Fourth Thursday Update
Thursday, April 24, 2014
Fasting Glucose: 96 mg/dl.
Glucose 1 hour after lunch: 100 mg/dl.
Weight: 196 pounds.
Blood pressure, resting pulse: 129/78 mmHg, 57Exercise: 5.4 mile run.
My fasting test was a little higher this morning than I thought it should be, so I did an especially tough (that is, hilly) run, and then had an especially low-carb lunch afterward. Result: glucose after lunch was scarcely higher than the fasting result.
These little adjustments do make a difference. The key to managing Type 2 is to make sure that, whenever you get a test result you don't like, you then change something to get a result you like better the next time. If your meter's less welcome results don't lead you to change anything, then your meter is just an electronic medium for depressing you. And that's what cable news is supposed to be for.
Diabetes: because it's there!
When you want to study the cause of Type 2 diabetes, there is clearly only one place you can go:
Yes, that's right: Mt. Everest.
Perhaps you're wondering what the world's tallest mountain could possibly have to do with diabetes. Have mountaineers been becoming diabetic as a result of their daring ascents? Well, not exactly. But it appears that some diabetes-relevant physiological changes occur in people making extreme high-altitude climbs, and there is something to be learned from it.
Earlier research has indicated that hypoxia (that is, reduced oxygen concentration in the blood, typically caused by travel to high altitudes) promotes insulin resistance. Some studies have seen this effect when test subjects went on a "simulated mountain climb" in a hypobaric chamber which reduced air pressure to the levels typical of a Himalayan expedition. But a new research project studied the impact of a real-life climb on Mount Everest, with climbers who were used to living at sea level. Some of the participants in the study only went up as high as the Everest "base camp", while others went all the way up to the 8848-meter summit (29,029 feet), and then returned to base camp for the last two weeks of the study period. Actually, "base camp" is a somewhat misleading term, considering that its altitude is 5300 meters (17,388 feet), which places it above all American mountains except for a couple of peaks in Alaska. Certainly everyone involved was experiencing hypoxia, whether they made it to the summit or not. There is not a lot of air up there, folks!
And what impact did this hypoxia have on the blood glucose of the climbers? None, really; glucose levels held pretty steady, without only very minor variations:
So is this evidence against the idea that hypoxia promotes insulin resistance? Not at all. Blood testing of the climbers showed clear evidence of insulin resistance. If their blood sugar didn't rise, it was because they were producing a lot of extra insulin to compensate for the resistance. Here's another chart, showing insulin levels in the climbers:
As the climbers reached very high altitudes, they lost much of their insulin sensitivity, and they had to produce a lot of extra insulin to compensate for it.
Why did the hypoxia experienced by the climbers result in insulin resistance? The researchers also found evidence of "oxidative stress" and inflammation caused by the reduction in blood oxygen; these things are known to promote insulin resistance.
But how can any of this be pertinent to Type 2 diabetes as most of us experience it (that is, at comparatively low altitudes)? Well, climbing Mt. Everest is not the only way to experience hypoxia. The researchers note: "Such findings are of possible importance to the pathogenesis of disease at sea level: there is renewed interest in the role of chronic hypoxia as a potential causative factor in the pathogenesis of insulin resistance. Indeed, chronic intermittent hypoxia (CIH) due to obstructive sleep apnea (OSA) may contribute to the development and progression of insulin resistance and diabetes. OSA appears to be a predictor of abnormal glucose metabolism in chronically sleep deprived obese adults."
OSA is a disorder in which you stop breathing when you fall deeply asleep, thus choking you and causing you to wake up desperately gasping for breath several times a night. OSA certainly played a role in the development of my own diabetes. I should point out here that there is good evidence that sleep deprivation, from any cause, can also promote insulin resistance. But the problem appears to be most serious when the sleep disruption is caused by a breathing disruption (and hence hypoxia).
Unsurprisingly, the researchers say they are especially interested in studying the biochemistry involved in hypoxia-induced insulin resistance to find out if they can use that information to produce new diabetes drugs. But maybe that's something you have to say if you want to get funding for your research.
I predict there will not be a great deal more hypoxia research that involves sending the test subjects up the dizzying slopes of Mt. Everest; it sounds like a pretty expensive and dangerous way to study blood chemistry. But if you were wondering whether or not oxygen is something you really need, I guess the answer is yes.
Feed a cold, starve a monkey
In the past, when I read about animal lifespans being prolonged by means of calorie restriction, I usually found (to my disappointment) that the animals in the study were not very closely related to humankind. They were typically worms or flies -- or even yeast, for heaven's sake (and the last time I checked, yeast were fungi rather than animals).
