5th Thursday Update
July 30, 2015
Fasting Glucose: 86 mg/dl.
Glucose 1 hour after breakfast: 131 mg/dl.
Weight: 198 pounds.
Blood pressure, resting pulse: 110/68 mmHg, 62 bpm.
Exercise: 8.3-mile hike
I'm taking some time off work this week, so I thought I had enough time to try doing one of my standard trail-running routes in the state park as a hike instead.
You end up doing as much total work either way, and perhaps you inflict just as much trauma on your joints. But it feels easier -- and I guess I've reached the age where "feels easier" becomes a very seductive phrase.
Breakfast of champions!
Breakfast tends to be a problematic meal for people with Type 2 diabetes.
The foods that we associate with the morning meal tend to be high in carbohydrates. There's a reason for that, of course: after the long overnight fast, your body craves carbohydrates. A lot of the sugar your liver stored up yesterday was doled out gradually during the night, to protect you from going into hypoglycemia. Now your body wants to replenish its provisions of stored sugar, and therefore wants you to have toast, and oatmeal, and orange juice, and hashed brown potatoes, and pancakes, and blueberries, and whatever other high-carb foods your kitchen can supply.
People with Type 2 diabetes tend to have trouble processing these sorts of foods without spiking their blood sugar, so a lot of diabetes patients see breakfast as a problematic meal which should perhaps be skipped altogether. Also, plenty of people (with or without diabetes) find that they "don't have time" for breakfast, and omit the morning meal from their daily routine -- probably thinking that skipping a meal is always a healthful practice. This phenomenon seems to be especially common in the United States.
Unfortunately, skipping breakfast has some surprising health disadvantages. It seems to promote obesity and cardiovascular disease, for example (although why that should be true is hard to say).
And now it turns out that skipping breakfast is an especially bad idea for diabetes patients. (This should not surprise us too much: every risk in life, short of the risk of being struck by lightning, has been shown by some study or other to be worse for people with diabetes.)
Researchers at Tel Aviv University have been taking a look at the impact of the American breakfast-free lifestyle on Type 2 diabetes patients, and the impact certainly doesn't appear to be positive. Apparently, fasting until noon "triggers major blood sugar spikes (postprandial hyperglycemia) and impairs the insulin responses of type-2 diabetics throughout the rest of the day".
It gets worse: "We theorized that the omission of breakfast would not be healthy, but it was surprising to see such a high degree of deterioration of glucose metabolism only because the participants did not eat breakfast... The researchers found that participants experienced extraordinary glucose peaks of 268 mg/dl after lunch and 298 mg/dl after dinner on days they skipped breakfast, versus only 192 mg/dl, and 215 mg/dl after eating an identical lunch and dinner on days they ate breakfast. This means that reducing the amount of starch and sugars in lunch and dinner will have no effect on reducing elevated glucose levels if diabetic individuals also skip breakfast."
But why would it be that way? Why would skipping breakfast have a negative impact on glycemic control during the rest of the day? Apparently because the beta cells in the pancreas (the cells which produce our insulin supply) tend to "forget" their proper function if they aren't used in the morning. The daily cycle seemingly "trains" the beta cells to function properly, and disrupting the cycle by skipping breakfast impairs the proper functioning of those cells, so that they don't produce enough insulin following a meal.
Still, it's hard not to be concerned about the glycemic impact of typical breakfast foods -- and also hard to find a quick-and-easy way to adjust breakfast to make it less high-carb.
Looking on the bright side, I have found over the years that my own endocrine system handles carbs better in the morning than it does later in the day. Today, for example, I had a comparatively high-carb breakfast (toast and yogurt) and only went up to 131 mg/dL an hour later, and that is close enough to "normal" (for a healthy non-diabetic person) for all practical purposes. Both the toast and the yogurt were lower-carb versions than average, but still: I can get away with more carbs in my breakfast than I could in my lunch or my dinner.
