The question & answer series below is intended to explain some issues which newly diagnosed (and not-so-newly) patients may need to see explained clearly.
What does the word "diabetes" really mean?
It really means "pissing". Actually, the Greek original is not that blunt (a literal translation would be closer to "passing through"), but pissing is definitely the idea. In medical jargon, the word diabetes refers broadly to disorders that cause overproduction of urine.
But isn't diabetes supposed to be about blood sugar rather than urine?
It's not always about blood sugar. If you have "diabetes insipidus", you produce a lot of urine, but your blood sugar is normal.
The name for disorders that raise your urine output and your blood sugar is "diabetes mellitus". Strictly speaking, it isn't correct to use the word "diabetes" as if it always meant the same thing as "diabetes mellitus", but everyone does it (doctors included), for the sake of brevity.
So what would the blunt translation of "diabetes mellitus" be?
And it's called that because...?
If your blood sugar level gets very high, your kidneys try to get rid of the excess sugar by flushing it out of your body through the urinary tract. Not only do you produce a lot of urine, but the urine you produce is sweet.
The term diabetes mellitus is very old. It dates back to a time when doctors were not able to measure blood sugar, but were able to notice that some of their patients produced urine which was sugary enough to attract ants and bees. They didn't know why anyone's urine would be sweet enough to attract swarms of insects, but they figured it had to be significant somehow. "Diabetes mellitus" seemed like a meaningful way to describe the condition. Unlike most antique medical terms, this one is still in use today.
So, if I'm not peeing all the time, it means my blood sugar is normal?
Sorry, no. That would be like saying "if I can walk, it means I'm sober". Your blood sugar can be elevated enough to harm you even if it's not elevated enough to make you take extra bathroom breaks.
Does everyone with diabetes mellitus have sugary urine?
Not if they manage to keep their blood sugar under control. It's only when your sugar level gets really high that you start to become popular with the bees. Of course, in ancient times, almost every diabetic was an uncontrolled diabetic, so anyone who had diabetes mellitus was pretty sure to be an interesting person to go camping with.
Why is the amount of sugar in my blood so important?
The chemical operations of a living human body depend on the presence of a certain level of sugar in the bloodstream -- no more, and no less. Destructive things start happening within the body if the blood doesn't contain enough sugar. Another bunch of destructive things start happening within the body if the blood contains more than enough sugar.
Which is more dangerous: low blood sugar or high blood sugar?
Low blood sugar can kill you in minutes, and high blood sugar usually takes years. So, in the short term, low blood sugar is the bigger threat.
On the other hand, the regulatory mechanism that prevents blood sugar from falling too low is pretty reliable. Not many people have a serious problem with low blood sugar. The regulatory mechanism that prevents blood sugar from rising too high is much more likely to fail, so millions of people have a serious problem with high blood sugar.
How can low blood sugar harm me?
Certain vital organs, and especially the brain, cannot keep functioning unless they are constantly supplied with chemical energy, and they obtain that energy by absorbing sugar from the bloodstream.
If the sugar level in your blood drops low enough, you will lose consciousness. If it drops a little lower than that you will die. Even if your blood sugar rebounds and you regain consciousness, an episode of this type can kill a lot of brain cells.
However, low blood sugar ("hypoglycemia") is, for most people, not likely to be a serious problem. We have all experienced the occasional mild episode of hypoglycemia, but in most of us the sugar level doesn't get nearly low enough to endanger us; it just gets low enough to make us feel bad for a while. The body is usually able to prevent the situation from getting any worse than that.
How does the body protect itself from low blood sugar?
Your liver maintains an emergency supply of sugar. If your blood sugar level drops too low, the liver releases a little of its sugar into the bloodstream to correct the problem.
This regulatory process is controlled by your endocrine system, which uses hormones (chemical signals) to adjust all sorts of conditions within the body (temperature, heart rate, growth, etc).
The particular hormone which raises blood sugar (by stimulating the liver to release some sugar into the bloodstream) is called glucagon.
How come I've never heard of glucagon?
Because it's rare for anything to go wrong with it.
Hormones are like airplanes: the ones that make the news are the ones that crash. There aren't a lot of people having a problem with glucagon, so nobody discusses it.
The hormone that reduces blood sugar is another story -- things go wrong with that one all the time, so the name of it is a much more familiar word. It's called insulin.
How does the body protect itself from high blood sugar?
When the blood sugar level gets too high, the pancreas releases insulin, which sends an urgent message to certain kinds of cells in the body, and especially to muscle cells. The message is: start absorbing sugar!
The muscles have a great capacity to absorb sugar and store it for future use -- but most of the time they don't do this, unless they are stimulated by insulin to do so. That is how the body intervenes when the blood sugar level is elevated: the pancreas releases insulin, the insulin stimulates the muscle cells, the muscles start soaking up sugar like sponges, and the sugar level in the blood begins to drop. When it has dropped enough, the pancreas cuts way back on insulin production, and the muscles stop absorbing sugar. By adjusting the amount of insulin it releases on a moment-by-moment basis, the pancreas can fine-tune the amount of sugar in the blood.
Unfortunately, this insulin-based regulatory mechanism is apt to fail. Millions of people have some kind of problem with insulin, and problems with insulin tend to be serious.
I should mention that there's another kind of cell, besides the muscle cells, that tends to absorb a lot of sugar when triggered by insulin to do so: the fat cells. The crucial difference here is that muscle cells burn up their stored sugar whenever you use your muscles. Fat cells don't burn sugar; they turn it into fat. Some people try to tailor their exercise programs to burn fat rather than sugar, but burning sugar is just as important: unused sugar within a human body is just fat waiting to happen.
How can high blood sugar harm me?
Excess sugar in the blood has the same sort of effect on your body that sugar in the gas tank would have on your car. Sugar is just too sticky; it has a bad habit of attaching itself to other substances. Having too much sugar in your system tends to gum up the works.
