“Our knees are not built to take this pounding.” I can’t count the number of times I heard this refrain from doctors and other healthcare mavens—all well-meaning, none of them runners. And, I must say, it made a lot of sense to me. How could repetitive pounding over hundreds of miles and for many years not cause damage? Before we answer this question, let’s take a look at the anatomy of the knee.
The structure of the knee
The knee is the joint between the femur (thigh bone) and the tibia (shin bone). The ends of the femur, tibia, and the back of the patella (knee cap) are covered with a smooth, slippery articular cartilage. This allows the knee bones to glide past each other when the leg is bent or straightened. Another more fibrous type of cartilage, called meniscal cartilage, covers the surface of the tibia making up the medial and lateral menisci (not shown in the picture below). They act as shock absorbers for the knee. Collagen, a protein, is an important component of both types of cartilage. The joint is also encapsulated in a membrane called the synovium, and the synovial cells secrete a thick, mucous liquid that nourishes the cartilage cells and lubricates the surface of the meniscus.
Any damage to the knee cartilage causes pain, the release of inflammatory factors, and eventual destruction of the cartilage. The end result is bone rubbing against bone. One of the hallmarks of a type of arthritis known as osteoarthritis (OA). Many experts tell you that OA, the most common form of the arthritic diseases, is the unfortunate result of the normal wear and tear that comes with aging. So, it is not surprising that running, what seems like the ultimate wear on the knee joint, has long been suspected as a cause of OA.
The facts are always right, it’s the interpretation that will trip you up
At one period of my research career, I was involved in the investigation of the biochemistry and immunology of connective tissue. I knew the process of damage to the cartilage and collagen down to the molecular level. That facilitated my falling into a common psychological trap: the bias of accessible information. When we are confronted with a problem for which we don’t have a ready answer, we tend to substitute that problem with another, for which we do have the answer. In behavioral psychology, this is called the availability heuristic.
In my case, the answer to the question of whether running caused OA was not readily available at the time. But I had a lot of related, if indirect information. Consider, for example, the presumption that OA is a wear and tear disease. In running, the force exerted on the foot (and traveling up to the knee and spine) by a 150 lbs person is an astounding 1,000 lbs! Cartilage treated in the laboratory with repeated pounding and macerating forces of 1,000 pounds results in the fraying of the hydrated bundles of collagen type II and proteoglycans, the molecular scaffold of cartilage. So no, we didn’t know specifically whether running caused OA, but the weight of the evidence seems compelling, doesn’t it? And yet…
Over the years, I kept on running long distances despite the pounding my knees took, joined by millions of other avid runners around the globe. Interestingly, when I looked around at the hundreds and thousands of fellow runners at the starting line of various races, I saw dozens of older people, some of them octogenarians, who had been running for many years—without any obvious signs of OA. But that, of course, is an anecdote and does not qualify as scientific evidence. So, what does science have to say?
Surprise, running may actually be good for you (and your knees)
There are many small studies, most of problematic design, that have looked at the question of a relationship between long-distance running and OA. In most of them, the results are equivocal. However, in a seminal series of studies by Dr. Nancy Lane and Dr. James Fries (now retired) of the Rheumatology Department at Stanford, they gave a definitive scientific answer to the question of whether recreational running over long periods of time eventually causes OA.
They followed 45 long-distance runners and 53 controls with a mean age of 58 (range 50–72) from 1984 through 2002 ( 18 years of follow-up!) with serial knee radiographs. Most of the subjects, both runners and non-runners, showed little initial radiographic changes. In fact, slightly more runners showed osteoarthritis in their initial radiographs than non-runners (6.7% vs. 0% for non-runners). However, by the end of the study, the runners did not have more prevalent OA (20% vs 32%, p=0.25) nor more cases of severe OA (2.2% vs 9.4%, p=0.21) compared to the non-runners. Note that if anything, runners showed less OA and severe OA than non-runners, but the differences were not statistically significant. Could a larger sample size make those differences statistically significant? Possibly. And, this is not just wishful musing; the biology of connective tissue suggests it.
Collagen and cartilage require weight-bearing activity in order to maintain their strength. In fact, with repeated exercise, they increase their tensile strength (defined as the resistance of a material to a force tending to tear it apart, measured as the maximum tension the material can withstand without tearing). The same is true for the tendons and ligaments that stabilize the knee joint. Furthermore, the synovium, the membrane that provides the lubricating fluid and nourishment to the joint requires weight bearing for its normal functioning. These observations suggest that, if anything, running should decrease, not increase, the prevalence of OA.
Related Content: What Really Works to Reduce Osteoarthritis Pain in the Knee?
Knee OA has doubled in prevalence since the mid-20th century
According to a paper in PNAS, knee OA has doubled in prevalence since the mid-20th century. The authors, Harvard anthropologists Ian Wallace and Daniel Lieberman, in a remarkable study, examined 2,576 American skeletons of ages >50 years old. They examined 116 native American hunter-gatherers, 60 early farmers from the prehistoric era (6,000-300 ago), 1581 skeletons from the early industrial era (1905-1940), and 819 skeletons from the modern post-industrial era (1976-2015). The radiographic marker of OA was the presence of eburnation (from burnish, to polish), the polished surface from bone-on-bone contact.
Comparing the two modern groups, the early industrial and the post-industrial, the rate of knee OA has more than doubled since 1940, from 6% to 16%. The researchers also had information about body habitus of the individuals that revealed even more depressing numbers. Of the early industrial group only 1% were obese (BMI >30) and 6% were overweight (BMI 25 -30). The post-industrial group (that’s us!) was quite different: 25% were obese and 24% overweight. Also, the post-industrial group was, on average, 6 years older.
So, there you have it. We live longer and we are more obese in the post-industrial group that suffers from more osteoarthritis. You might interpret these findings as proving that those are the reasons that we suffer more from knee OA. Not so fast. Using statistical analysis the researchers teased out the effect of BMI and age, and lo and behold, they found that the prevalence of knee OA is still more than double that of the pre-industrial group.
What might explain this unexpected observation? We don’t know yet. But if I may offer a tentative explanation, it comes back to running and weight-bearing exercise in general. We know that the more you do it, the more you inhibit the destructive influence of aging and inactivity. Perhaps a more sedentary lifestyle in the post-industrial compared to the pre-industrial group could be the explanation. But before we firmly place the blame on inactivity, as all researchers are wont to say: more studies must be done.
Dov Michaeli, MD, PhD
Dov Michaeli, M.D., Ph.D. (now retired) was a professor and basic science researcher at the University of California San Francisco. In addition to his clinical and research responsibilities, he also taught biochemistry to first-year medical students for many years.
During this time he was also the Editor of Lange Medical Publications, a company that developed and produced medical texts that were widely used by health professionals around the world.
He loves to write about the brain and human behavior as well as translate knowledge and complicated basic science concepts into entertainment for the rest of us.
He eventually left academia to enter the world of biotech. He served as the Chief Medical Officer of biotech companies, including Aphton Corporation. He also founded and served as the CEO of Madah Medica, an early-stage biotech company that developed products to improve post-surgical pain control.
Now that he is retired, he enjoys working out for two hours every day. He also follows the stock market, travels the world, and, of course, writes for TDWI.