In type I diabetes deficiency of insulin secretion caused by destruction of the islets of langerhans is the major abnormality. In type II diabetes, there is both insulin deficiency and insulin resistance. The association between these factors is not well understood.
The etiology of diabetes mellitus is a complex interaction of genetic and environmental factors. The strength of the genetic factor is very variable. Until recently, type I diabetes has been regarded as a disease of acute onset. Prospective studies have now shown that people may have islet cell antibodies for up to three years before the onset of diabetes. It has also been shown that children may have glucose intolerance before developing symptomic diabetes. These findings suggest that the clinical onset of type I may be preceded by a latend period during which islet cell antibodies and impaired glucose tolerance provide evidence of islet cell destruction. Two-factor virus infection and auto immunity appear to be important in causing destruction of islet cells. If susceptible individuals can be identified during the latent period, the possibility exists of arresting the destructive process. Type I diabetes is associated with disease of the microcirculation, which is responsible for the complications of retintitis, nephropathy, and some forms of gangrene and neuropathy. Electron microscopy studies indicate that the micro vascular abnormalities occur after the onset of the disease.

Type II Diabetes is associated with disease of the macro circulation, manifested by coronary artery and peripheral vascular disease. The fact that vascular changes often precede the onset of diabetes suggests that the metabolic and vascular changes occur independently. As mentioned above the relationship between hyperglycemia and the increased motility from cardiovascular disease is not clearly understood. The mortality rate is not fully explained by the known risk factors. Up to the present time, the life expectancy of patients with diabetes diagnoses before the age of thirty has been 30 to 50percent less than that of the general population. Death has been caused by renal disease in about 40 percent and by cardiovascular disease in most of the rest. There is increasing evidence that good control in type I diabetes is associated with fever renal and retinal complications, and this has now been made easier to accomplish by the introduction of insulin infusion pumps and frequent monitoring of blood glucose. The presence of microalbuminoria predicts renal disease many years later in both type I and type II diabetes. Photocoagulation in some types of early proliferative retinopathy can delay visual loss. The need for regular ophthalmologic screening of diabetics is now well established. Screening for microalbuminuria is not yet established as a routine procedure.
The high degree of concordance in identical twins suggests that genetic factors play an important role in type II diabetes and that clinical diabetes is unmasked by environmental factors mainly in genetically predisposed individuals. This unmaking of diabetes by environmental change probably explains the emergence of diabetes as a common health problem in many groups of North American, Indians and the natives of some pacific islands. About 80% of patients with type II diabetes are obese at the time of diagnosis. The strongest predictor of type II diabetes is Impaired Glucose Tolerance (IGT), as defined earlier. In allopathy, there is no evidence that it can delay complications or cure diabetes only natural medicines like unani is successfully treating diabetes.