These days, medicine is waxing optimistic about osteoporosis, announcing that there are more opportunities than ever before to make this crippling disorder a disease of the past. All that needs to be done is to overcome a few obstacles concerning treatment. But what these obstacles amount to are questions of basic safety and effectiveness - not least of which is whether some of the solutions to osteoporosis may actually cause the problem.
The most popular preventive medicine for osteoporosis - one of the great rationales for its use - is hormone replacement therapy (HRT). A number of studies indeed have shown that HRT retards bone loss in postmenopausal women. However, many of these results may be illusory. One early study puzzled HRT enthusiasts because it showed that women who'd used HRT lost bone faster that did untreated women once the hormone treatment was withdrawn (Lancet, 1979; ii:33.) But later research has demonstrated that you need to take HRT for at least seven years for a long-term protective effect on bone mineral, and even this may not be enough to protect women 75 years and older from fracture -t he age at which women are most at risk (N Engl J Med, October 14,1993).
What most people don't realize is that bone loss accelerates rapidly in women once they stop using estrogen, causing a 'catch-up' effect with those who'd never taken HRT. By age 80, women who had taken HRT for 10 years, starting soon after menopause, would lose 27 per cent of their initial bone density, while those never treated, about 30 per cent. The only solution would be to start on HRT once menopause began and to continue taking it for the rest of your life. This, of course, would have to be offset against your hugely increased risk of developing breast or endometrial cancer. It's well established that HRT increases the risk of breast and endometrial cancers, and that the longer a woman uses it, the greater the risk.
Contrary to what most doctors believe, estrogen only seems to have a temporary effect. Although it may decrease the rate at which old bone is torn down, formation of new bone eventually decreases in some three to five years, anyway. Indeed, one review of 31 studies on osteoporosis and estrogen concluded that estrogen did not have 'significant benefit' in slowing the onset of osteoporosis (Am J Med,1988; 85: 847-50).
A study comparing exercise alone with exercise plus calcium supplementation or exercise plus HRT in postmenopausal women with low bone mineral density (BMD) concluded that bone loss can be slowed or prevented by exercise plus calcium supplementation, or exercise plus HRT. Although the latter was more effective than the former in increasing bone mass, it also had more side effects. These included vaginal bleeding in 52 per cent of the women who hadn't had a hysterectomy, compared with less than a quarter of that in the exercise group and in the exercise-calcium group. Seven women in the exercise-HRT group needed a D & C. In addition, more than twice the women in the exercise-HRT group (47 per cent) had breast discomfort than the other two groups (N Engl J Med, Oct 24,1991).
Not all HRT studies have shown a positive effect. One study found that it didn't protect women with a history of osteoporosis even after 16 years of use (Ann Intern Med, 1995; 122: 9-16).
The other big question is whether estrogens or progestogens actually cause osteoporosis. Hormone replacement therapy usually consists of estrogen, or an estrogen-progestogen mixture, and there has been some concern over a possible link between progestogens and osteoporosis. One recent study found that women who had been using medroxyprogesterone as a contraceptive and then stopped increased their spinal bone density, whereas women who carried on using it, or who had never used it, did not (BMJ, Mar 12,1994).