Often doctors hear the question - ‘Doctor, my father has it. What are my chances? Do I get it?’ This question is very difficult to answer in most of the diseases unless there are certain proven facts that have been standardized with clinical trials and reports.

Diabetic susceptibility:
Type 1 diabetes is characterized by

* Its genetic inheritance

* Complete dependency on insulin treatment

* Young age onset

* Autoimmune destruction of beta cells in pancreas (Body defense cells called lymphocytes destroy own body cells)

* Development of ketoacidosis

Role of Autoimmunity :

Lymphocytes target beta cells in pancreas and destroy them slowly. So after sometime there will be no insulin in the body and the person develops diabetes. What triggers this self-destruction is not quite known but any external viral or toxic factor alters beta cells and makes them foreign to lymphocytes. So lymphocytes think that those are not own cells and destroy them.

Supporting this autoimmune theory there are antibodies detected in the person’s blood against beta cells, lymphocytes found in the pancreas causing insulitis and this type 1 autoimmunity is associated with other autoimmune diseases.

Role of Genetic Inheritance :

Type 1 diabetes has complex pattern of inheritance with susceptibility genes mapped to at least 20 loci. Most important is class II HLA locus. Certain HLAs are strongly associated with diabetes type 1.

95% of type 1 diabetics have HLA-DR3, HLA-DR4 or both. HLA-DQ genes are even more specific markers for type 1 diabetes (HLA-DQB1*302).

Family members of a diabetic are at increased risk for developing type 1 diabetes. Child of a mother with diabetes type 1 has a risk of 3%, where as the risk is 6% if father is diabetic type 1.

The risk between siblings is based on number of haplotypes shared between them. If one haplotype is shared risk is 6% and with two haplotypes risk increased to 25%. Risk with identical twins is 25 - 50%.

Role of Environmental factors :

There are many viral infections are thought to be triggering factors for the development of autoimmunity. Examples are coxsackie virus type B, mumps, measles, cytomegalovirus, rubella and infectious mononucleosis.

All these are not thought to be directly destroying the beta cells. But one proposed theory is : When virus infects pancreatic cells, the resulting cell damage cause release of beta cell antigens. Lymphocytes exposed to these antigens get sensitized and destroy beta cells.

Another proposed theory is viral cells produce antigens that mimic beta cell antigens so lymphocytes sensitized to these viral antigens destroys beta cells too along with viral cells.

Saying all that, there are experimental evidence to support these two theories and actual evidence that confirms them is lacking.

Above three factors works in classic type 1 diabetes in 90% of the cases. But in less than 10% of cases no reason will be found. And these type 1 diabetics are included under ‘Idiopathic’ group. Recently

it was reported that a mutation in the gene that is essential for the development of pancreatic islets is involved in these group of patients.

Tags: diabetic, diabetes, diabetic heredity, type 1 diabetes