There are 2 ways to get diabetes:
(1) For mysterious reasons, some peoples’ pancreatic beta cells, the ones that make insulin, disappear, often when they’re children. This process has no correlation with weight or anything else we can come up with. But the fact is, their bodies make essentially no insulin. This is often called Type 1 diabetes.
(2) Excess body fat for long periods of time causes some (but not all – another mystery) to become ‘resistant’ to insulin. These people produce plenty of insulin (to start off with), but their bodies don’t respond to it adequately. This is type 2 diabetes. (Note that some type 2 diabetics eventually stop producing insulin for unclear reasons, thus becoming more like type 1 diabetics).
In either case, there are 2 major consequences: (1) not enough glucose taken up by cells; (2) too much glucose in the blood. Interestingly, most of the major complications seem to come from (2) except when the blood sugar drops extremely low, which can quickly lead to death (DON’T TAKE INSULIN WITHOUT EATING!).
And in either case, the challenge is to keep the blood sugar from getting too high for long periods. This is mostly achieved by taking the proper amounts of insulin at the appropriate times. But it’s easier to prevent spikes by avoiding foods with a high glycemic index (GI). On the GI scale, sucrose isn’t so bad, simple starches are.
As far as weight control, it’s often the last thing a type 1 diabetic has to worry about – keeping weight ON is often the challenge as these people are chronically insulin-deficient. Type 2’s, on the other hand, can often gain much better control of, or even cure, their diabetes by achieving a normal body mass index.
Just to clarify the clarification (and add my two cents), it’s important to note that all not all obesity is the same. For example, someone with 5 kg of excess fat around their “gut” is more likely to get type II diabetes that someone with 10 kg of fat on their ass and upper legs (so-called “male vs. female obesity”, or “android vs. gynecoid” or “apple vs. pear”, etc. - this is where the waist to hip ratio becomes important)
On another note, you seem to be implying that the obesity causes the insulin resistance and, indeed, there is evidence for that. OTOH, there is also evidence (and nice physiology) to support the idea that insulin resistance comes first and then the obesity follows. Remember, insulin resistance is largely confined to the muscles of the body. So, if the muscles can’t accept glucose in response to the action of insulin, the blood glucose level rises until the pancreas is stimulated sufficiently to make enough insulin to overcome the resistance and drive the glucose into the muscles. But, if the person’s fat tissues are normally sensitive to insulin, or even resistant but to a lesser degree than the muscle tissue, the effect will also be to build up fat and cause obesity.
Finally, although I do agree that much is unclear, there is in fact a reasonable explanation as to why only some obese people develop diabetes, or even insulin resistance. As alluded to above, it involves the idea that where the excess fat is in the body is more important than how much fat there is. Again, fat around the waist is BAD, wheras fat that’s deposited in a more typically female distribution (buttocks and upper legs) seems relatively benign. Why is this?
To answer that question, I ask you to accept the following facts of metabolism:
“fat” is actually triglyceride. Triglyceride is made up of what are called free fatty acids (FFA) and glycerol. The fatter you are, the more triglyceride you have, and hence the more FFA you have floating around your bloodstream.
FFAs cause muscle tissue to “ignore” glucose and, instead of using that glucose for energy, use the FFAs instead (this is actually quite understandable on a bioenergetic basis especially when viewed in concert with the organism’s evolutionary need to conserve glucose for the brain during periods of starvation - a very common threat over the millenia).
FFAs also signal the liver to make glucose (this also makes sense from an evolutionary perspective, but let’s not go there now).
The effect of 2 and 3 are to raise glucose levels (the muscles aren’t using the glucose and the liver is busy producing it)
So, people with high levels of FFA will tend to have higher glucose levels (which, by the way, will stimulate insulin secretion. When things come to equillibrium, the net effect is high insulin and normal, or minimally-elevated glucose levels - a situation which resembles what goes on if insulin resistance is primary)
** and now the key **
fat in the gut region and fat in the buttocks or legs differ in two big ways:
gut fat (i.e.triglyceride) is fairly metabolically active (i.e. it is fairly easy for it to be changed back into FFAs and glycerol). Conversely, buttock and leg fat is quite inert. It tends not to dissolve back into FFAs and glycerol. Hey, just ask any woman how hard it is for her to get the flab off her ass and upper legs. Then compare to how (relatively) easy it is to get it off your gut (albeit usually only temporarily!)
==> gut fat, but not buttock/thigh fat, is a source of FFAs (which raises glucose as described above)
If/when FFAs are released from gut fat, they go right to the liver. OTOH, if/when FFAs are released from buttock/leg fat, they bypass the liver (so, FFAs from gut fat, but not gluteal/thigh fat, gives the liver a big signal to make glucose).
Taken together, 5 and 6 show that fat in the “gut” region, but not fat in the ass/legs will tend to cause high glucose & high levels of insulin.
I’ll finish by pointing out that the simple ratio of waist/hip is a POWERFUL predictor of not just diabetes and insulin resistance, but of atherosclerosis. It all comes together nicely. Coincidentally, just this week, the “Obesity Canada Clinical Practice Guidelines Expert Panel” said:
. For anyone interested, the entire thing is available for free here.
My lil’ body, which never ever had a pot, is trying to make one now. I’m well within all levels for weight/height, cholesterol, triglycerides, etc. etc. but I worry that this beginning of lard on the midsection is a bad sign. I know that overall weight loss will remove the objectional material from the gut area, but does the different quality of that fat make some methods better than others? I know that the body burns some things with some kinds of exercise and others with others - can you design a system for maximum burning of the nasty gut fat (and hopefully, therefore, avoiding diabetes)?
So I’m 140 pounds and slender, have been for 20 years, do I have the ok to eat a lot of sugar as long as I don’t gain weight? And brush my teeth often.
I’d say probably sure, although despite my confident-sounding post above there are lots of things we don’t fully understand about the relationship between diet and health. For example, while I think the approach of the anti-carb folks was totally nutty, there does seem to be something to the idea that higher glycemic index -> higher risk for ‘metabolic syndrome’ (any or all of a spectrum of things including diabetes, vascular disease/heart disease). While sucrose (table sugar) isn’t the highest on the glycemic index scale, it ain’t great.
A rule of thumb that seems to be holding up: the closer your food is to the state that it comes from nature, the better off you are. Sucrose is hard to find in significant natural quanitites, so it’s a safe bet that it isn’t good for you.