Looking for Loopholes in Nature
Monday, April 30, 2012
Fasting Glucose: 87 mg/dl.
Glucose 1 hour after lunch: 92 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 123/71 mmHg, 51 bpm.
Exercise: 4.6 mile run at lunchtime; yoga class in the evening.
Better Living Through Urination?
A few days ago, a search engine referred someone to this site who had typed "can you pee enough to keep your blood sugar regulated". My goodness. The mind reels.
The short answer is "no", of course -- but if I left it at that, I would be leaving unanswered the likely follow-up question, which happens to be more interesting than the original question: why can't you pee enough to keep your blood sugar regulated?
The kidneys filter certain substances out of the bloodstream, flushing them into the urine, while retaining others. To use the word "filter", though, suggests something a lot less sophisticated than the chemical sorting mechanism that is actually involved. The kidneys use "transporter" molecules to move some substances into the urine, while hauling others back into the bloodstream. (Subtances which aren't passed into the urine are said to be "reabsorbed", because the kidneys return them to the blood supply instead of eliminating them.) One substance which the kidneys do their best to reabsorb completely is glucose; after all, glucose is a crucial source of chemical energy, and the body never wastes chemical energy if it can help it.
SGLT2 and Glucose
In most people, the kidneys reabsorb something like 180 grams of glucose a day. The transporter molecule called SGLT2 is of special interest here, because it does nearly all the work involved in reabsorbing glucose. SGLT2 is very efficient at what it does; almost no glucose is lost from the blood supply, under normal circumstances.
However, there is a limit to what SGLT2 can accomplish. When blood glucose levels climb above the normal range, the reabsorption rate approaches the maximum that SGLT2 can provide. That maximum point is exceeded, once blood glucose levels get to about 200 mg/dl. Past that point, the kidneys cannot reabsorb all of the glucose back into the blood supply, and an increasingly large share of it passes into the urine. Also, at high levels of glucose in the blood, osmotic pressure increases the rate at which fluid passes into the urine, so that the bladder fills up faster and urination becomes more frequent.
That is why heavy production of sugary urine (sugary enough to attract ants and bees) is the classic symptom of diabetes. In fact, it's close to being the definition of diabetes ("diabetes mellitus" can be translated, at least by tactless persons such as myself, as "pissing honey", although I suppose there must be a more poetic way to say it).
Sugary Urine is Not Purposeful
Until recently, I misunderstood an important detail in this. I thought that sugary urine, occurring at high blood glucose levels, was a case of the body deliberately trying to shed glucose in order to restore normal glycemic control. I thought this meant the kidneys were trying to solve the diabetes problem -- and I wondered why they weren't doing a better job of it. Why did the kidneys wait until the glucose level got that far above normal before doing something about the problem? Why didn't the kidneys start releasing glucose into the urine as soon as glucose levels got slightly above normal?
It appears that I was looking at this issue in the wrong way. The body does not use the kidneys as a tool for driving down glucose levels. When glucose flows into the urine, it isn't because the kidneys are enacting emergency measures to get rid of it -- it happens simply because the kidneys have been pushed beyond the limit of their capacity to reabsorb glucose. The kidneys are designed to catch glucose and throw it back into the blood supply, and they never really stop trying to do that -- it's their job, after all. They aren't in the glcuose-lowering business (that's what the pancreas is supposed to do). However, in the case of uncontrolled diabetes, so much glucose enters the kidneys that there is no way for them to avoid spilling at least some of it into the urine.
Because the kidneys try their best to hold onto the body's available supply of glucose, their occasional spillage of the stuff into the urine does not look to me like much of a solution to the problem of diabetes. After all, most not-yet-diagnosed diabetes patients, who come in to the doctor puzzled about why they are suddenly urinating much more frequently than they used to, are expelling plenty of glucose in their urine... but they still have greatly elevated glucose in their blood.
And suppose you did try to pee your way to normal glycemia, by drinking gallons of icewater all day. Quite apart from the practical problem of never being able to let yourself get far from a bathroom, there is the problem of hyponatremia (taking in that much fluid can cause your sodium level to drop sharply enough to interfere with brain function, with painful and sometimes fatal results). I'm not saying that this approach would actually work for glycemic control -- I'm just pointing out that, even if it did work, it wouldn't be a very enjoyable way to live.
SGLT2 and Drugs
The pharmaceutical companies have lately been trying to use drugs to make the kidneys drive glucose levels down. The drugs in question are known as SGLT2 inhibitors, because they interfere with the normal functioning of those transporter molecules -- so that the kidneys lose a lot of their ability to rebsorb glucose, and the patient's urine becomes sugary even when the patient's blood is nowhere near as high as 200 mg/dl.
The experimental (and hard-to-spell) drug Dapagliflozin, which I wrote about in January 2012, is one of these SGLT2 inhibitors. The people who make it are having a hard time getting FDA approval for it, because of concerns about its risks (the data collected so far seem to indicate that Dapgrliflozin makes you five times likelier to develop certain forms of cancer, and that isn't what everyone looks for in a wonder-drug).
It may be that, somewhere down the road, SGLT2 inhibitors will be made safe (or will be proved to be safe in their present forms), and getting rid of excess glucose by dumping it into the bladder will become the standard way of solving the diabetes problem. But I'm not sure that we will describe that situation as "peeing enough to keep your blood sugar regulated". So I stand by my short answer: no, you can't pee enough to keep your blood sugar regulated.
Everyone likes to look for loopholes in nature. Isn't there a simple trick we can do to take care of this health problem? Couldn't we just pee more, or something?
I've heard people suggest, apparently in all seriousness, that it should be possible to lose weight by being cold. The body uses a lot of calories to maintain body temperature, after all. Why not turn off the furnace, sleep with the window open, and go outdoors without a jacket, all for the sake of losing weight? Well, maybe that would work, but it appears to work a lot better for arctic explorers than it does for Californians putting away their sweaters.
Nature isn't like the tax code; it doesn't have a lot of loopholes in it. And when we find something that looks like a loophole, we should try not to get too excited -- because it often turns out not to be solution we're looking for.
Photo from the Half-Marathon
There was a non-horrible photo taken of me at the Napa Half-Marathon on April 22, but I don't know that it's so non-horrible that I want to order a print of it. Even though this was from late in the race, when I was getting tired, I did manage to put on a brave smile. More than that we should not be asked to provide, under such trying circumstances.
Friday, April 27, 2012
Fasting Glucose: 91 mg/dl.
Glucose 1 hour after lunch: 95 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 124/70 mmHg, 58 bpm.
Exercise: 4.1 mile run.
A Pound of Cure
Thursday, April 26, 2012
Fasting Glucose: 87 mg/dl.
Glucose 1 hour after dinner: 115 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 113/69 mmHg, 61 bpm.
Exercise: 4.4 mile run at lunchtime; weight-training workout in the evening.
Training of Cardiologists: No Time for Prevention
You might be inclined to assume that medical students being trained to become cardiologists would receive a lot of education on the subject of how to prevent heart disease. Well, in that case, you would be wrong. Cardiologists in training are all taught about the pound of cure, but few of them are taught about the ounce of prevention.
In 2008 a group of medical organizations (the American Heart Association, American College of Physicians, and other big names in the field) became concerned about the one-sided education that heart doctors were receiving, and issued guidelines on the subject: minimum amounts of instruction which cardiology students should receive in various aspects of heart disease prevention, taught by instructors specializing in the subject.
Well, a group of researchers has now conducted a study to find out what percentage of cardiology training programs are satisfying the minimum requirement for training on the subject of heart disease prevention. The answer: 24% of them.
Why have so many of these training programs failed to meet minimum standards in this regard? The excuses offered have generally been "not enough time" and "not enough faculty members with expertise in prevention". I guess that last little problem says it all, doesn't it? Most medical schools lack faculty members with expertise in prevention. What do they think they're in business to do?
Well, like everybody else, they're in business to make money. And prevention is not where the money is. Those cardiology students who "don't have enough time" to study prevention do have enough time to learn how to put in stents, because procedures of that kind are well-compensated. Counseling patients on how not to need a stent are not well-compensated. According to the lead author of the study, Dr. Quinn Pack, "There tends to be more focus on the reimbursable procedures, as opposed to the things that, in my opinion, make a real difference to patients -- the medications, the diet, the smoking cessation and lifestyle changes."
In short, medical schools and their students are, inevitably, concentrating on what society pays them the most money for. And prevention ain't it.
I'm not sure I see a solution to this. Society favors cure over prevention because most of the people who make up society feel exactly that way. We're being stupid, of course, but that is how we see it. So, whatever bad things come of this, I guess we have it coming.
Taking it Up a Notch
During my weight-training workout this evening I added another 5 pounds to most of the exercises I was doing. You have to do that periodically. It's too easy to reach a comfort level and want to stay there. With weight-training, when you reach the point where you have no doubt at all about being able to finish all the reps in the sets you're doing, you need to move on and make it a little more challenging. It has to be hard enough that you're not absolutely sure you can do it. That's when the progress happens.
What Are We Measuring?
Wednesday, April 25, 2012
Fasting Glucose: 82 mg/dl.
Glucose 1 hour after lunch: 90 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 111/67 mmHg, 60 bpm.
Exercise: 5.2 mile run.
Measurement Is Hard!
I work in the test and measurement industry, so I'm more familiar than most people are with the difficulties involved in making an accurate measurement. I'm going to be talking about the hemoglobin A1c test in this light, but first I want to talk about measuring the speed of subatomic particles and the weight of a piece of fruit.
In September of 2011, a physics experiment (in which a particle accelerator at CERN in Switzerland fired neutrinos at a detector in Italy 450 miles away) made the headlines -- because the results appeared to show that the neutrinos arrived 60 nanoseconds earlier than they should have, and thereore must have traveled faster than the speed of light. Einstein's relativity theory ruled out faster-than-light travel, so this experiment was presented in news coverage as an earth-shaking (or rather universe-shaking) revolution in physics, because it meant that Einstein was wrong, relativity theory was flawed, time travel was theoretically possible, blah blah blah.
This sort of thing happens every year or two. The proving-Einstein-wrong industry has been keeping physicists busy for a century now, which is a pretty good run considering the lack of results. Every time someone thinks he's finally done it, he gets a lot of attention... up to the point when the error in his experimental setup is revealed. Then he wishes he wasn't getting quite so much attention.
In February, the explanation for those faster-than-light neutrinos turned out to be (suprise!) a measurement error. A loose GPS cable on a timing device caused it to get out of synchronization with other equipment. This threw off the experimental results, so that the particles appeared to be moving faster than they actually were. Fixing the cable problem caused the 60-nanosecond discrepancy in the timing to vanish. The reason the physicists didn't figure this out sooner was that they were looking for subtler errors, such as wrong values in an equation; it didn't occur to them that something as crude as a loose cable might account for the odd results they were getting.
I think that's a pretty good example of what a difficult challenge it can be to make an accurate measurement. There are a lot of potential problems involved -- a lot of ways to get it wrong. And it can be very easy to misinterpret your results, especially if you forget about the all-important distinction between what you think you are measuring and what you are actually measuring. That distinction might not exist, for a very simple sort of measurement (such as determining the width of a doorway with a measuring tape), but when the measurement technology gets any more sophisticated than that, you are typically measuring one thing which serves as a stand-in for a very different thing which you are more interested in.
Here's an example of the problem I'm talking about. Let's say you have a kitchen scale. An electronic scale, with a little digital readout. You put a piece of fruit on it. It reads "2.1 oz". Okay, does that piece of fruit really weigh exactly 2.1 ounces? Well, maybe. Probably pretty close to that, anyway.
But what you think you are measuring (the weight of the fruit) isn't what you are actually measuring. What you are actually measuring is a voltage. The weight of the fruit applies pressure to a strain sensor, which generates a small voltage proportional to the pressure applied to it. An analog-to-digital converter turns that voltage into a binary number, and a microprocessor runs that number through a lookup table which says that this particular number equals 26.9 millivolts... and that 26.9 millivolts is the voltage which this sensor is expected to produce when something weighing 2.1 ounces is sitting on the scale.