The main problem here is a chemical reaction called glycation (or "glycosylation"; I use the shorter version of the word). In glycation, sugar bonds itself to protein molecules in the body's various tissues.
Glycation is a problem because protein molecules have a lot of important jobs to do within the body, and they can't do their jobs properly if they have sugar bonded to them. Protein molecules are like hand-tools: their shape is crucial to their function. If the coins in your pocket were capable of welding themselves to your car keys, you would soon find that your keys had become useless. In biochemical terms, proteins that have become encrusted with sugar are pretty useless, too. Furthermore, glycated proteins tend to promote the formation of other harmful chemicals.
Once a certain percentage of the protein molecules in your body become glycated, degenerative health problems of various kinds begin to develop.
If the liver, muscle, and fat cells all store sugar, how come they aren't harmed by it?
They store it in a special, safer form. The reason blood sugar is so much inclined to bond itself to other substances is that blood sugar is in the form of glucose a "simple" sugar, meaning that it consists of individual sugar molecules, not chains of them.
An individual glucose molecule has, in effect, a pair of "hooks" that allow it to latch onto other molecules. This has advantages and disadvantages. On the plus side, a cell can very quickly grab a glucose molecule, pull it into the cell interior, and use it for energy -- which it couldn't do if that glucose molecule were chained to a bunch of others. The downside is that glucose, with its hooks always free, sometimes latches onto the wrong things and causes glycation.
When glucose is being stored (in muscle cells, fat cells, or the liver) the glucose molecules are linked together into a long chain (a sort of chemical Conga line), so that they don't have any hooks free to latch onto anything else. Sugar in this safe, stable form is called glycogen. When the body needs to take the sugar out of storage and use it, the glycogen chains are broken up into individual glucose molecules, and those are released into the bloodstream (hopefully in moderate quantities).
What exactly are the problems that glycation can cause?
There don't seem to be many problems that glycation can't cause. Because the body uses proteins for so many different purposes, glycating your proteins can create an endless list of medical problems.
The most common consequences of glycation include circulatory disorders (leading to heart attacks, ischemic strokes, and uncontrollable infections) and nerve damage (leading to numbness, tingling, chronic pain, and disabilities). Kidney and eye diseases are also common. But really, there's probably no part of your body that can't be harmed by glycation.
A new consequence of glycation was discovered recently: polyps discovered and removed during colonoscopies are a lot more likely to recur if your blood sugar is elevated (even slightly elevated --the so-called "pre-diabetes" level of elevated blood sugar is enough to make a difference).
The nastiest aspect of glycation is its tendency to sneak up on you. You can't feel it happening. It takes a long time for glycation-related damage to build up to the point that you start to have any symptoms. You can spend years glycating the proteins in your eyes, and doing nothing about it because you have no idea anything is going wrong there. If that happens, it may be too late to act when the problem finally becomes obvious.
But if everyone's blood has sugar in it, isn't glycation happening in everyone's body?
Yes, definitely. The question is, how much glycation is happening? Only a little bit is happening if your blood sugar is in the normal range. If your blood sugar is well above the normal range, glycation is happening at an accelerated rate.
But whatever the glycation rate is, doesn't it eventually build up anyway, and produce the same result in the end?
Actually, no. Under normal circumstances, the body is able to undo the effects of glycation, because the body recycles its proteins.
Over time, every protein molecule that is present in your body will be replaced by a fresh, new one with no sugar attached to it. (The old one is broken up into its constituent amino acids, and any attached sugar is stripped away.) For example, a given molecule of hemoglobin (an important protein in red blood cells) lasts about three months before it's recycled.
This recycling process goes on continually, and it prevents a gradual buildup of glycated protein. About 5% of a healthy person's protein (or at least their hemoglobin) is glycated -- and the percentage doesn't go up over time, because the protein recycling process is able to keep up with the glycation rate.
Unfortunately, the recycling process can't keep up with glycation if glycation is happening at an abnormally high rate. If your blood sugar is elevated, then proteins throughout your body are becoming glycated faster than the recycling process can replace them. Over time, the recycling process falls farther and farther behind, and a larger and larger percentage of your protein is glycated (8%, then 10%, then 12%, and so on). Meanwhile, a healthy person stays at 5% year after year.
Is there a lab test for glycation?
Yes. The "hemoglobin A1c" test isolates the blood-protein called hemoglobin, and determines how much of it is glycated. Glycated hemoglobin is known as hemoglobin A1c, hence the name of the test.
The rest result is a percentage, though it's not always stated that way. If the test result is quoted as "4.9", that means 4.9% (specificallty, 4.9% of your hemoglobin is in a sugar-coated state). The normal range is usually said to be as 4 to 6. The lab my doctor uses, however, defines 4.5 to 5.7 as the normal range. There isn't absolute uniformity among labs about how they test for hemoglobin A1c, so if your lab says the normal range for their test is something other than 4 to 6, take them at their word.
This test is often described as a measure of "average blood sugar". It can't really measure that. However, the A1c test result does give your doctor a good basis for estimating what your average blood sugar has been lately. The more heavily glycated your hemoglobin is, the higher your average blood sugar must have been over the last three months. (Hemoglobin lasts about three months before it is recycled, so the hemoglobin A1c test can't capture anything that was happening longer ago than that; also, the most recent month has more influence on the result than the previous two.)
The A1c test is not as simple or cheap as a blood glucose test, so doctors usually give it only to patients who have been diagnosed with diabetes mellitus. Most doctors give their diabetic patients this test once or twice a year. Although diabetic patients are more or less expected to score above 6 on the test, they are urged to keep the value below 7, because glycation-related health problems start to become common at that level.
The eye disease known as retinopathy provides an example of what the numbers mean in practical terms. The disease is common in poorly-controlled diabetics, but uncommon in everyone else. If your A1c level is just under 7, and it stays at that level for a decade, your risk of developing retinopathy during that time is about 5%. If the A1c level during that time was 11 instead, your risk of developing retinopathy would be 100%.