I guess I can understand why somebody wanting to perform experiments related to lifespan extension would want to focus on organisms that don't live very long to begin with. I mean, when you're extending the lifespan of yeast, for crying out loud, you can probably get your study pretty well wrapped up by lunchtime. But, convenient as they might be from a practical standpoint, experiments on worms, flies, and yeast might not tell us very much about human longevity. You're probably going to want to look at animals that are a little more human-like and live a comparatively long time.
But now scientists have been doing the same thing with our slightly closer cousins. A new study shows that monkeys, too, live longer if you keep them hungry. I don't know how much they enjoy it, but they live longer. And they don't develop the kind of chronic diseases (such as diabetes) that better-fed monkeys do. The lean-and-mean monkeys in the study had to live with a calorie input that was cut by about 30% from whatever was seen as normal. The control monkeys, who were allowed to eat as much as they wanted, had almost triple the risk of chronic disease. Staying hungry is apparently healthy, because it causes the body to go into a different kind of energy-management mode, with wide-ranging positive effects on health. Notice, in the picture below, that the underfed monkey on the left is aging a bit more gracefully than the indulged monkey on the right.
The study was not actually aimed at finding a healthful diet regime for humans; the point was to gather data which might lead to a better understanding of the underlying mechanisms which cause caloric restriction to promote health.
The benefits of caloric restriction are linked to regulation of energy, according to the study authors: "It affects how fuel is utilized. Caloric restriction essentially causes a reprogramming of the metabolism. In all species where it has been shown to delay aging and the diseases of aging, it affects the regulation of energy and the ability of cells and the organism to respond to changes in the environment as they age."
My own guess is that caloric restriction places an animal in the conditions which it typically would encounter in nature (that is, a constant struggle to get enough to eat); as those happen to be the conditions which the animal is biologically adapted for, it has a longer and healthier life when it is kept hungry. An animal won't live that way if it has a choice, but if it is forced to live that way it stays healthier longer.
Mighty few human beings will voluntarily live on the kind of restricted rations which made monkeys live longer in this study, but there is some evidence that it works for humans, too, when caloric restrictions are forced on them. Apparently the British civilian population experienced an improvement in health during the prolonged rationing of food during the second world war. The fly in the ointment is that the British people who lived through that don't seem to have enjoyed it one bit, and they got out of that mode of living as soon as they could. So, it's not clear if we can learn anything of practical use from the data collected in the hungry-monkey study.
Still, though: if someone can figure out exactly what the biochemical mechanism is that makes a hungry monkey a healthy monkey, maybe they can develop a hungry-monkey pill to give to us, so that we can gain the health benefits of near-starvation without the misery. I don't know if such a thing is possible, but I know it would be a big seller if it could be produced.
Third Thursday Update
Thursday, April 17, 2014
Fasting Glucose: 95 mg/dl.
Glucose 1 hour after lunch: 135 mg/dl.
Weight: 195 pounds.
Blood pressure, resting pulse: 126/76 mmHg, 59 bpm.
Exercise: 5.4 mile run.
My Run in Pictures!
It was a beautiful day and I went for a long hilly run at lunchtime. I decided to carry a camera with me and document the experience, for the benefit of any of you who have been thinking about going outside for a run but aren't sure what it would be like.
It turns out to be pretty hard to hold a camera while running without occasionally pressing a button on the thing without realizing you've done it. I somehow got the camera into a mode where it snapped photos every few seconds whether I was trying to take a picture or not. The result was a great many pictures of the ground, often with my hairy legs in the frame. This one was particularly good, as it reveals that my legs are so hairy, the hair is visible in the shadow I cast.
But I'm just going to show pictures of the scenery from here on.
My departure point is always the flagpole outside the building I work in. That's where I would meet up with running buddies, when I still had people to run with. My running buddies are sidelined with injuries currently, but my habit of starting there is pretty firmly established. Exercise is all about establishing habits and sticking to them.
I took the perimeter road out to the back gate of the company property. You see that ridgeline in the distance? I'm shortly going to climbing up to it, and running along it right to left. It's pretty intimidating if you think about it, so I try not to think about it.
California is not a very green place most of the year, so I try to enjoy the greenness when it's here.
Wild grass in California is light brown by early summer. Spring is the only time for it.
A nice aspect of running around here is that you always see a lot of other people out doing the same thing. Sadly, they're always faster than you.
She was so fast that she was breaking the sound barrier, as clearly evidenced by what the blast wave is doing to her hair.
As I start the long climb, I try to focus less on the ever-increasing steepness of the road...
...and focus more on the explosive greenness of the new leaves.
