As women navigate hot flushes, sleep issues and changing waistlines, there’s another quieter change that can often occur during perimenopause and post-menopause that deserves just as much attention: heart health.
While women often worry more about the visible signs of midlife and menopause, they are less aware of the hidden shifts in blood fats, blood vessels and metabolism that can silently raise the future risk for cardiovascular disease, the leading cause of death in women worldwide.
Women in their peri-menopause (i.e. from the time when periods start to become more erratic till one year after the complete loss of menstruation) and post-menopause become more vulnerable to cardiovascular disease because falling oestrogen levels trigger an unfavourable shift in blood fats, body fat distribution, blood pressure, glucose control, and inflammation.
This untimely cocktail pushes the heart and arteries under additional strain. By the late 50s and 60s, many women’s cardiovascular risk approaches – and in some respects exceeds – that of men of the same age, although the pattern and timing of disease differ between men and women.
Lipid metabolism made simple
We term “lipid metabolism” the way our bodies handle fats: from how we absorb them from food, to how they move through the blood, are stored, and are used up for energy our organs and cells need.
Because fat does not dissolve in water, the body packages it into tiny particles called lipoproteins that travel in our bloodstream. LDL particles carry cholesterol out to tissues; when there is too much LDL, or the particles are small and dense, they can more easily enter artery walls and help form plaques. HDL particles move cholesterol back from tissues and artery walls to the liver for disposal, which is why they are often called “good” cholesterol. However, their quality and function matter as much as their amount.
What changes at peri- and post-menopause?
Oestrogen has important protective effects on the cardiovascular system: it helps keep LDL (so-called bad cholesterol) lower, supports healthy HDL (“good cholesterol”), improves how blood vessels relax, and modulates inflammation.
Around the menopausal transition, ovarian oestrogen production drops sharply, and this is often associated with a rapid change in several metabolic pathways rather than a slow, gentle ageing process we would perhaps expect.
Large studies show that around and after menopause women develop higher total and LDL cholesterol, while HDL particles that are smaller and less effective at clearing cholesterol from arteries become more predominant. Triglycerides, a type of fat that circulates in our blood acting as one of our body’s main fuel stores, also increase post-menopause. This combination of fats creates what we call a more “atherogenic” or atherosclerotic plaque-promoting profile. When too many of these fats circulate in the bloodstream, they can build up in arteries over time, contributing to the development of fatty plaques that can gradually narrow the space for blood to flow. Eventually, they sometimes rupture and trigger a clot, raising the risk of heart disease and stroke.
At the same time, women are more likely to develop other cardiovascular risk factors:
- Weight gain, especially around the abdomen
- Higher blood pressure
- Insulin resistance.
All of the above further raise cardiovascular risk.
Modern studies on the collection of metabolites circulating in our bloodstream (metabolomics) confirm that over half of menopause-related metabolic changes are in lipid-related molecules, tightly linking this hormonal transition to cardiovascular risk.
How do women’s risks compare with men’s?
Before menopause, women generally have a lower risk of heart attack and stroke than men, helped in part by higher oestrogen levels and overall more favourable lipid profiles.
Data from large cohorts show that pre-menopausal women have lower total and LDL cholesterol than men of the same age, along with slightly lower blood pressure and better control of their glucose levels.
After menopause, this advantage shrinks or even disappears.
In a very large study carried out on British people, post-menopausal women actually had higher total and LDL cholesterol than similarly aged men, despite lower rates of other risk factors, such as smoking, hypertension and diabetes.
Clinically, women tend to develop cardiovascular disease (CVD) roughly 7–10 years later than men, but their risk accelerates sharply after menopause and ultimately converges.
Women are also more prone to certain presentations of heart disease, such as heart failure with preserved ejection fraction (where the heart looks as if it is pumping normally on scans, but is too stiff to relax and fill properly between beats), and microvascular angina (chest discomfort caused by problems in the heart’s small blood vessels). These forms of heart disease have historically been underrecognised and understudied.
Current approaches: lifestyle changes and lipid-lowering drugs
Across sexes, the foundations of cardiovascular prevention are the same:
For peri- and post-menopausal women, guidelines emphasise checking blood pressure, cholesterol and glucose, and acting early if these are abnormal, because the risk can increase quickly during this time.
Statins remain the mainstay medication for lowering LDL cholesterol and preventing cardiovascular events in people at increased risk. Large meta-analyses show clear benefits in women and men for secondary prevention (after a cardiovascular event such as a stroke).
