Progression Of Type 1 Diabetes

Type 1 diabetes occurs when there is an attack on the islet of Langerhans cells of the pancreas that results in the reduction and eventual stoppage of the production of insulin. This damage can occur because of an autoimmune response by the body or because of a viral attack or, less commonly, some type of trauma to the pancreas. Trauma to the pancreas can include injury in an accident or fall or because of a tumor within the pancreas. Not commonly, pancreatic injury to the specific beta cells that produce insulin may also happen because of specific types of chemotherapy drugs used to treat pancreatic cancers.

For most patients diagnosed with type 1 diabetes, the progression of the condition has already advanced to the point of noticeable symptoms. Prior to symptoms becoming evident, the destruction of the islet of Langerhans cells has already occurred.

Progression Varies

Regardless of the combination of genetic, environmental, medical or diet factors that are present, type 1 diabetes is a progressive condition. It starts with a trigger that causes, in most cases, the body to attack the beta cells of the pancreas as if they were foreign invading cells. The specific reasons this occurs can vary, but depending on the production of autoantibody-producing B cells in the body the damage to the pancreas, specifically the beta cells, can be slower and take years or it may be relatively rapid and result in the significant reduction in insulin production in just a few months.

Since initially there is still insulin being produced by the viable beta cells in the pancreas, there is time when the body may function as if insulin was being produced normally. This is often referred to as the “honeymoon” phase and will result in fluctuations in blood glucose levels as sometimes there may be insulin present and available to the cells and sometimes there may not be. For many children it takes approximately years for the symptoms to become continuous and significant enough for families to talk to the physician.

Internal Destruction Of The Pancreas

With the correct genetic and environment factors in place, a trigger occurs which starts the progression of the disease. The trigger is often linked to a virus such as the Coxsackie virus or Rubella, which causes the body to misinterpret the beta cells of the pancreas as part of the virus. This destruction is not immediate as there are literally over one million insulin-producing cells that combine to create of approximately 2% of the total size of the pancreas. The islet cells are actually scattered throughout the entire organ, so it is not a specific section of the pancreas. The antibodies to the islet cells begin to destroy those cells closest to blood supply vessels, then gradually invade deeper into the tissue of the organ.

As the level of insulin produced by the viable islet cells in the pancreas decreases, symptoms of diabetes begin to appear. Since this can be very gradual it is often difficult for the individual to pinpoint the specific time that a symptom developed. However, as the insulin levels continue to drop, and glucose regulation is not supplemented through the use of injected insulin, damage to the other tissues of the body increases.

The destruction of the beta cells of the pancreas continues either by autoantibodies or because of the specific virus. It is estimated that approximately 90% of all existing beta cells have to be destroyed before the body beings to show significant symptoms of diabetes. When antibodies are produced in the body they continue to attack the targeted cells, which in turn lead to complications with the attempt to implant healthy beta cells into the pancreas to regenerate insulin production.

Early Diagnosis Benefits

For patients that have an early diagnosis of type 1 diabetes, most of the significant concurrent medical conditions can be minimized or avoided. This is why regular check-ups and reporting any changes in hunger, thirst or urination are so important for children, teens and adults. Early diagnosis may also be instrumental in preventing the possibility of developing cardiovascular disease.  Studies have shown that moderate control of blood glucose levels resulted in significant reduction in the number of cardiovascular disease events, to include a reduced risk of stroke, non-fatal myocardial infarction and death. 2

Other research into reducing neuropathy, amputation of limbs, vision problems and kidney failure is similar. The earlier the diagnosis of type 1 diabetes and the more consistent blood glucose regulation is, the lower the risk of developing any of the concurrent medical conditions associated with the disease. This is very promising research for those with type 1 diabetes that may assume that these health risks cannot be avoided.

New advances in MRI (Magnetic Resonance Imaging) can allow doctors to survey lymphocyte inflammation and determine the level of inflammation and damage that has occurred at the time of diagnosis. 3  While still in the research stage this new technology could be instrumental in determining the viability of transplants and monitoring the autoimmunity factor within the individual. Increasing attention to the specific non-invasive options for determining the condition of the pancreas may also be essential in assessing a particular patient’s options with regards to transplants or therapies yet to be implemented in human patients.


1 Ostman, J., Lonnberg, G., Arnqvist, H. J., et al. (2008). Gender differences and temporal variation in the incidence of type 1 diabetes: results of 8012 cases in the nationwide Diabetes Incidence Study in Sweden 1983–2002. Journal of Internal Medicine , 386-394.

2 Nathan, D., Cleary, P., Backlund, J., et al. (2005). Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. The New England Journal of Medicine , 2643-2653.

3 Medarova, Z., Tsai, S., Evgenov, N., et al. (2008). In vivo imaging of a diabetogenic CD8+ T cell response during type 1 diabetes progression. Magnetic Resonance in Medicine , 712-720.

This article was originally published July 12, 2012 and last revision and update of it was 9/10/2015.