Is 2.1 ounces the actual weight of the fruit? Well, it is if the strain sensor really does produce exactly the same voltage as the lookup table expects it to, when a 2.1-ounce weight is applied.
But if the voltage actually produced by that strain sensor is higher or lower than it ought to be at that weight (perhaps owing to a temperature change, or some minor hardware defect), the measurement result is going to be wrong. For that matter, the sensor could be working perfectly, but somebody might have entered incorrect numbers into that lookup table. In either of those cases, the displayed weight is going to be inaccurate, because the required conditions for accurate conversion of the sensor voltage to a weight in ounces were not satisfied.
I'm not saying that there's anything wrong with designing a kitchen scale this way, or that kitchen scales are usually wrong. I'm just pointing out that the kitchen scale is right only if certain requirements are satisfied: the lookup table has to be free of numerical errors, and the strain sensor has to generate the same voltage, for a given weight, as the lookup table assumes it will. To put it another way, the thing we're actually measuring (voltage) has to have the expected relationship with the thing we think we're measuring (weight); if that's not true, the measurement result's not right.
In the case of those faster-than-light neutrinos racing from Switzerland to Italy, the scientists involved thought they were measuring speed. What they were actually measuring was the time difference between pulses on two pieces of equipment. This method could measure speed accurately, if the two pieces of equipment were properly synchronized. But they weren't, because of that loose cable, so there was a breakdown between what the scientists measured (timing of pulses) and what they thought of themselves as measuring (speed of particles).
It can be very important to remember the distinction between what you think you are measuring and what you are actually measuring -- and to remember the necessary conditions which have to be satisfied before you can reasonably say that one of those things equates to the other. If those conditions aren't actually satisfied, the results aren't actually meaningful.
What A1c Measures; What We Think it Measures
Which brings us to the much-misunderstood hemoglobin A1c test. Diabetes patients are often told that the A1c test measures "average blood sugar". This is not true.
What the test actually measures is the amount of hemoglobin in the patient's red blood cells that is "glycated" (bonded with sugar). Glycation is a kind of accidental, purposeless chemical bonding process which happens (usually at a slow rate) whenever protein is exposed to sugar. It's an undesirable accumulation, like rust on metal, or barnacles on the hull of a ship, or tartar on tooth enamel, and it happens simply because the ingredients are exposed to one another and sometimes they link up.
Because glycation is harmful, doctors need to know how much of it is going on; hence the hemoglobin A1c test, which examines one easily-collected protein to see what percentage of it is glycated.
Because everyone has at least some sugar in the bloodstream, everyone's hemoglobin experiences at least some glycation. (Nobody is ever going to take an A1c test and get 0% for a result.) However, the body replaces its hemoglobin and other protein molecules over time, recycling the old ones to make new ones that don't have anything undesirable stuck to them. Because of this recycling process, the amount of glycated protein in your body is not supposed to increase over time. About 5% of anyone's hemoglobin, when tested, will turn out to be glycated, but that percentage won't go up unless the glycation process accelerates, so that the body's recycling process can no longer keep up with it.
What would make the glycation process accelerate? Well, various things could, I suppose. Having a higher body temperature than average would accelerate it a little, but perhaps not enough to produce a measurable difference. The main thing that would boost the glycation rate to a measurable extent would be an increase in blood sugar. The more exposure to sugar your hemoglobin gets, the more glycated it gets. An increase in your average blood sugar will result in an elevated percentage of your hemoglobin being glycated.
For people with diabetes, the result on the A1c test will typically be above 6%, and if their diabetes is not well-controlled it will often be above 7% (or above 10%, for that matter). On the other hand, a drop in blood sugar will eventually bring the A1c result down, as the body's recycling process begins to catch up with the glycation process.
The point of the test is really to find out what your glycation rate has been lately, by checking out one easily-collected protein to see how much of it is glycated. Because the percentage of glycated hemoglobin rises or falls (gradually!) over time, as a result of changes in average blood sugar, the A1c result gives doctors a basis for estimating what average blood sugar has been over the past few months. (Owing to the limited lifespan of red blood cells, the A1c test does not reflect conditions more than 90 days in the past, and conditions during the most recent month exert an especially strong influence on the result.) However, it is not at all reasonable to say that the A1c test "measures" average blood sugar.
Average Blood Sugar and A1c
Certainly average blood sugar has an influence on the result of an A1c test. If your A1c went up, it almost certainly means that your average blood sugar went up. (By the same token, if the voltage from the strain sensor in that kitchen scale went up, the weight of whatever is on that scale almost certainly went up.) But to say that an A1c result of 7.0% is equal to an average blood sugar level of 154 mg/dl is like saying that 26.9 millivolts from the strain sensor in the kitchen scale is equal to a weight of 2.1 ounces. Maybe that's true, and maybe it isn't; there are some conditions that have to be satisfied before we can say with confidence whether it is true or not.
If we are going to say that an A1c result of X is equal to an average blood sugar of Y, what conditions have to be met? Well, here are two obvious ones:
The rate of glycation of hemoglobin, for a given average blood sugar, must be the same in all individuals and at all times.
The rate of recycling of hemoglobin must be the same in all individuals and at all times.
Unfortunately, actual human physiology does not satisfy either of these necessary conditions. Different people have different A1c results for the same average sugar levels -- either because they differ in their glycation rates or because they differ in their recycling rates (or both). It is well known that ethnic populations differ significantly in this regard. What do we make of this? If African-Americans get higher A1c results for the same blood sugar level than European-Americans, does that mean the former group are over-diagnosed with diabetes (as is often claimed), or that the latter group are under-diagnosed -- or both, or neither? It's hard to answer that, but it's easy to see why we shouldn't, given these confusing facts, call the A1c a "measurement" of average blood sugar.
Another issue that can have a big influence on A1c test results is medical treatment. This is especially true of hemodialysis, which dramatically alters the rate of hemoglobin recycling (and makes A1c results pretty much meaningless for certain patients with kidney disease). Some of the more outrageous research papers which claim that good glycemic control is harmful rather than helpful seem to have arrived at that conclusion partly by assuming that the A1c results of kidney patients on dialysis were as accurate as anyone else's (even though this is known to be wrong).
What Do We Do with the Uncertainties?
Please understand that I am not saying the A1c test is worthless, or that it doesn't tell us anything important. I'm just saying that we won't get any value out of it by pretending it measures something that it doesn't measure.
So what is it good for? Well, unless you are on hemodialysis, or some other treatment that distorts A1c results, you are pretty safe in assuming that an increase in A1c is bad and a decrease is good. A reduced A1c indicates a desirable trend in your glycemic control. That much connection between average glucose and glycated hemoglobin is valid.
But we shouldn't think that an A1c result can be mapped directly to a specific value of average glucose. Individual and ethnic differences introduce too much uncertainty into that, for this sort of thinking to be useful.
What the A1c result does indicate is glycation -- and glycation, not average blood sugar, is the real issue in diabetes management. We get it backwards if we think of glycation rate as significant only because it relates to average glucose; it would be more accurate to say that average glucose is significant only because it influences glycation rate.
What we really want to know
(or should want to know, anyway) when we look at an
A1c test result is how much harm is being done currently -- and glycation rate
is the best index of that. And the reason we want to know how much harm is being
done currently is that we want to do something about it, if we don't like the
answer. That, and not a doubtful equivalency between average glucose and
glycation rate, is what we should be focused on. But we won't focus on it until
we start focusing on what the test actually measures, instead of what someone
wants to pretend it measures.
Speaking of measurements that don't necessarily mean what we think they mean, today I turn 55. It is the oldest I have ever been, but I think I can get through this.
Bloggers and Big Brother
Tuesday, April 24, 2012
Fasting Glucose: 94 mg/dl.
Glucose 1 hour after dinner: 107 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 98/65 mmHg, 57 bpm.
Exercise: 4.5 mile run at lunchtime; weight-training workout in the evening.
Orwellian Tar Heels vs. the Blogosphere!
North Carolina -- always a good source of scary ideas about how state governments should be allowed to treat people -- is threatening a diabetes blogger with legal action and possibly jail. Steve Cooksey's blog about his diabetes, and about the diet that he uses to control it, is being investigated as an illegal enterprise. He is clearly giving people dietary advice -- and he is not a licensed dietitian!
Cooksey is a proponent of the "paleo" approach to diet -- a popular but much-criticized dietary movement which aims to recreate the diet that cavemen ate (on the theory that this primitive diet, whatever it was, is probably the diet to which human physiology is best adapted). Paleo dieters think that the chronic diseases which have arisen in modern industrial societies (including diabetes) are largely caused by a modern diet which is simply too different from humanity's ancestral diet for us to be able to adopt it safely.
Dieters vs. Dieticians
I don't know all the details of the paleo diet (if indeed there is a monolithic plan on which all paleo dieters agree), but I know that it concentrates on wild plants and lean meats which would have been available in the stone age, and avoids modern cultivated foods (especially grains) which would not have been.
The paleo-diet concept has been attacked from many different directions:
"It's impossible to figure out now what the human diet was like in the paleolithic era, so this whole idea is futile."
"It's possible to figure out what the paleolithic diet was like, but what you're eating is not like that."
"The paleolithic diet must have consisted of whatever was available in a given time and place, so it varied too much to offer us any specific model of nutrition."
"There's no reason to think that cavemen lived long, healthy lives, or that modern people will do so if they eat like cavemen."
"There's no point in adopting the paleo diet if you're not going to live the rest of the paleo lifestyle. If you have a desk job, and you buy your meat instead of hunting it with a spear, and you're not going hungry a lot of the time, then face it: you ain't paleo."
Dietitians generally hate everything about the paleo diet; when dietitians gather together to serve as panels of experts, they say that paleo is a fad diet, and probably the worst fad diet of them all. Their unified hostility is not enough in itself, I hasten to add, to confirm that this diet is a good idea, although some would argue that it's a promising sign.
Nutrition: Softer than Soft
Unfortunately, for certain practical reasons having to do with medical ethics and human rights, it is almost impossible to run a controlled experiment on nutrition and human health, so nutrition is a field largely devoid of hard facts and extremely rich in suggestive correlations which, if you are selective enough about which ones you include in your study, will support virtually any theory of nutrition you care to dream up.
In other words, nutrition is not a hard science. It is an extremely soft one. And, like other soft sciences (can you say psychology, boys and girls?), nutrition has a distinct tendency to codify prevailing assumptions as fact. This is especially true when billions of dollars are at stake. Why wouldn't nutritionists cling to prevailing assumptions, if it is known that any attempt to challenge prevailing assumptions would infuriate large agribusiness interests?
Clearly I am skeptical of "official" wisdom about what people should eat, but I am also skeptical of unofficial wisdom on the subject. If I were forced to summarize the state of existing knowledge about what makes for a healthy diet, I would echo what the screenwriter William Goldman said concerning the state of existing knowledge about what makes a good movie: "NOBODY KNOWS ANYTHING".
My view is that a healthy diet is one which works for you -- regardless of whether or not it would work for me. (Bear in mind that my definition of "what works" encompasses not only the effect of a diet if you stay on it, but your ability to stay on it, which is just as important.)
About Steve Cooksey
I haven't formed any particular opinion of the paleo diet theory in general, or Steve Cooksey's interpretation of it in particular, and I haven't been following his blog. However, I clearly have a reason to sit up and take notice when a diabetes patient who has found a way to get healthy that works for him, and shares information about this with other people who are interested in trying it for themselves, is treated as a criminal.
Cooksey reports great results:
he lost 70 pounds, got off the diabetes meds, normalized his blood sugar,
normalized his blood pressure, normalizes his lipids, got rid of a number of
nagging health problems, and became much more active and energetic. (Pretty much
my own story, really, although he ended up with a better "after" picture than I
This is, to put it mildly, not the typical trajectory of a diabetes patient after diagnosis. The great majority of Type 2 patients, receiving conventional medical treatment and following conventional dietary advice, (1) tend to get worse results over time rather than better results, (2) tend to add medications instead of getting off of them, and (3) tend to lengthen their list of health problems intstead of shortening it.