But then I get to the dreaded left-turn that leads up the really steep climb to the ridgeline.
Here again, I try to focus on the leaves, not the slope.
But it's hard to forget the steepness, not only from what your poor lungs are telling you, but from the sound of cars zooming downhill at you at out-of-control speeds.
During a long climb like this, you have to find something to distract you from how hard you're working. Plants bursting into bloom are always helpful.
Part of the reason I'm willing to climb all the way up to the top of this geological monstrosity of a hill is that I like the views that open up when I get up to the top.
There's always a feeling of accomplishment when I look down into the valley...
...and spot the red roof of the building I work in. it gives me a sense of accomplishment to realize I ran all the way up here from that distant building.
Up here I'm reminded that some people make a lot more money than I do.
I'm also reminded that some people work a lot harder for their money than I do. How long would I survive as a roofer, I wonder? Probably not very long.
And then comes the reward: a long downhill.
On the way down the hill, I like to observe the constantly changing little ecosystems as different kinds of plants go by.
They may be man-made ecosystems, but I enjoy the constant variety anyway.
Minute by minute, the atmosphere keeps changing. A lot of people complain that running is boring, but allowing yourself to be super-sensitive to the changes in your environment helps a lot. It helps me, anyway.
And then I'm inside the front gate of the company property!
And picking up whatever pollen they have in here that I didn't already coat myself with out there!
And soon I'm back at my building, for a quick shower and a return to the office to exchange e-mail with people in Scotland and China.
For me, my lunchtime run is not "a workout" in the sense of being a dull, tiring chore that has to be ticked off a checklist. It's more of a break; a little adventure. If you can learn to view your daily exercise that way, you'll have a lot less trouble doing it.
Resenting the Young
I recently read an op-ed piece by a guy who said that he was making his peace with the reality of growing older. He'd had to persuade himself that there was nothing wrong with aging. After all, it was nothing to be ashamed of. It was nothing to get depressed about. He was determined not to let himself become upset over his upcoming birthday.
Well, I was with him up to that point... but then he revealed that this upcoming birthday, which he was bravely refusing to become hysterical about, would be his 25th. At that point I wanted to smack him pretty hard.
Then I paused to analyze my reaction. One of the less admirable effects of growing older is that, if we don't watch ourselves, we can become absurdly resentful of young people simply for being young. How dare they? Nutty as it sounds to say it explicitly, a lot of us are always primed to feel as if it's somehow unfair that we're getting old while so many other people are young.
It's true enough to say that young people have something we don't have (youth), but there was a time when we had it, too, even though we don't have it now, and there will come a time when they don't have it either! So where does the unfairness come into this? It's not as if youth was something we never had a chance to experience even briefly, while the people who are young today get to luxuriate in it forever.
Probably some of the resentment we feel arises because it looks to us as if young people are enjoying their youth more than we enjoyed ours. This could easily be a false impression, though. Maybe they're dealing with problems we know nothing about, and they're not really enjoying themselves quite so much as we imagine. Also, it could be that our memory of our own youth is highly selective, and we mostly recall the problems we were dealing with at the time. The end result is that we think youth is a hundred times better for the people who have it now than it ever was for us. Youth was all about frustration and insecurity, when we were going through it; for them, it is fun, fun, fun! Oh, the unfairness of it all!
We need to give ourselves a bit of a reality check on all this. If we are no longer in possession of youth, it isn't because those who have it now stole it from us. And, although every generation of old people claims that "these kids today have it easy", changes in society and the economy, at least in America, have probably made life harder for the current crop of young people, not easier. (Higher education has become something close to a criminal racket, jacking up costs while the benefits erode, and dumping graduates into a life of heavy debt and unemployment. It wasn't always that way.) If young people are managing to be happy even while their society is systematically screwing them over, it's probably because they have developed resources of contentment within themselves. Unless it's the drugs. Anyway, the notion that young people have it easy today seems pretty doubtful to me. They have better phones, but that's about it.
It's also easy to feel that it's somehow unfair for us to be dealing with problems that young people don't have to deal with. Especially health problems. These young people don't have to go in for half the degrading medical screening tests we must endure, and they aren't saddled with managing chronic diseases. They don't have stiff muscles and sore joints. Their eyesight is fine, and so if their hearing, and if they engage in some unfamiliar sport or activity they're not going to be crippled by it the next day, or at least not as much as we would be. But once again, their advantage is temporary; we once had that advantage ourselves, and they will one day lose it. The only reason youth looks like an advantage at all is that the entire population doesn't experience it simultaneously.
