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The cause of knee damage may not be simply mechanical, some research suggests. (Sebastian Kaulitzki/Getty Images/Hemera)
The cause of knee damage may not be simply mechanical, some research suggests. (Sebastian Kaulitzki/Getty Images/Hemera)

Obesity and osteoarthritis: Without exercise, it's not just your knees that'll hurt Add to ...

The connection between obesity and osteoarthritis – a progressive degeneration of joint cartilage that affects 10 per cent of Canadian adults – seems obvious. Every extra kilogram of body weight puts an extra load of about four kilograms on your knees, for example, so the extra wear and tear erodes the joints. Simple and straightforward.

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But why, then, is osteoarthritis of the hand – containing non-load-bearing joints – also twice as common in obese people?

That’s the riddle at the heart of a debate currently flaring up in academic journals, between researchers who hold the traditional view of osteoarthritis as a product of purely mechanical forces, and those who believe that inflammatory signals triggered by conditions like obesity can play a key role. As evidence for the latter view piles up, traditional scapegoats like running are getting a new look – and a new long-term study of 90,000 people suggests that running may actually help, not hurt, your joints.

“For a long time [osteoarthritis] has been believed to be primarily mechanical,” says Dr. Richard Aspden, the head of the Musculoskeletal Research Programme at the University of Aberdeen in Scotland.

“However, the biological-origin camp are gaining ground. I guess the truth is probably somewhere in between.”

The key to the new view is that fat tissue isn’t just an inert substance that accumulates in inconvenient places in our bodies. Instead, it’s metabolically active: “a rich source of pro-inflammatory endocrine factors,” as Aspden put it in a 2011 review of the topic in the journal Nature Reviews: Rheumatology, which can trigger changes throughout the body, including in joints.

One example of the endocrine factors produced by fat tissue is leptin, best known as an appetite hormone. Researchers at the University of Michigan recently measured leptin levels in 543 middle-aged women. The results, which will appear in a forthcoming issue of Arthritis Case & Research, show that subjects with higher leptin levels were more likely to develop knee osteoarthritis during the 10-year follow-up period, even after adjusting the results to control for body weight.

Results like this have raised hopes that osteoarthritis could be treated by directly attacking some of these endocrine factors. Initial studies of this approach haven’t yet been successful (though a Belgian study published last year did show potential for slowing the progression of finger osteoarthritis), possibly because so many different hormones and other substances are involved.

Of course, it’s clear that mechanical factors also play a role in the disease. For example, one of the clearest risk factors is suffering an acute joint injury. That’s why studies of soccer and hockey players invariably show an elevated risk of developing osteoarthritis in later life: When athletes who have suffered acute injuries are removed from consideration, that risk mostly disappears.

In fact, studies now show that the traditional view of cartilage as an inert substance that can’t respond to extra demands is also incorrect. Regular exercise can actually lead to a thickening of the cartilage layer, whereas prolonged inactivity results in thinning cartilage – another example of the “use it or lose it” dictum.

All of this suggests that the results of another new study, to be published in Medicine & Science in Sports & Exercise, shouldn’t actually be surprising. Dr. Paul Williams of the Lawrence Berkeley National Laboratory in California has been following a huge cohort of runners and walkers since 1991, and his latest study analyzes osteoarthritis risk in 90,000 of them.

In brief, he found that those running more than 12 kilometres a week were 18.1 per cent less likely to develop osteoarthritis and 35.1 per cent less likely to need a hip replacement during the study’s 7.1-year follow-up, compared to those running less than that amount. Even those who ran considerably more – there were 863 subjects who ran more than 96 kilometres per week – had similarly reduced rates of osteoarthritis.

Previous studies have found essentially the same thing: A 2008 Stanford University study, for example, followed 45 runners and 53 matched non-running controls for 18 years; 20 per cent of the runners and 32 per cent of the non-runners developed knee osteoarthritis.

Further analysis of Williams’s results showed that the protective effect of running was almost entirely due to its role in lowering BMI in the subjects. Those who ran (or walked) more weighed less, and consequently had healthier joints. “The evidence seems to suggest [running] is good for you,” Aspden agrees. “Even when osteoarthritis has started, the suggestion is to keep exercising, albeit preferably low-impact – but gentle jogging isn’t ruled out.”

Williams’s study can’t determine whether it’s the lower weight or the fat-induced inflammation that’s more important; it will take years for scientists to reach any definitive conclusion in that debate. But the epidemiological evidence is already clear: Avoiding physical activity – even high-impact activities like running – in order to “preserve” your joints is a losing strategy.

 

Alex Hutchinson blogs about exercise research at sweatscience.runnersworld.com. His latest book is Which Comes First, Cardio or Weights?

Follow on Twitter: @sweatscience

 

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