5th Thursday Update

April 30, 2015


It's time once again for me to try answering the questions asked, at least implicitly, by people who were referred to my site after Googling various search strings.

"what is range for a1c test"

The hemoglobin A1c test determines how much of the hemoglobin (a protein in your red blood cells) is "glycated" (encrusted with sugar as a result of exposure to sugar in the bloodstream). The test result is a percentage, even if it's not stated that way on the lab report (in other words, if your result is 7.1, then 7.1% of your hemoglobin is glycated). The result of the test is a direct indication of the glycation rate (that is, the rate at which the sugar in your blood is creating unwanted bonds with protein), and an indirect indication of how sugary your blood has been, on average, during the past three months or so.

The reason the A1c test covers a period of 3 months, and no more, is that the body recycles its red blood cells, and they have a lifespan of about three months. Because almost no red blood cells are present in your blood more than three months ago, the test cannot reflect conditions longer ago than that.

The medical lab you use will cite a "reference range" for its particular version of the A1c test, indicating what range of values they consider normal. My lab calls the reference range 4.8 to 5.6%. My last A1c test result was 5.5%, so I made it into the normal range (though not with a great deal of headroom). Your lab may define the reference range differently, but not by very much.

"my a1c is 7.3 what does this mean"

It means 7.3% of your hemoglobin is glycated, which indicates your blood sugar has been too high, on average, in recent months. A result of 7.3% is high enough to give you an elevated long-term risk for various health problems which have been categorized as "diabetes complications" (eye problems, nerve problems, circulatory disorders, etc). For certain older patients, the long-term consequences of a test result of 7.3 might be regarded as less harmful than the short-term consequences of an attempt to reduce it, so in certain cases doctors will settle for a result of 7.3 rather than try bringing it down. But if your doctor hasn't said 7.3 is good enough in your case, you probably want to aim for a lower result -- in the normal range, or as close to the normal range as you can get without setting yourself up for hypoglycemic episodes.

Risk of diabetes complications rises as you get above 7.0%, and in fact it rises pretty steeply. If you're expected to be around for more than another year or two, I think you should be cautions about letting your A1c get very far above 7.

"normal a1c 0%"

No, actually, an A1c result of 0% would not be normal. I doubt if anyone has ever got a result of 0%, as it would indicate a complete absence of sugar in the blood, and that's not a situation anyone could survive for long.

"my a1c is 6.2 is that bad "
"how dangerous is a1c of 6.2"

An A1c result of 6.2% is considered elevated ("pre-diabetic") for a person who hasn't been diagnosed with diabetes -- a warning sign, in other words. But if you already have been diagnosed with diabetes, a result of 6.2 is considered good glycemic control. It may be a little high, but it's not likely to cause you problems unless you let it go higher than that. (I aim for a truly normal range, myself, but I'm a perfectionist, so don't listen to me.)

"is hemoglobin a1c 9.5 bad"


"I have an a1c of 6.2 am i pie diabetic"

Maybe you are a pie diabetic, but something tells me you meant to say pre diabetic. In which case, yes.

"does the a1c test each three month period equally"

No. The test is "weighted" toward the most recent month, meaning that conditions in your blood over the most recent month had more impact on the test result than conditions two months ago, and even more impact than conditions three months ago.

The reason for this is that blood cells are being recycled constantly. At any point in time, a lot of the red blood cells that were in your bloodstream 30 days ago are now gone, and even more of the cells that were in your bloodstream 60 days ago are gone. Younger cells, however, will all be captured in the test. On the other hand, younger cells won't have been exposed to blood sugar for as long, so the total glycation impact on them is reduced. Figuring all this out mathematically gets very complicated (certainly too complicated for me -- I was not exactly a stellar calculus student). In general, it's safe to say that any recent change in your glycemic control -- good or bad -- will have an outsized impact on the test result.

