Osteoporosis might not be the only culprit behind the increased risk of backbone fractures as we age. Researchers at Case Western Reserve University have discovered the very musculoskeletal features that evolved to let humans walk upright might also contribute to weaker spines.
Compared to apes, humans have larger, more porous vertebrae encased in a much thinner shell of bone. Just like broad heel bones and broad ends of the leg bones in humans, these vertebrae are specially designed for upright walking-they dissipate the impact of treading on two feet, protecting cartilage and spinal discs.
The design works well until men and women age and suffer natural bone loss-leaving them vulnerable to fractures and breaks, researchers say.
“In evolution, we have a great adaptation, but there is sometimes a tradeoff,” says Meghan Cotter, an anatomy instructor at Case Western Reserve University School of Medicine and lead author of the study. “The structure is great for walking around, but not good when you have osteoporosis.”
Apes, on the other hand, have much thicker vertebral shells to begin with-designed to provide stability for climbing and knuckle-walking. They can suffer comparable bone loss with age, but their vertebrae remain intact.
A major reorganization of the musculoskeletal system was required for early human ancestors to make the transition from walking on all fours to walking upright, the researchers say.
“We’re now living about twice as long as when the adaptation evolved, and that results in major problems,” Cotter says. “It highlights we are not perfectly evolved specimens.”
Cotter worked with former master’s student David Loomis, from the Musculoskeletal Mechanics and Materials Laboratory in the Department of Mechanical and Aerospace Engineering; professors Scott W. Simpson and Bruce Latimer, both with the university’s Center for Human Origins; and former Case School of Engineering professor Christopher J. Hernandez, who is now at Cornell University.
The team’s findings were published in the online journal PLoS One.
