When you read a list of potential diabetic complications, it looks as if all the complications are about equally significant. Nothing stands out. They all sound awful, of course, but you have no idea which ones to worry about most. And anyway, why worry at all? Aren’t you pretty safe from all of them, so long as you keep your glucose under control?
Well, not quite. One of those complications requires extra attention from you, because it takes more than glucose management to prevent it, and because the price of not preventing it is unacceptably high. This complication has the potential to blow up into a life-threatening emergency, suddenly and without warning. It’s absolutely necessary for you to take special precautions against it.

The complication I’m referring to is the so-called “macrovascular accident” — a medical emergency which occurs when an artery becomes blocked and, as a result, a vital organ is deprived of its blood supply. Usually this means a heart attack. However, the same sort of arterial blockage can also produce an ischemic stroke (ischemic strokes are the kind that are caused by blockage, not bleeding, within the brain). As the cause (and prevention strategy) for ischemic stroke is the same as for heart attack, so I'll treat them as a single issue.

I don't normally tend to dwell on the scary possibilities involved in diabetes, but I need to dwell on this one, for two good reasons: (1) you can can do something about it, if you understand the problem, and (2) a great many people don’t understand the problem, and don’t do anything about it (or don’t do enough).

Admittedly, anybody can have a coronary or a stroke, whether they have diabetes or not. However, as with so many other health problems that “could happen to anybody”, the risk is not evenly distributed throughout the population. Some people are likelier than others to have a macrovascular accident, depending on a variety of risk factors. One such risk factor, unfortunately, is diabetes.

The rate of coronary heart disease and ischemic stroke is definitely higher in people with type 2 diabetes than in people without it. What’s worse, good diabetic control does not, by itself, take care of the problem. Most of the added cardiac risk that comes with diabetes cannot be eliminated just by reducing your BG.

Because type 2 diabetes carries with it this heightened risk, and because glucose control by itself is not sufficient to eliminate the risk, you need to be more concerned about the possibility of a macrovascular accident than other people. I don’t mean you need to worry about it more than they do — I mean you need to do more about it than they do. So let me tell you about the problem. To avoid being depressed by it, stay focused on the reason I’m telling you about it: it’s a solvable problem.

What’s the real problem?

Perhaps it seems odd (even questionable) to put very a common arterial disease into the category of “diabetic complications”. Most other disorders which we think of as diabetic complications are common only in the diabetic population. They are rare in non-diabetic individuals (except as a consequence of extreme age).

Macrovascular accidents, by contrast, are anything but rare in the non-diabetic population. In fact, heart attacks are the leading cause of death in America. So is this really a diabetes-related issue? Even though the rate of macrovascular accidents is high among people with type 2 diabetes, couldn’t this be because people with type 2 diabetes tend to be at risk for other reasons, unrelated to diabetes?

A reasonable objection, and true in a way. People with type 2 diabetes do tend to have other cardiac risk factors (such as obesity, high blood pressure, and excess LDL cholesterol). However, even when you take those other risk factors into account, you are still left with an element of added risk which can’t be explained away in terms of factors unconnnected to diabetes.

But still — isn’t it strange that controlling BG doesn’t eliminate the risk? If the problem is really caused by diabetes and not by something else, then getting your average BG out of the diabetic range should fix the problem. So why doesn’t it?

Once again, a reasonable objection, and true in a way. Diabetes, in the strict sense of the term (chronic hyperglycemia) is apparently not the real problem. It seems that the real problem is insulin resistance -- or rather it is the hyperinsulinemia (excessive insulin in the blood) which the endocrine systems uses to overcome insulin resistance.

Too much insulin

If you are insensitive to insulin, your pancreas compensates for this by pumping out abnormally large amounts of the stuff. If your pancreas is able to produce enough extra insulin to overwhelm the body’s insulin resistance, your BG never rises above the normal range. If your pancreas is not able to produce that much extra insulin, you become diabetic. But either way, you probably have more insulin in your bloodstream than most people do, and that’s a problem.