"is 4.9 a good blood sugar level"

If you mean 4.9 mmol/l, that is equivalent to 88 mg/dL, which is a good fasting level. (Results after meals go higher than that.)

"graph of normal blood glucose"

The normal, non-diabetic glucose profile over the course of a day looks something like this:

Your assignment as a diabetes patient is to make your own glucose profile look like that -- or as much like that as you can make it look, under the circumstances.

Diabetes patients tend to get higher spikes than that after meals, but try to keep yours as close to the normal dimensions as you can.

" I'm diabetic and i want to know how to get rid of sugar in my urine"

Sugar in the urine is merely a side-effect of having too much sugar in the bloodstream. If you want less sugary urine, you need less sugary blood (see the graph above). Regular exercise, limitations on carbohydrates in the diet, and weight loss (if needed) are the most reliable remedies.

"is my sugar too low if i get the shakes and start wetting".

I am going to assume you meant to say "sweating", not "wetting".

Those are among the common symptoms of hypoglycemia. They are also among the common symptoms of giving a speech, acting in a play, making music in a concert, or engaging in a competitive sport.

Feeling hypoglycemic is very often a symptom of being hypoglycemic, but giving yourself a blood glucose test is the only way to find out for sure if that is what's happening to you, or if you're really just feeling bad for another reason.

"how to check if your urine contains glucose by mere looking"

You can't tell by mere looking.

However, you might want to try peeing on the ground and waiting to see if a swarm of bees arrive and pounce on the puddle. If you see a scene like this, it could be a sign of trouble.

"colonoscopy prep for nonmedicated diabetic"

I have some experience of doing colonoscopy prep as a nonmedicated diabetes patient. All I can say is that I made a decision to just follow the instructions as given. A colonoscopy is not something you have to do every day, or even every year in most cases. If the procedure calls for you to mix the laxative with large quantities of Gatorade, or something else sugary, just go with it. You'll be fasting at that point anyway, so no sugar is going to be getting into you in any other way.

A colonoscopy is an extreme situation, but fortunately it's also a temporary situation. If the prep pushes up your blood sugar higher than you like it, at least it's unlikely to have any lasting impact, because you won't be doing it again anytime soon.

Also, the sheer relief of having the colonoscopy over with will probably help you rebound quickly from any disturbance to your system that the experience caused you.

"how bad is glucose of 325"

Unacceptably bad. Harmfully bad. Work that down to something in the normal range, or close to it.

"yoga and lowered a1c test"

I go to a yoga class once a week, mainly as a means of healing the various aches and pains that come with exercising and ageing. But I don't think of it as a real workout, and I am skeptical that yoga alone would contribute a lot to reducing anybody's A1c result. However, certain kinds of yoga poses build muscle, and if you do them enough they might have an impact on A1c.

"glucose 99 pee a lot"

99 mg/dl doesn't seem to be nearly high enough to be causing polyuria (excessive urination). But when exactly are you getting a test result of 99? If that's your fasting result in the morning, but you go sky-high after meals, maybe your blood sugar is sometimes going high enough to produce that result.

High blood sugar is not the only condition that can cause polyuria, so if you can't see any reason to think high blood sugar is causing this, ask your doctor what else might be causing it.

"okay google are there any studies about too much beer drinking in men over 70 whether it causes more alzheimer's or dementia"

Google search strings should be brief. If they're not, they turn up results referring you to every website on earth (including mine). Also, a Google search phrase does not need to include a preamble such as "Okay, Google...".

I don't know anything about excessive drinking in men over 70 causing Alzheimer's disease or dementia. But I'm pretty sure it does cause drunkenness, along with a tendency to create excessively chatty Google search strings.

"if a doctor doesn't feel my urine analysis in front of you do you have a case"

I don't know what you're asking, exactly, but I'm pretty sure I don't want to understand it any better than I do.

Many aspects of modern society are more easily understood if you know that most people (or anyway most Americans) have a plan for retirement which hinges on either winning a lottery or suing somebody.