I wasn't skipping breakfast anyway, so I'm glad to learn that I was already doing the right thing.
4th Thursday Update
July 23, 2015
Fasting Glucose: 96 mg/dl.
Glucose 1 hour after lunch: 115 mg/dl.
Weight: 198 pounds.
Blood pressure, resting pulse: 112/74 mmHg, 64 bpm.
Exercise: 8.1 mile trail-run in the evening
Testing without test strips
Last week I wrote about the high cost of glucose test strips, and the increasing unwillingness of health insurers to cover them. So, it is encouraging to learn that an alternative technology for blood-glucose testing is on the horizon -- a technology which does not use test strips at all.
The new testing method not only doesn't require test strips, it doesn't require you to prick your fingers, either.
The new method involves nothing worse than bouncing an infrared laser off your skin, to see what wavelengths are reflected back. The method is called mid-infrared quantum cascade laser spectroscopy. The glucose level in the blood apparently determines which infrared wavelengths are strongly reflected and which are not. Glucose under the skin has a spectral "signature" which can be recognized, analyzed, quantified, and translated into a blood glucose level.
Not only does the spectral analysis yield a measure of blood glucose concentration, the measured results are accurate enough to meet the industry standard for glucose meters (within 20% of the actual value) and for most measurements are considerably closer than that (within 7% of the actual value).
Okay, so now I want to be able to by a mid-infrared quantum cascade laser spectroscopy glucose-meter, which doesn't need test strips or blood samples. There has to be a catch, though. Probably I will eventually find out that the first commercial model costs more than a pickup truck, so it will take a long time for the elimination of test strips to pay for itself. However, if I wait around for a year or two, Apple will probably introduce a version of it that costs only $1200 and tracks not only my blood glucose but the value of my retirement account and the extramarital affairs of my co-workers. I'll bide my time, and see what develops.
A submerged issue!
It's a peculiar aspect of medical history that effective remedies for a disease are sometimes discovered, then forgotten, then rediscovered. How could that happen? How would medical science "forget" that it had found a useful treatment for something? How could important information about a disease remain hidden for long intervals, like a whale, but rise to the surface occasionally?
It's not quite as strange as it sounds. Doctors know that enthusiastic early reports of an effective remedy very often fail to stand up under subsequent investigation. For that reason, doctors are highly resistant to excitement about alleged cures. If an ecstatic initial report is not followed up by further research confirming it, everyone is quite ready to assume that the claim turned out to be wrong -- and the whole subject is being quietly swept under the rug. Often that's a fair description of what happened. But sometimes the lack of confirmation indicates not that the treatment was shown not to work, but rather that no one believed strongly enough in the treatment to take on the burden of confirming that it did work.
A lack of follow-up is especially likely to happen if there is no known "mechanism of action" for the treatment. If you lack any theoretical grounds for expecting the treatment to work, it's hard to believe that the treatment really will work. Therefore, if research evidence seems to show that a particular drug is effective against a disease it wasn't designed to treat, but there's no clear reason why the drug would have that effect, the evidence can easily be forgotten about, and then rediscovered years later.
For example, clinical evidence that high doses of anti-inflammatory drugs alleviate Type 2 diabetes has been repeatedly discovered (by Ebstein in 1876, by Williamson in 1901, and by Reid, MacDougall, and Andrews in 1957). The anti-inflammatory drugs used were salicylates (aspirin and similar compounds), and the discovery that they had an impact on diabetes was accidental: patients who happened to be diabetic experienced a reduction (sometimes a dramatic reduction) in blood sugar while being treated with anti-inflammatory drugs for some other condition, such as rheumatic fever -- and their blood sugar went back up when the treatment was over.
