We can't avoid them entirely, and we probably don't even want to do everything possible to minimize them, because a life devoted entirely to risk-reduction is not the kind of life most people would enjoy. We have to strike a balance between what we want and how much risk we'll accept to get what we want. Not everyone strikes that balance in the same way. Some people tend to keep risk very low, even if it means giving up something they want. Some people want what they want, even if the risk involved in getting it is high.

Managing diabetes forces people to be constantly balancing the need for risk-reduction against the need to live a life that's satisfactory to them. It's all a gamble, and we are each free to figure out how much risk we're willing to accept. But having accepted a certain amount of risk, I don't think we should turn around and sue our doctors if the gamble doesn't pay off.

More Dietary Issues

Monday, January 6, 2014


Fat: the Good News

Well, well, well. Hot on the heels of last week's study complaining that metabolic syndrome patients aren't adhering to the low-fat diet recommended for them, we get a new study saying a low-fat diet isn't the best diet for at-risk people trying to avoid becoming diabetic. The study finds that the Mediterranean diet, which is actually high in fat, cuts the risk of Type 2 diabetes by about a third, compared to a low-fat diet.

Defenders of low-fat diets have a complaint: this wasn't a fair comparison between the Mediterranean diet and a low-fat diet, because the people who were put on a low-fat diet didn't actually comply with its requirements very well, so it wasn't truly low-fat, it was probably a pretty standard diet; it was only low in fat compared to the Mediterranean diet.

Well, this is the problem that always bedevils research on low-fat diets: most people find it hard to stick to them. If you are a health researcher, the low rate of compliance with low-fat diets is nothing more than an irritant. Why can't people just comply with the damned low-fat diet, so that we can collect a bunch of valid data on what sort of effect a low-fat diet would have, if we lived in an alternate universe where people found it easy to stick to a low-fat diet?

Perhaps I'm biasing the case a little by presenting it that way. But I don't think it's entirely irrelevant, when discussing different approaches to diet, to consider the ease or difficulty with which people adopt such a diet. And the issue is by no means limited to low-fat diets. Low-carb diets, if taken to the extremes which their advocates often recommend, can also be extremely difficult to stick to. A lot of people who think they won't miss baked goods, so long as they can have their barbecued ribs, end up lingering near a bakery as if they were at the grave of their beloved, and inconsolable in their grief. And although vegetarian diets are a bit easier to adhere to than low-carb or low-fat diets, they still present what we might call social challenges: they are the sort of diets that are easy enough when you eat alone, but considerably more difficult if you want to take some sort of place in society.

In terms of diabetes prevention, and in terms of glycemic control if it's too late for prevention, the carbohydrate in your diet is the one element which you clearly have to limit. Maybe not to the extent that Gary Taubes would want you to limit it, but it really does come down to a pretty simple rule: you must not take in more carbs than your system can absorb without an outsized blood-sugar spike being the result. If you can't eat a sandwich without your blood sugar spiking above normal, than sandwiches are not for you. That may be brutal, but it's the truth.

I was able to eat a sandwich today without an unacceptable spike (my blood sugar only went up to 115 mg/dl, and anything up to 125 is normal by any standard). No doubt the result wouldn't have been so low if I hadn't just done a hilly 5.3-mile run. But I knew what I could get away with under the circumstances, and what I couldn't get away with under the circumstances, and I was willing to live within those rules. If I get to the point that I can never eat a sandwich and get away with it, I'll have to stop eating sandwiches.

Well, if that happens, I'll deal with it. But I don't think I'm ready to go there before I have to. For the time being, I see carbohydrates as something I have to limit, not eliminate.

And I see fat as something I ought to limit a bit more than I have been lately, but certainly not something to restrict dramatically.


Dietary Issues

Friday, January 3, 2014


Naughty metabolic syndrome patients!

Researchers at the University of Eastern Finland have looked at people suffering from metabolic syndrome, and have found that these wicked, wicked patients are mostly not adhering to the dietary recommendations which have been given to them in the hope that they won't progress to Type 2 diabetes and cardiovascular disease.

Well, I'd be willing enough to join the researchers in condemning these patients, if they have been given an opportunity to prevent serious health problems and are throwing the opportunity away. But the complaints the researchers make about their diets don't seem especially relevant to me.

One complaint is that the great majority of the patients didn't keep their consumption of saturated fat under 10% of total energy consumption. Well, that's a tough target to hit, and the idea that it's important to hit it has been withering lately, owing to a lack of evidence to support it. I used to try to achieve that, but when I abandoned the idea (because it was difficult, and it interfered with more important goals, and it didn't seem to have a sound basis in the evidence), the cholesterol values on my lab report didn't go up. Apparently I can get a normal lipids profile regardless of what kind of fat I eat, so long as I keep exercising regularly and keep carbohydrate intake under control. So if the researchers are obsessing over this, they're worried about the wrong thing.

Speaking of carbohydrates, the researchers don't seem to have anything to say about carbohydrate intake. Since that is the most important dietary issue for people with metabolic syndrome, you'd think it would be worth a mention, wouldn't you? The fact that they don't address the issue at all makes me wonder how seriously I ought to take them.