So, if Cooksey is using an unconventional approach, and is doing better than most patients, it's hard for me to see why his unconventional approach is a menace to society. The conventional approach has an abysmal track record (you could do worse, but not much worse). And the conventional notion of a healthy diet is clearly too high-carb for diabetes patients -- and probably too high-carb for everyone else, too. As he is inclined to point out, if the North Carolina Board of Dietetics and Nutrition is doing such a fantastic job, why are 60% of the people who live in that state overweight or obese?
Cooksey has made public the official critique he received about his blog, including the red-inked reprimands on specific points:
Now he must take down his website, or heavily rewrite it so that he only mentions his own diet without recommending that anyone else try it. Otherwise, he faces a lawsuit by the licensing board, and (if he loses that) the possibility of 120 days in jail.
His web site originally included a link (now removed) to an offer of one-on-one support for a small fee; perhaps that was actually what provoked the licensing board to go after him. But they certainly objected to all the advice he offers for free, too, and his removal of the link has not persuaded them to back down. (He says he never made any signficant money from it to begin with.) The bottom line: he currently offers advice, free of charge, to any diabetes patient who wants to visit his site, and he freely discloses that he's not a doctor and his advice is based on his experience as a diabetes patient. But his site is still illegal in the eyes of the licensing board.
The Quack/Blogger Boundary
I can't pretend to have explored in Cooksey's site in great depth, in the short time since this story was brought to my attention, but so far I haven't found evidence that his site is anything other than what he says it is: the personal blog of a guy with diabetes who wants to share his experience since diagnosis. It just doesn't seem to me like an exploitive site. It seems like an opinionated site, yes -- but the last time I checked that wasn't against the law.
Now, I realize that there is a reason to go after people who sell things like fake cancer cures, or endanger the public health by publishing cooked-up information about imaginary connections between vaccinations and autism. But saying "I'm diabetic, and here's what worked for me"? Does the public really need protection from free speech in this area, especially when conventional diabetes therapy (and conventional dietary advice to diabetes patients) has so little to offer?
Cooksey's site includes (more often than mine does, I nervously report) the information that he isn't a doctor and he's merely sharing his own experience of managing diabetes. I fail to see why that is not an adequate shield for his First Amendment rights. (Or my First Amendment rights, come to think of it.)
In some situations there needs to be room for amateurs, because amateurs can and will say what the professionals can't and won't. Diabetes management is one of those situations. Reports about which drug was 8% better in clinical trials than some other drug are all very interesting, but sometimes you want to hear from somebody who gets normal results without drugs, just in case that information ever comes in handy. And you won't hear from that person if he's in jail, will you?
Glucose After Endurance Sports
Monday, April 23, 2012
Fasting Glucose: 102 mg/dl.
Glucose 1 hour after lunch: 114 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 119/77 mmHg, 55 bpm.
Exercise: 4.1 mile run at lunchtime; yoga class in the evening.
Glycemic Gyrations After a Long Race
Yesterday I ran a half-marathon in the Napa Valley (that's a race with a course that is 13.1 miles long). The weather was very warm, but I expected that, and was dressed for it, and was careful about staying hydrated.
One thing I should mention about long-distance races is that they don't start getting easier once you're over 50. My finish time was 2 hours, 11 minutes, 58 seconds. That is almost 2 minutes longer than the last time I ran a half-marathon, in July; it's a pace of 10:04. I felt some minor aches and pains during the race, but nothing bad. Afterwards I felt a bit footsore, and desperately needed a nap (luckily I got one), but I wouldn't say it was a terribly hard experience. I think I could have gone faster, if it hadn't been for a silly mistake: my Garmin GPS device had a dead battery (I thought I had charged it), so I wasn't getting any feedback on my pace, and I just didn't concentrate that much on my speed, and slacked off without realizing it.
It wasn't exactly inevitable that I would have a higher-than-usual fasting result the morning after I ran a half-marathon race, but it's not exactly astonishing either. The same thing happened the last time I ran a race of that distance, in July. There are two possible reasons why that would happen.
The more obvious explanation is that, after the race, I was extremely hungry, and I had a big dinner, with more carbs than I usually indulge in. In other words, the cravings induced by my running 13.1 miles earlier in the day were out of proportion with my actual needs, so I overcompensated for what was, in fact, only a modest carb deficit.
The alternative explanation is that, despite the big dinner, I went low in the predawn hours, and my system overcompensated for that.
Just a week ago I did a tough 12.6-mile trail run to get ready for the race, and the morning after that run my fasting level was 77. Perhaps this time, after a run which was slightly longer (and in which, because it was a race, I was running faster), I went hypoglycemic during the night and rebounded too far from that.
Looking back over my records, I've found that my fasting test the morning after an endurance challenge of this sort tends to swing to one extreme or the other -- either unusually high, or unusually low. And possibly the unusually high results are the aftermath of an unusually low one an hour or two earlier! Without CGM (Continuous Glucose Monitoring, an expensive technology which I don't have available to me), you can never be sure whether a morning high is just a high, or an overcorrected low.
Anyway, after a long race like that, I have learned to expect the unexpected, and I have also learned not to claim that I've been cheated when running for miles and miles is not rewarded with a good fasting number.
At least my post-prandial result after lunch was in the normal range -- so if the race knocked me out of whack for a little while, I think I recovered.
Starbucks to Phase Out Ground-Up Bugs!
Meet the cochineal, or Dactylopius coccus, a scale insect that lives as an
immobile parasite on a certain large cacti in Latin America. These
creatures don't exactly look colorful and exciting, but wait, there's
Once these insects are dead and dried, a fair chunk of their body weight consists of carminic acid -- that is, the strong red pigment known as carmine. People in Mexico and points south have long made red dyes by grinding up cochineal insects.
You'll never guess what this dye is mainly used for now: lipstick and food coloring!
This information hasn't exactly been secret up to now, but it hasn't been widely advertised, either. The Food and Drug Administration approves cochineal dye for use as a food additive, so there's nothing illegal about serving it, and what people don't know won't hurt them. At least, that was what Starbucks thought.
They've been using cochineal dye to color some of their fruitier drinks (such as strawberry frappuccinos) and desserts (such as raspberry swirl cake). But food activists, still riled up from their discovery of "pink slime" in ground meats, are on a roll now, and are exposing the use of all sorts of food additives which are legal but repulsive. Their wrath fell on Starbucks, and now the coffee-house chain has bowed to the pressure. Starbucks will be phasing out cochineal dye in their foods and drinks by the end of June -- and replacing it with lycopene, the red pigment which is found in tomatoes and may provide special health benefits to prostate-having consumers.
Of course, one possible way for Starbucks to give their strawberry and raspberry concoctions the color of strawberries and raspberries would be to use strawberries and raspberries, but I'm sure they would say there's some practical reason why this would be too expensive.
Still, I think they're missing a good opportunity here. Why not make two versions of each of these products -- a cheaper one which contains ground-up scale insects, and an expensive one which doesn't? Offering customers that choice, and watching their faces as they think about it, would have to be mighty entertaining, and would probably raise employee morale.
If I worked at Starbucks, I know I would jump at the chance to replace that tiresome question "room for cream?" with "room for bugs?".
BNP and Diabetes
Saturday, April 21, 2012
Fasting Glucose: 81 mg/dl.
Glucose 1 hour after lunch: 123 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 120/76 mmHg, 54 bpm.
Exercise: none (resting up for the half-marathon tomorrow).
Another Hormone to Fret About
Just in case you thought the question of what causes Type 2 diabetes was not quite complicated enough for your taste, and you wanted it to be more challenging, it turns out that there's another hormone you've never heard of which has something to do with this.
The hormone is called BNP. The acronym stands for B-type Natriuretic Peptide. To unpack the components of that:
The "B" in "B-type" stands for brain, but it's misleading: the hormone was first discovered in the brains of pigs -- but in humans it's produced mainly by the heart. What's that, you didn't know the heart could produce hormones? Apparently it can. And the heart produces more of this particular hormone when it needs help -- the hormone has healing effects, including a reduction in blood pressure.
"Natriuretic" means that the hormone causes the kidneys to expel excess sodium into the urine, as a means of reducing high blood pressure.
"Peptide" is a small protein molecule which, at least in this case, acts as a hormone.
People with abnormally low levels of BNP tend to have Type 2 diabetes.
Or should we say that people with Type 2 diabetes tend to have abnormally low levels of BNP?
Somehow or other, there is an association between diabetes and low levels of BNP, and researchers have been wondering which of these things is causing the other. A group of researchers at the University of Cambridge have conducted a study which concludes (although somewhat tentatively) that it is the reduction in BNP which is causing the diabetes, and not the other way around.
However, what the researchers haven't figured out is how a reduction in BNP could promote diabetes. They suspect that the patient's BNP level limits the impact of a gene variant ("rs198389") which is associated with Type 2 diabetes. In other words, having that gene variant puts you at risk for becoming diabetic, but whether or not that actually happens is determined by how high your BNP level is. If your BNP level is high enough, you're protected from the gene; if it isn't, you're not.
Okay, let's assume that is how it works. We are still left with the question of what determines whether or not you have enough BNP. Is that genetically driven, too? Or is there anything you can do about it?
Nobody knows. However, the BNP level tends to be low in obese people. So we're stuck with yet another causality problem! Does obesity depress BNP production, or does depressed BNP production cause obesity? That needs to be investigated, obviously. But if obesity depresses BNP production, and depressed BNP production increases vulnerability to the effects of the rs198389 gene variant, then at least that would explain the puzzle of how diabetes can be caused by both genes and lifestyle.
But, of course, I should pause here to acknowledge that BNP is only one hormone among many, and rs198389 is only one gene variant among many, that are known to be involved in Type 2 diabetes. This research cannot be the clue that unravels the whole mystery of the disease. It's just one more clue to add to the pile.
It's amazing how complicated diabetes is, in terms of what causes it and how it operates. The body's glycemic regulatory system involves so many hormones and genes, interacting in so many complicated ways, that it's hard to imagine we will ever get to the bottom of all this and be able to say, all right, now we really understand what causes diabetes and what's the best way to treat it.
I suppose some people, looking at this increasingly-complex tangle of genes and hormones that play a role in diabetes, conclude that this means the ultimate medication for diabetes will turn out to be a cocktail of 20 or 30 drugs, mixed together in just the right proportions to straighten out the whole mess. But what I conclude is that this means we cannot expect to find an ultimate medication for diabetes. It's like expecting to develop a chunk of computer code which, downloaded onto any PC, fixes whatever is wrong with it.
Diabetes, as a symptom, is simply the condition of having chronically elevated blood sugar. But diabetes, as a disease, is a scenario rather than a condtion. It is a chain of events, and the more we learn about that chain of events, the more complicated it turns out to be. But one thing is clear: it is a chain of events driven, very largely, by the way we live. Expecting to treat diabetes without changing the way we live is completely unrealistic.
The Patient-Centered Approach!
Thursday, April 19, 2012
Fasting Glucose: 93 mg/dl.
Glucose 1 hour after dinner: 67 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 123/73 mmHg, 60 bpm.
Exercise: 5.4 mile run at lunchtime; weight-training workout in the evening.
As my fasting blood sugar was above 90 this morning, and I like it to be below 90, I made a bit of an effort to drive it down today -- with two tough workouts: a hilly run at mid-day and a weight-training workout in the evening.
I didn't eat dinner until after the second workout, and while I was waiting after dinner for an hour to elapse, so that I could do a post-prandial test, I wondered if the test result was possibly going to be unusually low, simply because I felt that way.
Well, my goodness: 67! Apparently all that exercise drove me a little too far downward. I didn't want to fall further, so I ate some toast as a corrective measure.
I'm going to take it a little easier on exercise tomorrow -- I'll do some kind of light workout, but that's all. I need to store up a little energy for the half-marathon on Sunday.
The New Diabetes-Care Guidelines
The American Diabetes Association and the European Association for the Study of Diabetes have teamed up to produce a new set of clincal-practice guidlines entitled "Management of Hyperglycemia in Type 2 Diabetes: A Patient-Centered Approach". I'm not sure what diabetes care was centered on before, but it's patient-centered now. I'm sure you're as eager as I am to find out what that means.
