Saturation

Thursday, February 27, 2014

I took advantage of a break in the rain to take a tough, hilly run today, hoping that I could finish it before those very menacing-looking clouds in the west swept over me and started dumping rain. It worked out. I even got to relax in the outdoor hot-tub at the gym afterward, before any rain started falling. I'm pretty sure it will be a rainy day tomorrow, but I'll deal with that when I get to it.

 


Fat is fat -- or is it?

Fats are generally divided into saturated and unsaturated varieties (the difference has to do with the way the carbon atoms in them are bonded together, and how much hydrogen they contain). Looking at things above the molecular level, saturated fats tend to remain solid at room temperature, and typically come from animal food sources. Unsaturated fats tend to be liquid at room temperature and typically come from plant food sources.

(Note: "trans fats", also known as partially hydrogenated vegetable oils, are produced by an industrial process in which cheap vegetable oils are forced to bond with hydrogen under pressure. The purpose of this is to combine the traits of the saturated and unsaturated fats in a way that is useful to makers of processed foods; the downside of it is that hydrogenation twists the fat molecules out of shape, in a way which appears to have harmful effects on human health.)

For a long time it was believed that saturated fats raised blood cholesterol levels, and therefore promoted the buildup of cholesterol deposits on arterial walls, leading to blocked coronary arteries and heart disease. The public has been advised for decades to minimize saturated fats in the diet, and replace them with "heart-healthy" unsaturated fats. Evidence supporting this notion has been weakening more and more as researchers look into the matter, and some doctors say flatly that saturated fat has been "exonerated" as a cause of heart disease. This has had little effect, if any, on the recommendations given to the general public; the organizations that hand out such advice are not the sort of organizations that like to declare publicly that their earlier advice was wrong.

Speaking for myself, I no longer believe that saturated fat raises blood cholesterol. I have had ample opportunity to experiment with different diets in the years since my diabetes diagnosis, and I still get the same low cholesterol readings on my lab results regardless of whether my diet is centered around bacon or brussels sprouts. For me, what matters is how much I exercise, not what kind of fats I'm including in my diet; once I started a regular exercise program my cholesterol numbers dropped sharply, and haven't climbed back despite all sorts of different approaches to diet.

However, the mere fact that saturated fat doesn't appear to be the cholesterol-raising villain that we were told it was does not mean saturated fat has no other effects which might be undesirable. I am still willing to be told that evidence has been found for other reasons to minimize saturated fat in the diet.

A new study from Sweden claims to have found such evidence. Researchers Fredrik Rosqvist and Ulf Riserus induced 39 young adult volunteers of normal weight to gain 3% of their starting weight by eating 750 extra calories a day, in the form of high-fat muffins. But one group of volunteers ate muffins loaded with saturated fat; the others ate muffins loaded with unsaturated fat. The goal was to see if there was any difference in how this high fat intake affected their bodies, apart from the simple metric of weight gain. MRI scans were used to find out where, exactly, fat was building up on their bodies.

The result: "Despite comparable weight gains between the two diet groups, the surplus consumption of saturated fat caused a markedly greater increase in the amount of fat in the liver and abdomen (especially the fat surrounding the internal organs, visceral fat) in comparison with the surplus consumption of polyunsaturated fat. Moreover the total amount of body fat was greater in the saturated fat group, while, on the other hand, the increase in muscle mass was three times less for those who ate saturated fat compared with those who ate polyunsaturated fat. Thus, gaining weight on excess calories from polyunsaturated fat caused more gain in muscle mass, and less body fat than overeating a similar amount of saturated fat."

So there you have it. Saturated fat is apparently more likely to promote accumulation of liver fat and visceral fat -- both of which are associated with diabetes and heart disease -- than unsaturated fat.

It could be objected (and no doubt will be) that this study (1) is too small to support any bold conclusions, and (2) was rather extreme in the amount of fat it asked its subjects to eat, and therefore might not be relevant to those who eat saturated fat in less extravagant quantities. I assume further studies (and larger ones) will give us more confidence (or less) in what the Swedish researchers found. But it's not looking good for saturated fat at the moment. Perhaps my increasing difficulty with weight control in the last few years is the consequence of my decision not to worry about saturated fat, because it seemed to have no bearing on my cholesterol levels.

I confess that I checked to see what the two Swedish obesity researchers, Fredrik Rosqvist and Ulf Riserus, actually look like. I was sort of hoping they might look a little like this:

But it turned out that they look like this:

Apparently that's what the scientists look like in Sweden. What their soap-opera stars look like, I am unable to tell you.

 


Weight Training, Again

Wednesday, February 26, 2014

 


A rainstorm is currently interrupting our California drought (it won't be enough to make much difference in the larger scheme of things, but the rain is still pretty heavy), so I didn't feel like an outdoor run today. Instead I went to the gym.

As my neck is now fully recovered from the pain and stiffness of last week, and my shoulder is feeling better than it has in months, I thought I could risk doing a weight-lifting workout. It doesn't seem as if it did me any harm. And I didn't even hate it!

Hating it is my usual attitude, though, and that has been a bit of a problem for me. The experts all say that the ideal workout plan doesn't consist of aerobic exercise alone (usually running, in my case); one should do strength-building exercise as well. But my dislike of weight-lifting encourages me to find excuses for thinking I don't really need it. I keep coming back to the simple fact that I seem to be able to control my blood glucose with aerobic exercise alone. That being the case, why add another form of exercise which I find much less enjoyable?

The trouble is that the impact of aerobic exercise on me is immediate and measurable, while the impact of strength-training exercise is much less obvious. Aerobic exercise brings about an increase in insulin sensitivity in muscles tissues, which has a very rapid onset but fades slowly over a period of about 48 hours. During those 48 hours, and especially in the first 8 hours or so, glycemic control is significantly improved; the endocrine system is much better at limiting post-meal glucose spikes, because the glucose is so readily soaked up by muscle cells which have been reprogrammed by the workout to do just that. This phenomenon becomes pretty obvious if you test your glucose regularly. If I don't manage to do my usual lunchtime run on a workday, I can expect my glucose to go higher after lunch than it normally would. If I do an especially hard workout, I can usually count on unusually low glucose afterward. It's not an infallible system, but it certainly works a lot more often than it doesn't.

