Early menopause increases CHD risk
medwireNews: Women who experience premature or early-onset menopause before the age of 45 years are at increased risk of coronary heart disease (CHD) and cardiovascular and overall mortality, a review of the research indicates.
Given that as many as 10% of women experience natural menopause before 45 years of age, this finding “may have important clinical and public health implications”, says the team in JAMA Cardiology.
Agreeing with this, JoAnn Manson (Harvard Medical School, Boston, Massachusetts, USA) and Teresa Woodruff (Northwestern University, Chicago, Illinois, USA) say in a related commentary: “The recognition that women with early reproductive decline constitute a population at increased vascular risk provides important opportunities for early intervention in terms of both risk factor modification and, when appropriate, hormonal treatment.”
The researchers, led by Taulant Muka (Erasmus University Medical Center, Rotterdam, the Netherlands), identified 32 studies including 310,329 women.
Women with menopause onset before 45 years of age were a significant 1.50 times more likely to develop CHD than their peers aged 45 years and older. They were also 1.11 times more likely to develop fatal CHD, 1.19 times more likely to die from cardiovascular disease and 1.12 more likely to die from any cause.
Early-onset menopause was not associated with an increased risk of stroke or death from stroke, however.
For women experiencing menopause between the ages of 50 and 54 years, there was a 13% decreased risk of fatal CHD, compared with their peers younger than 50 years, and again there was no effect on stroke.
The researchers were keen to determine the effects of time since menopause on the risk of developing intermediate cardiovascular factors but, being reported on in just four observational studies and with inconsistent results, they only identified a need for further research on this and the mechanisms linking early menopause to adverse cardiovascular outcomes.
Early loss of ovarian function leading to endothelial dysfunction, inflammation, immune dysfunction and in turn vascular damage is thought to be one of the primary underlying mechanisms, notes editorialist Elizabeth McNally (Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA)
But she points out that age at onset of menopause is under genetic influence and suggests that “more direct molecular mechanisms may be responsible for the tie to cardiovascular disease, as defective DNA repair can alter immune and vascular health.”
Indeed, McNally and Muka et al both cite genome-wide association studies that have identified, and validated in additional cohorts, genetic polymorphisms linked to early menopause and cardiovascular disease that are involved in inflammatory response, oxidative stress and genome stability.
By Lucy Piper
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