The empirical classification of diabetes into standard type 1 and type 2 categories overlooks significant clinical heterogeneity within the South Asian population, creating a critical practice gap. Patients frequently receive sub-optimal empirical therapies because their specific pathophysiological drivers remain unaddressed. This diagnostic paradigm results in poor glycaemic control and unnecessary healthcare expenditure.

Addressing this clinical reality at the 4th World Congress on Cardio-Kidney-Metabolic Medicine (WCCKMM 2026) at The Leela, Mumbai, Dr V Mohan, globally renowned diabetologist from Chennai, explained that data clustering helps deconstruct this metabolic heterogeneity. The phenotypic divergence within South Asian populations necessitates a transition away from uniform treatment algorithms.

Dr V Mohan noted that data-driven clustering classifies Indian type 2 diabetes into four distinct phenotypes. These include severe insulin-deficient diabetes (CID) and insulin-resistant obese diabetes (IROD). Dr V Mohan clarified that his team was the first globally to report a combined variety, severe insulin-resistant and deficient diabetes (CIRDD), which represents the classic Asian Indian phenotype characterized by high triglycerides and low high-density lipoprotein.

The therapeutic implications of these distinct biological subsets are highly relevant to clinical practice. Dr V Mohan stated that mild age-related diabetes (MARD) shows the highest response rate to metformin. Conversely, individuals within the CID and CIRDD clusters exhibit severe secretory and resistance defects, meaning they do not respond adequately to standard metformin protocols.

Shifting the focus to monogenic variants, Dr V Mohan noted that maturity-onset diabetes of the young (MODY) patients are lean, possess strong family histories, lack ketosis, and do not require insulin. Identifying HNF4A or HNF1A mutations allows clinicians to stop insulin entirely and achieve excellent glycaemic control using inexpensive sulfonylureas.

Furthermore, diagnostic errors carry severe consequences in infantile presentations. Dr V Mohan observed that type 1 diabetes rarely manifests before six months of age; such cases typically signify neonatal diabetes. Dr V Mohan cited a patient with a KCNJ11 mutation who successfully transitioned from 14 insulin units to oral sulfonylureas, remaining insulin-free for over a decade.

Genetic screening avoids thousands of painful injections and reduces prohibitive treatment costs for families. Challenging traditional diagnostic paradigms, Dr V Mohan questioned why healthcare systems continue to treat all infantile and atypical adult diabetes with empirical insulin regimens when free genetic diagnostics and precise oral therapies are readily accessible to guide targeted interventions?

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