What it appears to mean, from my hasty review of this rather dense document, is that it's a waste of time trying to find the single best way to treat Type 2 diabetes, and then treat every patient that way... because patients vary, and the disease varies on a case-by-case basis. A doctor's approach should be adapted to each patient's particular situation.
The paper includes a list of key points:
Glycemic targets and glucose-lowering therapies must be individualized.
Diet, exercise, and education remain the foundation of any type 2 diabetes treatment program.
Unless there are prevalent contraindications, metformin is the optimal first-line drug.
After metformin, there are limited data to guide us. Combination therapy with an additional 1 - 2 oral or injectable agents is reasonable, aiming to minimize side effects where possible.
Ultimately, many patients will require insulin therapy alone or in combination with other agents to maintain glucose control.
All treatment decisions, where possible, should be made in conjunction with the patient, focusing on his/her preferences, needs, and values.
Comprehensive cardiovascular risk reduction must be a major focus of therapy.
Looking over this list, I know I ought to be gratified to see that diet and exercise get an enthusiastic mention, and near the top of the list at that. But, pessimist that I am, I can't help suspecting that this reference to lifestyle as "the foundation" of diabetes treatment is only a bit of obligatory piety, and that the authors' hearts are not in it. Judging from the rest of the paper, it appears that they think "treatment" really means drugs, and that a patient-centered approach (with "individualized" therapies) really means giving different patients different drugs.
There are four stages shown: the first is metformin (recommended here for all patients as the initial drug therapy). When that stops working, metformin continues but is supplemented by one other drug (five alternative families of drugs are shown). When that stops working, metformin continues and is supplemented by two other drugs (various possible combinations are listed). When even that stops working, the patient moves on to multiple daily injections of insulin.
Two things to note here: (1) the assumption of a gradually worsening condition which will have to be opposed by increasingly scary pharmaceutical firepower as time goes on, and (2) the seeming absence of lifestyle-based treatment.
Ah, but lifestyle is not absent! The legend "Healthy eating, weight control, and increased physical activity" is inscribed on the thin turquoise frame which surrounds all those ordered stages of drug therapy. Now, you could argue (and I supose the authors would argue) that placing lifestyle issues on the frame surrounding all the treatments symbolizes its over-arching importance -- you need to do it no matter which drugs you're taking! However, my actual belief is that lifestyle issues are placed on a thin frame outside the list of treatments because lifestly issues are not regarded as being treatments at all. (Yeah, yeah, yeah, you have to stay active and watch what you eat -- but let's talk about real treatment!)
As further evidence that lifestyle adjustments are not regarded as real treatment, we have this comment: "In most patients, begin with lifestyle changes; metformin monotherapy is added at, or soon after, diagnosis". Hmmm. Every stage of drug-based treatment is given a stated interval (usually 3 months) to prove itself; the doctor only moves on to the next stage if the current stage has failed to produce acceptable results within the stated number of months. But no such waiting period is given for lifestyle-based treatment. The doctor should start the patient on metformin "at or soon after diagnosis", without waiting around to see what diet and exercise can do for the patient. Why this difference of approach? It can only be because the authors think there is no point in waiting around to see how well the patient is served by diet and exercise. They take it for granted that diet and exercise won't work, even temporily. Metformin neeeds to be given a chance to show what it can do; jogging does not.
What's new in these guidelines, apparently, is the emphasis on figuring out which drug combination is right for different kinds of patients, on the basis of many different factors which can limit the efficacy or safety of particular drugs in particular individuals.
I don't think this is the revolution in thinking about diabetes care that I would have liked to see.
But let me return for a moment to those Key Points that I listed earlier. One of them kind of gets on my nerves:
All treatment decisions, where possible, should be made in conjunction with the patient, focusing on his/her preferences, needs, and values.
What bothers me about that is the phrase "where possible". Under what circumstances is it not possible to consider what the patient wants, in choosing from among a set of possible treatments? As a patient myself, I kind of like to preserve the distinction between a patient and a prisoner of war.
Surgery & Starvation
Wednesday, April 18, 2012
Fasting Glucose: 81 mg/dl.
Glucose 1 hour after dinner: 101 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 110/69 mmHg, 59 bpm.
Exercise: 4.5 mile run.
Alternatives to Bariatric Surgery for Diabetes
There have been more and more studies coming out lately which claim to show that bariatric surgery (various surgical procedures which cause people to lose weight because their newly-shrunk stomach won't accept much food) is a far more effective treatment for Type 2 diabetes than the usual pharmaceutical approach.
If the usual pharmaceutical approach were the only alternative to bariatric surgery, then the only reason not to make bariatric surgery the standard treatment for Type 2 diabetes would be the price tag: giving an expensive operation to millions of people (at least 20 million patients in the U.S. alone) would have to run into money. Oh, and there's also another issue: nagging concerns about what happens to such surgical patients over the years (including the concern that they will have to keep going back for more surgery).
However, there is a false dichotomy involved in presenting this issue as a simple choice between surgery and drugs -- as if no other options existed.
Most forms of bariatric surgery work simply by limiting the size of the stomach and therefore restricting food intake (the more radical surgeries also remove parts of the digestive tract entirely, so that digestion and hormonal signaling are altered). If even the less-radical surgeries result in what looks like a diabetes "cure" (normal glycemic control, and even restored beta cell function in the pancreas), why shouldn't the same result be achievable, without surgery, simply by going on a restrictive diet?
Some researchers set out to test that idea, and found that they could indeed get the same remarkable results with an extremely restricted diet and no surgery. The patients in this study had a diet which consisted of protein shakes supplemented by non-starchy vegetables, with a daily calorie count of about 600. Result: amazing drops in blood glucose, HbA1c, and triglycerides, and an amazing restoration of beta-cell function. So apparently calorie restriction is all it takes.
However... let us address the elephant in the room, if that is not too vivid a metaphor in this case: a diet which limits you to 600 calories a day is going to be incredibly hard to stick to through will power alone. The reason people are interested in bariatric surgery in the first place is that it forces them to do something that they find virtually impossible to do if they're not forced. It is telling that the diet study was tiny -- it involved only 11 participants, for crying out loud. If it were easy to get people to stick to a diet that restrictive, I think the study would have included a much larger patient population.
This study was strictly about diet, not exercise. I would like to see a similar study done, in which the diet is not nearly so restrictive, but a lot of exercise is involved. Perhaps such a study would reveal that, in patients willing to do enough exercise, it is possible to get remarkable results with neither surgery nor starvation required.
Playing It Safe with Exercise & Drugs
Tuesday, April 17, 2012
Fasting Glucose: 89 mg/dl.
Glucose 1 hour after lunch: 91 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 123/74 mmHg, 60 bpm.
Exercise: 4.1 mile run at lunchtime; weight-training workout in the evening.
After my slightly volatile blood sugar yesterday (a reaction, I'm pretty sure, to the gruelling trail-run on Sunday afternoon), my system seemed to be on more of an even keel today.
I had been rather stiff and sore yesterday, so I'm pleased to say that I was feeling much better today, and running didn't bother me. I think I'll do a longish run tomorrow if my schedule at work permits, and then dial it back a bit, as I get myself ready for the half-marathon race on Sunday. For the last few days before a big race, you don't want to push yourself very hard. Store up some energy and some non-hurting muscles, that's the plan!
Milnacipran Makes the FDA Watch List
From time to time the Food & Drug Administration releases a "watch list" of drugs which are under investigation because of reports that they cause medical problems -- problems serious enough that they might oblige the FDA to ban them, or at least to require changes in the way they are prescribed and labeled.
When an updated version of the watch list is issued, I tend to scan through it to see if there's anything on it that pertains to diabetes. At first I thought there wasn't, when I saw the list of 16 drugs that were added to the watch list today. But one of them (milnacipran, sold under the name "Savella"), which in some reports about the watch list is described as a treatment for fibromyalgia, is also used to relieve the pain of neuropathy (that is, damage to nerves caused typically by diabetes). If milnacipran causes trouble, a lot of people with diabetes are going to have that trouble.
So, what is the trouble with milnacipran? Or rather, what is the new trouble with milnacipran, as other issues have been noted before?
Well, apparently the new trouble with milnacipran is that it seems to cause "homicidal ideation". This is, in a way, a refreshing turnaround; the watchdog group Public Citizen asked the FDA to ban the drug in the past, on the grounds that it caused suicidal ideation. (The FDA declined to do so.) I will admit that I'm a little more afraid to have people taking drugs that make them want to kill others than to have people taking drugs that make them want to kill themselves. So, I guess I'm not surprised that the FDA took the first problem more seriously than the second, at least to the point of investigating the issue.
The list of possible side effects for milnacipran is by no means confined to destructive thoughts. Other effects to watch out for include nausea, vomiting, constipation, stomach pain, lack of appetite, weight loss, dry mouth, headache, increased sweating, dizziness, feeling of extreme facial warmth and/or redness, blurred vision, disturbed sleep, loss of sexual desire or performance, pain or swelling in the testicles, difficulty urinating, rash, itching, hallucinations, memory problems, weakness, seizures, inability to concentrate, confusion, difficulty walking without falling, fainting, coma, slowed or stopped breathing, fast or pounding heartbeat, extreme fatigue, jaundice, flu-like symptoms, and internal bleeding.
So no really serious problems, unless it is true that the drug makes you want to kill.
If the suspected link between milnacipran and the impulse to kill! kill! kill! holds up under investigation, I imagine the FDA will have no choice but to do something about the issue. Whether that will mean banning the drug or merely adding a "black box" label, warning the consumer that taking this medication may cause a tendency to slay, I don't know. If the latter solution is chosen, I hope the label will be shown not just to the pharmacist and the patient, but also to the patient's family, friends, neighbors, co-workers, and fellow-users of the public roads. If there are people around me whose doctors have been medicating them into a homicidal state, I feel as if I ought to know about it.
Monday, April 16, 2012
Fasting Glucose: 77 mg/dl.
Glucose 1 hour after lunch: 141 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 114/70 mmHg, 52 bpm.
Exercise: walking at lunchtime; aerobic workout and yoga class in the evening.
Aftermath of A Long-Distance Run
After the storms on Friday,
the weekend weather in Sonoma County was peaceful and sunny...
...and everybody was outdoors taking advantage of it.
I figured I'd better take advantage of it, too.
Ever-mindful that I have a half-marathon coming up on April 22, I've been trying to tuck some extra mileage into my running schedule lately, even though the weather has not been especially cooperative. As the weekend weather was good, I figured I should get in one last long-distance run before the race.
So, yesterday I went to the state park and did a very difficult trail run which, at a total distance of 12.6 miles, was very nearly the same length as the half-marathon (13.1 miles). The trail run was probably a lot harder than the actual race will be: the hill-climbs were much steeper, and the trails were were rocky and muddy. Also, in some places the trails were submerged under a swift-flowing stream (because runoff from Friday's storm was still coming off the hills). Fording one of these little streams, I stepped on a rock which looked flat and stable -- but it flipped over and threw me down on the rocks. Embarrassing! (Or it would have been, if anyone had been there to see it. Fortunately it happened in a remote area of the park, with no witnesses.)
I didn't injure myself significantly, but today I am sore in various places from that. That was why I didn't run today -- I figured I'd give myself a break and do a ligther workout in the gym after work.
It's hard to know where you cross the line between exercise as a health-promoting activity and exercise as trauma. I felt the need, going into the run, to give myself a real endurance workout -- not just to make sure I was prepared to handle the race next Sunday, but also to push my body well outside its comfort zone. I think there is therapeutic value in that. But you don't want to push yourself so far outside the comfort zone that you get into the injury zone.
The last two miles of the run were pretty hard -- I was feeling very tired, and perhaps also a little hypoglycemic. The feeling never quite got to the threshold of discomfort where I feel that I have no choice but to stop and take a glucose gel; I just felt hungry and tired. So, I completed the run, and waited until I got home (and had a shower) before I ate anything. And my dinner was not high-carb, either.
I assume that is why I had an unusually low fasting result (77) this morning. But it could also be why I had an unusually high post-prandial result (141) after lunch; I think my glycemic control system ran through some odd gyrations today, going low and then overcompensating and swinging high.
