Age Type 2<unk>  in youth brings a much higher prevalence of<unk>  like diabetic kidney disease, retinopathy and peripheral neuropathy than type 1<unk> , though no significant difference in the odds of arterial stiffness and hypertension. Poor glucose control In the early days of insulin treatment for type 1<unk>  there was much debate as to whether strict control of hyperglycaemia would delay or prevent the long-term<unk> . The work of Pirart suggested that microvascular<unk>  were less likely to occur in individuals with better glycaemic control. The issue was finally settled in 1993 with the publication of the<unk>  Control and<unk>  Trial. In the DCCT, subjects without prior retinopathy who maintained good glycaemic control for a mean of 6.5 years were 76% less likely to develop diabetic retinopathy than subjects with less strict control. Similar results were seen for microalbuminuria and peripheral neuropathy. The benefits of strict control of blood glucose were confirmed in longer-term follow-up by the DCCT EDIC study group. So far as macrovascular disease in type 1<unk>  is concerned, the same group reported improved outcomes for cardiovascular events in the group who had been managed by strict blood glucose control: in this group the incidence of any cardiovascular disease was reduced by 30% (95% CI 7, 48; P = 0.016) compared to the group with less intensive control and the incidence of major cardiovascular events (nonfatal myocardial infarction, stroke, or cardiovascular death) was reduced by 32% (95% CI −3, 56; P = 0.07). The situation regarding glycaemic control and<unk>  in type 2<unk>  is less clear cut than for type 1, though there is evidence from the United Kingdom Prospective<unk>  Study Group that strict blood glucose control is beneficial for both microvascular and macrovascular<unk> . In the original study a relatively modest difference in glycaemic control between the well-controlled and less well-controlled groups resulted in a 25% lower rate of microvascular<unk> . In follow-up studies from the same group significant relative risk reductions emerged for myocardial infarction (15%, P=0.014) and all-cause mortality (12%, P=0.007). Autoimmune processes Research from 2007 suggested that in type 1 diabetics, the continuing autoimmune disease which initially destroyed the beta cells of the pancreas may also cause neuropathy, and nephropathy. In 2008 it was even suggested to treat retinopathy with drugs to suppress the abnormal immune response rather than by blood sugar control. Genetic factors The known familial clustering of the type and degree of diabetic<unk>  indicates that genetics play a role in causing<unk> : * the 2001 observation, that non-diabetic offspring of type 2 diabetics had increased arterial stiffness and neuropathy despite normal blood glucose levels, * the 2008 observation, that non-diabetic first-degree relatives of diabetics had elevated enzyme levels associated with diabetic renal disease and nephropathy. * the 2007 finding that non-diabetic family members of type 1 diabetics had increased risk for microvascular<unk> , * such as diabetic retinopathy Some genes appear to provide protection against diabetic<unk> , as seen in a subset of long-term<unk>  type 1 survivors without<unk> .
Complications of diabetes
Paraneoplastic syndrome
Diabetic hypoglycemia
Complications of hypertension
Metabolic syndrome
Stress hyperglycemia
Idiopathic hypoglycemia
Ketosis-prone diabetes