what I learned
When I was in the hospital, the doctor and the nurses there started explaining to me what diabetes was, and how to treat it. I learned the mechanics of treatment, but exactly how it all worked, and how to compute what to do in different circumstances took me a long time to really understand. Here is my attempt to make it more understandable than it was presented to me. Now, this is little more than a basic overview of diabetes, but for now we’ll start here, and delve deeper in certain areas in later chapters. Diabetes is a little more complicated than what I am describing, because there are multiple pathways that cause effects in the body (it’s complicated and I don’t quite understand all of them).
What is a pancreas, and what is it supposed to do?
So, you probably already know that Type 1 Diabetics have a damaged pancreas, but what does a pancreas actually supposed to do that ours cannot?
Let’s start on a small scale, with individual cells. Every cell in our body needs energy. Our cells’ main way of creating energy uses the glucose found in the bloodstream. However, cells don’t take glucose from the bloodstream unrestricted, it has to be regulated, and that’s where insulin comes in. Insulin reaches cells through the capillaries, and essentially tells the cells “Open up! We got glucose rations for ya!” Using insulin, cells capture glucose from the bloodstream and use it right away, or store it as glycogen, a long chain of connected glucose molecules which is how glucose is stored in the body when not used immediately, but kept close at hand. Without insulin, cells can’t capture glucose from the blood, and two things happen. First, the cells start to starve and run out of energy, since they cannot replenish their glycogen supply. Second, the blood accumulates too much glucose. It may be counter-intuitive, but eating when your cells are starving won’t help, you need insulin to shuttle glucose into your cells. These two phenomena create all kinds of short- and long-term problems, and eventually kill you in a few days. So, insulin has the dual purpose of making sure our cells stay fed, and making sure we don’t have an overly high amount of glucose in our blood.
The insulin in our bloodstream all comes from our pancreas. When the glucose level in the blood (called blood sugar level, blood glucose level, or BG) goes up, the beta cells in the pancreas feel the increase in glucose (they have a glucose sensor), and immediately start releasing more insulin into capillaries that feed the large (hepatic) portal vein that goes straight to the liver and the rest of the body. Insulin is a hormone. As soon as the insulin reaches the liver and other cells across the body (such as all the skeletal muscles), they use it by capturing glucose and storing it as glycogen (or using it right away), thereby lowering your blood glucose across your body..
There is another group of specialized cells in the pancreas called alpha cells: they do more or less the opposite of beta cells. Where beta cells generate insulin that causes cells (particularly in the liver, but also in many other places, such as skeletal muscles, i.e. the muscles that you can contract voluntarily) to capture glucose, alpha cells generate another hormone called glucagon: glucagon causes glycogen in the liver to be released, as glucose, in the bloodstream. Alpha cells, like beta cells, are also able to sense glucose levels. We know that the liver carries a large quantity of glycogen reserve: it is our body’s primary fuel tank of glycogen. When BG goes low, alpha cells release glucagon, which causes the liver to release more glycogen as glucose in the bloodstream, which brings BG level up.
The pancreas is very efficient at regulating the amount of glucose in the bloodstream. When you are glucose-normal, your body maintain about 4 grams of glucose at all times throughout your blood, a glucose concentration of about 70-100mg/dl (in the US, that is, milligram of glucose per deciliter of blood), or 3.9-5.6 mmol/L (in Canada and Europe, that is, millimole of glucose per liter of blood).
At least, that’s how it works for glucose-normals. But, for us T1Ds, the system is broken.
How the pancreas doesn’t work for us T1Ds
Because I am a T1D, my pancreas is partially destroyed. My immune system recognizes my pancreas probably as a foreign entity, and is destroying my beta cells. As I am writing, my beta cells have now been gone for more than 4 years, although, periodically, a few of them try growing again before being quickly destroyed. If you have just been diagnosed, you likely still have some beta cells (we’ll talk about that later), but not enough to make all the insulin you need.
Because we don’t have beta cells, our pancreas can’t release insulin (or enough of it), so our body can’t regulate high BG and lower it on its own. And, even though we still have alpha cells, for some reason that is not well understood our body doesn’t do a good job at regulating low blood glucose either, so if we go too low our body won’t raise our BG on its own.
In both cases, the consequences are really bad for us:
- if we go too low for a couple of hours, we die. Our brain is a huge user of glucose: at rest, it consumes 60% of our glucose on an ongoing basis. Without glucose, our brain can’t function and dies quickly.
- In the other direction, if our BG remains too high for too long (that is if we don’t release enough insulin), our body starts making lots of ketones, our blood acidifies (DKA), our cell membranes fall apart, and we also die within a few days.
Growing up T1D 