I'm making this finding seem simpler than it seemed to doctors at the time. They didn't understand why anti-inflammatory drugs would have an impact on diabetes, and they considered it possible that what counteracted the patient's diabetes was not the drugs but the condition the drugs were treating. Could it be that rheumatic fever reduced blood sugar somehow? And why was this phenomenon seen only in patients with Type 2 diabetes, not Type 1? Everything about these clinical findings was confusing, and doctors did not know what to make of the situation, so they tended to forget about this discovery (and then make it again, decades later). They weren't able to fit it into any theoretical model of how Type 2 diabetes worked.
It now seems that what the researchers had stumbled upon (in 1876, and again in 1901, and again in 1957) was a connection between inflammation and Type 2 diabetes. Specifically, inflammation tends to promote "insulin resistance" -- a loss of sensitivity to insulin in the body's cells. (An understanding of this issue has been slow to emerge, because insulin sensitivity is extremely difficult to measure, and for many years it couldn't be measured at all.)
Insulin is supposed to trigger the cells to absorb glucose from the bloodstream, but insulin-insensitive cells don't do this (or don't do enough of it), and glucose starts accumulating in the bloodstream because the cells are not absorbing it. (The cells, and most especially the muscle cells, are supposed to act as sponges to soak up excess glucose in the blood -- which they do just fine, so long as the insulin-based triggering system is working properly.)
Declining insulin sensitivity is not the only factor driving Type 2 diabetes (declining insulin production in the pancreas can be part of the picture as well), but it's a very important factor, and in at least some patients it is probably the primary factor. Anything which tends to suppress insulin sensitivity also tends to elevate blood sugar; anything which tends to restore insulin sensitivity also tends to bring blood sugar down. (That is why exercise is so important for Type 2 patients: exercising muscles makes them more insulin-sensitive.)
Chronic inflammation is only one of various factors that tend to suppress insulin sensitivity (lack of sleep, lack of exercise, and obesity can also do it), but it's an especially important factor -- and even those other factors may suppress insulin sensitivity mainly because they trigger an inflammatory response in the body. So, if anti-inflammatory drugs alleviate Type 2 diabetes, presumably they do so because reducing inflammation restores the insulin sensitivity that the body's cells had lost.
That anti-inflammatory drugs have the effect of restoring insulin sensitivity, and therefore improving blood-sugar control, doesn't necessarily tell us that these drugs are the best way to treat Type 2 diabetes. Taking anti-inflammatory drugs in large doses can cause problems, and other methods of controlling blood sugar may be safer or more effective. There is reason to doubt that anti-inflammatories will be equally effective for all Type 2 patients (if you have Type 2, but in your case the problem is being driven more by diminished insulin production than by diminished insulin sensitivity, anti-inflammatories might not help you). Still, now that Type 2 diabetes is increasingly being seen as a disease driven largely by inflammation, there is growing interest in attacking Type 2 by finding ways to reduce inflammation.
For example, a recent study found that Type 2 patients treated with Salsalate (a salicylate drug used to treat rheumatoid arthritis) showed a reduction in blood sugar levels with an average drop of 0.37% in their hemoglobin A1c results.
Another study found that Type 2 patients given a stem-cell treatment designed to combat inflammation also experienced a significant reduction in hemoglobin A1c, although the numbers are stated with such maddening indirectness that I'm not sure how big the improvement was.
It's hard to say at this point exactly how promising anti-inflammatory treatment is, as an alternative to current methods of controlling Type 2 diabetes. But the disease is hard enough to control, for many patients, that adding to the available treatment methods is bound to be worth a try. Anti-inflammatory drugs might not be most effective option, for a lot of patients, but they might make a useful add-on to other treatments which are only partially effective.
If research into anti-inflammatory treatments for diabetes accomplishes nothing else, it will at least focus some attention on the inflammation issue in general. The issue may be submerged most of the time, but that doesn't mean diabetes patients shouldn't develop a healthy concern about it.
3rd Thursday Update
July 16, 2015
Fasting Glucose: 101 mg/dl.
Glucose 1 hour after lunch: 104 mg/dl.
Weight: 199 pounds.
Blood pressure, resting pulse: 117/68 mmHg, 67 bpm.