Lifting weights doesn't have that kind of immediate, obvious payoff, so I don't get much positive reinforcement from it. The research, however, says that the benefits are real. The CDC's article on strength training says that this kind of exercise has been shown to prevent or reduce the symptoms of many common health problems, including arthritis, osteoporosis, back pain, depression, and (of course) diabetes. Aerobic exercise may make your muscle tissue more insulin sensitive for a day or two, but strength-training gives you healthier muscle tissue, and more muscle tissue. Diabetes patients who lift weights certainly tend to have better glycemic control than those who don't. They also tend to be better at avoiding the frailty of old age: they are stronger, have better balance, are less prone to falls and injuries, and have tougher bones. They even have tougher hearts.

I am somewhat prone to injury and inflammation in my muscles and joints (as my recent troubles with neck and shoulder pain made clear), and although I have tended to see these things as excuses for not lifting weights, you could argue that they are signs that I need to be lifting weights. The aging process is only going to make those problems more frequent if I don't prevent them, and strength-training may be a necessary part of the prevention process.

As for why I don't like weight-lifting nearly as much as running, I suppose part of it is that weight-lifting requires a degree of focus that running doesn't. Unlike some people, who find running boring if the distance is more than a couple of miles, I welcome the automatic, continuous nature of running because it gives me a block of time that I can set aside purely for thinking. Weight-lifting isn't like that; the only thinking you're doing is about how hard this is and how much you wish you were already done with it. Tonight it didn't seem so bad; I kind of enjoyed it, even. Whether I can find a way to prolong that feeling remains to be seen!

 


Through the Looking-Glass

Tuesday, February 25, 2014

My very painful stiff neck from last week has now healed up nicely, and my right shoulder (which was also bothering me, though not as much as my neck was) is also feeling much better. So, on I go. The trick is not to hurt myself again. (Preventing that would be easier if I could know for sure how I got hurt before, but I will do my best to avoid further trauma.)

 


The surreal world of diabetes care

Whenever physician's organizations start to give doctors official guidance on how to take care of diabetes patients, I get the feeling that I am reading a surrealistic account of the goings-on in Lewis Carrol's Wonderland.

In this alternative universe, familiar things take on unsettling connotations because they are placed in strange contexts and combinations. The significance and priority of everything is disturbingly different from what we expect.

That was the feeling I had today while reading an article entitled Editorial Illustrates Shift Away from Glycemic Control in Diabetes Treatment. Oh, so we're shifting away from that, are we?

The article reports on an editorial in a publication called American Family Physician. I'm not a subscriber, so I'll have to assume that the article gives us an accurate account of what's in the editorial. But the bottom line, astonishing as it might seem to you (it certainly seems astonishing to me) is that controlling blood sugar levels is, apparently, no longer seen as a top priority.

Wait -- did I read that wrong? Since diabetes by definition means an out-of-control increase in blood sugar levels, it is hard to imagine how treatment of diabetes would not make it a priority to regain control of blood sugar levels. And yet we're told that other things matter more.

To quote the article: "An editorial in a February issue of American Family Physician proposes a simple way for physicians to communicate with patients about the best treatments for diabetes. The 'lending a hand' illustration reprioritizes treatment goals, based on research on mortality reduction, to convey that glycemic control is no longer the primary intervention. In order of benefit, to improve length and quality of life, patients with type 2 diabetes benefit from the interventions illustrated above, starting with smoking cessation".

The illustration referred to in the quoted passage is this:

"The 'lending a hand' illustration uses the fingers of an open hand to depict diabetes interventions from thumb to pinky in descending order of benefit, relative to complications and mortality. Smoking cessation is considered the most important intervention (the thumb). Blood pressure control, metformin drug therapy, and lipid reduction follow along the pointer to ring finger. Glycemic control, considered the least important intervention, is relegated to the pinky."

Why is glycemic control the least important intervention? "'Glycemic control is stuck in people's minds as the primary goal of treatment, but evidence has existed since the 1970s that other interventions are of greater benefit,' said senior author Allen Shaughnessy, Pharm.D., M.Med.Ed., professor of family medicine at Tufts University School of Medicine and fellowship director of the Tufts University Family Medicine Residency Program at Cambridge Health Alliance. Shaughnessy and colleagues wrote the editorial on their 'lending a hand' illustration to demonstrate the paradigm shift in treatment priorities. 'Lending a hand' emphasizes interventions that improve length and quality of life for those living with type 2 diabetes, in line with new guidelines from the American Diabetes Association and the European Association for the Study of Diabetes."

I can't help feeling that the 'Lending a Hand' concept gets things a little muddled:

  1. Smoking is not a diabetes-specific issue. And in America, at least, most people don't smoke. (The CDC found in 2012 that only 18% of American adults were smokers.) So, let me get this straight: the top-priority intervention for diabetes patients is one which is irrelevant to 82% of patients?
  2. Blood pressure control is a splendid idea, but for many people the best way to control it is by means of the same lifestyle changes which are required to control glucose.
  3. The purpose of metformin therapy is glucose control; why is the latter not only listed separately but given the lowest priority?
  4. Lipid reduction is a splendid idea, but for many people the best way to reduce it is by means of the same lifestyle changes which are required to control glucose.
  5. Controlling glucose is only the fifth priority intervention, yet controlling it through lifestyle adjustments (dietary choices plus regular exercise) will take care of priorities 2, 3, and 4. And priority 1 is largely irrelevant.

Yeah, yeah, I know: the program was designed by doctors who took it for granted that diabetes patients cannot or will not change their habits for the sake of their health. Also, they were rating the effectiveness of "interventions" not by how well they work if the patient does them, but by how well it works to ask patients to do them. The doctors are just trying to be realistic about what can be expected from diabetes patients: not much. Well, that may be true for the majority of diabetes patients -- but the majority of them don't smoke, either, and the good doctors saw no reason to take that into account. And perhaps more diabetes patients would make lifestyle changes if doctors presented it as necessary, instead of giving up on the idea before the patient even arrives in the examining room.

Here's an idea: most doctors have two hands, not one. Why don't they continue presenting the left-hand version above as the second-choice approach, explaining carefully that it has a poor track record of success (which it most certainly does), and reserve the right hand for lists of things that work better if you actually do them?

