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Before you think osteoarthritis (OA) has nothing to do with you until you’re older, learn why improving your health now could benefit your bones later. In fact, you might as well make this an even more productive learning experience by getting on a stationary bike or taking some vitamins while you read this. Yes, without frequent movement and proper nutrients, you’re more at risk for your joints to break down and possibly lead to chronic painful inflammation associated with OA. But, how can we be sure of that and how are researchers studying and deciphering these processes?
Man’s best friend has provided insight to uncover some important clues. Although only 12 percent of the human population aged 25 to 74 eventually develop OA, 20 percent of the general canine population also suffers from this chronic degenerative disease, according to Osteoarthritis Research Society International. And because canine joints pretty much work the same way as human joints, scientists have hypothesized, and now proven, that canine OA develops in a very similar way to human OA.
In 2002, Dr. Rondo Middleton, a senior research scientist at Nestlé Purina Research Center, collected cells from canine hip bones that had been discarded from hip replacement surgeries at Ohio State University. With a high-tech microscope slide known as a canine microarray, Middleton identified more than 300 differences between arthritic states, leading to a better understanding of how OA affected the canine body.
It was a game-changer to be able to identify and study the enzymes that were responsible for tearing down bad cartilage and building new cartilage, as well as the lifecycle of a healthy cell to an arthritic one.
“It allowed us to target the key players in the cells, rather than just the symptoms of the disease,” Steven Hannah, Head of Molecular Nutrition at the Nestlé Purina Research Center, says. “Prior to our studies, canine OA was understood to a certain degree. We knew damaged cartilage wasn’t being repaired correctly, but by letting the cell tell us what was happening to it, we could finally confirm that damage and inflammation were huge components of OA.”
So by finally proving what many assumed, Middleton and Hannah could now explore possible treatments for OA.
“We grew the cells in a petri dish, then caused them to move toward an arthritic state using certain molecular challenges. This model was used to examine nutritional candidates, such as omega-3 fatty acids, that might prevent the cells from becoming arthritic,” Hannah says. To confirm the anti-inflammatory properties of omega-3 fatty acids in not only petri dishes, but also arthritic dogs, Hannah and Middleton fed a diet rich in omega-3 fatty acids to dogs in a clinical study with collaborators at Colorado State University’s School of Veterinary Medicine. “And voilà the omega-3 fatty acids got to the joints like we thought they would and the arthritic dogs, by various means, told us they felt better,” Hannah says.
Now, scientists are able to study how such nutrients might play a preventative role in the development of the disease. “This work supports the idea that we don’t just necessarily need to throw medications at every issue, and we can actually minimize the amount of medical intervention if we leverage the nutritional management side,” Hannah says.
In other words, adding more fish rich in omega-3 fatty acids to the diets of both dogs and humans with OA may help reduce the amount of medicine they have to take later down the line. And for those without OA, it doesn’t hurt to eat some salmon for dinner tonight, or make it a weekly habit. It might help your bones later down the line.