Type 1 diabetes, or Insulin Dependent Diabetes Mellitus (IDDM), is a disorder characterized by”auto-destruction” of the pancreatic beta cells which produce insulin. Overtime, your body softly destroys these cells creating an insulin deficiency. IDDM seems to stem from an inherited defect in the immune system, triggered by some environmental factors. The specific cause of the disease remains unknown; however, scientists have isolated several things which could be linked to development of this disease.
IDDM
The objective of this review is to offer insight on where research is headed and what we know about the development of IDDM. Recent mapping of the human genome has opened several areas to explore in the area of diabetes research. Animal models and large population studies have contributed to some potential genetic links. The major histocompatibility complex (MHC) on chromosome 6 is a regulator of immune response as it recognizes “self” and “not-self” items in the body.
If something is viewed as foreign, the MHC will stimulate antibody production. Genes analyzed on the MHC are associated with IDDM, especially the human leukocyte antigen (HLA) class II alleles, DQ and DR. Although the HLA-DQ locus seems to be the best single marker for susceptibility among Caucasians, at least 40 percent of family-related diabetes cases have combinations of both DQ and DR alleles. DQ and DR alleles are nearly always found together on a chromosome and the threat is connected with them not being in balance.
Take into account
Many combinations are documented, some demonstrating both increased and decreased susceptibility, however it was difficult to find out the contribution of HLA-DQ independent of DR. The insulin gene region at chromosome 11 is also associated with IDDM risk. Studies conducted in the 1970’s established an HLA association and participation of IDDM when comparing siblings with the disease. When comparing the association between family members, results are inconsistent.
Current estimates indicate that HLA is 40-50% linked to genes passed down by family members. The risk of developing IDDM for a twin of a person who has the disease is about 70%, and this increases depending upon the particular HLA alleles that the twins share. When comparing the risk of developing the disease for first-degree relatives vs. US population, the threat is 1/20 and 1/300, respectively. Research in the region of HLA has been extremely tricky. Definitive answers can’t be drawn because not everybody holding these “vulnerable” genes develops IDDM. Actually, less than 10 percent of genetically susceptible people progress to diabetes, suggesting that other factors are responsible for development of the disease.
Research
Researchers have explored these other things, particularly environmental factors like early introduction of cow’s milk, dysregulation of the gut immune system, viral diseases, drinking water and a range of others. Several population studies have found a link between exposure to cow’s milk and increased risk for IDDM in genetically vulnerable individuals. A couple of studies also have shown an increased risk for babies exposed to cow’s milk or cow’s milk based formulas within the first 3 weeks, and also later in life.
It’s been found that babies fed cow’s milk had increased amounts of bovine insulin anti-bodies in comparison to those who were breast-fed. Bovine insulin is found in the milk of cattle. The antibodies binding to bovine insulin seem to cross-react with human insulin. Bovine insulin is deemed immunogenic as it differs from human insulin by 3 amino acids. Insulin-specific Compounds (ISA), those specific for IDDM, and increased T cell levels from exposure to cow’s milk are found in people taking diabetes related HLA risk alleles.
Did you know?
In some adults, development of diabetes has happened after infection with rubella. Although this poses a threat to susceptible people, vaccination programs have decreased the amount of rubella cases. There have been individual case reports of children developing IDDM after exposure to CMV. There have been recent research done showing that newly diagnosed people with IDDM were recently exposed to CMV. It’s been suggested that molecular mimicry might be partially responsible because CMV proteins share a similarity with a protein in the islet cells of the pancreas. Pak et al. found that about 20 percent of people with IDDM have CMV DNA from the islet cells.
Despite all this evidence but a large Swedish study found no correlation between CMV infection and risk for IDDM. Besides all this, vaccinations against the virus have reduced the incidence of CMV infections. Individual cases have been noted where those infected with EBV develop diabetes. However, IDDM growth as a consequence of EBV infection is most likely not responsible for the disorder in the vast majority of subjects. Little research and single cases aren’t enough to consider this a significant cause.
Final note
There have been reports of people developing IDDM after exposure to influenza, hepatitis A, varicella zoster, mumps, measles, rotavirus, polio, and Coxsackie A virus. Recent studies have found a positive association between zinc levels in drinking water and protection against diabetes. Magnesium levels in tap water have been shown to be linked to diabetes protection also, yet contradictory proof resides with this. The protections that zinc may provide is unclear. Despite potential relationships with heavy metals and diabetes, more research has to be done in order to ascertain the true relationship.
Of all of the evidence presented here, researchers have been unable to obtain the specific cause for development of IDDM. What we do know is that genetically susceptible people have an increased risk for diabetes. As displayed here, researchers have found genes that appear to predispose people to diabetes. Genes aren’t enough however, because not everyone with these genes develops diabetes. Environmental factors are another area of the picture. Whether it’s milk proteins, viral diseases, or impaired gut function, those who have hereditary susceptibility have a tendency to develop the disease after exposure to those. Identifying which variable is responsible has been difficult since precise mechanics of the human body are still unclear and tests to ascertain these things might not be specific or haven’t yet been created. Plus, isolating one factor isn’t reasonable since there are a whole lot of overlaps in immune functions and genetics.