 


Whiplash

Thursday, February 20, 2014

 


Rough Day

I'm suffering from a very stiff neck today, with very limited ability to raise my head up or turn to the left or right. This has happened to me a few times before -- and now it's happened again, for whatever reason. It's not hurting as much now as it was when I was trying (and failing) to sleep last night. I do think it's now getting better rather than worse, but I'm not feeling like spending a lot of time blogging tonight.

So, as a light diversion, I offer you the new invention the world has not been waiting for: sports recovery beer!

Yes, that's right: after a hard workout, you can help your system replenish its fluids and electrolytes...

...and also put your muscles into recovery mode!

All this just from drinking a can of beer!

The sports recovery beverage industry was already pretty questionable (the idea seems to be add more sugar back into your system than you are likely to have burned up while exercising). Sports recovery beer really takes it to the next level.

Apparently this product is not yet available -- it's a new business being launched in Canada. The launch might possibly be derailed by an inconvenient fact: the research says that muscle recovery is impaired rather than enhanced by post-workout alcohol.

But there's no denying that mood is enhanced by post-workout alcohol, so maybe they've got something there!

 


A Code for Everything, and Everything in its Code!

Wednesday, February 19, 2014

 


Hit by a turtle

Doctors have been fretting for a long time about a diagnostic coding system called ICD-10, and the fretting is getting louder as the deadline for implementing it grows closer. By October 1, 2014, doctors in the USA need to start using the ICD-10 codes when diagnosing any condition they treat -- or else their Medicare and Medicaid claims will go unpaid. That is the weapon that the Department of Health and Human Services (HHS) is planning to use to enforce adoption of the updated coding system (which, not very surprisingly, replaces something called ICD-9). And the HHS needs a weapon, because doctors are reluctant to adopt ICD-10. The original deadline for adoption was October 1st of last year; physician resistance was so strong that the HHS caved in and pushed the date out a year. They don't want to push it out again.

Other countries have been much less resistant to ICD-10, which was developed by the World Health Organization (WHO) in the early 1990s, and has been in use in many other countries for several years. Parts of Australia adopted it as long ago as 1998, and it has since been adopted in Canada, China, France, Germany, Korea, the Netherlands, South Africa, Sweden, Thailand, and Dubai. But in America, the deadline for implementation of the scheme has been pushed back repeatedly.

Why are doctors, or anyway American doctors, so unenthusiastic about using the ICD-10 coding system? Is it simply resistance to change, or to the heavy overhead (training, documentation, new software tools) involved in transitioning to a new system? Perhaps. But the complaint more often heard about the ICD-10 codes is that there are too damned many of them. The WHO went overboard in developing codes and sub-codes to identify every conceivable illness or injury which might bring someone to a doctor, and doctors like to point out the ridiculous abundance of codes for ridiculously specific problems. All in all, there are more than 14,000 codes in ICD-10, and the use of sub-codes to make them extra-specific expands the total further.

To give you an idea of how very specific the ICD-10 coding system can get, let us imagine you are a doctor, and you have treated a patient for a burn. But this is not just any burn -- this is a burn the patient received when her plastic jewelry caught fire. Well, the ICD-10 system has a code for that: X06.0XXA, "exposure to ignition of plastic jewelry, initial encounter". That phrase "initial encounter" does not, apparently, refer to the patient's initial encounter with the ignited jewelry, but rather to the doctor's initial encounter with the patient; for any follow-up visits, the code would be X06.0XXD, "subsequent encounter". And if the ignited-jewelry accident should lead to any long-term health problems after an apparently successful treatment of the original burn, then the code would be X06.0XXS, "sequela". Have we all got that?

However, we still have not exhausted the possibilities for burns caused by plastic jewelry. If the patient was burned by plastic jewelry which was merely melting, not actually aflame, there is another trio of codes for that. But from here on I think I'll leave off the letter suffixes, just because I'm already getting tired of the ICD-10 system myself, after working with it for only an hour. Let's just say that the code for burns caused by melted plastic jewelry is X06.1XX and leave the suffixes out of it.

Changing the subject to another source of serious harm, one might expect that asphyxiation caused by having one's head in a plastic bag could be covered by a single code, but here again there are many possibilities to consider. There's a big difference between putting your own head in a plastic bag deliberately, in a suicide attempt (T71.122), and having it done to you against your will, in a murderous assault (T71.123). Or it could be an accident (T71.121). Or the circumstances might be undetermined (T71.124). Still, it seems to me that, although a patient might care quite a lot about how, exactly, his head came to be inside a plastic bag, medical treatment (and Medicare reimbursement for it) would seemingly be the same in all cases.

And now we come to the subject you've all been waiting for: turtle attacks. The people who worked on the ICD-10 felt that W59-21X ("bitten by a turtle") was not good enough; it did not anticipate other potential injuries which might be inflicted by an aggressive turtle. Thus we have W59.22X ("struck by a turtle"). And, just in case the turtles think of another line of attack, we have W59.29X ("other contact with a turtle"). What intrigues me about that last one is that the developers of the ICD-10 didn't think that, plus "bitten by a turtle", pretty well covered the possibilities. They must have thought that being struck by a turtle was too common a source of injury not to give it a code of its own. Other animals which the ICD-10 people fear we might be "struck by" include chickens (W61.32X), ducks, W61.62X), raccoons (W55.52X) and fish (W56.52X).

More commonplace health problems are covered in even more detail; the list of diagnostic codes for diabetes (and for diabetes combined with various other problems, or manifesting various complications), runs to 25 pages. Picture yourself scrolling through 25 pages of this kind of stuff, trying to figure out which code is right for this particular diabetes patient receiving this particular treatment...

 

I'm not surprised doctors are reluctant to get started on implementing this new coding scheme. Whenever they finally do cave in and start using it, I wonder how much time is going to be frittered away on coding patients rather than treating them?

But what I really wonder is what kind of weekend retreats in lovely resorts the WHO people went on during the nine years they spent developing all those codes, and how drunk they were at the time the critical decisions were made. I picture them sitting around the pool, sipping drinks with tiny bamboo umbrellas in them, saying, "Hey, wait a minute -- what if the turtle doesn't bite you? What if it just hits you?". They left no stone unturned, those folks. Probably because they left no turn unstoned.


How Low-Carb is "Low-Carb"?

Tuesday, February 18, 2014

 


Wanting to cheat, and wanting to be cheated

The creative person looks at an extremely challenging problem and asks, "Is there some way I can solve this problem?". Then, after a little bit of struggle and frustration, the creative person asks, "Is there some way I can cheat at this, to create an appearance of having solved the problem?".

