Animal Studies Are Misleading
Animal Studies Say, ‘Smoke Up!’
In contrast to the opinions of physicians, the World Health Organization, and epidemiology studies on thousands of people, animal studies do not show that smoking decreases bone density. Dr. H. Wayne Sampson describes in the journal Alcohol Research & Health how animal studies have contradicted each other and how “recent research in animals … has failed to confirm the results of earlier studies that had reported a decrease in bone mineral density” following smoking or exposure to nicotine.16 These conflicting studies create confusion, despite clear evidence from studies on humans that link smoking to bone loss and increased fracture rates. It has long been known that cigarette manufacturers such as Philip Morris use conflicting animal data to confuse the scientific debate and undermine criticisms of their products.
In contrast to animal studies that give conflicting results, human studies offer clear answers. Moderate or heavy smokers lose 4 or 5 percent of their bone mass every 10 years—far more than most people do. Among other problems, this increased bone loss puts smokers at a 30 to 40 percent higher risk of having a hip fracture.17 The World Health Organization has confirmed the negative effects of smokinon bone density through a meta-analysis of epidemiological studies with a combined 60,000 subjects.18 The human data is clear and unequivocal.
Fluoride
Animal studies have repeatedly suggested that sodium fluoride (NaF) would be the biggest breakthrough in osteoporosis treatment. Animals injected with NaF showed increased bone mass, and researchers claimed that the drug could potentially eliminate osteoporotic bone density levels in humans. While NaF does increase bone mass in humans, it does not decrease fracture rates, and some doctors have argued that it actually increases the incidence of fractures. Additionally, the side effects of the treatment include abdominal pain and bleeding and severe acute pain in the lower extremities, a condition that was so debilitating that it was named “painful lower extremity syndrome.”19 These side effects—not predicted by animal tests—are so severe that it’s questionable whether NaF would be approved for use even if it did effectively treat osteoporosis.
In the case of NaF, animal studies mislead doctors because of a crucial difference between humans and most other animals: The bones of other animals do not fracture when they lose bone mass. Instead, animals’ bones tend to maintain their flexibility and resist becoming brittle.20 Osteoporosis researchers have spent decades debating the fluoride issue and have wasted massive resources because they chose to use animals to study a human disease.
Combination Therapies
Rat studies strongly suggested that combining two leading osteoporosis treatments—parathyroid hormone (PTH) and bisphosphonates—would produce a synergistic, beneficial effect.21 In rats, the two classes of drugs build and maintain bone strength far more efficiently when they are used together. In human clinical trials, however, there was no benefit to using the drugs in combination, and the data suggest that any bone-building effects might be less when compared with using PTH or bisphosphonates alone.22 This finding is a major setback for osteoporosis research because PTH/bisphosphonates combination therapy was widely seen as the next breakthrough in osteoporosis treatment as a result of the misleading rat studies.
Furthermore, clinical trials in women have found that estrogen therapy successfully combines with PTH therapy, contrary to the data from animal studies. Researchers are now refocusing their efforts on estrogen even though the use of estrogen in osteoporosis therapy has its own drawbacks in humans that were not seen in animal tests.
Hormone Replacement Therapy (HRT)
A main cause of postmenopausal osteoporosis is the reduction of estrogen that accompanies menopause. As such, estrogen therapy has long been used as the primary preventative treatment for postmenopausal osteoporosis. Unfortunately, hormone replacement therapies have been significantly over-prescribed because of misleading data from animal safety tests, which suggested that estrogen therapy would reduce arteriosclerosis, thus preventing heart attacks and strokes. Clinical trials conducted through the National Institutes of Health’s Women’s Health Initiative revealed that just the opposite is true.
The Women’s Health Initiative showed that estrogen and progestin therapies significantly increase rates of heart attack, strokes, and breast cancer in women. Undoubtedly, many women lost their lives because animal tests suggested that all menopausal women should take HRT. Additionally, osteoporosis treatment was dealt a blow because the mainstay of therapeutic treatment was revealed to be too dangerous for many women. Estrogen therapy is now making a slow comeback by using new low-dose therapies that remove much of the risk that is associated with traditional hormone replacement. Additionally, the crisis of HRT’s adverse effects has spurred the development of alternative therapies, such as biphosphonates, which would likely have occurred far sooner had there not been an overdependence on hormone replacement. Clearly, misleading animal tests severely stunted the development of safe and effective treatments for osteoporosis and caused killer diseases in women.
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16. H. Wayne Sampson, “Alcohol and Other Factors Affecting Osteoporosis Risk in Women,” Alcohol Research and Health 26(4) (2002): 292-8.
17. Janelle Miles, “Fed: Smoking Causes Bone Thinning, Researcher Says,” Australian Associated Press, 15 Feb. 2005.
18. Women’s Health Weekly, “Tobacco Use; Largest Study to Date Associates Smoking With Increased Osteoporosis Risk,” 15 Jul. 2004.
19. Michael Kleerekoper and Daniel Bernard Mendlovic, “Sodium Fluoride Therapy of Postmenopausal Osteoporosis,” Endocrine Reviews 14(3) (1993): 312-23.
20. Jee and Yao 195.
21. Roger S. Rittmaster et al., “Enhancement of Bone Mass in Osteoporotic Women With Parathyroid Hormone Followed by Alendronate,” The Journal of Clinical Endocrinology & Metabolism 85(6) (2000): 2129-34.
22. Corinna Kaarlela, “Combining Osteoporosis Drugs Produces No Added Benefit,” UCSF News Office, 20 Sep. 2003.
