In general, microbial diversity is associated with good health,1Blaser MJ, Falkow S. What are the consequences of the disappearing human microbiota?. Nat Rev Microbiol. 2009;7(12):887-94. meaning that the greater number of microbial species in the gut, the more resistant a person is to diseases such as rheumatoid arthritis.
In This Article:
- Connections Between the Gut Microbiome and Arthritis
- Gut Microbiome Health and Diversity
- Reduce the Risk of Arthritis by Improving the Microbiome
A Lack of Microbial Diversity (Dysbiosis) and Arthritic Disease
A person’s gut contains approximately ten thousand species of microbes. To put that in perspective: the average gut microbiome has about 3 million genes, while the human body is estimated to have approximately 20 thousand genes.2Ezkurdia I, Juan D, Rodriguez JM, et al. Multiple evidence strands suggest that there may be as few as 19,000 human protein-coding genes. Hum Mol Genet. 2014;23(22):5866-78.
If the normal diversity of microbes decreases or becomes imbalanced, it is called dysbiosis. Dysbiosis is associated with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and other autoimmune diseases.3Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol. 2009;9(5):313-23.
This association between dysbiosis and disease may help explain why many people with autoimmune arthritis report developing symptoms after disturbances in their gut microbiomes, such as taking antibiotics for chronic sinus infections or recovering from an infectious illness.
See The Science Behind Leaky Gut, the Gut Microbiome, and Arthritis
How the Gut Microbiome Becomes Unbalanced
Dysbiosis can begin at any time in life and occur gradually or suddenly:
- A newborn inherits its microbiome from its birth mother. For some people, an imbalance in the gut microbiome is naturally ingrained, beginning at birth.
- An imbalance can occur over time, influenced by environmental factors such as diet, medications (both prescription and over-the-counter), drinking alcohol, and smoking.
- An imbalance can occur suddenly, over days or weeks, as the result of an infection, the use of antibiotics, or another event.
See Improving the Gut Microbiome and Arthritis Symptoms with Diet
Dysbiosis can be diagnosed by testing a patient’s fecal sample(s), although the definition is not well laid out yet, and much more work is needed to make sure that this can be done effectively. Diagnosing dysbiosis is not a necessary or standard step for diagnosing autoimmune diseases.
Every Gut Microbiome is Different
Each person has his or her own unique gut microbiome, with variations in both microbe species and species’ relative proportions.
While each person’s gut microbiome is unique, general populations do share commonalities. For example, the gut microbiomes of people living in the United States are notably different than the gut microbiomes of people living in China, which is likely due to different diets. As such, vegans have different gut microbiomes than people who eat meat and dairy products.
See Foods for a Healthier Gut and Less Arthritis Pain
These differences support the notion that environment, lifestyle, and diet influence a person’s microbiome.
Some researchers hope that future research will show how medical treatments can be customized to a person’s gut microbiome. These treatments may involve dietary changes; tailored prebiotics or probiotics; and/or fecal transplants. For example, a person with rheumatoid arthritis may be prescribed a probiotic specifically tailored to his or her gut microbiome and immune profile.
- 1 Blaser MJ, Falkow S. What are the consequences of the disappearing human microbiota?. Nat Rev Microbiol. 2009;7(12):887-94.
- 2 Ezkurdia I, Juan D, Rodriguez JM, et al. Multiple evidence strands suggest that there may be as few as 19,000 human protein-coding genes. Hum Mol Genet. 2014;23(22):5866-78.
- 3 Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol. 2009;9(5):313-23.
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