Type 1: 90%–95% prevalence, onset over age 35, strong genetic predisposition with β-cell insulin production inability.

Type 1: 5%–10% prevalence, undernourished at onset, β-cells destroyed, eliminating insulin production.

Both types: Equal prevalence, similar onset age, shared absolute insulin deficiency.

Type 2: 5%–10% prevalence, onset in childhood/puberty, moderate genetic link with autoimmune β-cell destruction.

Type 2: Onset during puberty, absent obesity, defect in insulin resistance without β-cell decline.