An extreme workout disturbs the system and causes some short-term oddities, so it's a legitimate question to ask, whether it is "worth it" to push yourself that far. I tend to think that it is, but I can't prove it. My feeling is that, if I sign on to extreme exercise events (such as the half-marathon race on Sunday) once in a while, this will force me to stay in good enough shape the rest of the time to be able to do such things when I need to.
The real value of these exceptional events lies in the effect they have on what I the rest of the time! Yesterday's long run was hard on me in more ways than one, but the habit of keeping myself in a state of readiness to do very long runs has beneficial effects on me which I might not obtain otherwise.
Friday the 13th
Friday, April 13, 2012
Fasting Glucose: 90 mg/dl.
Glucose 1 hour after dinner: 132 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 122/73 mmHg, 52 bpm.
Exercise: 4.1 mile run.
On Friday the 13th -- the dopiest of all Special Occasions -- I'm seldom in a very serious mood. So, I think I'll just amuse myself, instead of launching into any kind of serious discussion of diabetes-related issues.
You know those decorated walls with holes for you to stick your head through, so that you can pose for a humorous photo, with your face seemingly atop the body of a person or animal? What the hell are those things called? Surely there is a word for them. But so far my web searches for the answer have turned up nothing plausible. Well, for some reason we have one of those in the office this week (I think someone is planning to use it to break the ice at a training event next month.) Anyway, it features a couple of boxers, so I posed for a picture with it this afternoon. I was planning to show it to you as evidence of my progress on the weight-lifting front, but I'm not sure the photo is absolutely convincing.
While I was posing for this, a sudden storm was exploding outside. Strange, as the weather had been nice when we'd gone running at lunchtime -- and weather in northern California is not nearly as volatile as it is in most other places. Sudden storms are a rarity here. When I got home (which is little more than a mile from my workplace, but 400 feet higher in altitude) I found the ground covered with what looked like patches of snow.
On closer examination the "snow" turned out to be a pileup of hailstones from the storm that hadn't melted yet.
Either that or it was tapioca.
Household Hints from 1887
At some point during my childhood, one of my sisters brought home a paperback book about witchcraft she had found at garage sale; it explained how to perform various magic spells. Immediately I wanted to try them out, and see if these spells really worked. However, the first few that I read called for bizarre ingredients, or for commonplace ingredients that had to be obtained under bizarre conditions. (It wasn't enough to just gather the mushrooms -- you had to collect them during a thunderstorm on Good Friday, or something like that, so that there really was no practical way to fulfill the requirements as written.) Frustrated, I hunted through the book, trying to find at least one magic spell that didn't have any impractical conditions attached to it, so that it would be easy for me to try it. But the entire book was that way. Every spell called for some prop or ingredient that I didn't have and couldn't get.
Nowadays, of course, I realize why the book had to be written that way. If the spells didn't involve unreasonable requirements, anybody could try them out, and discover that they don't work. Adding unreasonable requirements to the instructions you give is a very useful tactic to employ when you are giving advice and you don't want to take responsibility for it. So long as you're advising people to do something that you know perfectly well they won't do, you don't have to worry about them coming back to say that they did what you suggested and it turned out badly.
I think a lot of advice is given on this principle. So it is, I think, in the case of the household hints that I found in the Project Gutenberg on-line edition of "The White House Cook Book", an 1887 volume which purported to share the domestic wisdom of the wives of U.S. presidents with a wider audience.
In some cases the household hints included in this book are more notable for the problem being addressed than for the proposed solution to it (how many books of household hints today would offer advice on cleaning marble busts?). But what I mainly notice about these hints is the difficulty of doing what is being suggested, or even finding the ingredients required. It seems to be the book of magic spells all over again.
Anyway, I offer some of my favorite hints below, for whatever entertainment value they may provide.
Paint for Wood or Stone that Resists all Moisture:
Melt twelve ounces of resin; mix with it, thoroughly, six gallons of fish oil and one pound of melted sulphur. Rub up some ochre or any other coloring substance with a little linseed oil, enough to give it the right, color and thickness. Apply several coats of the hot composition with a brush. The first coat should be very thin.
Vinegar boiled with myrrh, sprinkled on the floor and furniture of a sick room, is an excellent deodorizer.
Destroy Moths in Furniture:
All the baking and steaming are useless, as, although the moths may be killed, their eggs are sure to hatch, and the upholstery to be well riddled. The naphtha-bath process is effectual. A sofa, chair or lounge may be immersed in the large vats used for the purpose, and all insect life will be absolutely destroyed. No egg ever hatches after passing through the naphtha-bath; all oil, dirt or grease disappears, and not the slightest damage is done to the most costly article. Sponging with naphtha will not answer. It is the immersion for two hours or more in the specially prepared vats which is effectual.
A small quantity of carbolic acid added to paste, mucilage and ink, will prevent mold. An ounce of the acid to a gallon of whitewash will keep cellars and dairies from the disagreeable odor which often taints milk and meat kept in such places.
Dissolve a ball of white beeswax, one inch in diameter, in half a pint of turpentine. Saturate the paper in this bath and let it dry two or three days before using.
Dip them for a minute or two in a kettle of boiling suds once a week and they will last much longer, making them tough and pliable. A carpet wears much longer swept with a broom cared for in this manner.
Polish or Enamel for Shirt Bosoms is made by melting together one ounce of white wax, and two ounces of spermaceti; heat gently and turn into a very shallow pan; when cold cut or break in pieces. When making boiled starch the usual way, enough for a dozen bosoms, add to it a piece of the polish the size of a hazel nut.
An Erasive Fluid for the Removal of Spots on Furniture, and all kinds of fabrics, without injuring the color, is made of four ounces of aqua ammonia, one ounce of glycerine, one ounce of castile soap and one of spirits of wine. Dissolve the soap in two quarts of soft water, add the other ingredients. Apply with a soft sponge and rub out. Very good for deaning silks.
Clean Marble Busts:
First free them from all dust, then wash them with very weak hydrochloric acid. Soap injures the color of marble.
To Remove old Putty from Window Frames, pass a red hot poker slowly over it and it will come off easily.
Take Rust from Steel Implements or Knives:
Rub them well with kerosene oil, leaving them covered with it a day or so; then rub them hard and well with finely powdered unslaked lime.
Scouring Soap for Cotton and Silk Goods:
Mix one pound of common soap, half a pound of beef-gall and one ounce and a half of Venetian turpentine.
Prevent Oil from Becoming Rancid:
Drop a few drops of ether into the bottle containing it.
A Good Polish for Removing Stains, Spots and Mildew from Furniture is made as follows: Take half a pint of ninety-eight per cent alcohol, a quarter of an ounce each of pulverized resin and gum shellac, add half a pint of linseed oil; shake well and apply with a brush or sponge.
Remove Paint from Black Silk:
Patient rubbing with chloroform will remove paint from black silk or any other goods, and will not hurt the most delicate color or fabric.
Colors in Washable Goods:
Soak them previous to washing in a water in which is allowed a tablespoonful of ox-gall to a gallon of water.
Ants that frequent houses or gardens may be destroyed by taking flour of brimstone half a pound, and potash four ounces; set them in an iron or earthen pan over the fire until dissolved and united; afterwards beat them to a powder, and infuse a little of this powder in water, and wherever you sprinkle it the ants will fly the place.
The following is a refreshing disinfectant for a sick room, or any room that has an unpleasant aroma prevading it: Put some fresh ground coffee in a saucer, and in the centre place a small piece of camphor gum, which light with a match. As the gum burns, allow sufficient coffee to consume with it.
Keep out Mosquitoes and Bats:
If a bottle of the oil of pennyroyal is left uncorked in a room at night, not a mosquito, nor any other blood-sucker, will be found there in the morning.
Scour Knives Easily:
Mix a small quantity of baking soda with brick-dust and see if your knives do not polish better.
Plush goods and all articles dyed with aniline colors, which have faded from exposure to the light, will look as bright as new after sponging with chloroform.
Put a little saltpetre in the water you use for your bouquets and the flowers will live for a fortnight.
Hellebore sprinkled on the floor at night. They eat it and are poisoned.
Carpets after the dust has been beaten out may be brightened by scattering upon them corn meal mixed with salt and then sweeping it off. Mix salt and meal in equal proportions. Carpets should be thoroughly beaten on the wrong side first and then on the right side, after which spots may be removed by the use of ox-gall or ammonia and water.
If oil-cloth be occasionally rubbed with a mixture of beeswax and turpentine, it will last longer.
Remove Mildew from Cloth:
Put a teaspoonful of chloride of lime into a quart of water, strain it twice, then dip the mildewed places in this weak solution; lay in the sun; if the mildew has not disappeared when dry, repeat the operation. Also soaking the article in sour milk and salt; then lay in the sun; repeat until all the mildew is out.
Take Ink out of Linen:
Dip the ink spot in pure melted tallow, then wash out the tallow and the ink will come out with it. This is said to be unfailing. Milk will remove ink from linen or colored muslins, when acids would be ruinous, by soaking the goods until the spot is very faint and then rubbing and rinsing in cold water.
Ink spots on floors can be extracted by scouring with sand wet in oil of vitriol and water. When ink is removed, rinse with strong pearl-ash water.
A piece of zinc put on the live coals in the stove will clean out the stove-pipe.
Hartshorn applied to the stings of poisonous insects will allay the pain and stop the swelling; or apply oil of sassafras, which is better.
Cutting off Glass Bottles for Clips and Jars:
A simple, practical way is to take a red-hot poker with a pointed end; make a mark with a file to begin the cut; then apply the hot iron and a crack will start, which will follow the iron wherever it is carried. This is, on the whole, simple, and better than the use of strings wet with turpentine, etc.
Buttermilk is invaluable in the treatment of diabetes.
Conflicting Health Goals
Thursday, April 12, 2012
Fasting Glucose: 94 mg/dl.
Glucose 1 hour after lunch: 113 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 123/74 mmHg, 55 bpm.
Exercise: 4.3 mile run at lunchtime; weight-training workout in the evening.
Does Good Glycemic Control Kill People?
There's been some extremely strange news developing in regard to heart failure. (As always, we must pause to explain that the confusing term "heart failure" doesn't mean what it says. The idea is not that the heart has stopped beating, but rather that the pumping action of the heart is weak and isn't moving enough blood volume through the arteries.) Anyway, heart failure is a common chronic condition, and many people who have that condition have diabetes, too.
It is always a tricky thing to manage two or more chronic diseases at the same time. What if the treatment that makes one of them better makes the other one worse? And if you are in that situation, how do you decide whether the positive effect of the treatment in one area is valuable enough to offset the negative effect of the same treatment in a different area?
Apparently this dilemma arises in people who suffer from both heart failure and diabetes. A new study from UCLA, reported in the American Journal of Cardiology, finds that, for heart-failure patients who also have diabetes, the two-year survival rate (in this case "survival" means neither dying nor requiring an urgent transplant) gets worse and worse as glycemic control gets better and better.
The paradoxical table below shows how the survival rate of heart-failure patients varies for different Hemoglobin A1c ranges (the patients are sorted into four "quartiles" -- that is, the ranges are chosen so as to get 25% of the patients in each range). Surprisingly, survival rates drop as A1c drops. That is, improvement in glycemic control is associated with lower survival rates, not higher survival rates. (Comparable figures for non-diabetic patients are shown here, too -- more on that in a moment.)
|HbA1c %||2-Year Survival %|
|7.3 - 8.5||60.7|
|6.5 - 7.2||41.5|
|6.1 - 6.5||51.1|
|5.7 - 6.0||60.6|
The range of variation in A1c is naturally much narrower in non-diabetic patients; the range of survival rates is also narrower, and shows no consistent pattern of correlation with A1c. (However, I can't help but wonder how a quarter of this group of "non-diabetic" patients come to have A1c results above the diagnostic threshold for diabetes!)
But back to the patients diagnosed as diabetic. Why would it be that the people with A1c results above 8.6% (indicating very poor glycemic control) would have a subtantial edge in survival rate, compared to patients with A1c results below 6.4% (indicating much better control)? I mean, when more than two-thirds of the "bad" patients survive and less than half of the "good" patients do, what is going on here? How do we interpret this?