"when you look at it"

So true!

4th Thursday Update

April 22, 2015

Yesterday I did a foolish thing, and scheduled my eye-doctor appointment on the same day as my dental appointment, so I spent the whole morning being examined and scanned. The proceedings included eerie NASA-style photos of my retinas (which resembled the surface of Mars), and a full set of dental X-rays. But nothing bad turned up, at either appointment!

The retinal scan was the test most likely to show evidence of diabetes-related problems, if I had any, but my optic nerves and arteries looked fine. (When I say they looked fine, I mean they looked fine to my eye-doctor. They looked creepy as hell to me. If that's what a healthy retina looks like, may I never see a diseased one -- especially if it's mine!)


More on the guidelines

Last week I wrote about the new Type 2 diabetes treatment guidelines from the American Association of Clinical Endocrinologists (AACE) and the American College of Endocrinology (ACE). I expressed my disappointment with the absence of any mention of exercise, and the generally depressing presentation of diabetes as a steady downhill progression, in which the patient will need more and more drugs at each faltering step on the road to hell.

There's another side to the story, though. What I was reviewing was the "AACE/ACE Comprehensive Diabetes Management Algorithm 2015" -- essentially a graphic flowchart illustrating the hellbound path. The algorithm can only give a shorthand indication of what doctors are supposed to do at each stage, and the easiest possible way to give a shorthand indication is to name a drug, so most of the algorithm looks like a pharmaceutical catalog. Maybe, if I saw the long-form document describing the Clinical Practice Guidelines, it would turn out to give a more nuanced (and less drug-focused) account of the diabetes-management process.

So, today I downloaded the 87-page document entitled "AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY – CLINICAL PRACTICE GUIDELINES FOR DEVELOPING A DIABETES MELLITUS COMPREHENSIVE CARE PLAN – 2015". (A somewhat lengthy title -- we'll call it the CPG from here on.) I figured there would be a little more meat to chew on in a long text document than in set of slides illustrating an algorithm. And there is.

This document aims to take a new, broader view of diabetes management: "The mandate for this CPG is to provide a practical guide for comprehensive care that incorporates an integrated consideration of micro- and macrovascular risk (including cardiovascular risk factors such as lipids, hypertension, and coagulation) rather than an isolated approach focusing merely on glycemic control." Okay -- so far, so good. A diabetes management program which aims to control your blood sugar, even if it sets you up for a heart attack, is obviously not the right approach.

Last week I reported that I searched the treatment algorithm for the word "exercise" and found no instances of it, but searches for "exercise" and "physical activity" turned up a lot of hits within the CPG.

Under 'How is Prediabetes Managed?', we read: "Prevention of T2D depends upon systematic lifestyle modifications including caloric intake reduction (e.g., 500 kcal deficit per day) and regular exercise (30 minutes aerobic work at least 5 days per week) to lose >7% body weight. Lifestyle management alone may be adequate for low-risk states and can reduce DM incidence by as much as 58%."

Under 'How are Glycemic Targets Achieved for T2D?', we read: "There is good evidence that regular physical activity improves glucose control in persons with T2D. Because physical activity is usually combined with caloric restriction and weight loss, as in combined lifestyle intervention programs, distinguishing the effects of increased physical activity alone from those of calorie restriction and weight loss is often difficult. However, studies on exercise alone show improved glucose control. Regular physical exercise -- both aerobic exercise and strength training -- is important to improve a variety of CVD risk factors, decrease the risk of falls and fractures, and improve functional capacity and sense of well-being. Physical activity is also a main component in weight loss and maintenance programs. Activity of at least 150 minutes per week of moderate-intensity exercise such as brisk walking (e.g., a 15- to 20-minute mile) or its equivalent (e.g., yoga, walking during golf, water aerobics, physical play with children, etc.), is now well accepted and part of the nationally recommended guideline for physical activity. For persons with T2D, recommendations include flexibility and strength training exercises in addition to aerobic exercise."

