The Truth About Osteoporosis
Osteoporosis literally means “porous bones,” a reference to the significant loss of bone density that defines the disease. Loss of bone density leads to brittle bones, which are at a high risk of fracture—in humans but not in animals. Osteoporatic bones frequently contain tiny fractures that lead to serious breaks during falls and other slight traumas. These major breaks typically occur in the wrist, spine, or hip, and the hip and spine fractures can be severely debilitating or even life-threatening.
An estimated 8 million American women suffer from osteoporosis. Women are twice as likely to develop the disease as are men and bear the vast majority of major fractures, including 80 percent of all hip fractures.1 These statistical differences between men and women are largely tied to hormonal differences between the sexes, particularly estrogen levels in women. While bone density can be lost throughout adult life, women typically suffer accelerated bone loss at the time of menopause, when estrogen levels decline. While genetics are certainly responsible for some aspects of bone loss, epidemiology has revealed that lifestyle choices are crucial to preserving bone density—making osteoporosis a disease that is largely preventable.
Animal experiments that address osteoporosis are crude and horrific. Common methods of inducing “osteoporosis” in animals include immobilizing their limbs in casts or suspending them by their hind limbs. Once their bones are weakened, experimenters inject drugs into the animals to see whether the drugs alter the amount of force that it takes to break the animals’ bones. Likewise, experimenters break animals’ limbs and then see which drugs help the bones heal. These procedures are excruciating and leave animals completely debilitated. Experimenters also cut out female animals’ ovaries to simulate menopause, but this method does not produce effects comparable to those that are seen in humans.
Using animals has produced little helpful information because, as Dr. A. Simon Turner of Colorado State University puts it, osteoporosis is “a disease that is restricted to humans [and is] a slowly progressive disease necessitating a study of several years’ duration to allow for a response to therapy.”2 Drs. W.S.S. Jee and W. Yao of the University of Utah note, “The rat, like other experimental animal models of osteopenia/osteoporosis, has no naturally occurring fragility fractures associated with the osteopenia.”3 Even when experimenters weaken animals’ bones, they don’t fracture in the same way that human bones do. Consequently, the artificial weakening and breaking of animals’ bones do not provide a legitimate model for a human disease that develops naturally over the course of a lifetime.
Osteoporosis was recognized more than 150 years ago by Sir Astley Cooper when he observed that hip fractures typically resulted from age-related reductions in bone mass and/or quality.4 Cooper made his discoveries through patient observation, not the manipulation of animals, and it is human clinical and in vitro research that continues to advance osteoporosis prevention and treatment today.
The Problems with Using Animals to Study Osteoporosis >>
1. C. Cooper, “Epidemiology of Osteoporosis,” Osteoporosis International 2 (1999): 2-8.
2. A. Simon Turner, “Animal Models of Osteoporosis—Necessity and Limitations,” European Cells and Materials 1 (2001): 66-81.
3. W.S.S. Jee and W. Yao, “Overview: Animal Models of Osteopenia and Osteoporosis,” Journal of Musculoskeletal and Neuron Interactions 1(3) (2001): 193-207.
4. Cooper 2
