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Key points: Human joints evolved a threefold cartilage deficit

1. Humans have significantly less cartilage-supporting molecules. Human cartilage contains roughly one-third the amount of glycosaminoglycans (GAGs) found in ape cartilage.

2. GAGs help keep cartilage healthy. These sugar chains bind water, helping cartilage remain hydrated, resilient and able to cushion joints.

3. The difference is not explained by body weight alone. Researchers found the deficit even in the elbow, which experiences less weight-bearing stress in humans than in knuckle-walking chimpanzees.

4. The deficit may contribute to osteoarthritis. The researchers suggest that lower GAG levels leave human cartilage more vulnerable to degeneration over time.

5. The evolutionary change may have occurred before humans and Neanderthals diverged. Genetic switches that regulate gene activity appear to have reduced the production of cartilage-supporting molecules in the human lineage.

6. The study examined human and ape cartilage. Samples included cartilage from 42 human donors and seven apes, including a chimpanzee and six other apes that had died in European zoos.

7. Genetic regulation appears to be a key factor. The researchers mapped genetic switches involved in skeletal development and identified a strong signal in the biological pathways responsible for producing GAGs.

8. The evolutionary reason remains uncertain. Scientists do not yet know whether reduced GAG production was a trade-off for another evolutionary advantage or a change that natural selection no longer prevented.

9. Human cartilage starts from a potentially less favourable baseline. The study suggests that this inherited GAG deficit may make humans more susceptible to cartilage damage as they age.

10. The findings challenge a traditional explanation of joint disease. Osteoarthritis is often attributed to the mechanical demands of walking upright, but the research suggests that the underlying chemistry of human cartilage may also play an important role.

Main takeaway: Human susceptibility to osteoarthritis may be partly rooted in our evolutionary history: compared with apes, we have substantially less of the water-binding molecules that help protect cartilage, potentially making our joints more vulnerable to degeneration.