There are several other places where exercise is recommended, often with specific reference to various diabetes-related health problems which exercise can ameliorate or prevent (such as hypertension, obesity, and cardiovascular disease).

Now, I should mention that the references to exercise, though numerous throughout the CPG, are more conspicuous if you're searching specifically for them than if you're not. If you just read the guidelines as ordinary text, exercise is something that comes up periodically amongst a great many references to drugs and weight loss. But the subject is mentioned repeatedly, and once ("studies on exercise alone show improved glucose control") it is even granted something like its actual level of importance. So, in regard to exercise, the new CPG is better than I expected, and considerably better than the "algorithm" document I was criticizing last week.

I haven't yet had time to evaluate the CPG in regard to other issues besides exercise, but I can already see that some of the ethical decision-making that went into the guidelines might leave a bit of room for argument.

For example, under 'Outpatient Glucose Targets for Nonpregnant Adults', we read: "Glucose targets should be individualized and take into account life expectancy, disease duration, presence or absence of micro- and macrovascular complications, CVD risk factors, comorbid conditions, and risk for hypoglycemia, as well as the patient's psychological status. In general, the goal of therapy should be an A1C level <6.5% for most nonpregnant adults, if it can be achieved safely). To achieve this target A1C level, FPG may need to be <110 mg/dL, and the 2-hour PPG may need to be <140 mg/dL."

Speaking for myself, I aim for a lower A1c than 6.5%, but I realize 6.5% is a time-honored treatment target; it is thought to present a low risk of diabetic complications. I should think you'd get a lower A1c than 6.5% if you hit the glucose targets mentioned above, but I realize everybody's different.

However, that qualifier "if it can be achieved safely" is a pretty large exception. The safety issue alluded to here is the risk of hypoglycemic episodes -- which are often induced by insulin and by glucose-lowering diabetes drugs of all sorts. When the only diabetes drug you're taking is exercise, the risk of hypoglycemia (or at least hypoglycemia severe enough to be harmful rather than merely unpleasant) is negligible -- a point which the authors of the CPG might have mentioned, and do not.

It concerns me that diabetes management is usually seen as a conflict between the need to control blood sugar and the need to avoid the harmful effects of treatment-induced hypoglycemia -- when there is a treatment available which does not induce a harmful level of hypoglycemia, and nobody wants to talk about it.

I also worry about the ethical compromises involved in the different recommendations for younger and older patients. "In adults with recent onset of T2D and no clinically significant CVD, glycemic control aimed at normal (or near-normal) glycemia should be considered, with the aim of preventing the development of micro- and macrovascular complications over a lifetime, if it can be achieved without substantial hypoglycemia or other unacceptable adverse consequences... A less stringent glucose goal should be considered (A1C 7 to 8%) in patients with history of severe hypoglycemia, limited life expectancy, advanced renal disease or macrovascular complications, extensive comorbid conditions, or long-standing DM in which the A1C goal has been difficult to attain despite intensive efforts..."

Don't get me wrong: I understand why younger patients need to be more careful about issues which have only a long-term health significance. I also understand why, in an elderly patient with other health problems, it might do more harm than good to chase a lower A1c result by means of heavy-duty drug treatment. But it's easy for a guideline which aims to be realistic about age issues to turn into a case of "we've decided you're old enough that we can stop trying now". Establishing an A1c goal in the 7 to 8% range sounds to me an awful lot like giving up. On the other hand, I'm not an endocrinologist treating a very old, very sick, very immobile patient, so I may not realize how powerful the impulse to give up might be in such cases.

From what I've seen of the CPG so far, my judgment is that it's better than I thought, even though the emphasis in it would have been different if I had been running the committee that came up with it.