Well, I'm sure there will be a faction arguing (as the same faction has argued before, especially in connection with ACCORD study) that good glycemic control is somehow inherently harmful. To hear them talk, you would think that merely to be in the normal glycemic range is enough to kill you. This makes we wonder how they think people manage to survive without diabetes, given that non-diabetic people live their entire lives in that oh-so-dangerous normal glycemic range.
A likelier explanation for the increased rate of death from heart failure, among diabetes patients maintaining tight glycemic control, is that whatever medications most of them are taking are doing them harm, either directly or by causing frequent hypoglycemic episodes which somehow stress the heart.
Even if it could be shown conclusively that out-of-control blood sugar does something positive in terms of preventing death from heart failure, I think that it does too much harm in other areas for hyperglycemia to be judged a good thing. (Supposedly smoking slightly reduces your risk of Alzheimer's disease, but no doctor recommends smoking on that basis, because of all the other problems it causes.)
It seems to me that what medical researchers ought to take away from this study (and ought to take away from similarly paradoxical studies, such as ACCORD) is not that glycemic control is bad, but rather that taking drugs is not the safest way to achieve glycemic control. Instead of abandoning the effort to control diabetes, because heart failure is a more immediate danger, maybe the right thing to do is to find a way to control diabetes which doesn't aggravate heart failure.
If that message ever does get through to researchers, and they start wondering what else to try, I'm here to help.
But Does It Work?
Wednesday, April 11, 2012
Fasting Glucose: 92 mg/dl.
Glucose 1 hour after lunch: 112 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 120/74 mmHg, 61 bpm.
Exercise: 6.6 mile run.
How Effective Is Metformin?
Considering that diabetes is one of the most common of all chronic illnesses (an estimated 350 million patients worldwide), and considering that the diabetes drug metformin has long been one of the most commonly-prescribed of all medications (42 million prescriptions in the United States in 2009)... you would think there could be no real doubt at this point about how effective metformin is as a treatment for diabetes.
Yessir, you would think that. But you would be wrong.
A recent meta-analysis of 13 studies of metformin efficacy came to the conclusion that we urgently need more studies of this subject, because the efficacy of metformin remains entirely unclear. Results of the studies were all over the map. They varied so much that it is possible the drug reduces all-cause mortality by 25% -- or increases it by 31%. For mortality specifically caused by cardiovascular disease, it is possible that metformin reduces it by 33% -- or increases it by 64%. As for "secondary outcomes", meaning health problems which weren't immediately fatal to the patient but were presumably not enjoyed (little things like heart attacks, strokes, heart failure, peripheral vascular disease, amputations, and microvascular complications), the meta-analysis was unable to confirm with any confidence that metformin made a difference one way or the other. The clearest signal to emerge from the data was a tendency for the combination of metformin and sulfonlyurea to makes things worse (certainly worse than either drug alone).
Now, an objection could be (and presumably will be) made, to the effect that these studies compared metformin to other treatment (not to doing nothing), and also that these studies defined efficacy in terms of people not getting sick and dying (not in terms of blood sugar being reduced). I think these objections are answerable.
First, the "other treatment" to which metformin was compared was in many cases dietary control, not medication with newer drugs, and we cannot simply assume that patients abandoned dietary control once they started taking metformin; therefore, the comparison between people taking metformin and people not taking it was probably fair.
Second, preventing people from getting sick and dying is a legitimate goal for any kind of medical treatment, and a reasonable criterion to use in judging efficacy. It is only natural for pharmaceutical companies to wish that drugs were evaluated only in terms of whether or not they improve someone's lab numbers, and never in terms of whether they improve someone's health -- because improving someone's health is a much more complicated assignment. Still, when all is said and done, people expect a medication to improve their health, and when that doesn't happen they are unlikely to find consolation in a lab report.
What are we to conclude from all this? Well, the authors of the meta-analysis seem to think that we can't safely conclude anything from such contradictory data. They note that the variability of results from study to study was "more than would be expected by chance", which is a scientist's way of saying "something fishy is going on here" without speculating about what that something might be.
If the study results point to metformin being highly effective, or maybe entirely ineffective, or maybe outright harmful... it all boils down to "we really don't know anything about metformin efficacy", doesn't it? The data yields no answer.
But sometimes no answer is a kind of answer. Call me unreasonable, but my expectation is that a genuinely successful therapy will yield unambiguous evidence of success. When studies contradict each other about whether or not an effect exists (for example, research into "psychic powers"), it typically means that the effect doesn't exist but some of the researchers want to think it does. There is an ugly possibility that the same pattern is occurring in the case of metformin studies, with the most positive results being found by the researchers who are most inclined to want or expect them.
Most people, of course, do not evaluate diabetes drugs in terms of long-term health outcomes. They look at the short-term impact on blood sugar, and put their trust in the assumption that, if you correct the latter, the former will take care of itself. The trouble is that it seems to matter how you correct the latter; choosing the wrong method may prevent your short-term accomplishments from yielding long-term rewards.
I face the same problem
myself, of course. What if my method of getting
short-term results doesn't yield long-term rewards? Well, that would be bad --
but I think there's some pretty good evidence in favor of doing it my way.
It was an unpleasantly over-stressed day at work, which actually made it a blessing rather than a curse that one of my running buddies wanted to run an extremely difficult route which we haven't done in over a year. An extra-stressful day can only be relieved by an extra-hard workout.
That route is a long run (6.6 miles) and involves an insanely steep hill-climb (the route goes up to a street called "Skyfarm", and it's called that for a reason). Because we're scheduled to do a half-marathon run on April 22, she figured we ought to work in some long runs as the date approaches. (I already started that, actually: on Sunday I ran 9.5 miles.) The skies today were gloomy and threatening, and it did rain on us a little bit. But the hard run felt good -- particularly the hot shower after it was done.
I came home and noticed that a
headline in yesterday's blog claimed that I had had some "glucose
adentures". "Adventures" was actually the word I'd had in mind. False
teeth played no role in my activities yesterday, so I corrected the spelling.
Glucose After 2 Meals
April 10, 2012
Fasting Glucose: 92 mg/dl.
Glucose 1 hour after lunch: 131 mg/dl.
Glucose 1 hour after dinner: 84 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 109/66 mmHg, 58 bpm.
Exercise: Gym workout (weight training and aerobic).
Post-Prandial Glucose Adventures of the Day
No wisdom to share this evening; I'll just report the glycemic outline of my day.
It was rainy, and I was just as unenthusiastic about going out in it at lunchtime as my running buddies in the office were. So, I knew I would be going to the gym after work instead.
Even though my lunch did not follow a run, as it usually does, and I was therefore not getting the sharp boost in insulin sensitivity which often enables me to get away with a starchier-than-average meal at lunchtime... I was hit pretty hard by carbohydrate cravings at lunchtime, and I ate a comparatively high-carb meal -- a taco plate at the cafeteria. Two tacos and some refried beans (no rice, at least -- I dodged that bullet). So, my post-prandial test result was higher than what I usually see. 131 is within my doctor's guidance, but 125 seems to be about as high as non-diabetic people go, and I usually try to score bonus points by staying under 125.
Anyway, 131 is just high enough to make me want to make up for it -- and prove to myself that I can do better. I was wondering how much lower my post-prandial result would be after dinner, if I did a workout first, and then ate a meal that was substantially lower in carbs. I tried the experiment (the workout featured both weight-training and aerobics, and the dinner featured roasted chicken breast, brussel sprouts, and milk). This time my post-prandial result was 84.
That's quite a drop, and as no medication is involved to cloud the issue, the comparison between those two results gives you some idea how much difference a workout makes, and how much difference it makes to limit your carbs.
And, once again, I noticed how much lower my blood pressure can be on an evening when I've done a weight-training workout. Doctors should emphasize that point to hypertension patients more; weight-training really seems to help with that.
Monday, April 9, 2012
Fasting Glucose: 86 mg/dl.
Glucose 1 hour after lunch: 116 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 123/75 mmHg, 51 bpm.
Exercise: 4.5 mile run at lunchtime; yoga class in the evening.
The Tipping Point on Weight Training
On Saturday something remarkable happened -- although it won't sound remarkable to you, so I'll have to explain what's remarkable about it.
What happened was that, even though I was having a busy day, and I was heading out of town, and it was supposed to be a rest day from exercise... I felt an urge to stop by the gym and do some weight-training. And the urge was strong enough that I actually stopped at the gym before leaving town, and did the workout.
What's remarkable is that I actually felt an impulse to go lift weights (on a day when I had already given myself permission not to exercise at all!), and that the impulse was strong enough to make me follow through on the idea. You see, even though I have managed to train myself to see aerobic exercise (usually running) as something I need to do, and even want to do... in recent years I was seldom doing weight-training with any kind of regularity (and when I did it, I didn't like it). Now and then I have felt a mild pang of conscience about not lifting, and have occasionally made a half-hearted acknowledgement that I really ought to get back into the habit. But I never really felt a spontaneous urge to go lift weights.
Lately I have started doing weight-training workouts more often, but until quite recently I have done them glumly, as a duty to be discharged, and certainly not as a hobby to be enjoyed. I doubt that anyone would have picked me out at the gym as the guy who was setting an example of rambunctious enthusiasm.
Maybe I finally did it enough for some kind of habit-controlling switch to get flipped in my brain. Maybe it was that I was finally starting to notice some enlargement of my arm muscles, and this was encouraging me. Anyway, I have somehow got into the mode of wanting to do strength-training.
Which is a good thing, because there are benefits to be had from it.
Strength-Training & Diabetes
The recognition that strength-training, and not just aerobic exercise, is important to good health in general (and diabetes management in particular) is a comparatively recent development in medicine. It used to be thought that aerobic exercise was all you really needed -- that strength training added nothing unique to the mix (apart from new opportunities for people to injure themselves). Diabetes patients, and older patients generally, were often advised against doing weight-training, largely because of fears (never really grounded in evidence) that the steep (but temporary) rise in blood pressure associated with strength training would pose a danger to such patients.
Also, strength-training (or
"body building", as it was usually called) had a bit of an image problem. It was
seen as the hobby of narcissistic jerks who didn't have enough sense to realize
when they had gone too far. Body-building was assumed to be about wild,
ridiculous excess. Anyone working on his biceps was assumed to be trying to
make them too big to fit in a shirt-sleeve -- or even in a pants-leg.
Well, there are guys like that, obviously -- and even girls like that. When you get that fanatical about what you're doing, you can go too far by miles. I'm sure these extreme boldybuilders think of themselves as icons of good health, and are puzzled to find that not everyone agrees. Why aren't people just admiring their accomplishments, instead of speculating about what all those steroids are going to do to them in a few more years?
Anyway, doctors are obviously not going to be in a hurry to endorse a form of exercise which they associate with a weird and reckless subculture. So, it's not surprising that the medical establishment took its time about concluding that strength-training can be good for your health -- and especially good for the very people (diabetes patients, and older patients generally) who were once being steered away from it.
But various studies in recent years have looked at the health-benefits of different kinds of exercise, and have concluded that the combination of strength-training with aerobic exercise is more effective than either type of exercise alone -- something like twice as effective, in terms of reducing average blood sugar. These studies include a Canadian study at the University of Calgary and the University of Ottawa in 2007, a study at the Louisiana State University in 2010, and other studies summarized in this Diabetes Spectrum review.
As Ronald J. Zacker writes in
the latter article:
"Physical fitness is composed of several components, including cardiorespiratory endurance, body composition, muscular endurance, muscular strength or power, flexibility, and balance/coordination. Each component of fitness has a unique role in the preservation of health. Whereas aerobic exercise primarily targets the cardiorespiratory endurance component, strength training appears to play a prominent role in many, if not all, of the other six components to physical fitness. In doing so, strength training has unique potential in helping to arrest much of the functional decline and disease progression associated with aging."
The gradual loss of muscles mass, bone mass, and balance over the years contributes greatly to the frailty of old age -- but we are not powerless to do anything about these losses; strength training is the best protection (perhaps the only protection) from them. Not only that, strength training reduces cardiovascular risk independently of other exercise done by the patient, and tends to reduce blood pressure (instead of increasing it, as doctors initially feared).