Extremely difficult scientific problems and engineering problems often attract the sort of person who is less interested in solving the problem than in receiving credit for solving the problem. This is where all those scientific scandals come from, with data manipulated (or outright invented) to make it appear that a scientific breakthrough has been made. That's why replication is so important in science -- and is such a problem for scientists who cheat. If your perpetual-motion machine only works when you're running it, then people are going to suspect that you haven't been totally honest about what's involved. If your medical experiment only yields positive results when you're collecting the data, then people are going to suspect that you have found a way to lose the bad results and keep the good ones. If a drug only seems to be effective when the research on it is being paid for by the maker of that drug, people are going to suspect that the fix was in from the start.

The urge to solve extremely challenging problems (or appear to solve them, anyway) is especially strong in the area of diet. People are always looking for some kind of magic formula for a weight-loss diet which doesn't make the person losing weight feel hungry. Every weight-loss diet book promises you that you won't feel hungry on this diet. However, history appears to show that diets which don't make people hungry don't make them lose weight, either. The problem remains unsolved, yet every new claim of a solution creates a new sense of hope that maybe this time somebody has finally nailed it.

Diabetes patients would like to solve a slightly different unsolvable dietary problem: how to create recipes for dishes which seem just like the high-carb foods we can't handle, yet are low in carbs.

The Holy Grail of diabetes recipes is the low-carb recipe that consists primarily of grains. It's a contradiction in terms, of course; grains are basically tiny pellets of starch. If you were going to make a low-carb rice recipe, how would you do it, apart from leaving out the rice? It's the perpetual-motion machine problem all over again -- a desire to cheat the laws of physics out of their normal consequences. People feel as if there has to be some way to trick nature into giving them the impossible: a rice dish that isn't high in carbs... even though rice consists mainly of carbs.

I was intrigued to see a dLife recipe today which claims to be a low-carb pilaf. Since pilaf is normally a rice dish, I wondered if maybe this was a pilaf made out of crumble cauliflower or something, but no: it's rice. Well, actually, one cup of basmati rice and one cup of quinoa. Quinoa has been promoted, especially to diabetes patients, as an alternative grain which is lower in carbs, but higher in protein, than other grains; this gives a superficial credibility to claim that this pilaf is Low Carb. The recipe is presented as follows:

Total carbs only 14 grams per serving? That seemed a little too good to be true. It made me wonder how the miracle was achieved. Is that quinoa stuff really low enough in carbs to make that big a difference? My independent nutritional research says that a cup of uncooked quinoa is 109 grams of carbohydrate and a cup of uncooked rice is 145 grams or worse; although 109 is certainly less than 145 grams, the carbohydrate total for the recipe is 254 grams (not including anything extra that might be contributed by the other ingredients), which seems like a lot. And it's not as if there's so much other stuff in the recipe that those carbs are going to be greatly diluted in the mix.  

So, at this point I'm wondering how the remarkably low carb count of 14 grams per serving was achieved. And then my eye finally zooms in on the detail that I should have checked first: serving size!

Okay: it's low-carb because, once you make the pilaf, you're only supposed to eat 1/18th of it. Well, that sounds perfectly realistic, doesn't it? I'm sure that, if you or I made that pilaf, that's exactly how much of it would be enough to satisfy us.

I didn't actually cook the pilaf, so I don't know how generous a 1/18th serving of it would be. But I used a kitchen scale to figure out how much 1/18th of 2 cups of grain (wild rice in this case) would be in its uncooked state. It turns out to be this much:

If you think that expansion during cooking would be enough to turn that pathetic little heard of grains huddled on the bottom of a bowl into a satisfactory meal, even with bits of red pepper and leeks tossed into the mix to magnify the richness of it all, then you have a lot more imagination than I do.

This kind of thing is simply cheating; end of story. Nobody is going to make a batch of pilaf and eat 1/18th of it. What's worse, most of the people who make that recipe will not even notice that they're only supposed to eat 1/18th of it. They'll see that blue "Low Carb" sticker and think that means there's no need to be cautious with serving sizes. This is a "Low Carb" food, after all! (A low-carb food which provides two-thirds of its calories in the form of carbohydrate -- you know, that kind of low-carb.)

What makes this kind of cheating dangerous, at least to my way of thinking, is that it's exactly the kind of cheating that we would like to accept uncritically. Low-carb rice pilaf! Thank goodness somebody finally found a way to make that! Don't spoil it by checking out the serving size!

 


President's Day

Monday, February 17, 2014

It's a holiday in the USA -- President's Day. Not one of the really big holidays, perhaps, but I do have the day off and I'm going to relax instead of blogging. I should be back tomorrow...



Targets

Thursday, February 13, 2014

I felt like I needed an long, hilly, extra-challenging run today, so I took one. Then my post-lunch test was unusually low (98), presumably because of the hard run. I've gone as high as 132 from very much the same lunch; I have to assume exercise made the difference.

 


A1c results vs. glucose results

Doctors usually give their diabetes patients a target hemoglobin A1c test result, and ask them to aim for that target. (The target is typically below 6.5%, or at least below 7.0%.) But the A1c test is intended for measuring long-term averages, and it is seldom administered more than four times a year. For patients to hit an A1c target result, they have to be working on day-to-day goals, not quarter-to-quarter goals. What should diabetes patients be aiming for in their daily glucose testing, to be sure they're on track for the A1c result they're trying to get next time?

Apparently there isn't a lot of uniformity out there regarding doctor's advice on what sort of daily glucose results patients should aim for, in hopes of getting the A1c result they're aiming for. Different patients get different advice, and that's probably not a good thing.

Some researchers in Massachusetts decided to do a study (based partly on data from continuous glucose monitoring devices) to find out which glucose testing results (on average) correlated with a given range of A1c results. The point is to give doctors a basis for creating more accurate clinical guidelines. There is a concern that some of the various current clinical guidelines are not right -- either they are too strict (setting patients up for frequent hypoglycemia episodes) or they are too loose (setting up patients for disappointing A1c results). What does the evidence say the actual guidelines should be?

"Mighty high" would be my summary, but I'm prejudiced. Here are the recommendations.

