Autoimmune diseases, including type 1 diabetes, are thought to involve chronic inflammation. Inflammation is a general term for the immune system's response to something, such as an infection or injury, and chronic means the response persists over time. At the cellular level, inflammation involves the release and increased activity of various immune system cells.
The inflammatory reaction in type 1 diabetes where the beta cells are attacked is called "insulitis." The immune system cells involved in the attack include various types of white blood cells (T-cells and macrophages), and/or the substances they secrete, including cytokines, nitric oxide, and free radicals (Cnop et al. 2005). (See the oxidative stress page for more on free radicals). Certain cytokines and other markers of inflammation may be associated with development of both type 1 and type 2 diabetes (Goldberg 2009). People with type 1 diabetes have higher levels of inflammatory markers than those without diabetes; even patients with good blood sugar control (Snell-Bergeon et al. 2010). A lot of researchers are trying to identify how exactly this inflammatory process works in the development of type 1 and type 2 diabetes: what cells are involved, and what their roles are (e.g., Cnop et al. 2005). As for why it happens in the first place, we don't know.
Cytokines are essentially messenger proteins that affect the behavior of other cells. There are various types of cytokines. Some cytokines can reduce inflammation, while other contribute to it: it is the pattern of cytokines that is critical in perpetrating autoimmune disease. Cytokines are secreted by immune system cells, and control the duration and strength of the immune response (Duramad et al. 2007). In type 1 diabetes, various cytokines act together in complex ways to induce beta cell death (apoptosis) (Gysemans et al. 2008). Cytokines can affect the expression of genes that are either protective or harmful for beta cell survival (Cnop et al. 2005). A number of environmental chemicals have been found to affect cytokine levels in infants and children, including volatile organic compounds, PCBs, organophosphate pesticides, and persistent organochlorines (summerized in Duramad et al. 2007).
A Chinese study found that inflammatory markers were higher in people with type 1 (including in adults) and type 2 diabetes, as compared to people without diabetes (Xiang et al. 2011). In fact, beta cells from people with type 2 diabetes showed signs of inflammation, which correlated with beta cell dysfunction (Butcher et al. 2014). Inflammation is associated with the development of higher blood sugar levels in people before they developed type 2 diabetes-- and this inflammation was not associated with increases in waist circumference (Klüppelholz et al. 2015).
Inflammation can spread from one area of the body to another. This process may be involved in type 1 diabetes, where inflammation in the intestine may spread to the beta cells in the pancreas (Vaarala 2002). Inflammation of the intestine has been found in both children with type 1 diabetes and in animal models of diabetes, and may contribute to the development of type 1 diabetes (see the diet and the gut page) (Vaarala 2008).
Interestingly, while signs of inflammation were present at the onset of type 1 diabetes, the levels did not change as the disease progressed over time (Reis et al. 2012). However another study found that in people with type 1 or 2 diabetes, after diagnosis, levels of inflammation were associated with blood glucose control and beta cell function, which worsened over time (Weber et al. 2015).
Omega-3 fatty acids reduce inflammation, and may be protective against type 1 diabetes (see the nutrition page). Vitamin D can also protect beta cells from cytokines may be able to reduce intestinal inflammation, and also may be protective against type 1 diabetes. Breastfeeding may also reduce inflammation, while stress, wheat, or cow's milk could increase it (see linked pages for sources). Yet interestingly, vaginal delivery, associated with a lower risk of type 1 diabetes in the child, may induce a beneficial form of non-chronic inflammation (see the gestation and birth page).
Some environmental chemicals have been found to induce inflammation in animals, including some air pollutants, arsenic, trichloroethylene, and nitrosamines. Whether the inflammatory processes induced by these chemicals could contribute to the development of type 1 diabetes is not known-- not all inflammation is created equal. Even closer to home, some chemicals have been found to produce intestinal inflammation in animals, such as some pesticides, bisphenol A, and cadmium (see the diet and the gut page for information and sources). Whether intestinal inflammation produced by these chemicals could contribute to the development of type 1 diabetes is also not known, but the possibility exists, and should be investigated.
Early life exposure to endocrine-disrupting chemicals can lead to inflammation later in life. In fact, one author suggests that this "misregulated inflammation is a common thread that links most significant chronic diseases and conditions across all physiologic systems as well as the associated comorbid conditions." (Dietert 2012).
Inflammatory processes appear to play a role in the development of type 1 diabetes, although how and why are still being worked out. A number of environmental factors may either protect against or contribute to the development of type 1 diabetes via their ability to protect against or contribute to inflammatory processes.
To see a articles on the role of inflammation in diabetes and obesity, as well as on various environmental factors that can cause inflammation, see my PubMed collection, Inflammation.