Diabetes is a condition in which the pancreas becomes unable to regulate the amount of the hormone insulin in the bloodstream. Without insulin, the body is unable to control the amount of glucose in the body (i.e. blood sugar). High levels of blood sugar, referred to as hyperglycemia, can damage the body’s tissues and be fatal if untreated. In fact, diabetes is the seventh-leading cause of death in the US, responsible for 2.9% of the total deaths in the county. There are two types of diabetes: type 1 and type 2. Type 2 diabetes is much more common and represents about 90% of all cases. Type 2 diabetes is usually caused by obesity, poor diet and lack of exercise, and is often preventable with healthy lifestyle choices. On the other hand, development of type 1 diabetes is not related to diet or lifestyle at all, is not currently preventable, and the exact cause is not currently known.
What is known is that the rates of type 1 diabetes have been growing rapidly in the last hundred years. Since the mid-20th century, the global rate of diagnosis of the disease has been rising by 3-5% per year, with an estimated 1-3 million people in the US afflicted. In the last few decades the incidence rate has jumped massively – from 1998-2010 it rose by 40%. This massive increase in such a short period of time suggests that the cause is somehow related to environmental factors, since genetic factors change too slowly and wouldn’t be responsible for such a large change in that short of the time frame.
An unlikely culprit behind the suspected rise in cases on type 1 diabetes: the improved living conditions since the industrial revolution. Before industrialization, people would take drinking water from a common source like a well, lake, or fountain. These sources were often contaminated with human and/or animal waste, so germs could spread quickly and easily. Some of the main pathogens spread in this manner were enteroviruses: viruses normally found in the intestines. Since we used to be exposed to these pathogens even in the womb, we would inherit defensive antibodies from our mothers. Eventually, we would develop our own antibodies, cementing our resistance to the viruses. The development of technologies like indoor plumbing and the spread of more hygienic practices (e.g. handwashing) has drastically reduced our contact with these pathogens. As a result, the rates of suspected enterovirus-related diseases, such as type 1 diabetes, has soared. For type 1 diabetes, it is expected that enteroviruses end up in the pancreas, where they can replicate and cause inflammation. When the body responds to this inflammation, pancreatic cells are damaged by the immune system. However, it is not expected that a single enterovirus is the cause; rather it is a complex reaction that causes the body to attack itself.
To test the hypothesis that enteroviruses were related to the onset of type 1 diabetes, researchers at Creighton University and the University of Nebraska Medical Center ran tests on a mouse strain called NOD (non-obese diabetic) that develops type 1 diabetes naturally. The researchers infected young mice with enteroviruses and compared them against NOD mice with no exposure to the viruses. The exposed mice ended up being less likely to develop the disease than the control mice that were not exposed. The early exposure to the virus is thought to spur the creation of regulatory T cells (Tregs) in the pancreas, which help fortify pancreatic cells and protect against the future inflammation and subsequent immune system attack. Interestingly, this effect was only present on tests in young mice; when the researchers infected older NOD mice with the viruses, they developed diabetes more often than the control group. The researchers suspect that the older mice already had pancreatic cells that were damaged, and the virus accelerated the damage before the production of Tregs could provide adequate protection.
The idea that early exposure to the viruses could proactively protect the pancreas from the onset of Type 1 diabetes led researchers to consider whether it is possible to use this interaction to develop a vaccine. The scientists hypothesize that an initial killed-virus dose, in which the host immune system is exposed to inactive copies of an enterovirus to develop antibodies against it, would be sufficient to provide initial protection against type 1 diabetes. Doses of an attenuated enterovirus (one that has been weakened to reduce its ability to cause disease) could then be used as boosters to improve immunity. Scientists in Finland are working on a killed vaccine for safety testing this year. Scientists are also working on ways to reverse the disease after onset. Researchers at Boston Children’s Hospital are trying to infuse the pancreases of diseased mice with stem cells to regrow damaged cells and stimulate the production of insulin.
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