📘 The autoimmune process and beta cell destruction

Your body destroys beta cells due to an identification error made by the immune system [1]. Normally, the immune system recognizes and protects your own cells, but in type 1 diabetes, it confuses proteins on beta cells with foreign invaders. It's as if your body's internal police were mistakenly arresting innocent citizens, confusing them with criminals.

This confusion can be triggered by a viral infection through "molecular mimicry" (similarity) [2]. The virus has proteins similar to those on beta cells, and after the immune system learns to attack the virus, it continues to attack your healthy cells as well [3]. Once started, the autoimmune process becomes self-sustaining and irreversible with current means.

Your immune system organizes a complex attack on beta cells [4]. Cytotoxic T lymphocytes (cell-destroying) are the soldiers that directly destroy cells, while helper T lymphocytes (helping the cytotoxic ones) coordinate the attack [5]. B lymphocytes produce autoantibodies that however do not destroy beta cells. Macrophages also come to the area to "clean up" cellular debris.

The attack is very specific. It targets only the insulin-producing beta cells in the islets of Langerhans, leaving intact the alpha cells (which produce glucagon), delta cells (somatostatin), and the rest of the pancreas [4]. It's like a surgically precise attack that destroys only the insulin factory, leaving the rest of the plant functional.

The destruction process can last from a few months to several years, depending on the aggressiveness of the autoimmune response and your age [6]. In young children, destruction is usually rapid, lasting from a few months to 1-2 years. In adolescents and young adults, the process can last several years, and in adults diagnosed with LADA, progression is slower, typically extending over 5-10 years [7].

During this "silent" period, you have no symptoms because the remaining beta cells compensate by producing more insulin [6]. Only when beta cell mass drops significantly (usually 60-90% loss, variable with age) does hyperglycemia appear and consequently the classic symptoms of diabetes. It's as if you had 100 employees in a factory, gradually some leave, the others compensate for a while, but when too few remain, production suddenly collapses.

With current technology we cannot completely stop the autoimmune process once started, but researchers are testing multiple promising approaches [8]. Teplizumab, recently approved for clinical use, can delay clinical onset by 2-3 years in people with stage 2 disease (autoimmunity and prediabetes) [9]. Other therapies under study include GAD vaccine, monoclonal antibodies, and beta cell implants obtained from one's own stem cells.

What you can do now is maintain excellent glycemic control, which reduces "stress" on the remaining beta cells and can thus slow their destruction [10]. Avoiding ketoacidosis and long periods of hyperglycemia is crucial. Participating in clinical trials, if you're eligible, offers you access to experimental therapies and contributes to finding a solution.

In the "honeymoon phase," when you still have functional beta cells, strict glycemic control is the best protection method [11]. Maintaining blood glucose between 70-140 mg/dl (3.9-7.8 mmol/L) reduces glucotoxicity and prolongs residual function [10]. Daily physical exercise also helps.

Immunomodulatory medications such as cyclosporine or anti-CD3 have shown temporary benefits in studies, but adverse effects limit their use [8]. It's important to discuss with your diabetes doctor about available options and not to try unproven treatments that promise miracles. The concept of "it can't hurt" is not valid and you can very easily harm (yourself), without meaning to.

Residual beta cell function is measured by blood C-peptide levels [12]. This is released in equal amounts with insulin by beta cells. A stimulated C-peptide level (after a meal) above 0.2 nmol/L indicates clinically significant residual beta function [13]. The test can also be done fasting, but is more informative after stimulation. C-peptide measurement can be repeated periodically to monitor the natural decline over the years.

Indirectly, you can suspect you still have residual function if you're in the "honeymoon phase" [11]. The external insulin requirement is small (under 0.3 units/kg/day) or even absent, blood glucose is relatively stable, and you don't produce ketone bodies despite missing doses. As beta cell function decreases, you'll notice increasing insulin requirements and ever greater blood glucose variability.

Yes, people with type 1 diabetes have an increased risk for other autoimmune diseases, a phenomenon called polyautoimmunity [14]. Approximately 15-30% develop chronic autoimmune thyroiditis (Hashimoto's), 4-9% celiac disease, and approximately 0.5% can develop adrenal insufficiency (Addison's disease) [15]. These conditions often form a polyendocrine autoimmune syndrome.

That's why your doctor will periodically check your thyroid function (TSH, ATPO antibodies) and screen for celiac disease (anti-transglutaminase antibodies) [14]. If you have unexplained fatigue, weight changes, digestive problems, discolored skin patches (vitiligo), or other new symptoms, report them immediately. The good news is that most people with type 1 diabetes do not develop other autoimmune diseases.