Type 1 and Type 2 Diabetes May Be Caused by the Same Underlying Mechanism

Through the years, there have been a variety of research initiatives that have looked at type 1 and type 2 diabetes as closely related conditions. Some even consider the two as being a part of a spectrum – where they are essentially, one and the same. This is called ‘the Accelerator Hypothesis‘.1 This hypothesis studies the relationship of BMI and age of diagnosis, and suggests that both conditions may be triggered by a degree of ‘fatness,’ and the same basic risk factors.  As controversial as this research is, through the years, the data have remained consistent with the hypothesis.


Now, new research out of Manchester University and Auckland2, suggests that type 1 and type 2 diabetes have the same underlying mechanism: they are both caused by the toxic clumping up of the hormone amylin around the pancreas’ insulin producing cells. This finding could lead to slowing down or a reversal for both forms of diabetes, with the development of drugs that could stop or slow down the forming of these clumps.

Amylin is a hormone that is normally produced alongside insulin, and helps regulate our body’s satiety signals.  When amylin gets produced, some of it ends up depositing around the pancreas’ beta cells which make insulin, where it then forms toxic clumps that end up destroying these insulin producing cells. When the cells die, the result is diabetes.

Research published by Professor Garth Cooper (based on 20 years of work) points to this being the cause of type 2 diabetes, and there is strong evidence with these newest findings that type 1 diabetes is caused by the same mechanism. The differences tend to be in age, and in the rate of onset of the conditions – in type 1, the toxic amylin deposits occur much more rapidly.

There could be potential medicines going into clinical trials within the next two years, and they will be tested on both type 1 and type 2 diabetes patients. The trials are planned with research groups in England and Scotland.

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