type 1 diabetes
Picture the pancreas as a factory whose only insulin-making machines are the beta cells. In type 1 diabetes, the body's own immune system mistakes these machines for enemies and destroys them, one by one, until insulin production grinds to a halt. Without the body's only key for letting sugar into cells, blood glucose climbs uncontrollably and lifelong insulin injections become essential for survival.
Type 1 diabetes is an autoimmune disease in which T lymphocytes selectively attack the insulin-producing beta cells of the islets of Langerhans, causing absolute insulin deficiency. It usually appears in childhood or adolescence but can begin at any age. Autoantibodies against beta-cell antigens — such as GAD65, IA-2, insulin, and ZnT8 — are detectable in the blood and serve as markers of the autoimmune process, often years before symptoms.
Because there is essentially no endogenous insulin, people with type 1 diabetes are prone to diabetic ketoacidosis if insulin is withheld, and they depend on exogenous insulin delivered by injection or pump together with carbohydrate counting and glucose monitoring. It accounts for roughly 5–10% of all diabetes. Although a genetic predisposition (especially certain HLA types) is required, environmental triggers are thought to ignite the autoimmune attack — but no single cause has been confirmed.
A 9-year-old develops thirst, frequent urination, and weight loss over a few weeks, arrives at hospital in ketoacidosis, and is found to have near-zero C-peptide with positive GAD antibodies — the classic presentation of new type 1 diabetes.
Absent C-peptide confirms the body has stopped making its own insulin.
A slowly progressive autoimmune form called LADA (latent autoimmune diabetes in adults) appears in adulthood and is often mistaken for type 2 diabetes at first; autoantibody testing distinguishes it.