Some patients get pretty grim A1c results. People with poorly--controlled diabetes can get above 12, or even 14. When things get that bad, and stay that bad for a long time, disability and early death become almost inevitable. So far, Ive been able to keep all my A1c test results in the normal range (my results have ranged from 4.8 to 5.4). I don't know how long I can continue to achieve that, but Im not going to give up on it easily.
So what about home test kits for glucose?
Everyone who has reason to suspect he has a problem with blood sugar should buy a glucose meter and take measurements often enough to be able to track what's going on.
These meters are not as good as medical lab equipment -- they have a "repeatability" problem, meaning that the same meter testing the same blood sample ten times in a row will give ten slightly different answers, with random variations above and below the true value. However, the errors arent very large, and because they are random in nature the error pretty much disappears during averaging of results. What you need to pay attention to is the average of your results, not the slight uptick that might occur on a given day.
There are two kinds of tests: "fasting tests" (taken right after you get out of bed in the morning, before eating or drinking anything) and post-prandial tests (taken at some specified time after a meal -- usually one hour or two hours). The fasting tests establish your baseline: this is how low your body is able to keep its blood sugar when no sugar is entering your bloodstream from the digestive tract.
The post-prandial tests establish how well your body is able to cope with the sudden influx of sugar into the bloodstream that occurs when a meal is being digested. These results will be at least a little higher than your fasting tests; how much higher they are gives a good indication of how much trouble your body is having controlling its sugar level.
What exactly is the normal
amount of blood sugar?
This is not as simple a question as you would think, so bear with me. First we have to straighten out the units of measurement.
The concentration of sugar in human blood is measured in two different systems of units. In American clinical practice, it is usually measured in milligrams of glucose per deciliter of blood, or "mg/dl".
However, America is out of sync with the rest of the world on this. Doctors in other countries (and scientists everywhere, including the U.S.) measure it in millimoles of glucose per liter of blood, or "mmol/l". The latter unit turns up a lot in literature about diabetes, so be aware of it. If you see a figure quoted in mmol/l, multiply it by 18 to convert it to mg/dl (that is, 5 mmol/l equals 90 mg/dl). Most glucose meters can be set to measure in either unit. From this point on I'm going to give examples only in mg/dl.
So what exactly does mg/dl mean? Look at it this way:
A milligram is an extremely small measurement of weight (an aspirin tablet weighs 325 mg).
A deciliter is 3.4 fluid ounces, which is about equal to an ungenerous serving of wine.
If your blood glucose level (usually abbreviated "BG") is 325 mg/dl, then a quantity of your blood equivalent to a small glass of wine would contain an amount of glucose that weighs as much as an aspirin.
I hasten to add that a BG reading of 325 is not normal. It's way too high. Only someone with a serious case of diabetes mellitus would ever have such a high concentration of glucose in his blood. Which brings us back to the question of how much is normal. Roughly speaking, the normal range is 70 to 120, but it matters when youre measuring it.
Blood glucose is not rock-steady, even in the healthiest person; it fluctuates over the course of the day. This fluctuation is unavoidable. Every time you digest a meal, glucose is dumped into your bloodstream. Every time you use your muscles, glucose is pulled out of your bloodstream. Because of these issues, the average healthy individuals BG rises and falls in roughly predictable waves all day long. However, the waves should not rise too high, or drop too low. The normal person's glucose profile looks something like the following picture:
The normal pattern is for BG to be pretty low when you wake up in the morning in the range of 70 to 99 mg/dl. After your first meal of the day, your BG increases, probably to a peak of 120 or less, and then falls. Subsequent meals cause another peak, followed by another decline. Work or exercise will also cause a decline. The whole range of variation during the course of the day is confined within a range of about 70 to 120.
By the way, that upper limit of 120 is a figure that I learned in a diabetes class, but I haven't seen it confirmed elsewhere. It may that most non-diabetic people go higher than that after a meal. I have seen 140 quoted as the upper limit of "normal" for a post-prandial test. There doesn't seem to be a clear consensus on this question.
How low is too low?
Dropping to the low 60s may make you feel bad, but it won't hurt you. (The possible symptoms of this are too numerous to list, but the more common ones include weakness, trembling, nervousness, and the urge to eat an entire wedding cake.)
Dropping to the low 50s will probably cost you some brain cells, and may lead to odd behavior. A friend of mine in this situation was observed by a coworker to be standing in front of a Coke machine for about 20 minutes, staring at it and trying to remember how it worked. When someone finally asked him if he was all right, he muttered incoherently, walked outside, and wandered into the field where the fire department found him later.
Dropping below 40 will probably make you lose consciousness.
Dropping below 30 will probably kill you.
Oddly enough, the unpleasant symptoms of mild hypoglycemia can be caused by any rapid drop in BG, even if you're only dropping from a high level to a normal level, not from a normal level to a low level. Diabetes patients who are used to being too high can feel like they're in crisis when they finally get their glucose back down where it belongs. (I know, because I experienced a little of that.) Fortunately, its a temporary problem. Once your body gets used to being in the normal blood glucose range, you feel a lot more comfortable there.
How high is too high?
This is one of those areas where confusion reigns because the goalposts keep moving, but here's my best shot at summarizing the situation.
The normal "fasting" BG (measured first thing in the morning, before breakfast) was once defined as <110 mg/dl. Then it became <105 mg/dl. Now it seems to be <100 mg/dl. Whatever the normal fasting level is defined to be, it's considered an indication of trouble if your fasting level gets any higher than that.
The fasting level at which the patient is considered to have diabetes mellitus used to be 140 mg/dl. That has since been moved down to 126 mg/dl. If you wake up in the morning with a glucose level of 126 mg/dl or higher, you are diabetic. Keep in mind that this number has little to do with medicine and a great deal to do with the politics of health care. Here's the deal: if your doctor wants to treat you for diabetes mellitus, your medical insurance company wants to see that your fasting glucose was measured at 126 -- otherwise they don't have to cover it. Unfortunately, that doesn't mean it's okay to have a fasting level of 125.