A1c Target,
%
Fasting BG,
mg/dL
Post-Meal BG,
mg/dL
Bedtime BG,
mg/dL
6.5 - 6.99 142 139 153
7.0 - 7.49 152 152 177

From my perspective a fasting test of 142 mg/dL is disturbingly high. I can't argue that the researchers are wrong to think it's consistent with an A1c result below 7%, because they have data on their side, and I've only got my intuitive judgment based on experience. Even so, I feel as if another issue is being ignored here: if your glucose levels are so high that your average fasting test is 142, isn't that going to have enough toxicity for your pancreatic cells to ensure that the situation gets worse over time? Part of the reason I've been much more conservative than that in my glucose targets is that I feel it keeps my glucose levels from drifting out of control. (After 13 years of unmedicated diabetes management, I still am in good control, so I don't think my experience should be dismissed.)

But I guess the fact that I have been taking the unmedicated approach means this study doesn't really apply to me. The researchers were looking at patients who are on insulin and/or oral diabetes drugs. For people in that situation, setting targets lower always carries with it a risk of triggering hypoglycemic episodes. These patients aim for their glycemic targets by adjusting their meds, and taking more meds means risking a low, so they're very cautious about it.

Today I got a lower post-prandial result not by taking an extra pill but by doing an extra-hard run. No hypoglycemic episode resulted. (I get lows quite infrequently, and they're never dangerous lows, just uncomfortable ones.)

It sure seems to me as if the unmedicated approach is the better one, if you can make it work. And I suspect more people would find a way to make it work if they weren't being discouraged from thinking it can work.

 


Simple Arithmetic

Wednesday, February 12, 2014

 


Freudian Headline of the Day

 


The Truth About Fiber!

Last week I mocked a study, payed for by General Mills, which found that Americans don't eat enough of the whole-grain products General Mills makes. "Many people, even health professionals, are confused about the relationship between whole grain and fiber," lamented the author of the study.

Well, if many people, even health professionals, are confused about the relationship between whole grain and fiber, maybe a brief examination of nutritional data for various foods will clear up some of the confusion.

First, let me begin by conceding that there is, indeed, a relationship between whole grain and fiber. The nature of the relationship is that whole grain foods contain fiber. Here's the breakdown on a slice of whole-wheat bread:

There, you see? There's fiber in that bread -- 2 grams of it. So, the relationship between whole grain and fiber is confirmed!

However, that "relationship" is not of the exclusive, monogamous variety that General Mills would have us believe it is. Fiber, that hussy, has been seen around town with plenty of other foods. Mr. Whole Grain may think he's the only thing in her life, but there's plenty of evidence to show that he's fooling himself about that.

I collected some data today on thirteen foods which I have seen recommended as good sources of fiber. But I wasn't content just to look at how much fiber was in each of them. For anyone managing diabetes, high-fiber foods need to be approached with a little caution, because high-fiber foods are often high-carb foods. So I also looked at total carbohydrate, and recorded the ratio of fiber to total carbs -- to see which foods were delivering the most grams of fiber per gram of carbohydrate. My results are in the table below, with the fiber/carb ratio shown on the right. I have listed them in order of increasing fiber/carb ratio, so the foods at the bottom of the table are the ones that contain the most fiber for a given amount of carbohydrate.

Food, Portion Total
Carb
Fiber Fiber/Carb
Ratio
whole wheat spaghetti, 1 cup 37 6 0.16
orange, 1 cup 21 4 0.17
whole wheat bread, 1 slice 12 2 0.17
apple, 1 cup 17 3 0.18
tomato paste, 1 cup 50 11 0.22
strawberries, 1 cup 12 3 0.25
brussels sprouts, 1 cup 8 3 0.38
split peas cooked, 1 cup 41 16 0.39
lentils cooked, 1 cup 40 16 0.40
broccoli, 1 large stalk 20 9 0.45
asparagus, 1/2 cup 4 2 0.50
raspberries, 1 cup 15 8 0.53
almonds, 1 cup 27 16 0.59

Golly, I'm not so sure the whole-grain foods are the champions when it comes to fiber/carb ratio. To get as much fiber from whole wheat bread as you would from a cup of raspberries, you'd have to eat four slices of bread and take in more than three times as many carbs as you'd get from the berries.

It looks to me as if the fiber superheroes are to be looked for in the produce department of your grocery store, not in the bakery department.

I think whole-grain baked goods have been outrageously over-promoted to diabetes patients, when it only takes simple arithmetic to show that they aren't that great a deal. Whole wheat bread is better than white bread (which provides only 1 gram of fiber per slice, not 2), but come on: the fact that a given food is better than something doesn't mean it's great. If whole wheat bread were better than raspberries, it would have something to brag about.

 


Bloodless Testing

Tuesday, February 11, 2014

 


Measuring spikes, not averages

I think of myself as keeping pretty good track of these things, but it turns out that there's a diabetes test which doesn't require a blood sample... and which I had never heard of before today, even though it's been available for several years. But maybe I shouldn't be too embarrassed about being in the dark about this test, because it's rarely ordered by doctors, so most of them apparently haven't heard of it either.

You would think that a diabetes test which doesn't require a blood sample would be a popular option, and more doctors would use it. The likely reason that the test isn't better known is that it's very awkwardly named.

The "1,5-AG" test measure a sample of saliva to see how much of a compound known as "1,5-Anhydroglucitol" is present in it. (Chemists are the only people on earth who think the middle of a word is a good place for a comma.) The amount of 1,5-AG in the saliva gives an accurate indication of how much is in the blood. And why does it matter how much 1,5-AG is in your blood? Well, the answer to that is a little complicated, but at least it's interesting.

The trouble with testing for diabetes by measuring how much glucose is in a blood sample is that the amount of glucose in blood is constantly fluctuating. A test of that kind can only capture a snapshot of a moving target; it tells you nothing for certain about what the person's blood glucose levels are like the rest of the time. A lot of diabetic people whose blood glucose skyrockets after a meal can continue to get normal-looking fasting glucose results for a long time; their diabetes might go undetected for years if the doctor keeps giving them screening tests that only measure fasting glucose. So, doctors have been looking for "biomarkers" to measure -- that is, chemical traces which reflect general trends in blood glucose levels over time rather than instantaneous glucose levels.