Disregarding the accident of timing, and examining a human life as a totality, the youth/age thing actually works out pretty fairly: everybody gets to be young, and everyone who doesn't die young gets to be old. So, if you're old, try not to think that young people are getting some kind of special favor just because they are in a state of youth. What they have that you don't have (youth) is something they only get to possess temporarily, exactly as you did. What you have that they don't have (comparative longevity) is something they might not be granted. For all you know, you might be the one who has an unfair advantage over them.
Thursday, April 10, 2014
Fasting Glucose: 98 mg/dl.
Glucose 1 hour after lunch: 121 mg/dl.
Weight: 196 pounds.
Blood pressure, resting pulse: 121/75 mmHg, 55 bpm.
Exercise: 5.4 mile run.
When a winning attitude makes you a loser
Some runners keep running as they get older, and others give it up. In some cases, people give up running because they develop knee problems or some other physical limitation which forces them to call it quits. But, contrary to popular impression, runners are not more prone to knee problems than other people, and plenty of runners are not stopped by a running injury -- they just stop. They decide to stop. But why do some runners make that choice, and others not?
A recent article in a running magazine discussed this issue, in light of research on the subject. It seems that runners who quit differ from runners who persevere over the long haul in one important regard: the quitters are the ones who are preoccupied with competitive goals. They want to see themselves getting faster and faster with each race they participate in. When they reach the point in life when the trend is unavoidably to get slower instead of faster, they ask themselves, "What's the point?".
Runners who have another motivation besides winning races -- that is, runners who find a way to value the activity of running for its own sake -- are the ones who keep at it. Slowing down over time doesn't make you ask yourself "What's the point?", if you never told yourself that running faster than somebody else was the point in the first place. The people who keep running late in life tend to be the people who are running because they get something out of it that has nothing to do with competition. And in terms of health, those are the runners who win out over the long term.
Most people who take up running -- or exercise in general -- as a way of getting their Type 2 diabetes under control are not likely to have unreasonable expectations of their own athletic performance. They don't expect to win the Boston Marathon, and in fact they probably don't expect to qualify to enter the Boston Marathon (non-runners tend to assume that anyone who wants to participate in that famous race can do so; the reality is that you have to prove yourself worthy by running another marathon faster than most runners are ever going to do it). If you're exercising to get your blood sugar under control, you're exercising for a higher purpose than winning races -- so you're more likely to keep at it.
Question of the day: why would researchers want to shove a fiber-optic cable into a mouse, and light it up inside?
Well, some people really don't like mice. But there's more to the story. The mice in this study had implants made of hydrogel (the same stuff soft contact lenses are made of), and the fiber optic cable lit up the gel with a particular wavelength of laser light to which certain molecules are sensitive. In this particular case, the gel was implanted with cells which react to that wavelength of light by producing a cascade of reactions which were expected to reduce blood sugar levels. When diabetic mice were rigged up in this way, lighting them up blue inside actually did reduce their blood sugar.
Obviously this technology is still a mighty long way from giving us any useful medical therapies for diabetes or anything else. But researchers are hoping, someday, to product medical implant devices which can stimulate the body to produce its own medications, so to speak, when they are needed. Sort of like a pacemaker, but not for the heart.
Of course, even today, it's already possible to stimulate reactions within the body which reduce blood sugar -- and you don't have to put an implant up your butt and fire lasers at it, either. But you do have to get out of the chair and move your body around a bit, so a lot of people still tend to regard it as an extreme measure.
It did sort of seem like an extreme measure to me as I was climbing the steepest hill on my running route today. But I still wasn't tempted to trade places with that mouse.
Science teachers and science popularizers tend to be haunted by the feeling that most people think science is uninteresting or unimportant, and that their audience has to be manipulated and tricked into taking it seriously. Because of this perceived need to make science seem important to people, the popularizers are always tempted to distort scientific ideas in the interest of selling them more effectively. I don't like this sort of thing, to be frank. To me, science is inherently interesting when it's presented for its own sake. Paradoxically, it becomes much less interesting when somebody is saying "here's a practical reason why you should care about this!", because the reason offered is usually unconvincing. And even if the reason offered seems convincing enough at face value, it's usually invalid, and sooner or later people find that out.
For years, the reason we were offered for why we should care about DNA (and the genes encoded in it) is that our individual DNA was the blueprint from which nature constructed us. Essentially we were told that we were our DNA, and our DNA was us. The genes encoded in our DNA determined everything about us. Our DNA was our identity, and also our fate. If we were destined to develop diabetes at age 42, it was written in our DNA. If scientists ever figured out how to make "clones" (two or more animals having the same DNA), they would be identical in every respect.
