Type 1 diabetes represents approximately 10% of all cases of diabetes and is often referred to as juvenile-onset diabetes. This type of diabetes is characterized by an autoimmune destruction of the beta cells, which leads to an inability to produce insulin, and a lifelong need for insulin treatment.
The peak age of incidence of type 1 diabetes is seen in childhood, but the disease may also occur at any stage of life, indicating the variation in the rapidity of the progression of the immune- mediated damage to the pancreatic beta cells that characterizes this condition. There is marked geographic and temporal variation in the incidence of type 1 diabetes, but as yet this has not given rise to clear aetiological hypotheses that have been supported by studies with individual- level measures of exposure.
Although it is widely proposed that type 1 diabetes originates from an interaction between environmental and genetic factors, there has been little progress in identifying the environmental agents that lead to disease. We know that antibodies to the Langerhans islet cells like islet cell antibodies (ICA), glutamic acid decarboxylase (GAD) and proteinthyrosinephosphatase (IA-2) is present at the start of the disease among 60-80% of the patients and it’s believed that the beta cell is exposed to an inflammatory environment that leads to or accelerates its death. Other theories includes virus infections, exposure to certain proteins in cow milk and strong psychological stress during yearly age.
However, by contrast, there has been rapid progress in understanding the genetic basis of the condition. The predominant genetic loci are HLA DQ8 and DQ2, which are found in 80 percent of children with type 1 diabetes in Scandinavia.
Although type 1 diabetes is called juvenile diabetes subtypes exists including preclinical type 1 diabetes in which there is evidence of autoimmunity before the onset of clinical diabetes and a form occurring after the age of 40 years, which resembles type 2 diabetes but shows serological evidence of autoimmunity and in which the patients eventually become truly insulin dependent. The latter form is called Latent Autoimmune Diabetes in the Adults (LADA).
Maturity Onset Diabetes of the Young (MODY) is an unusual monogenic subgroup of diabetes characterized by an early onset (usually before the age of 25 years). Unlike the type 2 diabetes of the young, there is no association with insulin resistance, hypertension or dyslipidemia. The underlying molecular genetics has been defined in most patients with MODY, and it’s now clear that there are distinct clinical phenotypes associated with the six etiological genes.
MODY accounts for about 1% of diabetic patients and most common causes are mutations in either transcription factors or the enzyme glucokinase. Changing life style factors, such as weight and physical activity will not prevent this condition.
Gestational Diabetes Mellitus (GDM), is characterized by a glucose intolerance first recognized during pregnancy. During the latter part of pregnancy the growth of the fetus is prioritized. The mother’s blood glucose levels are decreased and the insulin resistance increases. Normally, the pregnant woman is able to compensate this condition, however, sometimes the body of can’t compensate and this results in gestational diabetes. Diabetes resolves after delivery but is likely to recur in subsequent pregnancies and the lifetime risk of developing type 2 diabetes is about 30%.
Risk factors include obesity, family history of gestational diabetes and type 2 diabetes, macrosomic infants, unexplained stillbirths or neonatal death during a previous pregnancy.