Exercise: 6 mile run in the evening
My summer cold is slowly fading away -- all that's left of it is lingering cough, and there's not a great deal of that left. I'm no longer feeling weak, and I'm able to exercise again. My fasting tests are still a bit elevated from the after-effects of several days with little or no physical activity, but my post-prandial results are starting to look good, and I assume my fasting tests will soon do the same.
A complicated situation
My insurance company decided recently to restrict their coverage of glucose test strips. (They didn't warn me of their plans in this regard; they thought it would be more entertaining if I found out, after waiting line at the pharmacy, that the refill order I'd placed over the phone had not been approved.) So they've given me something to think about.
When I was diagnosed in 2001, my doctor told me to test twice a day (a fasting test and a post-prandial test), and ever since then, insurance has covered the cost of testing at a rate of two test strips per day. But it's 2015 now, and human knowledge of diabetes has progressed, apparently; it is now understood that one test per day is plenty. (Either that, or my health plan's knowledge of how to make itself more profitable by cutting benefits has progressed.)
Based on what I hear from readers, I should probably consider myself lucky that my plan offers any coverage for test strips at all. But if I want to continue doing two tests a day, as I have been so far, I must finance that indulgence myself. (I estimate the cost at $85 per month.) This has got me thinking about testing, and what it's worth, and how often we really need to do it.
I have no doubt that, if I complained to my health plan about their rationing of test strips, they would be more than ready to cite studies showing that testing doesn't help Type 2 patients anyway, or at least that it doesn't help them enough to justify the cost of keeping millions of diabetes patients supplied with test strips. I've seen these studies myself; they compare Type 2 patients who test more often to those who test less often, and they conclude that, on average, the glycemic control achieved by frequent testers is not much better than what is achieved by infrequent testers. Conclusion: testing doesn't help, or at least it doesn't help much. Why bother with it?
There are a lot of similar diabetes studies showing that various other things besides glucose testing don't help -- "lifestyle interventions", for example. But whenever these gloomy findings are presented to the public in a press release, I always find myself becoming angry at the way the conclusion is stated.
Typically, a study which supposedly shows that changes of lifestyle don't help turns out to show only that asking people to change their lifestyle doesn't help. It's not fair to say that exercise typically doesn't work, based on a study in which people were asked to exercise and most of them didn't.
Of course, doctors need to be realistic about therapies that have poor rates of patient compliance, but it's dangerously misleading to say that a lifestyle adjustment doesn't work, on the grounds that no improvement was seen in patients who were asked to make that lifestyle adjustment and, for whatever reason, didn't do it. I doubt very much that any study is ever going to claim a new drug doesn't work because there was no improvement seen in people who considered taking it but never did.
In the case of glucose testing, most patients who are asked to do it probably do it, but testing itself is not what is potentially helpful to the patient. Patients need to do more than just test their blood glucose and then get slightly depressed because it's up, or cheery because it's down.
The point of testing is to use the information for the purpose of making adjustments to your habits. You use testing to determine what works for you and what doesn't -- for example, which foods your system handles well, and which foods it doesn't. You use testing to figure out how your blood sugar responds to particular foods, and also to figure out how the impact is moderated by other factors, such as how much exercise you're getting, or how much sleep you're getting. You test in order to figure out what you're going to do differently tomorrow, to get a better result than you got today. A lot of patients don't use test results to steer the ship; they simply note, with a heavy sigh, that the ship seems to be drifting toward the rocks, and they wonder what their doctor is going to do about it -- when they ought to be figuring out what they themselves can do about it. If test strips are used only to get on record the sad particulars about how things went wrong, instead of being used to prevent things from going wrong, then in that case test strips are a wasted expenditure. But they don't have to be!
