Type 1 Diabetes – Etiology, Environment and Genetics

Diabetes is not restricted to a single type. One type of diabetes is an autoimmune disease while another type is due to lifestyle and environment. Diabetes afflicts thousands of people during their lifetime, but the least common form of this disease is type 1diabetes (T1D). In 2005, it affected some 340,000 persons in the United States.

What is Type 1 Diabetes (T1D)?

T1D is generally an autoimmune disease. It is used to describe a serious deficiency in insulin or a complete lack of insulin production. In the past, it has been known as insulin-dependent diabetes (IDD) or juvenile-onset diabetes.[1] Both terms were used to describe certain characteristics of the disease.

  • Individuals who develop T1D depend on insulin medication for the rest of their lives.
  • The age group most frequently diagnosed with T1D is under the age of 35. Many young people become diabetic with the onset of puberty. Of the 340,000 individuals with T1D in 2005, approximately half were younger than 20 years old. The disease can, however, affect individuals of all ages.

What Causes T1D?

This type of diabetes results when the beta cells found on the pancreatic islets of Langerhans are destroyed or damaged. As a result, they obviously are unable to function properly. The hormones designed to respond to changes in blood sugar levels cannot perform as they should. The result is insulin deficiency and hyperglycemia. Yet, the overall etiology of T1D is not as simple as this. It involves understanding the role the autoimmune system plays in the development of diabetes.

Diabetes as an Autoimmune Disease

An autoimmune disease is a type of self-destruction. It is one in which the body turns against itself, attacking its own tissues. The exact reason the body does so is not currently known. It is believed that the autoimmune system, while carrying out a specific function, damages or destroys the beta-cells islet cells responsible for producing insulin. It is known, however, that the autoimmune system is the major “effector” mechanism.[2] Specific triggers that precipitate the advent of T1D include:

  • Environmental factors
  • Genetic predisposition

Type 1 Diabetes and Environmental Factor Theories

One specific speculation concerning T1D concerns the geographic areas of incidence. The geographical areas reporting more cases of this form of diabetes are not in warm climates. In fact, statistically T1D is more common in colder climates. As a result, statistics indicate that while rates are highest in Finland and high in both Canada and the United States, they are low in Chile and Mexico.[3] It is theorized that colder or cool climates are more amenable to indoor living and, therefore, conducive to the spread of specific diseases that may act as stimulus for T1D.

In terms of environmental theories there are different hypotheses being investigated. One relates to possible increased exposure to disease without proper previous development of immunity. This is the “hygiene hypothesis.”[4]  Theories of this sort attempting to explain high rates of T1D in certain areas and its increasing rates in developed countries will require a lot more research.

Diabetes and Genetics

Diabetes is not present at birth (congenital). What may be inherited is a predisposition to contracting diabetes.[5]  What this means is that a genetic propensity for developing T1D exists but may lie dormant in your chromosomes while awaiting an agent (antigen) to trigger the disease. Research on twins has attempted to identify genetic factors that explain the development of T1D. It has been noted that when one identical twin develops diabetes, the other twin has a 50 to 60% chance of developing it too. If the twins are fraternal and not identical, the other twin’s chances are reduced to 8%.

Other research indicates the association between genetics and T1D. A mother with diabetes has a 3% chance of passing it on to her child while a diabetic father increases the likelihood to 6%. If both parents have T1D, the child has a 30% chance of developing diabetes.

A gene that has been identified as connected to diabetes is chromosome 6. It is called the human leukocyte antigen complex (HLA).  Not everybody with this complex develops T1D, and that is another medical mystery at this point. This clearly indicates the need for not only more research in general but for more studies to discover what specifically triggers the onset of diabetes using this HLA.

In all cases of an autoimmune disease, the immune system mistakes certain antigens for a virus and attacks them, destroying their ability to function properly, if at all. Some antigens that resemble beta cells may be certain common viruses. The possible culprits include:

  • Coxsackie virus
  • German measles rubella
  • Mumps virus
  • Rotavirus

The rapid attack on the beta cells resulting in their destruction may not result in immediate and significant effects. In fact, the destruction process may be slow.

T1D and Increasing Incidences

Research indicates that incidents of T1D, especially among younger children, are on the rise in developed countries where they have not been high in the past. Research in various countries has produced mixed results. There has been no definitive answer as to why the rate has continued to climb. Various theories have been put forth. They include:

  • Higher rates of Cesarean sections
  • Dietary factors (such as a deficiency in vitamin D deficiency, cow’s milk proteins becoming more commonly used and an increased ingestion of cereals)
  • Reduced  exposure to common childhood infections
  • Increased levels of childhood obesity[6]

All are up for debate and need a lot more research.

Conclusion

T1D is increasingly becoming a problem with younger children developing the need to live on insulin for the rest of their lives. While certain aspects of its etiology are becoming clear, no exact rationale for the appearance of the disease exists. Although the disease is inherited, it remains dormant, waiting for the stimulus that triggers it. More research is necessary if we are to understand how to prevent type 1 diabetes from creating a medical and personal issue for so many young individuals.

References

[1] Marcovitch, H (2006). Black’s Medical Dictionary 41st edition. Lantham, Maryland: Scarecrow Press.

[2] Van Belle, TL; Coppieters, KT; and Von Herrath, MG (2011). “Type 1 Diabetes: Etiology, Immunology, and Therapeutic Strategies.” Physiological Reviews J, 91 (1): 79-118.

[3] Masharani, U (2008). Diabetes DeMYSTiFieD. New York: McGraw Hill.

[4] Ma, RCW; and Chan, CN (2009). “Diabetes: Incidence of Childhood Type 1 Diabetes: A Worrying Trend” Nature Reviews Endocrinology 5 (October): 529-530.

[5] Dean, L; and McEntyre, J (2004). The Genetic Landscape of Diabetes. Bethesda, MD: NCBI

[6] Ma et al. (2009)

This article was originally published July 12, 2012 and last revision and update of it was 9/10/2015.