But then scientists did figure out how to make clones, and it turned out that animal clones sometimes had visible differences (color differences, for example). How could any such visible differences arise, if there were no genetic differences? Because the "blueprint" metaphor is oversimplified and misleading. The genetic code is more akin to a recipe -- a recipe which no two cooks follow in exactly the same way.
A recipe looks very specific when you see it printed in a cookbook, but in practice it will probably leave a lot of room for variations. Many recipes suggest possible substitutions (if you haven't got dried cranberries, raisins will do -- that sort of thing). And even if the recipe doesn't make such suggestions, cooks make substitutions of their own, for various reasons. "I'm not going to drive back to the store just for the nutmeg I forgot to buy. And anyway, I don't really like nutmeg. I'll just use a little cinnamon instead".
Even if every cook adhered strictly to the ingredients list, however, there would still be differences in the ingredients themselves (differences in the ripeness of fruits or vegetables, for example), and differences in how the ingredients were prepared. Can you and I really follow the same casserole recipe and end up with identical casseroles? Maybe your idea of "finely chopped" onions is more finely chopped than mine, and maybe your idea of "sauté until onions begin to brown" is browner than mine. Maybe your idea of "stir until it thickens" is thicker than mine. Maybe 45 minutes in the oven is different for my oven than it is for yours, especially if you live up in the mountains and I live on the coast (at high altitudes, water has a lower boiling point and cooking takes longer for that reason). Maybe the water from my well tastes different than the water from your municipal water supply. The recipe we're both following describes a process which we will both try to carry out in the same way, but it's not likely that our results will be so similar in taste and appearance that nobody could detect any difference between them.
Genes guide the development of a human body in the same flexible way that a recipe guides the development of a casserole. Your DNA determines which genes you have, but it can't entirely control gene "expression" -- how and when those genes are activated and deactivated. A human body exists within an environment, and it is affected by influences outside itself -- influences which turn genes on and off. This is especially true of a fetus in the womb. At that stage, two human bodies (mother and child) are engaging in a kind of chemical dialog which influences gene expression. That is why animal clones can differ in color -- they may have the same color-related genes, but those genes were not necessarily activated in the same way at the same stage of fetal development.
This whole complicated business of genes being switched on and off by an organism's interactions with its environment (the environment of the womb, initially, but the process continues after birth) is called epigenetics, and it is much more complicated (and difficult to study) than genetics itself. The Human Genome Project only gave us the ingredients list for the human recipe; how those ingredients end up being prepared is another matter entirely, and DNA is not really in charge of it.
Furthermore, neither genetics nor epigenetics control every aspect of life and health. Genes define our proteins, which of course is important, but proteins aren't everything (it's not as if we are made of protein and nothing else!). Also important: the "metabolites" -- compounds that are products of metabolism. (Metabolism is, roughly speaking, the set of chemical processes by which the body takes in food and water and air and transforms them into whatever functional molecules it needs). Understanding a disease (and hopefully treating it) involves understanding not only the genes involved, but the metabolites involved. The type and quantities of metabolites in the blood can change dramatically in the presence of disease, and although it's often hard to tell whether such changes are a cause or an effect of the illness, researchers cannot claim to have a good understanding of a disease if these changes in metabolites are not accounted for.
There are starting to be rumblings within the scientific community to the effect that researchers have become far too obsessed with genetics as the explanation (and potential cure) for all ills, and are neglecting other aspects of the problem. The DNA-is-everything narrative has been promoted to the public for so long that we have all grown up with it and become comfortable with it, and even scientists unconsciously assume it is valid.
Dr. Laura Reed, a geneticist at the University of Alabama geneticist, and lead author of a recent study on genetics and disease in fruit flies, is warning that researchers are relying too much on gene-centered methods of predicting and treating disease. "To augment the value of genetic data, the scientific community needs to add additional information from things like metabolomics – the analysis of metabolites within an organism. The Human Genome Project has been sold as something that is going to revolutionize medicine – that soon we will get our genomes sequenced, and we will be able to figure out exactly what diseases we are at risk for and, maybe, the best way to treat them. While it's true there are important innovations to come from that kind of information, it is much more limited than some may have hoped."
The fruit-fly study found that changes in diet had a comparatively small impact on gene expression, and a much larger (and apparently more medically significant) impact on metabolites. Dr. Reed thinks there is more to be gained, from a therapeutic standpoint, from focusing on the metabolites. Medical screening tests might more profitably look at metabolites than genes. "We can't expect to find a gene or just a few genes that explain any phenotype, including disease... It's unlikely that additional "miracle drugs" await discovery... The overall point of the paper is not a very popular idea, because it basically means things are much more complicated than we want them to be. But, that's reality. This does not mean that we can't incrementally improve things by understanding the genes that are involved, but, perhaps, a more expedient approach would be analyzing higher level traits, like metabolites, that might summarize what's occurring in the genome in ways more useful for diagnostic or treatment purposes."