The hemoglobin A1c test analyzes the hemoglobin in your red blood cells to see how much of it is sugar-coated; the test result is seen as an indicator of average blood sugar averaged over a period of about 3 months. (Red blood cells last about that long before being recycled.) Another blood test, the fructosamine test, analyzes proteins (mainly albumin) in the blood serum rather than the red blood cells, to see how much of that is sugar coated. Because proteins in the blood serum are recycled faster than hemoglobin in red blood cells, the fructosamine test is seen as an indicator of average blood glucose level over a shorter period (say, the past 2 weeks). The fructosamine test is not used nearly as often as the A1c test, but sometimes doctors use it if they want to assess the impact of a medication without having to wait 3 months for an A1c result. Generally, the A1c test is the preferred method of evaluating glycemic control averaged over time.

The good thing about the A1c and fructosamine tests (that they reflect average glucose levels rather than instantaneous levels) is also the bad thing about them: sometimes averages can be very misleading. (The fact that the average human being has one testicle and one ovary is a classic counter-argument to the popular assumption that "average" means "typical".) Just as average income within a population can be very misleading if a few rich people have most of the money, average glucose levels can be misleading if your blood glucose sometimes spikes very high after a meal, and then comes down pretty quickly. People who have recently developed Type 2 diabetes often exhibit that pattern: the only indication of trouble is that they go very high after a starchy meal, but (so far) they are still able to come down from that high pretty quickly, so the spike has little impact on their average glucose level. It's a sign of serious trouble, but the danger signal gets lost in the averaging process.

If doctors are going to screen for diabetes, and they want to catch cases of Type 2 diabetes at an early (and more correctable) stage, then it would be nice if there was a biomarker to analyze which reflected extra-high glucose spikes after meals, even in cases where the spikes are brief enough or infrequent enough to have little impact on an A1c test.

That's where 1,5-AG comes in. When a person gets high glucose spikes after a meal (say, 180 mg/dL), and glucose leaks through the kidneys into the urine, 1,5-AG leaks through the kidneys along with it. A person whose blood glucose goes that high fairly often will therefore experience declining levels of 1,5-AG in the blood (and in the saliva). A person with normal glucose levels will measure >12 ug/mL on the 1,5-AG test, but post-meal highs that occur with any frequency will bring the result below 12 (and even below 2, in extreme cases).

Some researchers are now advocating that the little-used 1,5-AG test should become a standard, non-invasive screening test, as it can detect cases of diabetes which would likely go undetected by any other screening method.

The 1,5-AG test probably doesn't have a lot of value for managing diabetes once you already know you have it, but I'm putting the information out there for whatever it is worth. Who knew you could be tested for diabetes without giving up anything more than your spit?

 


The "Why" Questions

Monday, February 10, 2014

My big crisis at work is over -- I finished in time for the software-release deadline. Now I'm trying to recover my equilibrium a bit...

 


But Why?

As anyone knows who has attempted to satisfy the scientific curiosity of an inquisitive child, one "why" question tends to bring on another, in an endless chain, which leads (sooner or later, and probably sooner) to an "I don't know" answer.

I do my best to follow the latest research studies on diabetes, and it seems as if a lot of these studies attempt to answer a "why" question, only to raise another.

For example, one recent study from Cambridge found that regular consumption of low-fat yogurt is associated with a 28% reduction in the risk of Type 2 diabetes.

But why? Why would consumption of low-fat yogurt reduce a person's diabetes risk? This study looked specifically at fermented dairy products (including yogurts and cheeses); as these products are good sources of vitamin K2, which has already been associated with a reduced risk of diabetes, the researchers speculate that the vitamin K2 in the low-fat yogurt might have a protective effect.

Well, maybe that's true. But if it is... why does vitamin K2 have a protective effect? Vitamin K2 is believed to preserve bone density and prevent calcification in blood vessels, but it's hard to see what that has to do with diabetes.

I'm sure this research will be cited by the people who sell yogurt, and also by the people who sell vitamin K2 supplements, but it might be more useful if we can figure out why yogurt, or perhaps the vitamin K2 it contains, has a protective effect against diabetes. (If it actually does: a correlation found in one study is not exactly absolute proof.)

Another study (at Lund University in Sweden) looked into the question of why diabetes patients who undergo gastric bypass surgery, for weight-loss purposes, typically experience a rapid normalization of their blood sugar. The answer can't be that blood sugar normalizes as a response to weight loss, because the normalization happens too fast -- often before the patient has actually lost any weight. So what is going on that causes blood sugar to normalize so rapidly in gastric-bypass patients?

The study involved pigs -- and only four of them, so it's not exactly overwhelming evidence. But what they found is that the pigs who had gastric bypass surgery had two changes start happening immediately in the pancreas: (1) the beta cells in the pancreas increased their production of insulin, and (2) the pancreas started growing additional beta cells.

Okay, but why? Why would gastric bypass surgery stimulate the pancreas to start producing more insulin, and start growing more insulin-producing beta cells?

It still seems to me that gastric bypass surgery is radical and creepy and unpleasant and carries unknown long-term risks. If there is a way to trigger those changes in the pancreas without going through major stomach surgery, maybe that would be the better way to go.

Anyway, "why" questions are always important, and always need to be asked... but they tend to just lead us to the next "why" question.

 


Who Gains?

Thursday, February 06, 2014

 


A useful bit of Latin

The Latin phrase cui bono means "to whose benefit?". It is a reminder to us to look for personal motives which might not be immediately obvious. If a man was murdered, think about who might have gained something by his death.

But the usefulness of the cui bono principle is not limited to homicide investigations in which it turns out that somebody is going to inherit a bunch of money from the murder victim. There are a lot of situations in which it's worth considering whether personal motives might be influencing people's ideas and decisions.

"Americans Need to Eat More Whole Grains, Study Suggests" reads the Medscape headline today, and immediately I'm thinking, cui bono? Who might benefit from having Americans eat more whole grains?

"Most children and adults in the U.S. are getting less than the recommended amounts of whole grains and dietary fiber, according to a recent study. Researchers found people who did eat the recommended three or more servings of whole grains each day also tended to consume the most fiber." So reads the report.

Then we get to the really interesting part. "Most people do not consume whole grains in amounts that can be most beneficial, also many people, even health professionals, are confused about the relationship between whole grain and fiber," Marla Reicks told Reuters Health in an email. Reicks led the study at the University of Minnesota in St. Paul. Her coauthors are all affiliated with General Mills, which funded the study."

