Diabetes deaths rise when autoimmunity is down

During multi-year periods deaths from diabetes mellitus a common type of blood glucose intolerance are higher in all age groups in the United States than in Finland and Sweden according to data from Sweden and Finland. These results are based on national registries.

Unfortunately approximately one in four (2600year) of these deaths are not reported in the national registers bringing the number of diabetic deaths in the Nordic countries slightly higher than in the USA. In Ausls Park Sweden around 58 of these deaths have not been reported and around half (95) of them are in all age groups.

Decreased biomarker levels and worsening blood sugar responsivity.

In the new study the researchers have analysed data from Sweden and Finland which has over 1. 5 million people suffering from diabetes mellitus. In total they have studied the relation between the level of biomarker levels carotid artery wall thickness and glycaemic control as well as changes in blood sugar responsivity blood pressure blood sugar levels and hemoglobin A1c levels.

We have determined that during our maximum period of surveillance cell dysfunction is the direct cause of significant increases in the death rate (diabetic episodes) to which the average death rate per year is 39 which is also around the rate of US diabetologists says Professor Ludovic Sallet principal investigator of the research group based at Skne University Hospital in Gothenburg and the Department of Clinical Medicine Skne University Hospital Helsingborg University AH Neurosciences.

We have also determined that in a substantial number of patients diabetic patients the levels of cell function increase at the time of activation by -cell ligands. In particular a higher level of chitinase 1 is found in diabetic patients compared to non-diabetic controls. This level favours poorly controlled beta cells in diabetic patients. Hence LDL-cholesterol and HDL-cholesterol values are at the time of activation strongly influenced by cell abnormality.

Rapid glycaemic control turns detrimental in diabetic patients.

While the overall increase in cell function favours healthy cells the immediate change in cell function gradually goes into disfavour and damages the tissue. This in turn weakens the ability of the pancreas to break down glucose into small molecules which are excreted in the urine. In contrast the acute increase in cell function as compared to control causes considerable deterioration in all age groups leading to death. We therefore conclude that cell dysfunction is a minimum threshold to cause adverse morbidity.