More pertinent to diabetes, people who combine the two types of exercise do a lot better at controlling blood sugar than people who avoid strength training. "Incorporating both types of activity appears to take advantage of differing mechanisms of action, enhancing insulin sensitivity and glucose disposal further than either activity could achieve alone."
So, I'm glad I am now finding it easier and more appealing to do weight-training -- since it's something I obviously need, whether I like it or not. In that situation, you might as well learn to like it!
Your (Implied) Diabetes Questions
Friday, April 6, 2012
Fasting Glucose: 84 mg/dl.
Glucose 1 hour after lunch: 120 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 120/69 mmHg, 55 bpm.
Exercise: 5.2 mile run.
Well, that's more like it: fasting result of 84, down from 100 on Thursday morning. I was more careful about the carbs yesterday, and because my ankle was feeling better I had a tougher workout in the evening; those two things together brought my fasting level back down where it belongs.
Today -- with the weather still clear sunny and clear -- I choose one of our more scenic (and hilly) running routes, and my ankle wasn't complaining afterward, so I guess I'm recovered.
It's time once again to review some of the phrases which people have typed into search engines recently, resulting in referrals to this site.
"how to not be hungry with a calorie deficit"
That's the answer everyone is looking for, and will never find. Asking how not to feel hungry when you're taking in fewer calories than you're burning is like asking how not to feel cold when you're crawling naked through snowdrifts.
I don't think you can have it both ways in this regard. Running a calorie deficit means being hungry. If you're not hungry, you are almost certainly not running a calorie deficit. That's why losing weight is so hard: you can't do it without feeling hungry a lot of the time, and people hate feeling hungry a lot of the time.
Yes, I know that most promoters of a weight-loss diet claim that, on their diet (unlike the other diets you've tried) you won't be hungry. For example, people who promote low-carb high-fat diets argue that high-fat foods make you feel more full than low-fat foods with the same caloric value. Perhaps that is true, and perhaps the hunger problem is therefore not as severe for people on that sort of diet. But my experience is that, no matter what I'm eating, if I'm running a calorie deficit, I'm hungry. Maybe my experience is atypical -- but if it were, then most people would find it easy to lose weight, wouldn't they? And I hear that most people aren't finding it easy to lose weight.
One fact which might be useful, though: the sense of thirst tends to become increasingly unreliable as we advance in years, and very often when adults are dehydrated, the need to take in water manifests as hunger rather than thirst. In other words, when you are feeling hungry, it may be that your body is really trying to get you to take in some water. So, when you're feeling hungry, your first response should be to down a big glass of water, because sometimes that will be enough to make the feeling go away. I'm not claiming this is a miracle cure, but sometimes it's helpful.
"urine ate by ants = pregnant"
Well, here we are again. I seem to have become the internet's go-to guy for information about sugary urine attracting insects.
That phenomenon has been recognized for many centuries as a symptom of diabetes mellitus (and practically the definition of diabetes mellitus, as that phrase can be roughly translated as "pissing honey"). However, lately, I have been seeing a lot of these search strings in which people are implying that urine which attracts swarms of insects is a sign of pregnancy, not a sign of diabetes. I don't know where this is coming from -- is there a folk belief in some culture or other, to the effect that pregnancy sweetens a woman's urine?
Well, some women develop "gestational diabetes" during pregnancy, and that would be enough to get the insect world interested. But gestational diabetes is the exception rather than the rule; so far as I know, pregnancy by itself is not enough to win you any followers who go on six legs.
"why does urine a bit sweet and im not diabetic"
Sweet urine is a typical indication of poorly-controlled diabetes (sugary blood leads to sugary urine, as the kidneys try to get rid of the excess sugar by excreting it).
However, I'm not sure there is any mechanism which will make your urine sugary even when your blood isn't, unless you are taking a drug (such as dapagliflozin) which is designed to produce that effect. Perhaps there is a disease which blocks glucose reabsorption in the kidney, bringing about the same effect as dapagliflozin in the absence of the drug -- but if there is such a disease, I haven't heard of it.
So, I'm skeptical. Your two claims (that your urine is sweet, and that you don't have diabetes) seem incompatible with one another. I'm guessing that one of these claims is probably wrong.
"what does fasting hemoglobin of 6.2 mean for non diabetic"
It probably means that you are not going to be non-diabetic much longer.
Reasonable people can disagree about where the upper limit for the "normal" Hemoglobin A1c range is, and where the diagnosis point for diabetes ought to be, and what the range in between those two points should be called. But, by most definitions, an HbA1c result of 6.2% is higher than would be seen in a patient whose endocrine system is functioning completely normally.
In other words, your endocrine system is starting to have difficulty maintaining normal glycemic control. This situation has a built-in tendency to get worse if you don't do anything to turn it around -- and the longer you wait to do something about it, the harder it will be to turn it around.
Another thing I would like to see turned around is the popular notion of "diabetic" and "non-diabetic" as absolutely distinct categories, with no gray area in between them. Most people seem to think that, so long as they can squeak by as not quite meeting some arbitrary definition of "diabetic", they've got no problem, nothing to worry about, and no work to do. They're wildly wrong about this.
"victoza had kept my glucose numbers down but now they're climbing"
Victoza is a GLP-1 analog. That is, Victoza is an injectable, fake version of a naturally-occuring peptide hormone which (1) diminishes the release of stored sugar from the liver, (2) stimulates production of insulin, and (3) increases sensitivity to insulin.
Naturally-occurring GLP-1 is released by the body in fine-tuned amounts, and only when it is needed. Fake GLP-1 (such as Victoza) is injected in a great big dose which is supposed to last you all day. So, it's a fairly blunt instrument, and it can be hard for the body to tolerate (it makes a lot of people feel sick), but it does clobber blood sugar fairly well.
I don't know why Victoza would work for you and then stop working, but I have a reasonable guess: any drug which operates (at least in part) by stimulating your pancreas to produce insulin is going to lose effectiveness after the maximum insulin-producing capacity of your pancreas declines. Whether or not this is a case of the drug "wearing out" the pancreas, or a case of the pancreas losing productivity for some other reason, I don't know -- but whatever the explanation for the problem is, once your pancreas isn't able to make as much insulin as it used to, Victoza isn't going to work as well for you as it used to.
Also, if your sensitivity to insulin has declined for some reason (weight gain? insufficient exercise? the aging process?), Victoza isn't going to work as well for you as it used to.
Bear in mind that diabetes drugs operate by interfering with a complex system -- and if the system itself changes, the effectiveness of the drug changes. Suppose you found that your gas mileage wasn't as good after you moved from the plains of Nebraska to the mountains of Colorado -- in that situation, would you blame your car, or would you think that the altered terrain was making it harder for your car to get the same results as it used to? If your Victoza isn't getting the mileage it used to, it could be that the terrain inside you has altered.
Healing & Drugs
Thursday, April 5, 2012
Fasting Glucose: 100 mg/dl.
Glucose 1 hour after dinner: 113 mg/dl.
Weight: 186 pounds.
Blood pressure, resting pulse: 116/72 mmHg, 60 bpm.
Exercise: Gym workout (aerobic and weight-training).
The Walking Wounded
A fasting level of 100 is not what I wanted to see this morning, but I must admit that I expected to be at least a little elevated. Because of my sore ankle, I was comparatively inactive yesterday. I did get a minimal amount of exercise, but it was much lighter exercise than I usually do, and I was not moving around a lot otherwise. And, looking back on it, I had too much to eat, and too many carbs, for the circumstances.
One of the great drawbacks to having diabetes is that, the more you feel in need of "comfort food", the less your system is ready to absorb any food that is especially comforting.
The good news: today my ankle feels fine. The whole episode seems almost unreal to me. After the initial injury on Tuesday at noon, I didn't hurt until 2 AM Wednesday (but then it hurt like crazy). The injury healed rapidly over the course of the next 24 hours, and when I got up this morning I felt entirely recovered.
Naturally, I was tempted to go back to running today, especially as it was another beautiful sunny day. Still, I figured that would be rushing things just a little. Instead I took the same lunchtime walk as I took yesterday (faster this time), and in the evening I had a tougher workout at the gym (weights and the stair-climber). My ankle still felt fine afterwards. I'll try running tomorrow, and see how that goes.
Diabetes Management: Drugs, Drugs, Drugs!
A doctor named Matthew Mintz did a blog post entitled "Is It Time To Stop Using Sulfonylureas?", and was surprised at how controversial his views on the subject proved to be. An opinion poll which accompanied his blog got a result which was almost evenly split between those who thought these particular oral diabetes drugs had outlived their usefulness and those who thought it was best to keep using them because they are cheap and they have been around long enough for doctors to know their limitations.
He received 51 comments on his blog post. Most, perhaps all, of these comments came from doctors -- doctors whose mastery of spelling and grammar was not notably superior to what we see in on-line forums generally, whether the subject is pharmacology or auto racing. One of the doctors referred to diabetic progression as "unrelentless", apparently combining the words "relentless" and "unrelenting" (which mean the same thing) to form a new word which seemingly means the opposite of either. Then other doctors took up this coinage and used it without embarrassment. It seemed clear enough to me that they thought "unrelentless" meant "relentless". But, come on: how hard is "un"?
Anyway, the whole discussion was interesting to me more for what wasn't said than for what was. The word "exercise" appeared precisely once, in a long and meandering dialogue about competing approaches to diabetes management. So did the word "diet" -- and in the same place. Here's the quote: "It might be possible to spare patients insulin if we can preserve beta cells with diet, exercise and combinations of therapies which include metformin and TZD's". Even in the one sentence where lifestyle enters the conversation, it is assumed that lifestyle changes will be combined with drugs.
Along the way, Dr. Mintz (who had started the conversation) noted that half the people who use either sulfonylureas or metformin lose control of their blood sugar within three years -- and almost all of them have lost control within nine years. You might think that this evidence of the failure of popular diabetes drugs would cause doctors to wonder if some other approach might be worth looking into. But their reaction seems to be that, if you tried drugs and it didn't work out well, you just didn't choose the right drugs. The question is not which approach to diabetes management works best, but which combination of drugs works best.
This kind of drug-centered chatter among doctors drives me crazy. I'm sure they think it is justifiable for them to focus entirely on meds, because "everyone knows" patients won't adopt any other approach. But what if the reason patients don't adopt any other approach is that doctors so seldom talk about any other approach? The assumption that patients won't exercise or lose weight tends to become a self-fulfilling prophecy. Why should you do something as difficult as that, when your doctor clearly thinks it won't work as well as drugs?
Exercise & Injuries
Wednesday, April 4, 2012
Fasting Glucose: 88 mg/dl.
Glucose 1 hour after lunch: 100 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 121/75 mmHg, 61 bpm.
Exercise: Gym workout (aerobic).
When Exercise Hurts
It was once taken for granted that what people needed, when they were recovering from an illness, injury, or surgery, was lots and lots of rest. The less time a recuperating patient spent out of bed, the better!
This assumption remained in place until experiments began to reveal that extended rest has harmful effects on the body, and tends to delay recovery instead of promoting it. These days, hospital patients are asked to be up and around quite soon after surgery, to avoid the hidden dangers involved in excessive rest. On the other hand, hospital patients are not asked to do gymnastics after surgery -- they are simply asked to do certain light-weight activities which won't overstrain them. The goal is a level of physical activity that is neither too much nor too little.
Finding that ideal compromise is not always easy to do. If I have an illness or injury that interferes with my ability to exercise, I try to get active again as soon as I possibly can, because I think that's the quickest route to recovery -- but it's never easy to be sure I'm not overdoing it, and creating more trouble for myself. What makes this an especially difficult issue for me is that I rely on exercise to keep my blood sugar in control; I therefore have a strong motivation to stay active even when I'm in compromised state. This means that I tend to push myself to exercise as usual, unless I'm absolutely certain I can't handle it.
While I was running yesterday, I had a mishap for which there must be a name, because it happens often enough to runners (or at least to this runner). But I don't know the name of it, so I'll just have to describe it to you. What happened was that I put my left foot down on the edge of a hole in the pavement, and my foot tilted violently into the gap, putting a sudden heavy strain on my ankle. I don't really know for sure, but based on where it hurt, I think what I put a particularly hard strain on was the trans-crural ligament.
