Unlike type 2 diabetes, type 1 is not linked to diet, as it has a both genetic and environmental origin. While the triggering virus has been around for thousands of years, the disease only started creeping up in the first half of the 1900s, and dramatically ros in the 1950s. One reason for this historical increase in the incidence of Type 1 diabetes could be linked to improved sanitation in our developed world.
This is known as Strachan’s idea, or more commonly as the hygiene hypothesis. In 1989, he was the first one to link the rising rates of allergic illnesses in the UK with improvements in living standards since the industrial revolution. He hypothesised that somehow the exposure to bacteria and viruses in the first years of life, would protect against the conditions showing up later.
Although Type diabetes is not an allergic illness whatsoever, the same idea is there for diseases like Type 1 diabetes and Polio. Various hypotheses suggest that early exposure to pathogens and infections can enable the body to learn how to deal with both bacteria and viruses.
Type 1 diabetes is when the body mistakenly destroys its own cells in the pancreas (islet cells), which makes the hormone insulin. This is very important because it enables the body to use glucose for energy. Diabetes 1 usually strikes before the age of 20, and can cause a very early death.
Now there might be a solution to this problem: scientists have recently discovered that the enterovirus - specific virus responsible for type 1 diabetes - can either prevent or instigate the illness in mice, depending on the age of infection. It works as such:
Three different tests were done on three different mice.
The first mouse was free of genetic vulnerability to type 1 diabetes, and when infected with an enterovirus, it readily fights it off. As a result, the islet cells in the pancreas are able still able to continually produce insulin.
The second mouse was one with genetic predisposition to type 1 diabetes, and because of its old age, it is likely to have its islet cells in the pancreas already damaged by the spontaneously generated autoimmune T cells. In this case, the enterovirus can quickly reproduce in the islet cells and further damages them, reducing the production of insulin. This example would show, that the enterovirus was triggering the onset of type 1 diabetes, where it was easily and quickly developed.
The last mouse also had a genetic predisposition, but was a lot younger. Because of its age, the autoimmune attack is not yet under way, with still healthy islet cells. Here, when infected, the enterovirus prompts the production of regulatory T cells, also known as Tregs, which suppress the generation of autoimmune T cells, fortifying the pancreas against type 1 diabetes. As can be seen, the enterovirus protected the mouse from developing type 1 diabetes, instead of triggering it.
If the same results can be confirmed in humans, a vaccine based on a group of viruses commonly excreted in feces could potentially prevent type 1 diabetes. Although science doesn’t know yet what exact enterovirus is involved in the onset of diabetes, scientists hypothesize that vaccinating with multiple types of enteroviruses can offer the most protection. This would be so as the approach could stimulate the numerous exposure humans used to have with enteroviruses throughout life, accumulating protective immunity.
It is very encouraging, that a vaccine approach against type 1 diabetes is now finally under way and even more efforts are in the works to reverse type 1 diabetes after its onset. In the US alone doctors diagnose 40,000 new patients with type 1 diabetes in one year. With this dramatical increase in the incidence of type 1 diabetes, using certain measures to make it as rare as it once was could benefit millions.