Obesity-Related Gut Bacteria Could be the Real Culprits in “Wear and Tear” Arthritis
Arthritis and joint pain are common afflictions in the obese. However, new research suggests that this may not be due to stressed joints, as widely believed. Instead, the real cause may be body-wide inflammation triggered by the bad gut bacteria that thrive in obese people.
Osteoarthritis is a common side effect of obesity and the greatest cause of disability in the US – affecting 31 million people. Often called “wear and tear” arthritis, osteoarthritis in obese people has long been thought to be a consequence of undue stress on the joints.
However, researchers at the University of Rochester Medical Center have found evidence that the gut microbiome (which is heavily influenced by diet) may be the driving force behind this type of osteoarthritis.
The researchers fed mice a high-fat diet much like a Western “cheeseburger and milkshake” diet. After 12 weeks on the high-fat diet, the mice became obese and diabetic. Their body fat percentage nearly doubled compared to control mice, which were fed a low-fat, healthy diet. The colons of the obese mice were dominated by proinflammatory bacteria, and almost completely lacked beneficial probiotic bacteria (such as Bifidobacteria).
The scientists monitored the gut microbiomes of the mice. They found that changes in the gut microbiomes coincided with signs of body-wide inflammation, including in their knees.
The researchers induced osteoarthritis in the knees of the mice by mimicking a common sports injury (known as a meniscal tear). Interestingly, the osteoarthritis progressed much more quickly in the obese mice than the healthy mice, with almost all of their cartilage disappearing within 12 weeks of the tear.
Remarkably, the effects of obesity on gut bacteria, inflammation, and osteoarthritis were completely stopped when the high-fat diet of the obese mice was supplemented with a common prebiotic, called oligofructose (inulin). The knee cartilage of the obese mice receiving the oligofructose supplement was indistinguishable from that of the lean mice.
The growth of good bacteria, such as Bifidobacteria, was boosted by the prebiotic. In turn, the good bacteria took over and crowded out the bad bacteria. Consequently, the body-wide inflammation was reduced, which slowed the loss of cartilage from the injured knees.
The oligofructose even made the obese mice less diabetic!
There was, however, one thing the supplement didn’t change: body weight.
Obese mice given oligofructose remained obese. Thus, bearing the same load on their joints, yet their joints were healthier!
Simply reducing inflammation was enough to protect joint cartilage from degeneration, supporting the idea that inflammation, not “wear and tear,” drives osteoarthritis and joint degeneration.
Unfortunately, we don’t yet know if the same bacteria that protect the mice from obesity-related osteoarthritis are the same in humans.
The researchers are now planning to move their study to humans.
Eric M. et al. Targeting the gut microbiome to treat the osteoarthritis of obesity. JCI Insight, 2018; 3 (8) DOI: 10.1172/jci.insight.95997