Beta-Cell Classification of Diabetes and the Egregious Eleven: Logic for Newer Algorithms/ Processes of Care The Role of Newer Anti-Diabetes Medications.

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Beta-Cell Classification of Diabetes and the Egregious Eleven: Logic for Newer Algorithms/ Processes of Care The Role of Newer Anti-Diabetes Medications in Reducing CV Risk and Outcomes in Patients with Diabetes: Diabetes Medications May be a Cardiologist’s Best Friend Stan Schwartz MD,FACP Affiliate, Main Line Health System Emeritus, Clinical Associate Professor of Medicine, U of Pa. 6105472000 1

Current T2DM Guidelines But limits therapeutic options in Type 1 Based on ‘old classification’ of DM

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Current DM Classification Failing (Certainly appropriate with knowledge available when current classification adopted) BUT WE’VE LEARNED SO MUCH MORE Immune destruction of β-cells / and Insulin Resistance is used as basis of distinction between T1D, and T2D and all other sub-types of DM Diagnosis is often imprecise Flatbush DM- present in DKA- ‘turn out to be T2DM’ LADA- Adults who look like ‘typical T1DM’ Antibody positive who look like ‘T2DM’ T1DM with Insulin Resistance (like T2DM) Ie: Complicated by extensive overlap yet distinct differences in etiology and phenotype The four types of diabetes include: The typical child with type 1 diabetes; Early onset of type 2 diabetes, particularly in non-Caucasian groups; An atypical form of diabetes sometimes with fluctuating insulin dependency, seen in African Americans; and The very rare “maturity onset diabetes of youth” (MODY), which has been found to be related to identifiable genetic mutations, transmitted in an autosomal dominant pattern, and virtually always in Caucasians.

β-Cell Centric Classification of Diabetes: Implications for Classification, Diagnosis, Prevention, Therapy, Research INSULIN RESISTANCE Environment G E N E Epigenetics Inflammation/ Immune Regulation Polygenic Monogenic β-Cell secretion/mass FINAL COMMON DENOMINATOR CLASSIFY PATIENT BY CAUSE(s) of Beta-Cell Dysfunction In EACH Individual

β-Cell Centric Classification of Diabetes: Implications for Classification, Diagnosis, Prevention, Therapy, Research INSULIN** RESISTANCE Environment* G E N E Epigenetics Inflammation/ Immune Regulation Polygenic Monogenic β-Cell secretion/mass FINAL COMMON DENOMINATOR *Environment=Genetic suceptibility to eg: viruses, endocrine disruptors, food AGEs, Gut Biome **Insulin Resistance= Centrally Induced, Peripheral, Stress Hormones, Gut Biome

Phenotypic Presentation is defined by: Slope = ‘Natural History’ over time,i.e.,RATE OF β-cell LOSS. Slope is not linear in either T1DM or T2DM, and may be intermittently relapsing, remitting, stabilized, and improved. Complete loss of β-cell mass may never be reached, especially if newer agents better preserve β-cells. 100% − 0% − Severity = β-cell loss of mass Pre-Diabetes = FBS ≥100, PPG ≥140 All DM = FBS ≥126, PPG ≥200 Critical β−Cell Mass % β−Cell Mass Disease Modification I I I I I/ ≈ / I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I Increasing Age Age at presentation = tipping point when the combined gene effect / environmental trigger is exposed as phenotypic hyperglycemia

G E N E INSULIN RESISTANCE Vasculature Environment Inflammation/ Pathophysiology of Cardio-Vascular Disease Involves the Same Etiologies/ Pathophysiologic mechanisms of Diabetes/Hyperglycemia : Implications for Classification, Diagnosis, Prevention, Therapy, Research INSULIN RESISTANCE Environment G E N E Epigenetics Inflammation/ Immune Regulation Polygenic Monogenic Vasculature FINAL COMMON DENOMINATOR CLASSIFY PATIENT BY CAUSE(s)/Mechanisms of VASCULAR Dysfunction In EACH Individual

G E N E INSULIN RESISTANCE Vasculature Damage Environment Pathophysiology of Cardio-Vascular Disease Involves the Same Etiologies/ Pathophysiologic mechanisms of Diabetes/Hyperglycemia : Implications for Classification, Diagnosis, Prevention, Therapy, Research INSULIN RESISTANCE Environment G E N E Epigenetics Inflammation/ Immune Regulation Polygenic Monogenic Vasculature Damage *Environment=Genetic suceptibility to eg: poor diet,lack of exercise, sleep disorders,, food AGEs, Gut Biome **Insulin Resistance= Centrally Induced, Peripheral, Stress Hormones, Gut Biome