If you are in the "borderline" region of 100 to 125, your doctor has a bit of a problem: he's not allowed to say that you're diabetic, but he can't tell you that there's nothing wrong with you, either. Lately, doctors have dealt with this problem by referring to the borderline region as "pre-diabetes". They hope their patients will hear this term and realize that it means "in the process of becoming diabetic". In reality, their patients hear it and think it means "not nearly bad enough to be called diabetic".
The medical reality underlying the politics of the issue is that "pre-diabetes" is diabetes. It may be the earliest, mildest phase of diabetes, but it's still diabetes. There simply isn't any way that your blood glucose level would be creeping above the normal range if your insulin-based regulatory system was working properly. If you're elevated at all, it means your body is struggling with insulin resistance and not quite winning the battle, so there is definitely a problem to be addressed. Also, when you are in this earliest and mildest stage of the disease, you have your best opportunity to reverse it. The longer you wait to do something about elevated BG, the harder it will be to do something about it, and the greater the risk that some harm will be done which can't be undone.
I've been talking about the fasting level, because diabetes mellitus is usually defined in terms of that, and rules about what's normal or not normal are usually defined in terms of that. What about post-prandial tests? This area is more murky, at least to me. My doctor told me at the start to try to keep post-prandial BG under 150; he said this was a "hard target" but that I should at least try to get there. Maybe that means 150 is considered the upper limit of the normal level, and he wanted me to aim for that even if it wasn't necessarily practical. On the other hand, maybe its a looser standard that is given to people with diabetes. I don't know why this issue has to be so murky, but it is.
What causes the breakdown of the mechanism that is supposed to prevent high BG?
There is more than one way for this regulatory mechanism to break down. Therefore, more than one disease can cause the condition known as diabetes mellitus (which is really more of a symptom than a disease).
What are these diseases that cause diabetes mellitus?
There are two common ones: "juvenile" diabetes (now called Type 1) and "adult-onset" diabetes (now called Type 2). There is also "gestational diabetes", which occurs in pregnant women, but that seems to be virtually the same thing as Type 2 (except that it is somehow being triggered by the physical changes that occur during pregnancy).
Is the age of onset the only difference between Type 1 and Type 2?
No. In fact, that's the one area where the two diseases are becoming more alike (Type 2 is reportedly becoming common in children and adolescents.) In most other ways the two are quite different.
What exactly is Type 1?
People with Type 1 have lost the ability to produce insulin. They lose it suddenly, completely, and permanently, as the result of an auto-immune reaction. (That is, the immune system goes haywire and attacks one of the bodys own tissues as if it were an invasive organism.) The particular tissue that is attacked in this case is the pancreas, specifically the "Beta" cells in the pancreas (the cells which produce the body's insulin supply).
Why was Type 1 formerly called "juvenile diabetes"?
The immune reaction that causes Type 1 typically occurs in childhood. It rarely happens any later than age 25.
Why doesn't Type 1 begin later in life?
Probably because the immune reaction is triggered by some commonplace environmental factor (a virus, a pollen, a type of food, something like that). Only a few people have a genetic predisposition to react unfavorably to this environmental factor. Whatever the environmental factor is, it is so frequently encountered that the people who are predisposed to have a bad reaction to it are likely to do so pretty early in life. Although no one is sure what the environmental factor is that triggers the reaction, a likely suspect is cow's milk. In countries where breast-feeding is standard and dairy foods arent, Type 1 is seldom seen.
When the term "juvenile diabetes" was coined, it caused no confusion, because there weren't any mature adults with the disease (no one survived it that long), and because "adult-onset diabetes" was not seen in young people. In modern times that situation has changed. Medical breakthroughs have made it possible for people with "juvenile" diabetes to survive into old age. Lifestyle breakthroughs have made it possible for children to develop "adult-onset" diabetes. Because these terms have become so confusing, they are seldom used any more. To be sure, "Type 1" and "Type 2" are not very meaningful (and they sound as if they were coined by Doctor Seuss), but at least they are merely uninformative, not misleading.
What happens if your body can't produce insulin?
The muscles can't absorb glucose, or at least they can't absorb nearly enough of it, so the glucose accumulates in the bloodstream and builds up to extremely high levels. (The kidneys start dumping the glucose into the urine, but this doesn't get rid of it fast enough.)
In this situation, a lot of the calories you consume simply go to waste, because digestion converts most of what you eat into glucose, and a lot of the glucose is being dumped out in the urine instead of finding its way into the cells that need it. Because calories are being wasted in this way, people who can't produce insulin tend to become thin. They also, of course, suffer greatly from the health problems that are caused by high rates of glycation.
It is not possible to live very long without insulin. Therefore, if you can't produce insulin on your own, you have no choice but to take regular injections of the stuff. Before injectable insulin was available, people used to die from Type 1 in a few months.
Why does insulin have to be injected? Why not take it as a pill?
Digestion breaks down insulin, so taking it orally is not an option. Other methods of taking it have been tried (inhalers, for example), but injection seems to work best (insulin pumps are just another means of injection).
Is there any other way for people with Type 1 to control their blood glucose?
A pancreas transplant would do the trick, but it's a difficult operation and it's seldom done. Most people with Type 1 have no choice but to take insulin injections -- which is too bad, because injecting insulin is a fairly crude method of adjusting blood glucose and it's easy to overcorrect.
People who take insulin shots have to be very careful not to take more than they need at a given time -- which requires them to be very sure about how much they do need, and that's not as easy to judge as you might think. A friend of mine who takes insulin shots has had life-threatening emergencies because the amount of insulin he took after dinner was too much for what he had eaten.
What exactly is Type 2?
Type 2 is a form of diabetes mellitus that is caused not by a lack of insulin but by a loss of sensitivity to insulin. Type 2 patients can still produce the stuff; their bodies just don't respond to it properly.
