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Stanley Schwartz Part 1, Introduction and Types of Diabetes




In part 1 of this Exclusive Interview, Stanley Schwartz talks with Diabetes in Control Publisher Steve Freed during the AACE 2018 convention in Boston about the classification of diabetes and the learnings that have happened since first creating the various diabetes designators.

Stanley Schwartz, MD, FACP, FACE is an Emeritus Associate Professor of Medicine at the University of Pennsylvania.

 

Transcript of this video segment:

Freed: This is Steve Freed and we are here at AACE 2018 in Boston. And we’re here with a special guest, Dr. Stanley Schwartz. [Freed to Schwartz] Maybe you can just start off and just give us a little bit of history of what you do and where you do it.

Schwartz: So, I was 32 years at University of Pennsylvania. Now, Emeritus Clinical Associate Professor in Medicine. I was a DCCT Principal Investigator, saw lots and lots of patients. In the past seven and a half years, I’ve had a single solo practice in the Philadelphia area. I’ve actually been more academic since I left the university because now I control my time and not anybody else telling me what to do. And in that regard, I’ve written about 28 papers in seven years, and traveling the world, traveling the U.S., and locally speaking about my new ideas about how we should be organizing and treating — recognizing diabetes and preventing complications.

Freed: We’ve seen a lot of changes over the last years, specially probably the last 10 years. And I was wondering, you know, there used to be two types of diabetes. And now it’s changed, and then there were five, and now we’re talking about 11, but they’re all based upon beta cell issues. Maybe you can talk a little bit about the different types of diabetes.

Schwartz: Well, the current classification: type 1, type 2, LADA, which are the big ones, that have been used in the past 5-10 years, were based on old information. Type 1 was immune destruction of beta cells. Type 2 was insulin resistance. And LADA, they didn’t really know what it is but it suggested immune destruction but in the older patient. When I was asked how do we diagnose diabetes by the ADA, about three years ago now, it took me about three nights before I had the epiphany that says, “The current classification has failed.” And that’s because we’ve — not because they were wrong, but because we’ve learned so much more. And in that regards type 1 patients, 30% to 50% of them now we recognize had insulin resistance. And about 15% of type 2 patients have islet cell antibodies, a sign of immune destruction or inflammation of the beta cell. And LADA turns out to be predominantly type 1 genes. But their expression is delayed, if they surprisingly have type 2 genes. So, we’ve just learned so much more. So, to me, there is only one disease, and that’s hyperglycemia, right. And the real question is what’s causing the damage to the beta cells that results in hyperglycemia? And we’ve recognized 11 mechanisms of hyperglycemia that we gave the story “Egregious Eleven” to. And 6 of these mechanisms are things that damage the beta cell, the muscle liver fat or related to insulin resistance, the brain which results and centrally controls peripheral insulin resistance as well as sympathetic tone. And we know about the gut biome which can damage the beta cell, and by the way, cause insulin resistance. And we also know about inflammation. So, there you have 6 that can damage a beta cell. So, you have 6 mechanisms that damage a beta cell. And then once you have a damaged beta cell, you have 5 results of that damage: reduce insulin, increase glucagon, increase glucagon resistance, reduce amylin which means that the stomach is going to empty faster and raise the sugar. And all those, will cause minor hyperglycemia, results in up-regulation of a protein, SGLT2, in the kidney, which exacerbates hyperglycemia. So, given that logic, it tells us how to take care of patients with diabetes. One, you can implement precision medicine. You can implement Patient-Centric Medicine, in the sense of figure out with appropriate markers, what’s causing the disease in that individual patient, and then use the least number of drugs in combination that treats the most number of mechanisms of hyperglycemia. And that’s the principle surrounding the Egregious Eleven. And the side correlate of that is don’t use drugs that damage the beta cell. So, there’s no logic for sulfonylureas. There’s no logic — even though it’s somewhat less to use with glutamide. And maybe the surprising answer is if you can avoid it, and we’ve written a paper that says, “You should be able to avoid the use of insulin in 90% of your type 2 patients.” So if you can avoid it, don’t use insulin. Because insulin gives you — when you inject it in the periphery, results in obligatory hyperinsulinemia. Hyperinsulinemia means weight gain, which means increased triglycerides and cytocide that damage the beta cell. So, even insulin can damage the beta cell. So, we’re not using sulfonylureas that cause hyperglycemia. We’re not using insulin where both those can damage the beta cells. And we’re using combinations of the newer agents that treat the most number of mechanisms of hyperglycemia.

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