People who are diagnosed with type 1 diabetes must work hard to keep their blood sugar levels balanced and may be more at risk of ketosis or hypoglycemia. This is because the beta cells in their pancreas no longer produce insulin. So, they must use injections to help their bodies make use of all of the glucose.
Too much insulin and they have low blood sugar. No insulin at all and they get sick from hyperglycemia and ketosis.
If you’ve been diagnosed with type 1 diabetes, you may be wondering what made your pancreas stop working. Well, the exact causes of this disease are not clear.
Potential Causes Of Type I Diabetes
Research has shown that there is a genetic factor in the development of this disease. In fact, some people who will never be at risk of developing Type 1 due to not having the right human leukocyte antigen (HLA). There are multiple HLAs associated with type 1 diabetes.
These antigens are used by the body to trigger an immune response which normally doesn’t cause a problem. But, when people with a genetic disposition to Type 1 get sick with a virus that carries the same or similar antigens as the beta cells in their pancreas, the body’s immune system goes a little haywire.
As the body learns to recognize and attack the virus that is infecting it, the body can also start to see those beta cells as a foreign invader. Your immune system responds by attacking the beta cells, which over time kills your pancreas’ ability to produce insulin.
Essentially, type 1 diabetes is an auto-immune disorder.
What are some of the viruses that can trigger the development of Type I?
- measles
- mumps
- rotavirus
- coxsackie b virus (b4 strain)
There may be other viruses that also carry similar antigens. Additionally, some research indicates that feeding cow’s milk to an infant may also have a connection to developing this disease. However, this is not agreed on by all researchers.
[expand title=”References“]
Type 1 Diabetes Facts and Tips. URL Link. Accessed June 7, 2017.
Type 1 Diabetes Causes. URL Link. Accessed June 7, 2017.
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