No doubt, from a clinician's viewpoint, I am insisting on a meaningless, hair-splitting distinction between saying that a given diabetes-management practice doesn't work and saying that asking patients to adopt it doesn't work. Who cares, really? At the end of the day, most patients are not going to do any better if you ask them to exercise, reduce carbs, and test regularly -- because the average patient won't follow through on those things, at least not enough to get a significant benefit. So why not save ourselves a bunch of extra words, and simply say that exercise, carbohydrate reduction, and regular testing don't work? What's the harm in putting it that way?
The harm arises from our old friend, the self-fulfilling prophecy. If you take a dismissive attitude toward diabetes-management techniques which you think patients won't follow, and you even go so far as to say they don't work anyway, then of course patients won't follow them, and won't get any benefit from them.
My personal difficulty here is that, as a diabetes patient keeping his blood sugar under control (for 14 years, so far) by means of behavior modification rather than medication, I am distinctly in the minority. Most patients aren't doing what I'm doing, and probably fewer of them will try it over time, as the official message people are hearing from the health-care industry in general is that the things I'm doing don't work.
The things I'm doing don't work if you don't actually do them; there's no arguing with that. And I suppose there's no arguing with the assumption that a lot of diabetes patients won't do them (although I think more patients would do them if they were given more encouragement than they usually are). But is it strictly necessary for the health care industry to take a one-size-fits-all approach, and (because testing doesn't help the average diabetes patient) restrict access to test strips even to patients who have a proven track record of using them effectively -- and staying off meds as a result?
Surely I've saved my health plan a few dollars over the past 14 years, by not being on any diabetes drugs. My doctor told me, several years back, that he would have had me on five meds by that point if I'd done nothing more than what the typical patient does. I'm not sure what those five meds would have been, or how much they would have cost, but it seems a safe assumption that they'd cost more in combination than the test strips which are currently the only thing I'm getting from the pharmacy.
Admittedly, after 14 years of experience, I know the game well enough to be able to maintain control with less frequent testing. But one test a day is pretty minimal feedback for a beginner, who is trying to learn the art of blood-sugar control in a hurry. There's a lot to learn, and the more data-points you take in, the faster you learn it. Maybe the health industry could compromise, and give more test strips to novices who are still trying to get a good basic grasp of the principles involved -- even if we suspect a lot of them won't get a good basic grasp of the principles involved?
Look, I realize that plenty of diabetes patients aren't going to do what's necessary to get the problem under control. But let's not punish those who are willing to do what's necessary. And more of them will be willing to do what's necessary, if they're not told that it won't work.
2nd Thursday Update
July 9, 2015
Fasting Glucose: 84 mg/dl.
Glucose 1 hour after dinner: 114 mg/dl.
Weight: 199 pounds.
Blood pressure, resting pulse: 136/83 mmHg, 56 bpm.
Exercise: None (sick day)
Not a good week...
A particularly nasty summer cold is cutting a swath through my workplace; last weekend I came down with it and it's proving to have real staying power. It reached some kind of peak last night, with a throat-burning cough which seldom let me relax. Tonight the cough seems to be receding, but I feel so exhausted with it that any exercise -- even going for a walk -- seemed out of the question today.
My blood sugar is surprisingly well controlled under these challenging circumstances, but that's partly because I'm aware of being in a compromised state, and I'm cutting carbs accordingly (dinner was just baked chicken and vegetables). Blood pressure is up, however, so I hope I'm feeling better tomorrow, and can get in a real workout.
I don't know how much energy I have for writing a blog post tonight, but I'll do what I can.
Three bad things are worse than no bad things
Diabetes, Heart Attack, and Stroke a Lethal Combination says the Medscape headline. They cite a JAMA report of a study finding that "Among 689,300 people... follow-up at about 13 years revealed that those who had a history of diabetes, stroke, or MI were about twice as likely to have died as those who had none of those cardiometabolic conditions. With two of them, the death rate quadrupled, and with all three, the death rate was eightfold."
I'm not sure that, even if this research had not been done, anyone would be doubting that it's a health risk to have diabetes, or a stroke, or a heart attack, and a worse health risk to have two of those, and an even worse health risk to have all three of them. But I suppose it was necessary for someone to look into it, and see how much difference there is between having one of these problems and having more of them.