Another complaint they have is that 65% people in the study were taking in too much salt. I can't get too excited about that one either. Apparently about 20% of people are "salt responders" and will develop high blood pressure if they take in too much salt -- so doctors want everyone to cut salt intake way back, to make sure they're capturing that 20% of the population for whom this matters. I think the salt thing has been overblown -- if you can keep your blood pressure under control without restricting your salt intake, I'm not convinced that you need to condemn yourself to eat bland food for the rest of your life. Anyway, the relevance of this to Type 2 diabetes seems doubtful to me.

Also: most people in the study didn't hit the target of taking in 25 to 35 grams of fiber per day. That's rather a lot, it seems to me; it's hard for me to believe that not hitting that aggressive target is going to have a huge impact on potential progression to Type 2 diabetes.

In short, the researchers seem to be very focused on issues that have a questionable relevance to heart disease and diabetes, while they ignore the issue (carbohydrate intake) that is clearly relevant.

I guess my main reaction to this study is: so what?


"Because of Futility"

Thursday, January 2, 2014


Periodontal care & glycemic control

Periodontitis (inflammation of the gums) has long been regarded as a problem for people with Type 2 diabetes, because inflammation of any kind tends to suppress insulin sensitivity, and periodontitis is a chronic condition which keeps people in a constant state of inflammation. Although this might not "cause" diabetes exactly, it certainly makes it harder to keep blood sugar under control; it has long been assumed that proper dental treatment would improve glycemic control in diabetes patients who have periodontitis, by making them more sensitive to whatever amount of insulin they are able to produce. Some small studies appeared to show that dental treatment can indeed improve glycemic control.

And now a somewhat larger study involving 514 participants, published in JAMA, is throwing cold water on all this. The study compared glycemic control in diabetes patients who received treatment for their periodontitis ("scaling and root planing plus chlorhexidine oral rinse") versus patients who didn't.

The study continued for 6 months and was then abandoned "because of futility". The treated patients showed some improvement in their periodontitis, but in terms of glycemic control (as judged by the hemoglobin A1c test) they showed no improvement over the untreated patients.

The study's conclusion: "Nonsurgical periodontal therapy did not improve glycemic control in patients with type 2 diabetes and moderate to advanced chronic periodontitis. These findings do not support the use of nonsurgical periodontal treatment in patients with diabetes for the purpose of lowering levels of HbA1c."

As a dental patient with a long and frustrating history of periodontitis, I have some thoughts on this.

First, speaking as a veteran of "root planing", I am surprised to find that procedure described as "nonsurgical". If that's not surgical, what is? Root planing is not exactly aroma-therapy, you know.

Second, periodontitis is a difficult condition to get under control, and it takes time to make progress on it. I'm not surprised that six months was not enough to bring about a reduction in A1c results.

Third, although the treated patients are described as showing improvement in their periodontitis, the quantitative measures of improvement as reported sound awfully modest to me. For the gum "pockets" to be less deep than before is welcome, of course, but when the depth is only reduced by about a quarter of a millimeter, that sounds to me like a patient who is only starting to make progress. If you haven't made more progress than that, then the inflammation is still there, and we shouldn't expect an improvement in glycemic control at this stage.

Obviously, periodontal treatment isn't going to work as a short-term solution to the problem of elevated blood sugar. But that doesn't mean periodontal treatment won't benefit a diabetes patient in the long run, once the periodontitis has been more successfully treated.

I think diabetes patients should be aware of all the factors that work against good glycemic control -- even those factors which we can't address in the short term. With any luck, we'll be alive and dealing with these issues in the long term.


Apparently, it really is 2014!

Wednesday, January 1, 2014

I don't know how to explain this rationally (it's not rational, which may be the root of my difficulty), but I never could quite accept "2013" as a valid year. It sounds fictional -- as if I had only ever seen it in the pages of a science fiction novel. Every time I wrote it down over the past 12 months, I squinted at it, wondering if it wasn't a mistake. But 2014 somehow seems like a real date. I can write a check with a 2014 date at the top without thinking that maybe the bank will refuse to cash it on the grounds that there is no such year. So, that alone gives me a reason to feel good about the new year!


Holiday prescription: go take a walk

If you've had a little more to drink on New Year's Eve than you would normally consider sensible and healthy, the idea of exercising on New Year's Day might seem a little too challenging. But it can be done!

Maybe the reason some people's exercise programs fall apart is that they think they have to be operating at 100% capacity to exercise at all. If you're not absolutely bursting with energy, exercise is not for you today! Might as well stay home, and rest up for the day when you start to feel more frisky. (Unfortunately, for people who don't exercise regularly, that day never comes. Resting up doesn't get you ready to exercise again; it gets you ready to do some more resting.)

Exercise is never more useful to you than when you are trying to help your body recover from the indulgences of the holidays. The catch is to choose a kind of exercise which is serious enough to count as a real workout, but not so intense that you simply can't face doing it today.

My prescription for a holiday (or post-holiday) workout is a good long walk, preferably in a very pretty place. My chosen place today was the Bear Valley trail at Point Reyes National Seashore. The trail stretches through 4.2 miles of woods before it reaches the coast.

With all that lush foliage going on for four miles, it's a little startling when you finally reach the rugged California coastline.

But once you get there, you can pose for a dignified portrait, looking like someone who would never indulge in alcohol on New Year's Eve.

Also, you get to see all the other holiday hikers who have made it all the way out to the coast, to prove that they can do it even on New Year's Day.

Also, you get to see all of Mother Nature's other creatures, who don't treat this day any differently than another.

Anyway, that's what works for me on New Year's Day!

Your mileage may vary...


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