Based on that description, you would think that Type 2 would be just as severe as Type 1. Here's why it isn't: the loss of insulin production in Type 1 is total, while the loss of insulin sensitivity in Type 2 is partial. If you have Type 1, the insulin-based regulatory mechanism has broken down completely; it's an all-or-nothing situation. If you have Type 2, the mechanism is still limping along, doing its best; it's a matter of degree.
What is the result of this loss of insulin sensitivity?
Certain kinds of cells (and particularly muscle cells) are designed not to absorb glucose from the blood unless they are stimulated to do so by the presence of insulin. If these cells are insensitive to insulin, they don't absorb glucose, or at least they don't absorb enough of it, even when insulin is present. The cells do absorb some glucose, but they absorb less glucose for a given level of insulin than they ought to.
Why doesn't the pancreas just produce more insulin, to compensate for the reduced sensitivity?
It does. This is called "compensatory hyperinsulinemia", which means that the body releases abnormally large amounts of insulin until the cells start absorbing enough glucose. It's as if the body has become slightly "deaf" to insulin, so the pancreas is obliged to start shouting to get the message across.
So that solves the problem, right?
Sort of. For a while. Unfortunately, there are a couple of serious problems with compensatory hyperinsulinemia as a strategy for staying healthy.
First of all, there is a limit to how much insulin a pancreas (even a healthy pancreas) can produce. When your sensitivity to insulin is declining, the amount of insulin that it takes to compensate for the problem gets larger and larger. Eventually, a point is reached where the pancreas can't make enough extra insulin to do the trick, and the glucose level starts rising above the normal range. That is the point at which Type 2 can be diagnosed. Before that point, the problem is hidden.
Second, it is not a good or safe thing to be chronically overdosing on insulin, no matter how much you seemingly "need" it. Insulin in abnormally large doses causes inflammation of the arteries, which leades to heart disease. Because of the harm excess insulin can do, insulin insensitivity is a serious problem by itself. Even if it hasnt made you diabetic yet, it can still set you up for a coronary. It is now believed that this is the explanation for a great many heart attacks that happen to people who didn't know they were at risk for such a thing. The terms "syndrome X" and "metabolic syndrome" refer to a complex of health problems that relate to insulin insensitivity, with or without diabetes.
In a sense, people whose insulin resistance develops into Type 2 are lucky -- they know they have a problem, so they can do something about it. People who can make enough extra insulin to hide the problem aren't going to know what hit them when it finally does.
Is insulin insensitivity the same thing as "insulin resistance"?
Yes, but I don't like the term insulin resistance, so Ive been putting off using it.
What's wrong with the term "insulin resistance"?
We use the word "resistance" to describe defiance, rebellion, refusal to cooperate. We don't use it to describe a loss of sensitivity. No one calls numbness "touch resistance". No one ever refers to hearing loss as "sound resistance".
Insulin resistance is a stupid term, because it doesn't communicate the real point: it matters very much how sensitive to insulin you are, and this sensitivity is subject to change. Whoever invented the term insulin resistance had a tin ear for language (or should I say that they were language resistant?), but everyone uses it, so I guess I will use it here from this point on.
So what causes insulin resistance?
After spending decades investigating this question, scientists finally seem have arrived at a consensus: nobody has a clue.
To be fair, we do know about some things which are strongly associated with insulin resistance and appear to cause it -- but exactly how and why they cause it is far from clear. Those things are:
Abdominal fat. I say "abdominal fat" rather than "body fat" because it seems to make a difference where the body stores its fat. People whose fat is concentrated around the abdomen rather than the hips have the greatest risk of becoming insulin resistant (and the more fat they have there, the greater the risk). It seems that abdominal fat is able to function like an organ, or even like an endocrine gland. It exchanges hormones with the rest of the body. Somehow or other, it has the ability to reduce the body's sensitivity to insulin. It doesn't necessarily take a very large amount of abdominal fat to make this happen.
Sedentary living. People who don't exercise have a heightened risk of insulin resistance. You might think that this is really just the abdominal-fat issue in disguise: after all, there's a lot of overlap between sedentary people and overweight people, regardless of whether they got fat because they didnt exercise or they stopped exercising because they got fat. However, inactivity seems to play an independent role in causing insulin resistance. No matter how fat or thin you are, exercise bosts your insulin sensitivity, and going without exercise depresses it.
Inflammation. Anything that causes inflammation, such as a chronic infection, seems to promote insulin resistance. The rate of Type 2 diabetes is very high among people with periodontal disease, apparently because the inflamed gum tissue releases compounds into the bloodstream which promote insulin resistance.
Genetics. Some people have genes which seemingly enable them to use the energy in food more efficiently. On the plus side, this seems to make them good at surviving prolonged hunger, but it also heightens their risk of developing insulin resistance when food is abundant. (One theory says that these genes provide an adaptive benefit in regions that have frequent famines, hence the relatively low gene frequency in Europe; another theory says Europeans were the first people in the world to start eating refined grains, so they started losing these genes as an adaptation to an altered diet.) Whatever the reason for the existence of these genes, and their unequal distribution across the globe, the genes alone usually won't drive you into diabetes. However, there are apparently at least a few fit, slender people who exercise regularly and eat right and still develop Type 2 diabetes; in these people, genes alone can make it happen.
Other causes: Insulin resistance is also promoted by various transitory disturbances such as dehydration, having a fever, and emotional stress. Stress may not actually be all that transitory, come to think of it; some people are stressed out pretty much all the time. Unfortunately the stress response causes inflammation in the circulatory system, which of course promotes insulin resistance.
But how do we know that the cause of insulin resistance isn't just bad genes and nothing else?
We know it because of (among other things) the example of the Pima Indian tribe, which straddles the US/Mexico border. The genes for insulin resistance are extremely common in that gene pool; almost everyone has these genes. In the old days the genes used to help them survive frequent food shortages; now it makes them insulin resistant.