However, it does seem a tiny bit obvious that, if any one of those three problems doubles your mortality risk, adding a second problem doubles the risk again, and adding a third problem doubles the risk yet again. It's sort of like doing a study to find out the combined height of three tables, each four feet tall, if you stack them on top of one another. Could it be the three of them stacked up would be twelve feet tall? (There's no telling, until somebody does a study!)
This reminds me of a study I read once which tried to determine if people were more disabled if they had two bad knees than if they had just one bad knee. The researchers concluded that having two bad knees was worse (and by a factor of two, in case you were wondering how much difference the second bad knee made).
Now I guess we need to do a meteorological study, to see if there's more total precipitation after four days of rain than after two days of rain (and how much more).
Coffee -- not a cause of diabetes (or much else)!
A Danish study has determined that coffee consumption seems to have no relation to one's risk of developing diabetes. The researchers, at the University of Copenhagen, report that "coffee neither increases nor decreases the risk of developing lifestyle diseases such as obesity and diabetes". However, it seems to me that the researchers attacked the problem from a surprising and questionable angle.
The researchers seemingly weren't looking at coffee consumption directly -- instead, they looked at genes.
Wait a minute -- genes? What do genes have to do with this?
"The researchers have designed a unique study, where they have looked into a number of genes that affect our desire for coffee. If you have the special coffee genes, you may be drinking more coffee than those not having the genes. This allows the researchers to see whether a higher coffee consumption increases or decreases the risk of developing lifestyle diseases. 'We can now see that the coffee genes are surprisingly not associated with a risk of developing type 2 diabetes or obesity. This suggests that drinking coffee neither causes nor protects against these lifestyle diseases'."
It is news to me that there exist such things as "special coffee genes", and that those of us who are highly dependent on our morning coffee are that way because of something in our genetic code. I'm more or less willing to buy the claim that certain genes are more common among people who drink a lot of coffee. However, it seems to me unjustified to leap from there to a conclusion about the effects of coffee consumption, based on nothing more than people's genetic signatures.
Of course, I understand why scientists would want to make that leap. Doing a study which quantifies how much coffee people are actually drinking (as distinct from how much coffee people say they are drinking) is very difficult, but genetic testing is very easy. Couldn't we just use the genes (which are easy to verify) as a stand-in for coffee consumption (which is hard to verify)? Well, yes, we could do that... if we don't want to be careful not to introduce obvious sources of error into the study.
I'm going to keep drinking coffee anyway, of course -- I'm just concerned about this kind of thing becoming accepted practice in research.
A few study authors are very busy...
The BMJ, formerly the British Medical Journal, before they decided they just wanted to be a set of initials (remember Prince?) has published a study of studies. Specifically, they looked at medical articles reporting the results of clinical trials of diabetes drugs published between 1993 and 2013. Of the thousands of authors involved, fewer than 1% accounted for 32% of the articles, and fewer than .01% of them accounted for 10.5% of all articles.
So, articles on clinical trials for diabetes were dominated by a pretty small cadre of researchers. Almost half of them are directly employed by the pharmaceutical industry. Of the articles which could be assessed for conflicts of interest, only 6% were considered "fully independent".
In a Medscape article on the BMJ report, a professor of medicine named John B. Buse (apparently himself a prolific author of such studies) took the time to be interviewed... and to protest too much: "I do think that the speculation about how and why people do this kind of work is off-target. There is a world-view that if science is paid for by a commercial interest that it is probably tainted and at least should be viewed with caution and…those people who have done that work should always be treated with suspicion of their motives. At least among the colleagues I work closely with in the US on multicenter trials, they do take this work very seriously, with great effort and tremendous integrity."