Cui bono? Who benefits from this? General Mills, the company that makes its money selling grains to the American public. And General Mills, by a wild coincidence, is funding the study that says American need to buy more of what they're selling!

Is there anything else we need to know about this "scientific" study of the health benefits of whole grains, which was paid for by a corporate grain-merchant? Not that I can see.

Science that is funded by someone who has a financial interest in getting a particular result is not science. It is a parody of science. It needs to be recognized for what it is -- and called out for what it is.

 


Supplement Fever

Wednesday, February 5, 2014

 


Accepting that enough is enough

Even in the ancient world, people were aware of a disease known in Latin as "scorbutus". It was a disease which developed in people who were forced to subsist on extremely limited diets, most typically on long sea-voyages (because only a few types of foods, such as salted meats and dried grains, resisted spoilage long enough to be taken on such voyages). The disease was also seen in soldiers and prisoners forced to adopt similar diets. If your diet included no fruits or vegetables, sooner or later you would develop scorbutus.

And scorbutus was a pretty bad problem. It attacked the skin and other connective tissues, such as the gums. People with scorbutus developed spots on their skin which later became open sores. Their gums deteriorated (with resulting loss of teeth) and they bled from their mucous membranes. They became exhausted and immobilized, and eventually they died. Taking a long sea voyage put you at a very high risk of dying from scorbutus before the journey was over.

We now know that scorbutus is caused by a deficiency of a compound which, in honor of its role in preventing scorbutus, is called "ascorbic acid". These days we call it "vitamin C" (and we call scorbutus "scurvy"). Vitamin C is abundant in fruits and vegetables, but you can't get it from the sort of foods that were available to sea-voyagers in the old days.

Fun fact: sea-voyagers weren't the only ones who didn't get enough vitamin C. Aristocrats used to think that plant foods were for commoners, and they ate a diet so meat-centered that they were often deficient in vitamin C themselves. King Henry VIII suffered chronically from scurvy, and he wasn't the only royal who had that problem.

In 1753, a Scottish surgeon named James Lind demonstrated experimentally that scurvy could be treated with citrus fruits. Eventually the Royal Navy adopted the practice of taking limes on its ships, and adding lime-juice to the sailor's grog. (British sailors became known as "lime-juicers" as a result; the term was eventually shortened to "limeys" and applied to British people in general.)

But why was vitamin C so important? Why did people develop such a terrible disease if they didn't get any of the stuff in their diets?

It turns out that vitamin C is required for the synthesis of collagen, an essential protein in connective tissue. If collagen cannot be synthesized, then the body cannot carry on its normal task of refurbishing connective tissues. As a result, the skin and gums and other connective tissues cannot be kept healthy; they gradually fall apart.

Interestingly, most animals don't have this problem, because they are able to make their own vitamin C. But some animals, notably the monkeys and apes (a category which includes us), are unable to make vitamin C because they lack an enzyme (L-gulonolactone oxidase) which is needed for the job. Why don't primates have the enzyme needed to make vitamin C? Presumably because primates subsist on diets which include fruits and vegetables (gorillas are almost exclusively vegetarian), so it hasn't been historically necessary for primates to be able to make their own vitamin C. Nature did not foresee the day when a particular primate species would leave Africa, colonize northern Europe (where seasonal availability of plant foods is problematic), and start going on long voyages aboard ships loaded with barrels of flour and salt pork.

Now, the lesson we should have learned from all this is that the human body needs certain compounds to keep itself in a healthy condition, and if it can't make those compounds for itself, then the human diet needs to include an adequate supply of those compounds. The lesson some people actually did learn from all this is: vitamin C is magic! The more you have of it, the healthier you will be! Some very intelligent people (Linus Pauling, for one) have taken up this attitude, and have recommended massive doses of vitamin C as the best way to prevent not only scurvy but pretty much everything else. The undeniable existence of deficiency diseases has convinced a lot of otherwise-sensible people that, for some naturally-occurring compounds, there is no such thing as "enough". We should not trust a varied diet to give us sufficient quantities of those substances. Everyone (even if they are not taking part in 15th-century voyages of exploration and subsisting on flour and salt pork) must take supplements!

This attitude has been great for the supplement industry, but has it been great for humans? Some say no. Late last year the Annals of Internal Medicine published a report entitled Enough Is Enough: Stop Wasting Money on Vitamin and Mineral Supplements. Their conclusion: the evidence says that the popular vitamins and supplements do not actually help prevent the health problems they are expected to prevent, and in some cases cause health problems. So why take these things?

The report does say that vitamin D supplements are possibly worth taking (vitamin D deficiency is a real phenomenon, and possibly a serious problem for some people), but for everything else there's no obvious advantage to be gained by taking the stuff.

Still, regardless of what the evidence shows, a lot of people find it hard to let go of the idea that, if vitamin deficiency is bad, vitamin over-sufficiency has to be good. Well, look at it this way: if too little blood sugar is bad, does that mean too much blood sugar is good?

The fact that the body needs a certain amount of some substance found in commonplace foods does not mean that the body will benefit from taking in more of that substance than it requires.

 


February Q & A

Tuesday, February 4, 2014

 

More of my impulsive answers to the questions raised by internet searchers, referred here by Google of late...

  • "a1c of 6.2 is it diabetes"
  • "how serious is a1c of 6.2"
  • "my a1c results were 6.2. is that bad"
  • "is 6.2 a1c diabetes"

For some reason, 6.2% is the most common hemoglobin A1c test result for people to ask about on Google. What answer should they be given?

The diagnostic threshold for diabetes on this test is 6.5%. Does that mean anything lower is normal? Unfortunately, no.

The normal range is said to extend, or was once said to extend, up to 6.0%. The lab I go to now calls the normal range 4.8 to 5.6%. So if you're higher than "normal", but not high enough to be "diabetic", what are you to make of your situation? What is this medical limbo you've landed in?

It's usually called "prediabetes", a term which doctors think patients understand to mean "Emergency! Do something to change this, before it gets worse!". Patients understand it to mean "Don't worry about this, because if it was serious they'd call it diabetes".