So, there you are. Life is complicated. Health is complicated. Disease is complicated. DNA isn't everything.
...but sometimes change is necessary, and I need to make a change in my approach to blogging.
When I started this as a daily blog six years ago, I did so partly out of curiosity: could I actually write a daily blog, and think of something new to say in it each day? And if so, how long could I keep such a thing going?
The answers to those two questions seem to be "yes" and "for about six years".
You might think that the chore of writing a daily blog would become less burdensome for me over time, as the familiarity of the task made one me more skilled and efficient at it. Maybe that would be true, if my blog were about any and every subject -- whatever was in the news, whatever I'd heard or read or experienced lately. But when your blog is about a specific subject (even a complicated one, such as Type 2 diabetes), it becomes increasingly difficult over time to find anything new or interesting to say about that subject.
Most of my blogs are triggered by the latest research findings on diabetes, and let's face it: most research on diabetes these days can be summarized in exactly the same way every time: "A team of researchers at the University of [obscure Scandinavian town], in collaboration with a team at [prestigious university in the U.S. or U.K.] has identified a previously-overlooked [gene / protein / hormone / metabolite] which is [more abundant / less abundant] in people with diabetes than it is in people without diabetes. Animal experiments showed that [enhancing / suppressing] this molecule [triggered / alleviated] diabetes in obese rats. Could this molecule be a promising drug target? Researchers say more study is needed, please send them lots and lots of money right now." I feel as if I have been writing some variation on that summary at least once a week for the past year.
As for the ordinary practical details of daily diabetes management, I think I've discussed them so many times that it makes me feel a little silly to discuss them again, trying to present them differently. I try to come up with something original to say, and often become tense and frustrated and blocked, and stay up late at night trying to produce some kind of blog entry I can post without feeling ashamed of it. I'm not getting enough sleep as a result, and I know that's not good for me.
Having come this far with my web site, I don't want to give up blogging entirely, but I have to be honest: I can't face doing it on a daily basis any more. Lately I've been skipping most Fridays, and even that hasn't been enough of a relief.
What I'm going to try instead is to do a weekly blog that's updated on Thursday night. I'm hoping that whatever I write in that Thursday post will be longer, more detailed, and more thoughtfully chosen than the sort of thing I've been posting in daily blogs. We'll see how well I pull that off. It could be that being relieved of the burden of daily blogging will give me a renewal of enthusiasm for writing the weekly installments.
Anyway, it's a change I really have to make, and I'm making it as of this week. Let's see what I come up with between now and Thursday night!
Picking a Winner
Thursday, April 3, 2014
Fasting Glucose: 89 mg/dl.
Glucose 1 hour after lunch: 101 mg/dl.
Weight: 197 pounds.
Blood pressure, resting pulse: 115/72 mmHg, 56 bpm.
Exercise: 5.4 mile run.
Finding the right foods
I often describe Type 2 diabetes as a kind of hobby. At first it seems like the kind of boring, awful hobby that no one in his right mind would take up. But once you've had it foisted on you, you might as well act like it was your idea in the first place and its fascination is inexhaustible.
Within the hobby of diabetes management are sub-hobbies, and perhaps the most rewarding of these is the endless quest to find a really satisfying food that doesn't spike your blood sugar. Ideally, it would also meet certain other criteria, such as being cheap, or readily available, or easy to make at home. But just finding a delicious food that doesn't drive your blood sugar through the roof is enough of a challenge right there.
And I don't mean a single ingredient in a meal, I mean something that qualifies as a meal pretty much by itself. A hamburger patty isn't going to drive your blood sugar through the roof, but on the other hand, you're probably not going to eat a hamburger patty with no bun and no starchy accompaniments (such as fries), so a hamburger isn't the kind of thing I'm talking about. I'm talking about a food that is satisfying and complete on its own terms, and includes a balance of protein, fat, and carbs, and still doesn't spike your blood sugar. Finding a food like that is not necessarily easy, as you may have noticed.
Part of the reason it's not easy is that it's hard to be sure, simply from what you have read about a food or what nutritional data you've been able to gather on it, what impact it is going to have on your blood sugar. And by "your blood sugar", I mean literally your blood sugar -- as your personal response to a given food might differ from someone else's. Experimentation is the only way you're really going to figure out what sort of meals your system can deal with, and what sort of meals it can't.
