Type 1 diabetes (often called Juvenile Onset Diabetes) is categorized as a childhood or young adult disease but can in rare instances occur at a later age. Diabetes symptoms sometimes begin out of nowhere and can develop over just a few days. If the sufferer does not have a family history of the disease, the possibility of diabetes may not even be considered.
Fortunately many of the common diabetic symptoms are similar to the more controllable form of the disease, Type 2 diabetes. Only 5-10% of the people expressing the classic diabetic symptoms will in the end be diagnosed with Type 1 diabetes.
Type 1 diabetes sufferers have high blood glucose levels because their body does not have enough of the hormone insulin. This happens when the immune system attacks the insulin-producing beta cells in the pancreas and destroys them, causing the pancreas to make little or no insulin. The body needs insulin to use sugar, which is the basic fuel for cells. Insulin allows the sugar in the blood to enter the cells. No one knows why type 1 happens.
Previous research has suggested that children exposed to the insulin which can naturally be contained in cow's milk may develop antibodies to insulin. It is possible that in some genetically susceptible children, a continuous, even small-dose early exposure to bovine insulin in cow's milk may lead to loss of tolerance to insulin and subsequent Type 1 diabetes. Interestingly, one study found that in cases where the child had a diabetic mother rather than a diabetic father, this effect was less marked. [Science 155:26, June 26, 1999]
According to the "Rotterdam Study" reported in the journal Neurology, diabetes mellitus may not only damage the function of the eyes, limbs, kidneys, and heart – it may also impair the function of the brain and hasten the process of senile dementia.
The Rotterdam Study is a large, ongoing prospective analysis which tracked dysglycemia and dementia in over 6,000 individuals over age 55. The researchers found that diabetes mellitus nearly doubles the risk of developing both vascular dementia and Alzheimer's disease. Diagnosis of diabetes was based on World Health Organization criteria using a glucose tolerance test.
A related editorial called Alzheimer's a possible "brain-type diabetes". Besides damaging important blood vessel networks and increasing the risk of small "silent" strokes deep inside the brain, dysglycemia may be directly involved in the development of the neurofibrillary tangles, the clumping of nerves and fiber tissue inside the brain characteristic of Alzheimer's.
The researchers noted that advanced glycation end products (AGE), proteins damaged by chronically high blood sugar levels, are commonly found inside these tangles. "In brains of AD patients the receptor for AGE appears overexpressed," they noted. "Activation of this receptor leads to increased oxidative stress that may result in cellular damage."
Diabetes also disrupts insulin signaling to other cells in the body. This altered signaling may increase the activity of a neuronal enzyme that stimulates phosphorylated tau proteins to build up, a key trigger mechanism cited as one of the earliest signs of Alzheimer's.
NOTE: This study strongly suggests the important potential role of glycation products and insulin response, not just glucose levels, in causing degenerative disease.
Relatives of people with Type 1 Diabetes, as well as the sufferers themselves, run a risk of developing celiac disease. The resulting inflammation and tissue damage reduces vitamin B12 absorption and may lead to Pernicious anemia, which occurs in approximately 1 in 50 adults with Type 1 Diabetes.
Signs of Type 1 Diabetes, as it progresses, may include dry skin, blurred vision, unexplained weight loss and a thin, malnourished appearance.
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