What causes T1DM?

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The defining feature of type 1 diabetes mellitus (T1DM) is the presence of autoimmunity against the cells of our body that produce insulin, that is, the beta cells of the pancreas. The autoimmune activity against these cells causes deterioration of the insulin producing function over time. As soon as the insulin producing reserve lowers below a individual threshold, the patient will develop clinical diabetes. This may also depend on other factors, such as insulin resistance or individual susceptibility to beta cell function loss.

In most cases, antibody levels are high, such as anti-GAD, anti-IA-2A or anti-ZnT8 antibodies, but, in about 5-10% of cases, antibody levels are negative. Some studies suggest that there is still autoimmunity in these cases, but it is not know whether there are other antibodies or other forms of autoimmunity.

The younger the patient develops T1DM, the more severe is the clinical presentation. Severe cases of T1DM will present themselves with rapid weight loss, increased thirst, increased urination and, in children, failure to grow. If the person is not treated, a severe complication of T1DM will emerge: diabetic ketoacidosis. This state of extreme insulin deprivation is fatal in a few days if not immediately treated. Until the 1920s, patients with T1DM invariabily died of ketoacidosis. When insulin became available, a once fatal disease became a chronic disease.

Older patients, in particular patients above the age of 40 years old, may present themselves with milder forms of progression. In some cases, the patient may have T1DM for several years without developing ketoacidosis. This happens because older patients lose their insulin producing function slower than younger patients, so they will have a milder but still progressive form of diabetes. We should suspect that a patient older than 40 years old may have T1DM if the patient has no excess weight and no familiy history of diabetes, particularly if there is a personal or family history of autoimmune disease.