Why does it matter how much insulin is in your blood? That is not completely understood, but it seems that excess insulin is not good for your arteries — it has a scarring effect on arterial walls. This scarring promotes the formation of cholesterol deposits. (There is controversy about this issue, actually. Speaking as an amateur observer of the scene, I can only say that I think those who attribute diabetic coronary risk to excess insulin have made a strong case.)

The harmful effects of excess insulin can occur in the absence of diabetes — for the simple reason that excess insulin can occur in the absence of diabetes. Many insulin-resistant people are able to secrete enough extra insulin to keep their glucose levels down. They can pass a diabetes test, but something is wrong nevertheless. Such people can develop coronary heart disease even though they don’t seem to be at risk for it. The whole “Syndrome X” (or “Metabolic Syndrome”) phenomenon of insulin resistance as a cause of arterial problems was discovered by researchers who were attempting to discover why heart attacks sometimes happen to the “wrong” people.

Coronary heart disease

It seems to me that I shouldn’t talk about coronary heart disease without first providing some explanation for the very peculiar name of the condition. Coronary means “crown-like”. The arteries that supply blood to the heart muscle come together and enter the heart at the top, forming a “crown” of blood vessels; because of this appearance, they are called coronary arteries. Yes, I know that’s a ridiculous reason for calling them coronary arteries, but that’s what they’re called. (Just be glad the arteries don’t enter the heart at the bottom; God only knows what doctors would want to call them in that case.) Anyway, if one of the coronary arteries becomes blocked, a section of heart muscle is deprived of its blood supply — and all hell breaks loose.

How can the heart run out of blood?

Let me confess to a conceptual problem I have always had about this issue, which I suspect that others must share with me: how can the heart, of all unlikely muscles, possibly run short of blood? Isn’t the heart a hollow vessel filled with blood? I mean, for heaven’s sake, the blood is right there! Why doesn’t the heart muscle just soak it up?

I have no doubt that, to experts on physiology, such questions seem almost unthinkably naive. It probably doesn’t occur to them that anyone could be dopey enough to look at the matter this way. Because it doesn’t occur to them, they never try to explain the matter. Which is too bad, because a lot of us need to have it explained.

I’m not sure I am the right person to step in and explain it for them, but I’ll do my best. It isn’t enough for a muscle to have blood next to it. The chambers of the heart might be full of blood, but the heart muscle doesn’t benefit from that. Muscle tissue, like any other tissue, requires that blood be distributed to it, through a complex network of blood vessels, branching out into microscopic vessels called capillaries, so that blood is delivered to every cell in the tissue. No tissue can survive without these networks of tiny blood vessels. Even tumors require them, which is why cancer researchers are always looking for ways to block formation of new blood vessels (and therefore prevent tumor growth). Anyway, heart muscle can’t just absorb blood directly from the chambers of the heart; it relies on a network of blood vessels, and that network is furnished with blood from only one source: the coronary arteries. Each artery in the “crown” serve a particular section of the heart muscle, and failure of any of them is going to cause serious trouble.

The blockage may be complete, or it may be partial, but whenever a section of heart muscle is not receiving as much blood as it needs, its functioning will be impaired (not a good thing) and its tissues will be damaged (definitely not a good thing). This alarming situation is called a heart attack. The amount of damage that results depends on which arteries are blocked, to what degree they are blocked, and how much stress the heart is under at the time. Even a partial blockage can be devastating if the heart is working hard, and therefore needs significantly more blood than the half-blocked artery can deliver.

What blocks the arteries?

Blockage of arteries is typically caused by arteriosclerosis. This is the famous “hardening of the arteries”, in which the arterial walls become thickened and inelastic. The common variety of arteriosclerosis is called atherosclerosis, which is caused by the buildup of cholesterol deposits. (For all practical purposes, you can regard these two words, which look so much alike anyway, as interchangeable; I will use the term atherosclerosis.)

The buildup of cholesterol deposits on arterial walls is a gradual process, constricting the flow of blood through the arteries more and more over time. However, it can also produce changes which are anything but gradual. If there is a lot of deposited material on the wall of a large artery, a piece of it can flake off the arterial wall, and become lodged in a smaller artery downstream. Also, the breaking-off of this piece of deposited material may wound the blood vessel, causing an obstructive blood clot to form. Either way, this sort of event can lead quite suddenly to a complete or near-complete blockage of an artery (and to a heart attack which seems to come out of nowhere, perhaps when you’re sitting peacefully in a reclining chair, minding your own business).