3rd Thursday Update

April 16, 2015


The Usual Approach

When I read about how doctors are being told to treat Type 2 diabetes (that is, by official medical organizations which establish guidelines for diabetes care), I always get the feeling that I have stepped through the looking-glass, into an alternate reality which bears little resemblance to my own experience with the disease. Everything the doctors are focusing on seems unfamiliar to me; everything I am focusing on goes unmentioned.

Yesterday the American Association of Clinical Endocrinologists (AACE) and the American College of Endocrinology (ACE) issued their updated guidelines for optimal care for patients with type 2 diabetes.

This document is in algorithm form -- that is, it consists of flowcharts guiding the physician through a sequence of actions which basically amount to adding more and more drugs as the patient does worse and worse. To be fair, "Lifestyle Modification" is the label prominently applied to the first step in the process, for all patients. But the second step (depending on how bad the patient's hemoglobin A1c test result is at diagnosis) is determining how many drugs to start with, and when to start adding more of them.

In other words, "Lifestyle Modification" is a vaguely-described jumping-off point for all patients, after which the algorithm assumes the patient will also need drugs, and will need more and more of them over time. That "Progression of Disease" arrow at the bottom of the chart tells the real story here: the patient is expected to get steadily worse, and the doctor's task is to keep track of this grim trend, in order to determine how many drugs the patient needs at each point in the inevitable downhill slide.

This isn't what my own experience of the disease has been like. Fourteen years after diagnosis, I'm on no medications. My most recent A1c result (last month) was in the normal range (5.5%). Today my fasting test was 83 mg/dl, and my post-prandial result was 123 (and that was before I'd even had my exercise for the day). Clearly the disease has not "progressed" in the normal way for me, if my inevitable decline hasn't taken me any further downhill than this since 2001.

The "Lifestyle Modification" aspect of the algorithm is the only one relevant to my experience of managing the disease, but even here, I find little that I can relate to, in terms of anything I'm doing now. The creators of the algorithm seem to be using "Lifestyle" as a code-word for "weight loss". Exercise is not mentioned. And I mean it is literally not mentioned. I tried running a search of the PDF file, in case exercise was mentioned and I missed it, but it came up blank.

This is bizarre to me. Exercise has been the cornerstone of my approach to diabetes management. I have collected enough glucose test data on myself to know that exercise reliably boosts my insulin sensitivity and allows me to keep my glucose test results (and ultimately my A1c test results) within the non-diabetic range. Exercise is what it's about. Exercise is what keeps me from participating in the downhill slide which the algorithm assumes is the fate of every patient. Isn't exercise worth of a little more attention than the endocrinologists are giving it?


A modest proposal

Here's a thought: if your research finds that "Maternal exercise significantly improved male offspring's insulin and glucose metabolism whereas female offspring showed only modest improvement", and the headline under which the research is presented reads "Male offspring get most benefit from pregnant mother's exercise", and the photo with which you illustrate the story looks like this....

...then the mothers in the study had better not turn out to be a bunch of goddamn mice.


Late sunsets

I'm still taking advantage of the late sunsets these days to get out into the real world after work. It's a healthy thing to do, if you get the chance to do it.


2nd Thursday Update

April 9, 2015


But how does it work?

In 1897, the Bayer company in Germany started synthesizing a medication known as acetyl salicylic acid (wisely renamed "aspirin" for marketing purposes). The new drug was known to be effective as an anti-inflammatory, as a pain-reliever, and as a fever-reducer. What wasn't known was how it worked. For a very long time, aspirin's "mechanism of action" remained mysterious. Eventually, the British researcher John Vane was able to show that aspirin worked by suppressing production of prostaglandins (lipid compounds which served a hormone-like function, as signalling molecules). Vane won the Nobel Prize for this work... in 1982.

