Type 1 diabetes (T1D) is an autoimmune disease that was traditionally thought to be passed down genetically through families. But more recent data has shown that most Type 1 diabetics do not have a family member with the disease, and only a small fraction of those with the genetic predisposition for T1D actually develop the disease, suggesting that there must be factors beyond genetics at play.
We know that our environments can interact with our bodies in ways we do not fully understand to either protect us from or propel us towards certain diseases. Environmental factors can be anything from what we eat and drink to the things we touch and the air we breathe.
In the case of Type 1 diabetes, consider one of the most basic ways of interacting with your environment: breathing in the air around you. Maybe on one not-so-lucky but not completely uncommon day, you breathe in and contract a virus. When you are infected and overcome a viral infection, your immune system normally adapts to become stronger. However, there are some strains of viruses (i.e. enteroviruses), that, when attacking a person with a genetic susceptibility to T1D, can promote inflammation in the insulin-producing part of the pancreas and may instigate the development of Type 1 diabetes (Filippi 2008). The virus’s effect on the body is dependent on the individual, the stage of life when the infection occurred (i.e. infancy, adolescence, adulthood), the strain of virus and many other factors, creating a cloud of ambiguity around the causal relationship between exposure and disease state.
You may be thinking, “Sure, I can see how environmental factors triggered T1D in that case, but the person in question still had a genetic predisposition to the disease – so doesn’t that make it a genetic illness?” If you are asking this question, you are absolutely right – but you might be surprised to learn how a genetic susceptibility can be created in the first place.
Environmental factors like Vitamin D and ambient air pollution exposure are all suspected of playing a role in the development of T1D. While research has not consistently proven a direct pathway here, we do know that exposure to some of these elements can actually cause epigenetic changes, which represent how your genetics are expressed. For example, maybe your mother had zero family history of Type 1 diabetes and lacked the susceptibility genes to the disease, but she grew up in Los Angeles, where she spent years driving a convertible up and down the busy freeways, increasing her exposure to harmful air pollution. This exposure could have caused methylation to parts of her DNA, leading to an epigenetic change that could be passed on to you, potentially predisposing you to T1D. So while you are genetically predisposed to the disease, the predisposition itself could have been caused by environmental factors in the first place.
Scientists are uncovering more and more correlations like these between our environments and our health, but the connections remain largely unclear and uncertain. This is partially due to the lack of accurate data streams in the research studies, (i.e. partially due to inaccurate patient self-reporting health outcomes, different experimental methods for testing and different measurement devices, inability to adequately characterize PM composition (is it VOCs? Dust? Microbes? Type of microbes?) etc.). If we could better understand and characterize the environment around us, perhaps we could better understand the cause and effect relationships that lead us to autoimmunity.