What it actually means, if I may speak candidly instead of in code, is that your endocrine system is starting to lose control of your blood sugar, but things haven't got bad enough yet for the situation to be called diabetes. The sooner you do something to bring your blood sugar back into the normal range, the likelier it is that you can then keep it from drifting into the diabetic range. Waiting until you get to 6.5%, and are officially diagnosed as diabetic, will make it harder get on top of the situation.

  • "doctor does not believe that i have diabetes"
  • "people don't believe in diabetes"

Maybe diabetes is like Tinkerbell: everyone has to clap to show that they believe in it, or it will die!

As I've mentioned before (as recently as yesterday), diabetes is so poorly defined a term that people are pretty much free to believe in it or not, as the mood strikes them. But if you think you have problem with glycemic control, work hard it controlling it, regardless of whether anybody else (including your doctor) is calling it "diabetes".

  • "diabetes medicated vs non how do you feel"

We humans don't have much sensory awareness of our blood sugar level. If it goes low enough, we can get weak and shaky, but if it's only slightly low, or normal, or slightly high, or pretty seriously high, we feel about the same regardless. So, being non-medicated for your diabetes doesn't make you feel a particular way, regardless of whether your approach is working well or poorly. My own non-medicated program is very much exercise-based; because I exercise 6 days a week, I feel good pretty reliably.

Being medicated for diabetes can certainly change how you feel; those drugs have side effects. The most common side effects are diarrhea and nausea. I'd have to be mighty satisfied with how well the drugs were controlling my diabetes before I'd be willing to make chronic diarrhea and nausea a part of my life. But, to be fair, not everyone gets those side effects; some people tolerate diabetes drugs quite well.

  • "i'm depressed i have type 2 diabetes"
  • "i'm a new diabetic 2. will i go into a coma."

Being diagnosed with diabetes does tend to depress people, and I think one of the causes of that depression is a feeling of helplessness. That's why I think taking the charge of the situation, and actively managing your own diabetes (rather than passively letting your doctor manage it) is the best way to get over depression triggered by the diagnosis.

I can't promise that you'll never in your life go into a coma, but it doesn't seem as if it ought to be high on the list of concerns of someone newly diagnosed with Type 2 diabetes, especially if they're planning to control the condition without meds. Diabetic coma can result from an extreme low (induced by taking too much insulin) or from an extreme high (as a result of losing control of blood sugar entirely). I've had diabetes 13 years now, and I've never even come close to anything like that, and it's something I spend zero time worrying about.

  • "what does a little bit of sugar in the urine mean"

It's hard to know what "a little bit" means, but any sugar at all in your urine is abnormal, because the kidneys normally return all the blood sugar that flows through them to the bloodstream, allowing none of it to pass into the urine. Sugar in the urine means either that your blood sugar is significantly above normal (so the kidneys can't return all of it to the bloodstream as they should) or that you have some kind of kidney disease.

  • "stress and a1c results"
  • "what can over stressed times do to a a1-c blood test"
  • "stress ha1c"

Apparently a lot of people like to think that stress can elevate hemoglobin A1c results -- that is, falsely elevate them, causing your A1c result to go up even if your blood sugar does not.

As the A1c test simply measures how much of your hemoglobin has sugar bonded to it, it's not easy to imagine a scenario under which your A1c result would go up even if your blood sugar didn't. Stress doesn't have the magical power to make your hemoglobin molecules bond with sugar molecules.

Conceivably stress could indirectly elevate your A1c result... by elevating your blood sugar. This could happen. Stress causes you to produce "stress hormones" (such as adrenaline and cortisol), which tend to suppress insulin sensitivity, thus raising blood sugar. Stress can also interfere with sleep, with the same result.

So, if your A1c is up and you think stress is playing a role, than by all means do whatever you can to combat stress. But never use stress as an excuse for pretending that a rising A1c does not represent rising blood sugar!

  • "what kind of insects come out of the urine of diabetes patients"

Hallucinatory ones.

You're a bit confused: insects are said to be attracted to the sugary urine of diabetes patients -- they are not said to emerge from it.


I'm back, sort of

Monday, February 3, 2014

 


My week

I'm still dealing with the end-of-project crisis at work which made me give up on blogging last week. It's probably foolish, and maybe even impractical, for me to return to blogging before I've met the project deadline (Friday, unless I have to work through the weekend to solve problems I can't solve by Friday night). But I don't like to neglect the blog, so I'll do my best to post some new content this week. I may have to be less long-winded this week, though.

 


Not Really Diabetic

A reader of long standing, who has stabilized his A1c results in the range of 5.4 to 5.9% (without going on meds), reported to me today that he finds himself questioned frequently by people who don't believe such a thing is possible for anyone who has diabetes. They suggest to him either that he's lying about not being medicated (since an unmedicated diabetes patient obviously could not do as well as he's done) or else that he doesn't really have diabetes. He finds this frustrating, but he has become used to it.

Considering how much higher his A1c results used to be, I would say that he was not labeled frivolously as diabetic. He more than met the diagnostic criteria. That he later reduced his blood sugar to non-diabetic levels, without help from the pharmacy, does not mean he was never diabetic in the first place.

Clearly there are worse problems for a diabetes patient than dealing with people who think they don't really have diabetes because they're doing too well. But his experience does illustrate a problem which arises from a conflict between the way "diabetes" is defined and what most people (including doctors) think the word really means.

Strictly speaking, to be diabetic is to have abnormally elevated blood glucose levels on a persistent basis. If your blood sugar is not abnormally elevated on a persistent basis, then you're not diabetic.

But "diabetes" as most people (including most doctors) use the term refers to whatever underlying problem in your endocrine system is giving you a tendency toward elevated blood sugar... and will drive your blood sugar to abnormally high levels if you don't keep fighting it. Diabetes in this sense is considered chronic and incurable. There is no such thing as getting rid of it. You can only control it. And you must not speak of "curing" it! Once you're diagnosed as diabetic, you're always diabetic.

I'm willing to concede that the underlying problem in the endocrine system which pushes people in the direction of diabetes is not a "curable" problem. But it's unfortunate that the seemingly boundless vocabulary of medicine does not have room in it for a term which describes diabetes patients who have normalized their blood sugar. They're not "cured", but neither do they meet the diagnostic criteria for diabetes.

Some diabetes patients are well-enough controlled that, if their medical records were lost, a new doctor would not be able to tell that they had it. Maybe we don't want to call them "cured", but we ought to have a term for them other than "diabetic".


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