There's something a little alarming about a drug being widely used for decades even though scientists don't know how it works. If you think it doesn't matter whether or not we know how it works (so long as we're pretty sure it does work), think again. Even if a drug has an established track record of effectiveness and doesn't seem to be dangerous to most people, it probably has undesirable side effects which are more dangerous to some people than others. If doctors understand how a drug works, they will be better able to identify situations where taking the drug is too risky. (For certain patients, aspirin is too risky, but it took doctors an awfully long time to figure that out; they might have figured it out sooner if they figured out how aspirin works sooner.)

Or, to look at the situation in a more hopeful light, if doctors understand how a drug works, they will be better able to identify other diseases which are potentially treatable with that drug, even though the drug is not currently prescribed for that purpose. It is often discovered, usually by accident, that a drug intended for one condition is also useful in treating a completely unrelated condition; such discoveries could more easily be made if the drug's mechanism of action were better understood.

Some diabetes drugs have been poorly understood in terms of how they work -- including the most widely-used diabetes drug of all, metformin. It was clear enough that metformin somehow prevented the liver from releasing excess amounts of glucose into the bloodstream, but how it did that was not clear at all. Some new research from Toronto explains the drug's action largely in terms of its interference in a signalling pathway between the small intestine and the liver. Specifically, metformin stimulates the small intestine to produce more AMPK (a signalling molecule which it produces when glucose concentration is rising). This, in turn, sends a message to the liver: stop releasing stored glucose into the bloodstream! I'm simplifying this a bit, but that's the basic idea.

We usually think of chemical signalling within the body as something which is accomplished entirely by hormones produced by the endocrine glands (such as the pancreas). But researchers are finding that there's a lot more to it than that. The small intestine, and even body fat, can become involved in the process, detecting changes in blood chemistry and sending out chemical signals which aren't exactly hormones but function more or less the way hormones do. Apparently the liver relies, at least partially, on AMPK released by the small intestine to determine how much stored glucose should be released into the bloodstream at any given time. In people with Type 2 diabetes, the amount of glucose the liver releases is typically too much (because impaired insulin sensitivity, and reduced insulin production, are causing the blood to be too glucose-rich to begin with). Metformin, it seems, causes the small intestine to produce more AMPK than it normally would after a meal, and this warns the liver to release less glucose than it normally would.

The same researchers also found another intestinal signalling pathway which can reduce blood sugar (this one involves resveratrol, a compound found in red wine). Researchers are now hoping that their newfound knowledge of these signaling pathways will lead to development of medications which work better than metformin and resveratrol do. (Or will at least be more profitable than they are.)

Well, that's one way of looking at it. But there is another way of looking at it: instead of finding a way to make the small intestine tell the liver to release less glucose (because the body can no longer deal with the amount of glucose the liver normally releases), we could attack the problem a little more directly. After all, the amount of glucose the liver normally releases would not be too much, if we increase insulin sensitivity (mainly through exercise) or if we reduce the amount of glucose the digestive tract is releasing into the bloodstream (mainly through carbohydrate reduction in the diet). Where those two things fail, it may indeed be necessary to interfere with the chemical conversation that goes on between the gut and the liver. But if you can make those things work, then no drug is needed.

All sorts of factors determine how much glucose is in your blood, because all sorts of factors influence (1) the rate at which glucose is being released into the bloodstream and (2) the rate at which glucose is being extracted from the bloodstream. Some of those factors you can control directly, simply by making adjustments in the way you live your life. Drugs only need to come into it when those adjustments are not sufficient to correct the problem.


More on the gut/diabetes connection

Remember how I said above that a drug intended to treat one condition can turn out to be useful in treating another condition? And that it's easier to figure this out if you understand what the drug is doing?

Further research out of Toronto suggests that insulin resistance in Type 2 diabetes is, at least to some degree, triggered by inflammation in the intestinal tract. The researchers reasoned that drugs designed specifically to suppress inflammatory diseases of the intestinal tract (such as Crohn's disease) might therefore be effective as a treatment for Type 2 diabetes. And what do you know? It seems to work.

At least, it works in obese mice. Well, it's a start!