It felt pretty painful when it happened, but I've found in the past that I usually recover best from that kind of thing if I keep right on running. So, I did keep right on running, and my ankle started feeling better, and pretty soon I had forgotten about the injury. During the rest of the day my ankle felt fine. In the evening, when I went to the gym for a weight-training workout, it didn't even occur to me to go easy on my ankle; I did the usual leg-press exercises. The workout didn't bother me. My ankle didn't hurt after I got home from the gym, either. I went to bed thinking I had no ankle problem of any kind.
Then I woke up at 2 AM with an ankle hurting and lighting up the room with its evil red glow.
It was a bit shocking how sore my ankle had become since I'd fallen asleep. It was hard to find a way to position my foot so that it didn't hurt. I dreaded what would happen when I got up in the morning -- would I even be able to walk on it? Was I going to need to get hold of some crutches? What was going to happen to my exercise program? How long would it be before I could work out again -- and what would happen to my blood sugar in the meantime? I didn't get a great deal more sleep after that; it's during the predawn hours that I am especially prone to dwelling on worst-case scenarios.
After the sun finally came up, I nerved myself to get out of bed and assess my condition. Well, it wasn't as bad as feared -- I found that I could walk, although with a limp. Also, after a few strides, my ankle would settle into the rhythm of walking and the limp would diminish greatly. I could climb stairs. I could get around. I could go to work. But it was pretty clear that this was not going to be a running day for me. Even just standing around, my ankle would sometimes have a painful little spasm if I put my weight on it at the wrong angle; running would obviously be stressing it far too much.
However, I didn't necessarily feel like spending the whole day indoors. The wet gray skies we've been having lately turned to pure blue this morning, and the sunlight was glistening on all the rain-washed greenery that had sprung up in the past few weeks. I very much wanted to go outside at lunchtime. Finally I decided that I should try going for a walk. I could walk cautiously and slowly, pretending that I was a very old man recently released from the hospital. I thought that the walk would probably make my ankle feel better rather than worse, when all was said and done.
Well, it did seem to work out that way. The walk was not vigorous enough for me to see it as aerobic exercise, but it had to have some exercise value (it did involve hill-climbing). And when I was done, my ankle felt better rather than worse. (But I wrapped an ice-bag around it when I got back to my desk, in case I had strained it more than I realized.)
Although I wasn't ready for running, I didn't think I needed to give up having a workout today. So, I went to the gym after work, and used an elliptical training machine on which your feet just slide forward and back, with your upper body doing more of the work. That was fine; it didn't bother my ankle at all.
Then I sat in the hot tub, and held my ankle up against a particularly vigorous hot-water jet, hoping that the vibrations involved would have a relaxing effect on it. I don't know if that theory was valid, but my ankle feels pretty good now, and I'm hoping it will feel even better tomorrow.
Now, the way some people would have handled a day like this would be very different. They would not have gone to the gym, or gone on a walk, or even gone to work -- they would have called in sick, stayed at home, and rested all day with their feet up. There is no way for me to rewind the day now, and re-live it in that restful state. Therefore, when I express the opinion that my ankle would be feeling worse now if I had done that, I cannot begin to prove it. But even if I'm wrong in thinking my ankle would be feeling worse now if I had done that, the fact remains that my ankle feels much, much better now than it did this morning. So, in making the effort to stay as active as I could under the circumstances, I'm pretty sure I made the right choice.
However, if I'm unable to walk tomorrow, I'll have to think again about my decision-making process!
Sitting Ducks: the High-Risk Lives of the Sedentary
Tuesday, April 3, 2012
Fasting Glucose: 97 mg/dl.
Glucose 1 hour after lunch: 87 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 118/72 mmHg, 60 bpm.
Exercise: 4.1 mile run at lunchtime; weight-training workout before dinner.
I didn't like my fasting test result of 97 this morning (I prefer to keep it below 95), so I had a very low-carb dinner to nudge things back in the right direction. It worked: I got a post-prandial result of 87. Having two kinds of workouts today helped with that too, no doubt.
I'm getting more comfortable with weight-training now. It isn't as hard to drag myself to the gym as it had been for a long time. I'm sure I would prefer to stick to aerobic exercise only, if that was all I really needed in terms of health. But experience (and various studies) suggest that any exercise program which doesn't include strength-training is incomplete.
Too Much Sitting
For a long time I have been assuming, and asserting, that I am no longer a sedentary person because I work out regularly. However, "sedentary" does not necessarily mean that you never exercise. Even if you work out daily, you can still be sedentary in the sense that you spend a lot of your time sitting (usually while staring at a glowing rectangle). Regardless of whether the glowing rectangle that is holding your gaze is a TV screen or a computer monitor, and regardless of whether the time you spend in front of it is leisure time or work time, that time has to be counted as sedentary time. And by that reckoning, I spend several hours a day in a sedentary state. The fact that I spend an hour working out in the middle of all that is not insignificant -- it does help -- but it doesn't nullify the harmful impact of sitting down for hours every a day. When you walk, or even stand up, your leg muscles are constantly working (and removing glucose and fats from the bloodstream); this doesn't happen when you are seated.
One study, reported recently
in the Archives of Internal
Medicine, found that too much sitting shortens your life -- regardless of
whether you are exercising during another part of the day. The study (conducted
in Australia) looked at 200,000 adults older than 44 years, and found that
all-cause mortality increases as the number of seated hours per day increases.
People who reported sitting for 11 hours a day or more were 40% more likely to
die during the study period than those who reported sitting less than 4 hours a
day -- even when other factors that contribute to mortality were adjusted for.
Apparently, sitting down for extended periods is harmful, even if you exercise frequently. The extra risk associated with extended sitting continues to be associated with it, regardless of whether you are thin or fat, and regardless of whether you exercise. The study authors suggest that people who work at a desk should create opportunities to get up (standing while on the phone, for example) as frequently as possible.
I am restless enough that I
tend to find excuses to get up frequently anyway -- at least when I'm at the
office. At home I'm a lot more inclined to get comfortable with prolonged
slouching in front of the computer, especially when I'm desperately trying to
think of a topic to address in my blog. I guess I'd better think of a way to
interrupt myself often at home, too.
One Nation Under Statins: Cholesterol Drugs for All!
Monday, April 2, 2012
Fasting Glucose: 91 mg/dl.
Glucose 1 hour after lunch: 110 mg/dl.
Weight: 185 pounds.
Blood pressure, resting pulse: 122/72 mmHg, 56 bpm.
Exercise: 4.5 mile run at lunchtime; yoga class in the evening.
I guess we knew it was going to come to this, sooner or later: some physicians are pushing for the idea that the best answer to the question "which patients should get statins?" is "all of them!".
The American College of Cardiology held its 61st Annual Scientific Session in Chicago last week, at which Dr. Benjamin Galper of Columbia University presented the results of an analysis of five strategies for identifying and treating coronary risk factors. ("Treating" in this context means "prescribing statins"; other methods of preventing heart disease were apparently not considered.) The conclusion: the best plan is simply to give high-dose statins to everybody, regardless of whether they have many risk factors, few risk factors, or no risk factors.
It's a little hard to tell exactly what Dr. Galper's "analysis" consisted of. It's described as a "Markov-chain Monte Carlo statistical analysis of 30 years based on the costs of testing and statins and the expected number of patients classified as moderate or high risk shown in the trials of the screening strategies." Dr. Galper refers to it as a "simulation". Anyway, we're not talking about an actual clinical trial, following patients being treated differently over a long period, to see how the actual health outcomes compare. It is a summary of what Dr. Galper and associates think would have happened, if such an experiment had been run. And the conclusions relate mainly to cost-effectiveness -- the statins-for-all plan is seen as the best because it is expected to save the most lives for the least money.
So what exactly are statins, anyway? They are a class of drugs that are used to reduce levels of cholesterol in the blood. They work by inhibiting an enzyme called HMG-CoA reductase, which is crucial to the formation of cholesterol. The statin drugs essentially mimic HMG-CoA reductase, and take its place without performing its function, so that less cholesterol is formed (within the liver) and released into the bloodstream. The higher the statin dosage, the less cholesterol your liver can produce. The most frequently prescribed of the statin drugs (atorvastatin, sold as "Lipitor") is the best-selling drug in pharmaceutical history (in 2008 alone, Pfizer sold twelve billion dollars' worth of the stuff).
Now, let me point out that cholesterol is not necessarily a toxic subtance which we would all be better off without. The body has uses for cholesterol (it's used in building cell walls, for example), so you don't want get rid of it entirely. You just don't want to have excessive amounts of it. Mevastatin, the first of the statin drugs (developed in Japan in the early 1970s) apparently went too far in this regard; the drug caused muscle deterioration and other dangerous effects, and it was never approved for use as a medicine. Later statins, such as atorvastatin, reduced cholesterol without overdoing it, and were soon very widely prescribed. Still, given the complexity of the cascade of reactions we are messing with here...
...it would be almost amazing if no unplanned effects resulted from taking statins. Various worrisome side-effects of statins have been noted (such as headache, muscle pain, and an increase in the risk of diabetes and liver disease). Proponents say these are not common enough to be of concern.
Other problems with statins have been reported, and I'm afraid I have to go with anecdotal evidence in this case, which is what we are usually urged not to do. I can't help it in this case: I happen to know three people well (all of them men, though I don't know if that's significant) who were prescribed statins and stopped taking them (over their doctors' strenuous objections) because they couldn't bear the way they felt when they were taking these drugs. What they reported to me was a combination of fatigue, weakness, and a feeling that they were literally about to die (one of these men was even "putting his affairs in order" to ease his wife's transition to widowhood). Perhaps it is this kind of thing that Dr. Galper has in mind when he says: "The actual rates of true adverse events [with statins], even looking at millions of people treated, are relatively low."
True adverse events? Sounds like the No True Scotsman logical fallacy to me! Why would anyone talk about "true adverse events", unless they are looking around for an excuse to dismiss most adverse events as figments of the patient's imagination? I assume that a true adverse event, for a statin advocate, would be one which is objectively measurable, not a subjective account from some whiny patient who claims to feel like he's dying when he takes statins. That's not a true adverse event! It is dangerously easy to dismiss the patient's experience of taking a medication, if the experience mainly affects how they feel. However, given that cholesterol is used in brain and nerve tissue, isn't it only to be expected that a drug which interferes with cholesterol synthesis might affect the way people feel -- perhaps intensely?
But then Dr. Galper lets slip something remarkable: he says that, from a public-health standpoint, it may be difficult to implement a strategy in which the bulk of the US adult population is placed on a high-dose atorvastatin -- because statin-therapy compliance rates are often as low as 20% to 40%.
Huh? The compliance rates are 20% to 40%?
Think about it: here is the most prescribed drug in pharmaceutical history, and the majority of the patients it is prescribed for won't take it. Hmmmm... why do you suppose that might be?
Could it be that those patients who react badly to statins, and feel terrible when they take them (even though they are not having true adverse events, mind you!) are more numerous than physicians would like to admit? There most be some reason why a majority of the people who are given a drug which is supposed to save their lives won't take it, and the most reasonable hypothesis is that it degrades their quality of life in some way.
Dr. Galper also mentions (rather recklessly, it seems to me) that one reason to give statins to everyone is that a great many people develop coronary heart disease without having identifiable risk factors for it -- so, to make sure all those people are protected as well, doctors should give statins to everybody. Well, hold on a minute here. One of the traditional risk factors for coronary heart disease is high cholesterol. I know that plenty of people without high cholesterol have heart attacks -- but how would it protect them to give them a drug for high cholesterol, if they don't have high cholesterol? What exactly would the statins be doing for those people?
And, since statins have so far not been prescribed for people who don't have high cholesterol, how do we know what's going to happen when we give statins to people whose cholesterol isn't high? Shouldn't there be clinical trials to see if this causes new problems for people -- problems that nobody knows about yet, because the conditions necessary to create those problems won't exist until we start giving statins to large numbers of people with normal cholesterol?
The whole idea of prescribing a drug for the entire adult population seems to me reckless and fanatical. I mean, what is this -- a cult?
"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!)