Common-causes-of-autoimmune-disease-explained

What Really Causes Autoimmune Disease?

The immune system, when functioning properly, protects the body from infectious diseases caused by bacteria, fungi, viruses, and parasites. Infectious diseases can range from more common illnesses, like a cold or the flu, to less common and even fatal illnesses, like HIV.

The immune system is a complex and vital system that works to maintain optimal health. Sometimes, a trigger can cause the immune system to become overactive and actually attack healthy cells in the body — this is referred to as autoimmune disease. There are more than 100 types of autoimmune disease, each of which affects a specific part of the body or, in some cases, the entire body. Some of the most common examples of autoimmune disease include type 1 diabetes and rheumatoid arthritis. In this article, we’ll introduce some of the causes associated with autoimmune disease.

Stress

A recent study has found a link between stress and the development of autoimmune disorders. In this study, researchers analyzed more than one million people from the Swedish population using census data and registries that indicated prescription medications and medical diagnoses. The study tracked the health of more than 100,000 individuals diagnosed with a stress disorder and compared their risk of developing an autoimmune disorder to individuals who did not have a stress disorder. Scientists found that individuals diagnosed with a stress disorder were more likely to develop an autoimmune disorder compared to individuals without a stress disorder.

A Gut Imbalance

The gut (or the gastrointestinal tract) plays an important role in maintaining the health of the body’s immune system. Certain tissue found in the mucosal layer of the gut, called lymphatic tissue, constitutes 70 percent of the entire immune system. Moreover, the diverse colonies of microorganisms in the gut, called the gut microbiome, interact with the gut’s mucosal layer to maintain the integrity of the immune system. An imbalance in the gut microbiome affects the body’s immune system and has recently been linked to the onset of autoimmune disease.

Exposure to Toxic Substances

Evidence shows that certain substances in the environment and even certain medications can increase the risk of autoimmune disease. A well-cited example is the onset of a musculoskeletal disease that affected hundreds of people after ingesting contaminated cooking oil in Spain in 1981.

Infections

Multiple studies have shown that autoimmune disease can be triggered by infection from bacteria, virus, or parasites. Scientists believe this can happen in one of many ways, including:

Molecular mimicry: Molecular mimicry occurs when a pathogen (like bacteria, a virus, or a parasite) shares structural similarities with one or more of the body’s own cells. In addition to attacking the pathogen, the immune system starts to attack healthy cells that are similar to those of the pathogen.

Sustained immune activation: A persistent infection or chronic infection can trigger autoimmune disease. This occurs when an inflammatory response is sustained by the immune system for a long period of time.

One or More Factors Can Initiate Autoimmune Disease

Autoimmune disease can develop from one or a combination of the factors outlined in this article, in addition to others not mentioned here. There is also a genetic factor involved that increases a person’s risk of developing certain autoimmune diseases. Having one or more of these risk factors does not guarantee the onset of an autoimmune disease, but it may increase the likelihood that one will develop.


Resources:

https://www.mayoclinic.org/diseases-conditions/infectious-diseases/symptoms-causes/syc-20351173
https://www.stanfordchildrens.org/en/topic/default?id=all-about-the-immune-system-90-P01665
https://www.webmd.com/a-to-z-guides/autoimmune-diseases
https://www.health.harvard.edu/blog/autoimmune-disease-and-stress-is-there-a-link-2018071114230
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433529/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433529/
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