Symptoms of Diabetes mellitus

 

The main symptoms of diabetes are:

·Increased thirst because the water potential of the blood is lowered by the extra glucose.

·Producing of a lot of urine because of drinking a lot and because the glucose in the urine prevents the reabsorbing all the water they would otherwise do.

·Extreme tiredness because the cells of the body are unable to take up the glucose from the blood.

·Weight loss because glucose is not being taken into the cells but is being excreted in urine.

·Genital itching and regular episodes of thrush because of the glucose in the urine.

·Blurred vision because glucose accumulates in the lens lowering its water potential so that it absorbs water and swells making the person shortsighted.

 

These symptoms develop suddenly in Type I Diabetes (TID) and slowly in Type II Diabetes (T2D) which is usually less severe.

 

Before diabetes could be treated, sufferers from TID usually went into a coma and died within a few days.  People with T2D lived longer but suffered from other problems caused by the high levels of glucose in their blood which damages small blood vessels. (These problems may still affect people with diabetes because it is difficult to control it perfectly.)

·The retina can be damaged (diabetic retinopathy) leading to blindness.

·The kidney can be damaged leading to kidney failure.

·The nerves can be damaged (neuropathy) so that feeling is lost and wounds go unnoticed.  This is most common in the feet and may result in ulcers and infection that eventually requires amputation.

·There is an increased risk of heart attack or stroke.

 

 

Type I and Type II Diabetes

Type I diabetes (T1D) used to be called insulin-dependent diabetes mellitus or juvenile onset diabetes.  Type 2 diabetes (T2D), used to be called non-insulin-dependent diabetes mellitus or late onset diabetes.

Although insulin was discovered in the 1920s physicians continued to be perplexed by the remarkably different forms of diabetes mellitus. The difference between insulin-sensitive and insulin-resistant forms of the disease was noted in 1931, but the first direct evidence that TID was due to deficiency in insulin occurred in 1951 when a method of measuring insulin in a patient’s blood was developed.  This was followed by the finding that diabetic pancreases (examined after death) contained nearly undetectable levels of insulin, relative to controls. Meanwhile, physical anthropologists utilized somatotyping to distinguish two groups of people with diabetes: Type I -thin juvenile patients and Type II -older patients with excess body fat. 

Immunology emerged as an important new field in the 1950s, and diabetes came under scrutiny as an autoimmune disease in the 1960s and 1970s.   It is now known that TID is an autoimmune disease caused when the person’s immune system responds inappropriately to a viral infection such as a cold.  As well as attacking the virus, it also attacks and destroys the beta cells in the islets of Langerhans which make insulin.  To develop TID people also need to have a particular gene (or genes) that makes them react like this.  Not everyone with this genetic make-up will develop TID because they might not get an infection that causes the immune system to attack the beta cells.  TID is treated with insulin and diet.

T2D is caused by the body becoming insensitive to insulin.  This is usually the result of a long term, excessive intake of carbohydrates and a genetic predisposition.  It used to be thought of as a disease of late middle age but there are now examples of children developing this form of diabetes.  T2D is treated by diet; insulin is not used because these people usually have too much insulin in their bloodstream. However, after an extended period of excess insulin secretion, the pancreas may lose its ability to produce insulin and a Type II diabetic may then become insulin dependent.

Child diabetes time-bomb warning

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