Your “first”

Most of us are used to injuring our muscles occasionally, and then waiting patiently (or impatiently) for them to heal and start working properly for us again. But injuring heart muscle is not quite the same thing as spraining your ankle. You can’t wrap an Ace bandage around your heart, limp around gingerly on it for a while, and wait for it to start feeling better so that you can use it again.

Your heart muscle needs to keep working for you constantly, at full efficiency, day and night, for your entire life. Your heart never gets a vacation, and it isn’t allowed any sick days. Whether it is injured or not, it has to keep on working just as hard as ever. You can easily survive an injury to your back muscles, abdominal muscles, or leg muscles, but injuring heart muscle is not something you can afford to take a chance on. Not even once.

Please do not imagine (as some people apparently do) that your “first” heart attack will be a kind of wakeup call or learning experience for you. It’s true that a lot of people who have a first heart attack manage to avoid having a second one, but in many cases they achieve this not because they learn from the experience, but because they die from it. Sorry, but it’s true. More than a third of all heart attacks are fatal. I don’t know about you, but I just hate the sound of that. I don’t ever want to play a game of chance that has worse odds than Russian Roulette. If you don’t want to play it either, you should do everything you can to avoid having your first (and potentially final) heart attack.

How much risk?

No human being has zero risk of heart disease. However, some people carry a lot more risk than others, and it isn’t just because they inherited the wrong genes. The biggest risk factors that most people face relate to the way they live, and are therefore controllable. To a large degree, we choose the amount of heart attack risk we are going to live with.

If you are stuck with a major risk factor that is beyond your control, the thing to do is to compensate for it, by taking extra care to reduce whatever risk factors are not beyond your control. By doing this, you may be able to level the playing field, so that your total risk is no worse than the average person’s (and maybe better).

Cardiac risk factors are usually expressed as multipliers of the “normal” risk (that is, the risk faced by a healthy person with no special problems, no bad habits, and no family history of heart disease). In other words, if a particular condition carries a cardiac risk factor of 2, then having that condition doubles the normal probability of developing coronary heart disease.

The good news is that the “normal” risk is reasonably low. The bad news is that a lot of us add so many multipliers to the “normal” risk that we are essentially heart attacks waiting to happen.

I should add that when two risk factors are combined, they magnify each other disproportionately. A pair of small risk factors can have more impact when you combine them than you would expect. When it comes to risk factors, the whole is greater than the sum of the parts.

How much risk does diabetes add? It is hard to set a precise value on the diabetes risk factor, because people with type 2 diabetes usually carry several other risk factors as well. They are more likely than non-diabetics to be obese, to be sedentary, to have high blood pressure, and to have an unfavorable cholesterol profile. These additional cardiac risk factors complicate any attempt to evaluate the risk of diabetes alone. But for what it’s worth, one reasonable estimate of the diabetes risk factor (based on a large, long-term German study) is 2.5, meaning that diabetes by itself makes you two-and-a-half times as likely as a healthy non-diabetic person to have a heart attack.

Hold on! Don’t panic. I know that sounds awful, but let’s put that number in perspective.

People who don’t have diabetes, but who do have a bad lipids profile (a very common sort of person, in our society), carry a risk factor of sixteen. If they have a bad lipids profile and high blood pressure, this combination (which is by no means rare in our society) carries a risk factor of twenty. In other words, diabetes may be a risk factor, but it’s a relatively small one. The really big risk factors are things that you can do something about.

Sadly, many diabetics don’t do anything about those non-diabetic risk factors. As a result, they end up with a combination of risk factors that is much, much worse than diabetes alone.

Many people have diabetes plus high blood pressure; that combination is more than three times as dangerous as diabetes alone.

Many people have diabetes plus a bad lipids profile; that combination is more than eight times as dangerous as diabetes alone.