Of course, to some degree, you can figure out how a dish is likely to affect you. If it involves a mound of steamed white rice the size of a throw pillow, it's going to spike you; you already know that much without having to conduct any experiments. Sometimes, though, a dish which seems pretty iffy can work out. And if it turns out that you actually love that dish, that's a victory.
One very satisfying dish that I've found works for me is a Mexican stew known as pozole (or, north of the border, as posole). It's peppery red soup with pork and hominy, and it's long been a favorite of mine.
Because of the hominy in it (a starchy ingredient for sure), I would have expected pozole to have a bad effect on my blood sugar, but it never seems to.
Judging form the nutritional data I can get hold of, hominy isn't exactly a low-carb food...
...but, on the other hand, it isn't nearly as bad as rice:
Presumably the reason pozole doesn't spike me is that the hominy isn't as carbohydrate-dense as other grain foods, and also that the total amount of hominy in a bowl of pozole is not huge; there's a lot of broth and meat in it as well, and sometimes non-starchy vegetables as well. Attempting a nutritional analysis of pozole is difficult, because there are many ways to make it, but supposedly the total carb content of a bowl of it is something like the carb content of one slice of whole-grain bread.
The main difficulty I have with Pozole is finding it. Even Mexican restaurants don't always have it (some of them just make it on Sunday). And it's the sort of dish that, if you want to make it at home properly, you'd better be willing to devote most of your day to it. Some recipes promise that they will enable you to make pozole without a big time investment, but those are the kind of recipes that replace every ingredient with something else, and result in a dish which only looks like pozole. So, I'm always on the lookout for pozole made the right way -- that is, by somebody else.
So, if I go to a Mexican restaurant (not always the ideal place for a diabetes patient to be), I always check to see if they have pozole today. And at the fancy grocery near my house, which has a big deli section with house-made soups, I always check to see if they have pozole. Which, yesterday, they did, so I bought a pint of it in a plastic container, brought it to work with me today, and heated it in the microwave for lunch. Delicious, satisfying -- and my post-prandial test an hour later was a mere 101. Of course, it helped that I had just done a tough, hilly run. But pozole never seems to spike me very much. At least, it doesn't so long as I don't accompany it with starchy extras, which is why it's a shame that Mexican restaurants (where I'm likeliest to find pozole) always place high-carb temptation on the table in front of me, no matter what I order.
My point here is certainly not that you should start eating pozole. For all I know, it has a bigger impact on your blood sugar than it has on mine. My point is that you should experiment (by means of post-prandial testing) on various foods, to discover the ones which don't spike you, but don't leave you feeling cheated, either. These foods aren't easy to find, but it's worth taking the trouble.
Does anything not cause diabetes?
Wednesday, April 2, 2014
Fasting Glucose: 89 mg/dl.
Glucose 1 hour after dinner: 112 mg/dl.
Weight: 197 pounds.
Blood pressure, resting pulse: 121/69 mmHg, 59 bpm.
Exercise: 5.2 mile run.
As molecular analysis tools become more and more sophisticated, researchers are finding it easier to compare blood samples of people with and without a disease, and search for chemical differences between them. What it amounts to is taking one chemical at a time and asking: do people with disease X have the same amount of this chemical as people without the disease? If not -- if they have a lot more of it, or a lot less of it -- than maybe the disease is caused by having too much or too little of this stuff. Knowing that, we may be able to develop a drug to treat the disease.
However, identifying a difference in the abundance of a blood component between people with and without a disease does not mean you have identified the cause of the disease. If people with diabetes have more of a given protein than people without diabetes, is that because having too much of that protein causes diabetes? Or is it because having diabetes (or being the sort of person who's likelier to have diabetes) causes you to produce more of that protein?
So, a second stage in the investigation is required, in which you find a way to cause a laboratory animal to have more or less than the normal amount of the suspect compound, and then wait to see if they develop the disease. This kind of experiment is typically done by means of some kind of genetic modification of mice which causes the mice to produce more than usual, or less than usual, of the compound under suspicion. The researchers then watch to see how this modification affects the risk of the disease being studied.
University of Toronto researchers were studying more than 300 compounds in blood, and looking for changes in the abundance of blood compounds in people with Type 2 diabetes and in pregnant women with gestational diabetes. They were particularly looking at "changed metabolites" -- compounds altered by the body's processing of them. They found that one particular metabolite, an altered fat compound known as CMPF, was more abundant in diabetic than non-diabetic people. They also found that CMPF is absorbed by the insulin-producing beta cells in the pancreas, and once that happens, insulin production is degraded.