A further note on eggs

Only last week I was writing about the pros and cons of egg consumption, as it related to diabetes. The day after I uploaded that, some new diabetes-related egg news was published. It is mighty hard to keep up with this stuff.

New research from Finland suggests that regular consumption of eggs reduces the risk of developing Type 2 diabetes (reportedly by 37%).

Of course, it's necessary to be cautious in interpreting these results. The test subjects in the study were men, and middle-aged or older; the findings would need to be confirmed, and would need to be seen also in young men and in women, before we could conclude that "eggs prevent diabetes". It could be that the egg-consuming men in the study, who had lower diabetes rates, also had something else in common which protected them. Could it be that they were simply having lower-carb breakfasts, and this made the difference? It's too early to tell. And does this finding have any relevance to people who already have Type 2? Again, it's too early to tell.

But I'm glad that the research seems to support my judgment that eggs are probably more helpful than harmful to people with (or people at risk for) Type 2 diabetes.

In any case, it is always best to be cautious about accepting sweeping conclusions based on the results of a single study...


1st Thursday Update

April 2, 2015


Eggs, good or bad?

Notions of which foods are healthful, and which are not, tend to evolve over time. Every few years, a new food is singled out, in reports claiming that it either cures a disease or causes one. (Actually, the claim is usually that it cures, or causes, half the diseases known to medicine.) Whether the food in question is being presented as a blessing or a curse, we are told that sinister vested interests are trying to keep the public in the dark about what has been learned.

During the period when such notions are popular, it can be difficult to imagine that there will ever be a time when they will be recalled as amusing relics of more primitive era, when people would believe anything.

Which brings me to the subject of eggs.

Eggs have been demonized in years past as a cause of heart disease, and although they have lately been exonerated to a large extent, they are still regarded with some suspicion -- particularly as a problematic food for diabetes patients. Which is annoying, because eggs are seemingly a real gift to diabetes patients in most respects.

For one thing, eggs are very low in carbohydrate -- which is not something you can say of every breakfast food. Most of the foods you would think of having in the morning -- including toast, cereal, and orange juice -- deliver heavy loads of sugar to the bloodstream shortly after you eat them. Eggs do not do this.

Eggs are primarily a source of protein -- and "complete" protein, meaning the sort of protein which includes all of the amino acids humans require. Eggs also provide certain vitamins (including vitamin D) which are hard to find in other foods. And, although eggs are not exactly a convenience food, as they need to be cooked, they are the quickest-cooking food around, and the process doesn't require a lot of culinary skill. (I mean, if you aren't capable of scrambling eggs, you probably shouldn't be allowed to drive, either.) So, here we have a low-carb, high-protein breakfast food that's quick and easy to cook. What's not to like?

What has given eggs a bad reputation is that they are also rather high in fat and cholesterol, and accordingly have been seen as a food which increases the risk of heart disease.

It is exceedingly difficult to discover, with anything like certainty, which foods (and which ingredients in those foods) actually contribute to heart disease. Because we don't raise human beings in cages and perform controlled experiments on them (by strictly regulating what they can eat), we have to fall back on the messier and less reliable process of asking different sorts of people what they eat, and believing them, and comparing their health outcomes. Many, many sources of error and bias creep into the process, and the result is a bunch of studies which agree poorly with one another (but agree rather well with what the researchers running each study were expecting to find). Because this process is such a mess, it can take decades for a clear picture to emerge; until then, we're stuck with contradictory evidence and we have to make an educated guess about who's right.

A lot of researchers have been gathering a lot of evidence over the years about diet and heart disease, and the general trend over the years has been for researchers to find less and less evidence that cholesterol consumption in general, and egg consumption in particular, play a significant role in causing heart disease in otherwise healthy people.

Part of the reason for this appears to be that prior assumptions about how dietary fat and cholesterol affected a person's lipid profile were either overstated or simply wrong. Trans fats (that is, natural fats which have been altered by artificial hydrogenation) are strongly associated with heart disease, but natural fats and cholesterol in the diet apparently are not.

