This transcript has been edited for clarity.
This is the first in a series of videos in which I'm discussing how to diagnose diabetes. In the past, when I trained, it seemed as though this was simple. First, there were people who didn't have diabetes. There were people with type 1 diabetes who basically had an absolute deficiency of insulin. Then there were people with type 2 diabetes who both didn't make enough insulin and also had insulin resistance. The world was simple. We treated those types of diabetes differently and there wasn't much confusion.
There's also prediabetes, which I'm not discussing, and both pre–type 2 diabetes and pre–type 1 diabetes. Ideally, we'd prevent people from developing overt diabetes if we diagnosed them earlier.
The American Diabetes Association Standards of Care classifies diabetes in this way. First, they say type 1 diabetes is due to autoimmune beta-cell destruction, usually leading to absolute insulin deficiency. This includes latent autoimmune diabetes of adulthood (LADA). LADA is a form of type 1.
I think there's subtlety here because there are people with type 1 who don't have measurable autoantibodies. There are people with LADA who are treated much like they have type 2 diabetes, at least for a while. We know from the Joslin 50-year follow-up study that people with type 1 diabetes after 50 or more years may still make a little bit of measurable C-peptide.
In theory, type 1 diabetes is autoimmune beta-cell destruction that leads to insulin deficiency. Type 2 diabetes is due to a non-autoimmune, progressive loss of adequate beta-cell insulin secretion, frequently on the background of insulin resistance and metabolic syndrome. I'm going to point out that metabolic syndrome can occur in anybody, and I have many patients with type 1 diabetes who also have metabolic syndrome. I think that's a separate issue for many of our patients, but it's very important because it confers a higher risk for cardiovascular disease.
Then there are subtypes of diabetes due to other causes. Frankly, these are the patients that I see most often. There are patients who have monogenic diabetes syndromes such as neonatal diabetes and maturity-onset diabetes of the young (MODY); diseases of the exocrine pancreas such as cystic fibrosis and pancreatitis; patients who are post-pancreatectomy; patients who have drug or chemically induced diabetes, such as with glucocorticoid use; people who are treated for HIV/AIDS; and those who have organ transplants. There is gestational diabetes, which is diabetes diagnosed in the second or third trimester of pregnancy that was not present prior to the pregnancy and tends to go away after the pregnancy but confers an increased risk for type 2 diabetes in the future.
Almost everything we do depends on the patient's clinical status and how they respond to treatment, not necessarily just based on a label. There is no single specific test that separates people with type 1 diabetes from type 2 diabetes. Islet autoantibodies can be present in every type of diabetes, from type 1 diabetes to type 2 diabetes to MODY. There are people with type 1 diabetes who don't have measurable insulin autoantibodies.
We know that diabetic ketoacidosis, although we think of it occurring in people with type 1 diabetes, can occur in people with type 2 diabetes. C-peptide levels can be high or normal in people with type 1 diabetes at the onset of their diagnosis, although a very low C-peptide level generally determines that someone does have type 1 diabetes. I have patients who are post-pancreatectomy with a very low C-peptide level, < 0.6, although they are not actually considered as having type 1 diabetes because it's not autoimmune, even though that's how they behave clinically.
Finally, in people who have MODY, which you might think is the simplest form of diabetes because it's a monogenic gene defect, you can see different phenotypic expressions in terms of their glucose levels. For example, I have a family where three sisters have exactly the same genes, but the oldest has normal glucose tolerance, the middle sister has impaired glucose tolerance, and the younger sister has diabetes and is on treatment with a sulfonylurea agent. Even the same genes can be expressed differently.
To help deal with this confusion, I am providing three additional videos to help you understand how I assess the types of diabetes and how to treat people clinically. The most important lesson I tell my patients every day is that your body will tell us what it needs because I often can't predict the course of an individual's diabetes. I can't tell them if and when they'll end up on insulin, but I can follow people and treat them based on what they need at that moment in time. Thank you.
Anne L. Peters, MD, is a professor of medicine at the University of Southern California (USC) Keck School of Medicine and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.
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Cite this: Anne L. Peters. Diagnosing Diabetes: Not So Simple - Medscape - Oct 13, 2023.
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