Think about what this means if you have many different risk factors. If you start with diabetes, and you add high blood pressure... and you add abnormal lipids... and you add obesity... and you add lack of exercise... then the end result is going to be an absolutely crushing burden of coronary risk. (Advanced players add cigarette-smoking to these other risk factors.) You really can’t live your life under that kind of burden.

You need to get to work immediately on eliminating whatever risk factors you have besides diabetes. Diabetes itself you can live with. What you cannot live with is diabetes combined with a mountain of needless additional risks.

What you can do

Obviously it is important to do everything you can to avoid injury to your heart muscle. But what can you actually do?

Glucose control isn’t enough by itself to protect you from heart disease, but fortunately there are several other things you can do, and should do, in order to cut your cardiac risk down to size.

Get strong

One thing you can do is to strengthen the heart and the cardiovascular system in general.

Like any muscle, the heart is strengthened by using it in a way that challenges its performance capacity — specifically, by doing aerobic exercise which forces the heart to pump considerably more blood than it does when you’re at rest. The eventual result of this kind of exercise (if you do enough of it, over a long enough period) is that your heart becomes more powerful and your arterial system increases its capacity. Your heart can move more blood with each contraction, so that it doesn’t have to pump as fast as it did before. Your average pulse rate and your average blood pressure both decrease. In other words, your heart no longer has to work as hard as it once did for a given level of physical activity. This is definitely a good thing — it makes your heart less vulnerable to injury as a result of partial arterial blockage.

However, strengthening the heart is not enough. It may make your heart more capable of coping with partial arterial blockage, but that’s not exactly an ironclad guarantee of safety. You need to do what you can to prevent arterial blockage from occurring in the first place, and to reduce whatever deposits have already accumulated on the walls of your arteries.

Reduce your insulin levels

Because excess insulin is believed to have a damaging effect on your arteries, you want to do whatever you can to reduce it. Unfortunately, you don’t have any direct way of telling what your insulin level is. Insulin is highly variable and difficult to measure, and it usually is not measured outside of a research setting. You are most unlikely to receive from your doctor any information at all about what is going on with your insulin levels. However, there are four things you can do that will have the effect of reducing the amount of insulin your pancreas needs to produce:
  • Control your intake of carbohydrates.
  • Lose excess body fat.
  • Increase your muscle mass through strength training.
  • Get a lot of exercise.

Maintain a healthy lipids profile

You want the LDL/HDL ratio (that is, the ratio of “bad” cholesterol to “good” cholesterol) to be as low as possible, so that you don’t develop harmful deposits on arterial walls. Here’s how to do it:
  • Get most of your fat calories from unsaturated (preferably monounsaturated) fat.
  • Minimize consumption of saturated fat.
  • Avoid consumption of trans fat (hydrogenated oils).
  • Get a lot of exercise.

Combat the effects of glycation

You can minimize the harm caused by glycation in your system by keeping your BG under control and adopting a healthy lifestyle generally.
  • Moderate your intake of calories, particularly carbohydrate calories.
  • Include fresh fruits and vegetables in your diet (because of the anti-oxidants they contain).
  • Get a lot of exercise.

Control your blood pressure

Hypertension (high blood pressure) is a notorious risk factor for heart disease and other ills. It is also notoriously common among diabetics. You need to get your blood pressure down to the normal range and keep it there. (Be aware, by the way, that accepted notions of what is “normal” are revised downward periodically.) Reducing blood pressure is notoriously difficult, even with medication — but it is not nearly so difficult if you do the following:
  • Lose excess body fat.
  • Avoid excessive consumption of coffee and other stimulants.
  • Avoid excessive consumption of alcohol.
  • Learn to control stress, anger, and impatience.
  • Get a lot of exercise.
Doing these things will very likely to bring your blood pressure down. Maybe it won't come down so much that you don’t need medication, but at the very least it will probably allow you to reduce the amount of medication you need to take, and that’s always worth doing.

More about blood pressure

Your heart forces blood into your arteries more or less the way a tire pump forces air into a bicycle tire. Your arterial system, like a bicycle tire, is designed to operate within a certain range of pressure.