Even though cholesterol in the blood certainly matters, dietary cholesterol turns out not to have the kind of impact on blood cholesterol that researchers had assumed. Most of the cholesterol in the bloodstream is manufactured by the body, not consumed directly. And the cholesterol in eggs is particularly ineffective in raising human blood cholesterol, because another substance present in eggs (phosphatidylcholine, also known as lecithin) inhibits cholesterol absorption.

However, some researchers still see a problem: lecithin is transformed by bacteria in the gut into another substance known as TMAO, and TMAO has been shown to cause arterial disease (in mice, anyway), so even though the lecithin in eggs blocks absorption of cholesterol, the lecithin might be ultimately be harmful to us, on balance, because of what our gut bacteria will turn it into.

As you can see, this stuff gets very complicated. Once researchers start getting down to the level of which molecules get transformed into which other molecules by bacteria, you know you're not going to get a simple, yes-or-no answer to the question, "are eggs bad for us?".

Leaving aside the arguments about individual molecules and what they do, what do the available studies tell us about whether people who eat eggs get more heart attacks? Well, the studies are not wonderfully consistent in their results, but the consensus appears to be that eating eggs in moderation (defined as maybe six eggs a week) does not significantly increase cardiovascular risk in healthy people.

But of course there is a catch! That phrase "in healthy people" is meant to exclude diabetes patients already at heightened risk of heart disease. It appears that eggs present more risk to the cardiovascular health of people with diabetes than they do on people without diabetes. This is in keeping with the general tendency of anything undesirable (with the possible exception of lightning strikes) to happen more often to diabetes patients than to anyone else.

So what's a diabetes patient to do? Give up the advantages of eggs (an easy-to-cook, low-carb, high-protein breakfast food), or hold on to those advantages and live with the apparent risk that they can cause trouble for diabetes patients?

I can't tell you what you should do, but here's how I see it: I am dealing with the diabetes-associated cardiovascular risk by exercising, and for as long as I've been doing that (14 years now!) I've been able to get very good results on my blood cholesterol tests, even though I've been eating a diet that includes eggs. So I think I've lowered my heart-attack risk enough that I can afford to have eggs for breakfast. I do not think I'd be doing my heart any favors to have a bowl of high-carb cereal instead. Eggs for me, thank you!

What got me thinking about eggs tonight is that I found out one of my neighbors, who raises chickens, has a local door-to-door delivery service for eggs. I figured I might as well take advantage of this convenient way of getting the freshest possible eggs, so I signed up. On Tuesday I got my first dozen. They are indeed of high quality. But I have to admit I was a little startled to see how thoroughly the label on the carton had been personalized....


Walking wounded

Last week I had a relapse of the same pain in the same place in the same foot that had been plaguing me a month ago, so I decided to take a break from running for several days, and walk instead. I found that hiking, particularly on hilly routes, seemed to make my foot feel better rather than worse. I decided to wait, this time, until my foot felt entirely normal (not just less sore) before going back to running. Fortunately, the current combination of late sunsets and warm weather is making evening hikes feasible.

And there certainly are nice places to go for a long, hilly walk around here. These pictures were taken on a walk yesterday, towards sunset:

Today my foot finally felt normal, so I decided I was ready to risk doing a long trail-run today. (I took the day off work, so I knew I had time for it.)

It was a nice run, and I think I got away with it -- my foot wasn't hurting at the end of it. The real test will come later -- is it going to hurt when I wake up tomorrow morning? We'll see. I'm icing it tonight just to improve the odds that it won't decide, while I'm sleeping, that I need to be punished for running on it today.

Another good thing about the run was that I didn't run out of energy during it, despite the distance (9.4 miles). You might expect that taking a break from running will reduce your stamina, but sometimes it seems to increase it.


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