But not everyone in the tribe has insulin resistance. On the Mexican side of the border, the lifestyle of the Pima indians involves more working and less eating; compared to their relatives on the US side, they are more active, less fat. They also have a much lower rate of insulin resistance. On the US side, by contrast, almost all the adult Pima Indians develop Type 2 diabetes. The lifestyle differences between the two sub-populations are the only relevant differences between them that anyone has been able to identify.
It's important to remember that, no matter what unfortunate genes you might be stuck with, you don't have to be stuck with your habits -- and your habits matter as much as your genes do.
Does eating a high-carbohydrate diet increase the risk of Type 2?
It sounds like a reasonable guess, and a lot of people think it's true. Proving it's true is mighty difficult, though. Researchers have looked for a connection between high-carb diets and Type 2, and they haven't been able to find one.
It's doubtful they would find such a connection if it was there; most research studies on the health effects of dietary differences are fatally undermined by reliance on what people say they eat instead of what they actually eat. A much-publicized study of a group of nurses claimed to find that it doesn't make any difference how much fat you eat; this bold claim rested entirely on a modest reduction in fat intake which one subgroup claimed to have made, even though we know (from the amount of weight they gained) that they couldn't possibly have been describing their eating habits accurately. In short, research on dietary differences is a hopeless mess, and it's hard to draw any conclusions from it.
A high-carb diet might not cause Type 2, but researchers have found a very strong connection between high-calorie diets and Type 2. Clearly, eating too much can make you diabetic, even if (as far as anyone can tell so far) it doesn't make much difference whether your calories are coming from baked goods or bacon.
I hasten to add that, once you have become diabetic, it certainly does matter how much carbohydrate you take in.
What is the genetic connection between Type 1 and Type 2?
There doesn't seem to be any connection. Different diseases, different causes, different genes. Both types have appeared in my family, but this is most likely a coincidence (and not a very wild coincidence, considering how common Type 2 is now).
Is insulin resistance permanent once you develop it?
It's not exactly permanent, but it's certainly persistent. Increasing your sensitivity to insulin tends to be a slow and gradual process. It's as if, once your body becomes insulin resistant, it wants to stay that way, and you have to work patiently on the problem to overcome it.
Whether it is possible to restore insulin sensitivity all the way to normal is unclear. You can get it close enough to normal to push your BG back down where it belongs, but that may or may not be a full solution to the problem. If you boost your insulin sensitivity to the point that your body can keep its BG in the normal range, but you don't boost it to the point that your body no longer needs to give itself an insulin overdose, you still have a problem to work on.
People who have been diagnosed with Type 2 have an increased risk of coronary heart disease, and controlling BG does not eliminate much of this increased risk, because so many of these people still have elevated insulin levels (which doesn't do their coronary arteries any favors).
Because insulin levels are hard to measure, and outside of a research lab they aren't measured, you aren't going to get any feedback from your doctor on what's going on with your insulin level. You pretty much have to fly blind here. The safest thing to do is to assume that, even if your BG is normal, there is still an underlying insulin-resistance issue to be dealt with, and you still need to be very dedicated about daily exercise and weight control in order to boost your insulin sensitivity as much as you possibly can.
In one sense, insulin resistance is permanent: if you have ever had it, then you know you are genetically predisposed to it. Your body "wants" to become insulin resistant, in other words, and it will drift in that direction if you do nothing to prevent it. You will always have to keep an eye on this issue.
If insulin is so bad for
your arteries, why doesn't it hurt people with Type 1 who inject it all the
People with Type 1 only inject enough insulin to give them normal insulin levels -- the levels that they used to produce before they lost the ability to produce any insulin at all. The circulatory system can tolerate insulin in normal quantities.
Type 2 patients who go into hyperinsulinemia to compensate for insulin resistance are constantly pumping out abnormally large amounts of insulin; that's when insulin starts to be a problem.
Can Type 2 "turn into" Type 1?
Not really, but a lot of people talk about this happening. Let me put it this way: Type 2 can turn into Type 1 if you're willing to change the definition of Type 1.
Normally, Type 1 is defined as auto-immune disease which attacks the pancreas and destroys the patient's ability to produce insulin. If you drop that definition entirely, and declare that Type 1 means any situation in which the patient can't control BG without injecting insulin, then in that limited sense Type 2 can turn into Type 1.
If you have Type 2 for a long time, and you don't control your BG very well (so that glycation is doing harm all over the body), one of the consequences is that the amount of insulin your pancreas can produce tends to decline. Just at the point where you are needing more and more insulin to overcome your resistance to the stuff, your body starts producing less and less of it. It may be that insulin production declines with age anyway, but it certainly declines when excess BG is glycating and damaging your pancreas (an effect sometimes referred to as "glucotoxicity").
Type 2 patients who get into this unfortunate situation often take insulin shots, and some people say that this is an example of "Type 2 turning into Type 1". This seems to me like a misuse of language, but nobody asked me, and there are indications that doctors are getting on board with this kind of talk. Sometimes doctors refer to Type 1 as "IDDM" (insulin-dependent diabetes mellitus) and Type 2 as "NIDDM" (non-insulin-dependent diabetes mellitus), as if the only difference between the two diseases was the available treatment options.
What's kind of creepy about giving insulin to Type 2 patients is that (a) they may already have more insulin in their blood than their arteries can tolerate as it is, and (b) the dosages they're given are often bigger than anything that would be given to a Type 1 patient. I suppose that doctors have no choice but to treat a really bad case of Type 2 in this way, because getting BG under control is more urgent than getting insulin under control. Excess BG can cause a wider range of health problems than excess insulin can, and probably will cause them sooner. (On the other hand, excess insulin causes coronary heart disease, and that's what people with Type 2 usually die from.)
