For a long time I have held the belief that type 1 (T1) diabetes should have a different name. “Diabetes” as our country knows it is mostly type 2 (T2). And truthfully, it makes sense; 90-95% of the diabetes population in the United States has type 2 diabetes. So it isn’t surprising that most people don’t know the key differences between T1 and T2. The thing is though – they are so very different! My personal opinion is that the general population, as well many clinicians, would have a better understanding and awareness of how each disease was alike yet unalike if they had different names.

Let’s start with T1, because well….#livinthattype1life. T1 is characterized by an absolute loss of insulin. What makes insulin, you ask? The beta cells! Beta cells within the pancreas secrete insulin and release it into the blood stream as needed, typically in response to the presence of glucose. In T1, there has been an autoimmune attack; the beta cells have been destroyed. Beta cells are little miracle workers, and when they cease to exist, the effect is devastating. It is widely believed that something environmental (like a virus) causes the body to attack itself. The arena of research on T1 is vast and growing rapidly; we are not always certain of the cause or precipitating factor for the onset of type 1, but we know the result is an irreversible insult to the immune system.

In the early part of diagnosis, the individual with T1 may experience a “honeymoon” phase; this honeymoon period is marked by some insulin production. You can understand why this might be associated with something seemingly positive like a honeymoon – there are a few beta cells left, and they are producing some insulin. But – do not be fooled! These beta cells are not producing enough insulin to sustain life; the individual would likely enter DKA were it not for supplemental exogenous insulin (insulin from a source outside the body). In my experience, people use the honeymoon term a little too loosely; the only real way to confirm one is actually honeymooning is by measuring insulin production; this can be done through simple lab-work.

So with this eventual total loss of insulin production, the glucose in the blood stream has no where to go. Normally, insulin enters the blood stream, swoops up the glucose and takes it into the cell to be used as energy. So, in T1, we’ve got to provide exogenous insulin to get that glucose where it needs to go. Are you starting to see why glucose variation happens so easily in T1? The insulin dose has to match the amount of glucose exactly in order to have a “normal” blood sugar result. Unlike T2, there is no endogenous insulin to supplement and assist this process of blood sugar normalization. The only readily available treatment for T1 diabetes is insulin in the form of multiple daily injections from an insulin pen or vial or an insulin pump; again, I stress that insulin is the only treatment option. If you encounter someone claiming to have T1DM but they are not on insulin, they are not T1, unless they fall into the very small group of individuals that have undergone pancreatic transplant or are part of a research project that is studying alternative treatments. Research is looking at all sorts of treatment options, but they are still being studied and available to a limited few (I am particularly excited about stem cell research related to beta cell regeneration!).

Let’s briefly discuss insulin resistance, which is a topic that will be heavily discussed in the next post comparing T2 to T1. Can a type 1 experience insulin resistance? Yes! The topic of insulin resistance in T1 should be a separate post in and of itself; briefly, as an example, the higher the blood glucose is, the more resistant the body is to insulin. To simplify – basically, my body responds quickly and drastically to even a quarter of a unit when my BG is 100; that quarter of a unit won’t do shit when my BG is 300. There are numerous ways in which the T1’s body can face insulin resistance; certain foods, types of exercise and illness can precipitate an increase in insulin resistance.

That pretty much breaks down the patho of T1. This is certainly not an all encompassing explanation, though. The processes happening at the cellular level are so intricate and incredible. This here is intended to be a down and dirty description of what’s happening in T1. The next blog post will be on T2 pathophysiology. 

*You’ll notice in my writing that I use words like typically, most often, usually, most of the time, etc. – this is because there are no absolutes in diabetes. If you are an individual reading this that does not fall into the “usual” group, I hear you. I understand that there are always outliers.

Cheers,

Kelly