So, you see: if he says his cronies do their work very seriously, with great effort and tremendous integrity, then conflicts of interest need not concern us. The usual scientific concerns about eliminating sources of systemic bias don't apply. Why is it even necessary to do controlled experiments? When the integrity level hits "tremendous", we have clearly progressed beyond those sordid realms in which personal bias can influence conclusions.
What people mean by the distinction between "hard" science and "soft" science is that, in some fields, standards of scientific rigor are strict, and in other fields they are not. If medical research gets any softer than this, Starbucks can sell it as a smoothie!
1st Thursday Update
July 2, 2015
Fasting Glucose: 89 mg/dl.
Glucose 1 hour after dinner: 117 mg/dl.
Weight: 198 pounds.
Blood pressure, resting pulse: 118/70 mmHg, 66 bpm.
Exercise: 8.4 mile trail-run in the evening
Health -- in theory and practice
I've said it before, and I'll say it again: when you have diabetes, you become your own science-fair project. And it's really important to get an "A" on the thing!
Perhaps you didn't want to become a science-fair project. Perhaps you would have preferred to leave the science to those who are more temperamentally suited to that kind of thing. Unfortunately, you don't really get a choice in the matter. Some people are born scientific, others achieve it, and still others have it thrust upon them.
Anyway, like it or not, if you've received a diagnosis of diabetes or prediabetes (the distinction is about as meaningful as the distinction between "visibly pregnant" and "pregnant but not showing yet") you're a scientist now. That means you need to think like a scientist, at least to some degree.
For one thing, you need to understand the distinction between "theoretical" and "experimental" science. The reason you need to understand the difference between those two things is that most diabetes patients try to take the theoretical approach, but the experimental approach is the one that will actually help them.
Theoretical science is blackboard science -- the kind that can be done without a laboratory, by working logically from first principles and developing a mathematical model that fits with what is already known. Experimental science, on the other hand, is about setting up a situation in which the predictions of a theory can be compared with reality, to see if the predictions accurately describe what happens. To put it bluntly, theoretical science is about coming up with a plausible story, and experimental science is about checking the story out to see if it's true. Both kinds of science are necessary to the overall scientific enterprise -- somebody has to check the stories, and somebody needs to come up with stories to check -- but there's an unfortunate human tendency to value the theoretical side over the experimental side.
There are certain social considerations which make theoretical science more appealing than experimental science. If you're doing your science at a blackboard, and not in a laboratory, you don't have to get your hands dirty trying to get the equipment working right, and you don't have to let mere engineering problems distract you from the pure intellectual beauty of theoretical work. Experimental science seems a little less prestigious -- it's the blue-collar side of science, and a lot of people would prefer to stay away from it.
The trouble is that the pure intellectual beauty of theoretical work is not actually worth anything, if it can't be confirmed. It isn't enough that your theory is ingenious, original, consistent, convincing, and makes a good fit to the equations. It must also make a good fit to reality, in a way which experiments can confirm.
"If it doesn't agree with experiment, it's wrong" said Richard Feynman, a theoretical physicist by trade who was an experimentalist by nature. He knew that even the most beautiful theory was only as valuable as it was verifiable. In 1986, he served on the Rogers Commission, which investigated the explosion of the space shuttle Challenger during a cold weather launch. He grew weary of theoretical discussions about whether the freezing weather during the launch might have impaired the resiliency (and thus the sealing integrity) of the O-rings on the solid rocket boosters. So, in the middle of a hearing, he startled his fellow commissioners by performing an experiment in front of them. He clamped a piece of O-ring material, chilled it in ice-water, removed the clamp, and observed that material didn't spring back to its original shape when it was chilled in that way. The designers of the O-rings might have assumed, on theoretical grounds, that the O-rings would remain springy enough to function normally in cold weather, but Feynman's ice-water experiment said otherwise. If it doesn't agree with experiment, it's wrong.
A good theory generates predictions about how things work -- predictions which experiments will confirm. A bad theory generates wrong predictions, or no testable predictions at all. Nobody would have been impressed by Newton's theory of gravitation if he had made no specific, testable predictions about the force and acceleration of objects in free-fall (or if he had made predictions that turned out to be wrong).