However that may be, I still think it's crucial to keep a clear distinction between Type 1 and Type 2, because patients need to think about them differently. If you have Type 1, circumstances beyond your control have caused you to suffer a complete and permanent loss of the ability to produce insulin, and the only thing you can do about it is to give yourself shots. If you have Type 2, on the other hand, you're confronting a vastly different problem: very probably, your habits of living have made you insensitive to insulin, a problem which you can reverse by changing your habits. In terms of how you deal with them, the diseases could not be more different, and losing sight of those differences would be a very dangerous thing.
What can I do to become more sensitive to insulin?
The most important things you can do are to shed excess weight and exercise regularly.
If excess abdominal fat reduces your sensitivity to insulin, getting rid of that fat increases your sensitivity to insulin. Losing five pounds can easily be enough to see some kind of noticeable reduction in BG.
Exercise, particularly if it is challenging enough to make you sweat a lot and feel sorry for yourself, boosts insulin sensitivity. This effect lingers for at least 24 hours, and perhaps 48, so if you exercise daily you're pretty well covered. Also, during exercise the muscle cells, because of their continual expansion and contraction, soak up sugar through a mechanical process which doesn't depend on insulin -- you get a lot of glucose transferred to the muscles "for free", so to speak, during exercise.
Some supplements are said to increase sensitivity to insulin. The one for which there is the most evidence is cinnamon. Some studies say it helps. At least one study says it doesn't. Some people take a capsule of it every day. I did for a while, but I got to a point where I could get good BG numbers without it. It's hard to say whether I progressed to the point that I stopped needing it, or I was merely mistaken in thinking it had been helping me in the first place. Still, if you like cinnamon on your toast or in your oatmeal, why not? It's not going to hurt you, and at least one study says it will help.
How much exercise does it take to fight insulin resistance?
Everyone's case is different, so you pretty much have to work this out experimentally. Obviously, you have to do whatever amount of exercise will keep your BG within normal limits. Test your BG daily; if your fasting level is 100 or more, it means you need to exercise more (unless it means you need to eat less). In this situation, either increase the amount of exercise you're doing, or reduce the amount of food you're consuming, or both, until you start getting better results.
I would recommend working out at least 5 days a week, and 6 if you possibly can. Don't take two days off exercise in a row, because the boost in insulin sensitivity that results from exercise fades quickly.
A workout should last at least 30 minutes, and it shouldn't be too easy. If you finish your workout with a dry T-shirt, that is nature's way of letting you know that whatever you were doing for the last 30 minutes wasn't enough.
Some authorities say a workout should be 60 minutes rather than 30, but I hesitate to mention it because I don't want to discourage beginners who think 30 minutes is alredy enough of a challenge. I should confess here that, when I started my exercise program in 2001, I couldn't handle 30 minutes of aerobic exercise. I would get on a stair-climber or exercise bike at the gym, and exercise until I thought I was about to die. At first that meant 15 minutes, and after a week I moved it up to 20. After about a month I moved it up to 30 minutes. After about 5 years I ran a marathon; it's funny how far you can go if you keep making small incremental improvements. Not that people with Type 2 need to become marathon runners, but even the most out-of-shape people can make remarkable gains over the long haul if they keep on challenging themselves and remain patient with the process.
A lot of Type 2 patients can get a significant benefit from light exercise (walking, say). It's certainly better than no exercise at all. However, because of the extra cardiac risk that comes with being insulin resistant, you really want the cardiovascular benefits that come with aerobic exercise. This is especially true if you also have high blood pressure (and most Type 2 patients do have a problem with that). So, my bottom line is: go for a walk if that's really all you can do today, but go for a run (or a swim, or a bike ride) if you can possibly fit it in.
Weight-lifting is also recommended for patients with Type 2, because it's helpful in terms of glucose control to have a good amount of muscle mass (you can think of your muscles as sponges for soaking up glucose -- the bigger the sponges, the better). Also, weight training tends to make whatever muscle tissue you have more sensitive to insulin. However, if you feel that you have to choose between aerobic exercise and weight training, because you can't make time in your day to do both, I think the aerobic exercise will do more for you.
The trick is to learn to think of exercise as a routine aspect of your daily life, like bathing or brushing your teeth -- not as a hobby activity that you'll do if you're in the mood and you have time for it. The truth is that, at least at first, you will never be in the mood for it, and you will never have time for it. You have to stop thinking that it matters whether you want to do it or not. This is easier said than done, but it's not impossible. It helps a lot of you have exercise buddies, because it's easier to show up and do a workout if you promised someone else to do it with them. Admittedly, this is bound to be harder if you live in a place that has cold winters. Running and cycling in the snow are not attractive options to most people. Joining a gym, or buying a home treadmill, might be good practical solutions.
Another thing to keep in mind: exercise never feels good during the first few minutes. The body needs to convert over to a different kind of energy-burning process when you're working out, and the conversion process is not instantaneous; it takes about five minutes. During those five minutes, you're doing something that the body isn't ready to support, and the result is that those five minutes can feel awful. The less you are accustomed to exercise, the worse those five minutes feel. With experience, this problem is reduced, but I doubt that it ever goes away entirely. The trick is not to become demoralized because you feel bad at the start; even great athletes probably feel bad at the start. They don't let it bother them, because they know they can work through it.
Are there medications for insulin resistance?
Yes. Lousy ones, if you ask me.
Certain kinds of diabetes drugs can increase your sensitivity to insulin, or reduce your blood sugar in other ways (interfering with carbohydrate digestion, for example). I'm not sure I'd call them wonder drugs, though. They produce a lot of unpleasant side effects (such as chronic diarrhea and the occasional sudden death). Some of them seem to increase your risk of a heart attack (or at least don't reduce it), which is pretty ironic given that heart disease is the biggest risk associated with diabetes, and reducing that risk should seemingly be the main goal of diabetes therapy. Also, diabetes drugs usually have to be taken in combination, so that you're taking various expensive pills all day and suffering the side effects of each one. (My doctor tells me that, if I had done what most Type 2 patients do, he would have had me on five meds well before now.)