For primary prevention (before any event occurs), the evidence of benefit in women is less robust than in men, and some analyses suggest that absolute risk reductions may be smaller. However this remains an active area of research. Regardless, women who meet established criteria for statins are still less likely than men to receive them or to stay on therapy – a major implementation gap that extends to other lipid-lowering drug classes, as discussed below.
Menopausal hormone therapy (MHT)
For many years, oestrogen was thought to be a heart-protective therapy, but clinical trials and their overall analysis have painted a more complex picture. MHT is prescribed primarily to relieve troublesome menopausal symptoms: hot flushes, night sweats and vaginal symptoms, and also helps prevent bone loss and fractures. It is not a heart-prevention pill, but its relationship with cardiovascular risk is relevant for any woman considering it.
Our understanding of MHT and the heart has changed substantially over the past two decades. Early large trials raised alarm, but they largely studied women who started hormones in their 60s, long after menopause, using older formulations. When the data were re-analysed by age at the time starting treatment, and newer studies focused on women closer to menopause, a more reassuring picture emerged: for healthy women who begin MHT before 60 or within about 10 years of their final period, cardiovascular risks appear low.
Some studies suggest possible cardiometabolic advantages, but the evidence for hard clinical benefits such as fewer heart attacks or lower mortality remains inconclusive, and MHT is therefore not recommended as a cardiovascular prevention strategy.
Timing and formulation matter.
Modern MHT uses low-dose oestradiol, preferably via the skin (patches or creams) rather than taken orally, since transdermal oestrogen bypasses the liver and avoids the increase in clotting factors associated with oral preparations. Starting hormones around the time of menopause looks very different from starting them in the late 60s or 70s, when baseline cardiovascular risk is already higher.
Current guidelines from menopause societies in North America and Europe recommend a personalised approach: using the lowest effective dose, reviewing risks regularly, and making decisions jointly with a clinician who understands both a woman’s menopausal symptoms and her cardiovascular profile.
In late 2025, the US Food and Drug Administration began removing the broad warnings that had linked MHT to cardiovascular disease, breast cancer and dementia across the board, describing those old labels as misleading when applied to healthy women in their 50s (this regulatory change occurred after the primary literature for this article was gathered). The most prominent warning that remains is for endometrial cancer with oestrogen-only therapy in women who still have a uterus, underlining the importance of using an adequate progestogen alongside oestrogen in those cases.
Newer cardiometabolic therapies
Several newer drug classes offer promising additional tools, especially for women with obesity, diabetes or very high cholesterol.
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), such as semaglutide, were first developed for diabetes but are now also used for obesity. A large analysis of clinical trials found that GLP-1 RAs reduce blood pressure and lower the risk of myocardial infarction, with
neutral effects on stroke. The landmark SELECT trial showed that weekly semaglutide (at 2.4 mg) reduced major cardiovascular events by about 20% in people with obesity and existing CVD but without diabetes, an advance that is already changing clinical guidelines.
For people whose LDL remains high despite maximally tolerated statins, PCSK9-targeting molecules (monoclonal antibodies) can lower LDL by around 50–60% and have been shown to further reduce cardiovascular events.
Recent sex-specific analyses indicate that women and men achieve similar LDL reductions and cardiovascular benefits from these drugs.
Unfortunately, as with statins, women are somewhat less likely to receive them in practice – illustrating a persistent treatment gap across lipid-lowering drug classes that warrants urgent attention.
Where is research heading?
The trend is towards a more personalised approach.
Current priorities include better understanding of how menopause-related lipid and metabolite shifts translate into plaque formation, and identifying which women are at greatest risk so that prevention can be more personalised. There is also a call for more trials designed from the outset to answer sex-specific questions, including optimal use of statins, GLP-1 RAs, PCSK9 inhibitors and MHT across different menopausal stages – particularly large randomized controlled trials powered to detect differences in clinical events (heart attacks, strokes, deaths) that can establish whether the promising but inconclusive cardiovascular signals seen in studies using surrogates as endpoints and observational studies translate into robust evidence that is guideline-changing.
For now, the key message is that cardiovascular disease is not just a “man’s disease”, and that peri- and post-menopause is a crucial window to analyse your risk factors, adjust your lifestyle and diet, and, when appropriate and with your medical specialist’s recommendation, use evidence-based medications to protect your heart and blood vessels in the long-term.
The AXA science philanthropy is now part of the AXA Foundation for Human Progress, which brings together the commitments of AXA Group and Mutuelles d’Assurances in the fields of Science, Nature, Solidarity, and Culture. Before 2025, the global science philanthropy was held by the AXA Research Fund, which has supported over 750 projects around the world since its inception back in 2007. To learn more, visit Axa Foundation for Human Progress.
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