There is always a danger that scientists will get too wrapped up in the theoretical side, and lose interest in confirming their beautiful abstract ideas experimentally. Physics, for example, appears to be entirely bogged down these days by "string theory" -- the notion that subatomic particles are ultimately made of tiny, vibrating, multi-dimensional fibers, the existence of which we cannot verify even in principle. Some scientists worry that string theory is just an armchair speculation, and that nothing will come of it because it doesn't connect to reality. (They also worry that it's popular among physics professors because it is "safe": if there's no way to test it, then there's no risk that your work on it will ever be proved wrong.) I have to confess I feel some nostalgia for the days when physicists were working on ideas that had real-world implications, even though the implications were sometimes dangerous ones. Maybe I should take comfort in the thought that, if string theory has no link to reality, at least nobody's going to use it to make the next super-weapon (we're not like to have to worry about terrorists getting hold of a String Bomb.)
For that special group of amateur scientists known as diabetes patients, there is a similar danger of being too much seduced by the theoretical side, and disregarding the important work of running experiments to see whether the theory checks out.
Many diabetes patients do their best to keep up with the state of expert opinion about how diabetes patients should manage the condition and protect their health -- but they become frustrated by the inconsistency of expert opinion in these matters. Which expert should they trust? Who's got this right?
Science at its best is not really about finding an exert you trust and believing what that expert says. Science is supposed to be about finding a story which seems plausible and testing it to see if it's right. You can't just ignore the experimental side.
Well, for some kinds of health problems that you might someday need to manage, you have no choice but to ignore the experimental side, because you have no means of gathering experimental data. However, one advantage diabetes patients have over patients managing other sorts of problems is that, in the case of diabetes, experimental data is easy to collect. All you need is a glucose meter and willingness to use it.
Admittedly, telling you to test your blood glucose regularly makes the situation sound simpler than it is. You have to be invested enough in the data-gathering process to pay attention to the way your glucose results fluctuate under various conditions, so that you can see patterns emerging which reveal what "works" for you, and what doesn't. But if you're willing to collect the data, and observe how other factors affect it, you can learn a great deal in a comparatively short time.
If you are committed to testing, and learning from the results, you can learn things which would otherwise remain obscure to you. For example:
- How much carbohydrate can you take in without spiking an hour later? (Don't ask an expert --ask your glucose meter.)
- How much exercise do you really need, and what kind? (Experiment with different kinds of exercise, and different amounts of exercise, to see what gives you the best glucose results.)
- Is it okay for you to eat rice so long as it's brown rice? (Test your glucose an hour after eating brown rice, to see if your system copes with that better than it copes with white rice -- and try not to feel crushed if it turns out to make very little difference.)
A lot of the suggestions that are made to diabetes patients need not be taken at face value. Most of them can be tested -- not necessarily to find out if they work, but to find out if they work for you.
For example, I read an article today claiming that the glycemic impact of a meal is altered by the order in which you eat the different foods involved in the meal. Supposedly, if you start with the low-carb foods and finish with the high-carb ones, the latter will have significantly less impact than if you eat them first. I offer no opinion about whether this claim is valid, but it certainly wouldn't be hard to check it out. Suppose you start having a standardized breakfast on Saturday mornings -- bacon, eggs, and toast. Check to see whether your post-prandial glucose results are significantly lower if you eat the toast last than if you eat it first. I don't know how qualified or intelligent are the people making that recommendation, but even if they're geniuses, they might be recommending something not because it always works, but merely because it works in more cases than it fails. If I'm going to be one of the cases in which it fails, I need to know that -- and experimentation is the only way I'm going to find out.
It's very easy for diabetes patients to feel helpless because they can't figure out which expert to believe. The way out of that problem is not to find the right expert, but to set up the right experiment.
"NOT MEDICATED YET"
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!)