Maybe the drugs would be worth all these disadvantages if they were actually more effective than, say, jogging -- but they aren't. Exercise boosts your insulin sensitivity better than drugs will, without side effects and for free. The drugs are what you fall back on if you're too disabled to exercise.
Even if you find that exercise alone is not enough to keep your BG under control, and you have to be medicated, that doesn't mean you can then give up exercise. You will still need to do the exercise, in part to protect yourself from the cardiovascular problems associated with Type 2 (an area in which the drugs will give you absolutely no help). In fact, you probably have to exercise more if you are taking the drugs, because you not only have to work out to protect yourself from what insulin resistance is doing to your heart, you now have to work out to protect yourself from what the drugs might be doing to your heart.
Since you're going to have to do the exercise anyway, you might as well get really serious about it, so that you can control your BG without having to take expensive dangerous pills that give you diarrhea. At least, that's how I feel about it; but clearly a lot of people disagree. According to my doctor, most Type 2 patients just want to take pills for it, from the very beginning. (They don't do so well with that approach, but he is seldom able to persuade them to see thing differently.)
By the way, if you read any grim articles about Type 2 which portray it as a condition that inevitably gets worse and worse over time, keep in mind that those ugly stories are about the kind of Type 2 patient who doesn't exercise, doesn't give up any bad habits, and relies on pills to take care of the problem for him. If you take that approach, the disease does tend to get worse and worse over time, but you don't have to take that approach.
How do different foods affect BG?
Maybe I should begin by saying that, when you are trying to solve the problem of insulin resistance, and trying to get your BG back down where it belongs, how much you eat (that is, how many calories) is probably more important than what kind of foods you are eating. I'm not saying it doesn't matter what you eat -- I know it does -- but comparing foods tends to distract people from the real issues.
I think some people with Type 2 tend to spend too much time thinking about hair-splitting distinctions between one food and another (do chickpeas have a better "glycemic index" than pinto beans?), when it would make more of a difference if they just ate slightly smaller helpings of either. Losing weight and exercising will both do a lot to improve your insulin sensitivity; choosing between brown rice and red potatoes won't.
That said, here are the basic facts about food and BG:
A small fraction of the fat you eat (maybe 10 or 15 percent) is converted to glucose, but this happens very slowly, over a period of about eight hours. Impact on BG: very small. However, fat tends to slow down digestion, which limits the impact on BG of everything else in the meal.
A larger fraction of the protein you eat (maybe half) is converted to glucose, over a period of about four hours. Impact on BG: fairly small.
100% of the carbohydrate you eat is converted to glucose, and rapidly, over a period of an hour or less. Impact on BG: large.
Eating just about anything will make your BG go up shortly afterwards, but carbohydrate is the major player here, since all of it is turned to glucose, and it's digested rapidly (also, most people eat more carbohydrate than protein or fat). Eating a high-carb meal dumps a lot of glucose into your bloodstream in a hurry. The more carbohydrate there is in a meal, the faster and higher BG rises, particularly if the carbohydrate isn't combined with fat. (Dry toast will probably spike your BG more than toast with peanut butter would, even though the total calorie count is lower.)
Of course, as soon as you start eating, the pancreas starts releasing insulin to reduce the inevitable BG spike. If you are insulin-resistant, your cells won't respond to the insulin vigorously enough, so that your BG goes higher than it ought to, and stays high longer than it should. A lot depends, therefore, on how much carbohydrate is included in a meal.
Actually, anyone gets a BG spike after a meal, but in a healthy person it doesn't go very high. Typically 120 mg/dl. Maybe 150 after something sugary. But in people with Type 2, it can easily go to 200 or more. I was told to try to keep my post-prandial (that is, 'after a meal') BG readings below 150. I was also told that this was a "tough target" but I should try anyway. It wasn't long before I was able to do it. Once, I blew it and shot up to 212 after a meal, because I had eaten a small container of "lite" yogurt, which turned out to have contained an amazing quantity of sugar (which raises interesting questions about the meaning of "lite").
Depending on how sensitive you are to insulin, there is going to be a certain amount of carbohydrate per meal that your system can cope with; exceed that amount, and you are going to see a big increase in BG an hour later. However, the more you are able to increase your insulin sensitivity through weight loss and exercise, the more carbohydrate per meal your system will tolerate.
I used to think it was crucial to choose low-carb foods so as to get the lowest possible BG after a meal. Lately I have begun to think that this approach is a distraction from the real issue (insulin resistance), and maybe even a way of hiding from the real issue. Keeping your BG within normal limits is a good thing, but you shouldn't do it as a kind of cover-up. Suppose you decide that it's no longer possible for you to eat potatoes, and by shunning them you are able to get good BG tests after a meal. That's all well and good, but that seemingly successful approach may blind you to the fact that it should be possible to eat potatoes, and if you could boost your insulin sensitivity a bit, it would be possible.
People have to do what works for them, and if your BG is high, I agree that it's important to get it down where it belongs as soon as possible. However, you shouldn't forget that your larger goal is to become more insulin-sensitive, so that you can eat "normal" foods without having to worry about it. Some foods (such as restaurant desserts with names that include the word "decadence") are perhaps never going to be okay for you to eat, but a potato really ought to be. For the long term, therefore, the way you want to be thinking is not "which foods should I give up forever, so that my BG doesn't spike too much after dinner?" but rather "what can I do to improve my insulin sensitivity, so that I can eat a satisfying meal and not have to worry about it?".
Generally speaking, it is best to avoid heavily processed foods, especially if they contain "trans fat" (partially hydrogenated oils) or high-fructose corn syrup. Also, you want to get down as much as you can on saturated fat (usually that's in meat and dairy foods). Vegetarianism is, at least in principle, the simplest way to "eat safe" when you have Type 2, but given that ours is a very carnivorous society, there are a lot of practical and social obstacles that make it hard to be a vegetarian. Still, you can at least try to eat more plant-based food and less animal-based food. Except for a few items such as coconut oil, almost all plant foods are safe bets unless you eat them in excessive amounts.