Exceeding the upper limit of that pressure range can be damaging. The physical stress that it puts on the arterial walls produces a kind of inflammatory response, and this encourages the formation of cholesterol placques. To avoid that, you need to check your inflation pressure periodically. Doing that is pretty easy, in the case of bicycle tires (they have an external valve to which you can connect a pressure gauge); it’s less easy in the case of arteries.

But how would you estimate the pressure in bicycle tires if you had no pressure guage? By feel, of course. You could squeeze the tires to see how much they resisted the extrenal pressure you were applying to them. Something roughly similar is done to measure blood pressure: a cuff is wrapped tightly around your arm, and inflated so that the arm is squeezed. The external pressure is increased until it restricts the circulation of blood in your arm. (This reveals how much opposing pressure your heart is applying to your arteries.)

The standard device for doing this is called, at least in books on the subject, a sphygmomanometer. (In conversation, most people avoid this term, for some reason, and call it a blood pressure cuff instead).

Whatever you call it, the device is an inflatable ring which surrounds your arm and is pumped up with air until it squeezes the arm hard enough to cut off the circulation briefly. The pressure in the cuff is then reduced slowly until the blood circulation resumes, and at that moment the pressure in the cuff itself is measured. Actually, the pressure in the cuff is measured twice, first when blood begins to flow again, and then when the flow becomes unrestricted (those two moments are identified by characteristic sounds heard in a stethoscope inserted under the cuff). Therefore, the results of a blood pressure measurement are always given as a pair of numbers: 149/97, for example, or (if you’re lucky) perhaps 119/77. The units represented by these numbers are “millimeters of mercury” (abbreviated mmHg), a pressure unit that refers to the mercury column that is used in clinical sphygmomanometers.

Because the pressure in the cuff is decreasing during the interval between the two measurements, the second of the two measurements is always smaller than the first. Your pressure might be 140/90, but it’s never going to be 90/140.

That part about timing the measurement by recognizing sounds in a stethoscope makes it sound as if measuring blood pressure is something of an art, and perhaps not an art which the average person can master. You don’t need to worry about that: digital devices which take the measurement automatically are available at your local drug store, and they’re not extremely expensive.

Systolic & diastolic

The first and higher number is called systolic pressure, which comes from the word systole, meaning contraction. This is what your arterial pressure rises to — briefly — during a pulse; that is, the systolic pressure is the pressure during the instant that the heart is contracting and forcing blood into the arteries.

The second and lower number is called diastolic pressure, which comes from the word diastole, meaning dilation. This is what your arterial pressure drops down to between pulses; that is, the diastolic pressure is the pressure during the interval when the heart is expanding and filling up with blood, prior to the next contraction. You will often hear that the diastolic reading is the more significant of the two, but apparently that is a gross simplification of a complex issue. The advice from the experts is to regard both numbers as important, and to try very hard to keep both of them within the normal range.

“Normal” pressure

Ideally, what should these numbers be? What are the healthy, normal values for systolic and diastolic pressure? That’s a surprisingly tricky question, because the definition of “normal” blood pressure has been changing lately — in a downward direction.

It used to be said was that normal blood pressure was anything below 140/90 (although people with diabetes were urged to aim for numbers substantially below this limit). It now appears that the limit itself needs to be lowered.

On May 14, 2003, a coalition of medical organizations and agencies called the National High Blood Pressure Education Program Coordinating Committee issued a new set of recommendations in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. (I’m sorry to make you read titles of such ludicrous immensity, but I don’t know how else to refer to these organizations; apparently they don’t go in for nicknames.)

Anyway, the NHBPEPCC, or whatever the hell you call it, concluded that the upper end of the so-called “normal” blood pressure range is in fact an unhealthy place to be. They are defining blood pressure ranges as follows:

  • below 120/80 (normal)
  • 120/80 to 139/89 (prehypertension — lifestyle changes recommended)
  • above 139/89 (hypertension — medication recommended)
The “prehypertension” zone is a new concept. There is growing evidence that blood pressure in this range significantly increases the risk of heart disease and other health problems. So far, medication is not being recommended for people in the prehypertension zone, but doctors are now suposed to warn their patients that blood pressure in this range is really not “normal” and that they should be adopting a more active lifestyle (and perhaps losing weight, too) in order to reduce it.