Commentary by Bruce Ettinger, MD, NCMP
Over the past 10 years, the Study of Women's Health Across the Nation (SWAN) has provided us with an astonishing number and variety of studies based on observation of 3,302 women transitioning from premenopausal to postmenopausal status. In the area of skeletal health, prior SWAN reports have described how falling serum estradiol levels signal an increase in bone turnover that, in turn, accelerates age-related bone loss. SWAN defines trans-menopause as the period 1 to 2 years before 2 years after the FMP.
Quantitatively, these transmenopausal changes have been shown to be modest and brief—specifically, about a 30% increase in bone turnover, with a resulting increase in the annual rate of bone mineral density (BMD) loss of about 2%. SWAN has also shown us that over the long term, the median annual bone loss is approximately 1% (ie, a cumulative 11% in the spine and 9% in the hip).
The current SWAN report assesses bone turnover in 918 women undergoing a natural menopause at a median age of 51.3 years. Data on these women were available for about 6 years before and 6 years after the FMP. During the 2- to 3-year transmenopausal period, the bump in bone turnover was greater among thinner women (BMI <25) than heavier women (BMI >30). However, these differences dissipated within a few years after the FMP. Additionally, differences in bone turnover among different ethnicities were largely explained by BMI.
Should these findings alter our management of women transitioning through menopause? The simple answer is no—for the following reasons:
The modest and self-limited changes in bone turnover and BMD should allay concerns about catastrophic bone loss occurring in otherwise healthy women transitioning through menopause.
Given the variability in bone turnover markers and BMD, small changes in bone turnover and BMD would be difficult to reliably detect in individual women.
Should these findings alter our perspective on preventing bone loss? I would like to tentatively say yes, for the following reasons:
To return a transitioning or postmenopausal woman’s bone turnover to premenopausal levels requires only a modest antiresorptive drug effect.
When prevention of bone loss is appropriate, I suggest we avoid potent antiresorptive treatments that typically suppress bone turnover by 60% to 80% and instead consider those with milder effects, in the range of 30%. That would fit the profile of low-dose hormone therapy or selective estrogen-receptor modulators.
With accumulating evidence of harm (atypical femoral fractures) linked to excessive suppression of bone turnover, it would be prudent in the setting of prevention to seek physiologic restoration of premeno-pausal bone turnover rates.