They tested the effects of CMPF in mice by modifying the mice genetically to block the action of the transporter molecule which draws CMPF into beta cells. Doing this prevented the harmful effects of CMPF on insulin production by the beta cells. So, apparently, gestational diabetes and Type 2 diabetes can be triggered by CMPF being absorbed into beta cells -- and could be prevented by blocking such absorption. Make a pill to do that and you get rich!
If any drug treatments do come out of this, don't hold your breath waiting to see them tried on pregnant women. The danger of birth defects makes researchers very cautious (at least since the thalidomide fiasco) about testing drugs on expectant mothers. Type 2 patients would surely be the first to get a chance to try out such treatments.
However, it's worth remembering that this kind of research story turns up all the time. Some hormone, protein, or other molecule turns out to be unusually abundant (or scarce) in people with diabetes, and the pharmaceutical companies look for ways to suppress (or boost) the body's production of that molecule. But it's a long journey from there to a safe and effective treatment. And why are there so damned many kinds of molecules that are unusually abundant (or scarce) in people with diabetes? There seems to be no end of ways for something to go wrong chemically in a human body and produce diabetes as a result.
Does everything cause diabetes, for crying out loud?
The Worm Turns
Tuesday, April 1, 2014
Fasting Glucose: 88 mg/dl.
Glucose 1 hour after lunch: 112 mg/dl.
Weight: 196 pounds.
Blood pressure, resting pulse: 107/69 mmHg, 54 bpm.
Exercise: Gym workout in the evening (aerobics).
Another day of heavy rain, but with no breaks this time. I just couldn't make myself go out for a run in it. I went to the gym after work instead (very much a second choice, but better than nothing) and sweated on the stair-climber for a while. Tomorrow's supposed to be clear, though, so I hope I can look forward to a run in the sunshine.
Could a sea-worm offer a diabetes cure?
Diabetes researchers are cautiously excited by Australian reports that the sting of a rare sea-worm found in the Great Barrier Reef might have the surprising effect of triggering a remission of Type 2 diabetes.
The creature in question is a "polychaete", or segmented worm. Like many such worms, this particular polychaete (Spirobranchus fatuus) has an elaborate, frond-like apparatus for snagging edible debris from seawater. Unlike most such worms, the apparatus is extremely colorful, and is capable of inflicting a sting very much like that of a jellyfish or fire-coral. Australian scuba-divers exploring the Great Barrier Reef have learned to avoid touching them.
Scuba-divers from more distant locales have not learned to avoid touching them, which is how a British tourist with Type 2 diabetes came to be stung by one... and then returned home to England to enjoy an unexplained reduction in his blood glucose (his hemoglobin A1c result dropped from 8.4 to 6.1, and his doctor eventually took him off the oral diabetes drugs he had been taking). Perhaps his remarkable case would never have come to light, had he not been the older brother of a professor of medicine at Leeds University, who decided to take a closer look at the matter.
Research is extremely preliminary and small-scale at this point, but a tiny study (involving only 11 diabetes patients) found that deliberate exposure to the sting of Spirobranchus fatuus brought about a measurable reduction in HbA1c results in most of the patients, and a dramatic reduction (the researchers are hesitant to use the word "cure") in 4 of the 11 test subjects.
The reason why is not at all clear. Little is known about the toxin employed by this colorful sea-worm, but like most natural venoms, it is a complex brew, involving many different chemical components. It could be years before we know which ingredient in the mix fights diabetes -- if indeed any of them do. (Some questions have been raised about the reliability of the Australian reports so far.)
Until any of this solidly confirmed, we can only watch and wait -- and hope that we have an answer before Spirobranchus fatuus (which is thought to be endangered owing to a worldwide decline of coral reef habitats) is no longer around to help us get to the bottom of the matter.
You can find more details on this strange story here.
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Reading the Stats
What this is about
I am going to use this space to report on my daily process of staying healthy -- what I'm doing, and what results I'm getting, and how I interpret the connection between the two.
I am not trying to taunt anybody, by reporting better results than they are getting themselves. I'm doing this to provide encouragement, not irritation.
Regardless of what your own health situation is now, you can probably pick up some useful ideas by tracking what I'm doing, and seeing what the results are. I don't mean that you should do whatever I do, or that imitating my behavior will get you the same results I get. We all have to figure out what works for us. Let's just say that I'm giving you an example of some things to try, and they might help. If they don't, try something else!
One word of warning: I sometimes participate in endurance sporting events (including "century" bike rides and the occasional marathon), but please don't assume that you would have to participate in extreme sports to get the kind of results I'm getting. Most of the year I'm not working out nearly that hard, and I still get very good results. For some people, vigorous walking may be enough. (But if it isn't in your case, don't cling to the idea that it ought to be enough -- do whatever it takes to get good results!)