This one is personal. And that is exactly why I need to write it.

Women cardiovascular risk is assessed, communicated, and responded to too often inadequately – and a recent paper on women, lipids, and cardiovascular disease made that plain once again. Not because the science does not exist, but because it has not been adequately translated into clinical practice or into the conversations women are having with their doctors.

Cardiovascular disease remains the leading cause of death in women. Yet women’s risk is still too often missed. The fastest relative rise in atherosclerotic cardiovascular disease mortality is now occurring in women aged 45–64 — the exact cohort in which perimenopause, hormonal transition, and a lifetime of accumulated cardiovascular exposure converge. This is not a statistical footnote. It is a clinical emergency hiding in plain sight.

I want to address that here, as both a clinician and as a patient.

My own picture

I am a former elite athlete. Lean, disciplined, physically active, and deeply engaged with my own physiology for the better part of two decades. From the outside, I look like someone at low cardiovascular risk.

My ApoB, Lp(a), and LDL-C are slightly raised. And they matter.

This is precisely the kind of finding that gets minimised in clinical conversations — particularly for women, particularly for those who look and function like the picture of health. The reflex is to attribute elevated lipid markers to diet. To suggest dietary modification and monitor. To contextualise the numbers as “not concerning” given an otherwise healthy lifestyle.

That reflex is not always wrong. But it is frequently incomplete. And the incompleteness is doing harm.

Why cholesterol is not simply a diet story

Cholesterol and associated lipid particles respond to a web of factors that have nothing to do with how many eggs someone ate last week. Genetics plays a major role — Lp(a) in particular is almost entirely genetically determined and lifestyle cannot meaningfully modify it for the vast majority of people. Hormonal environment shapes lipid metabolism significantly. Inflammatory load, liver function, thyroid status, cortisol, recovery patterns, and life stage all sculpt the lipid picture in ways a simple dietary conversation cannot address.

For women specifically, cardiovascular risk extends beyond traditional markers to a set of female-specific factors that most standard risk assessments ignore entirely: pregnancy complications, gestational diabetes, hypertensive disorders of pregnancy, PCOS, premature menopause, chronic kidney disease, autoimmune inflammatory disease, and diabetes. Each carries independent cardiovascular significance, and standard frameworks consistently undercount how common these are in women.

Female lipid biology: dynamic, not static

Lipids shift significantly across a woman’s life — during adolescence, pregnancy, breastfeeding, and menopause. Male-derived reference ranges do not capture this. Lp(a) rises in pregnancy and again around menopause, with high Lp(a) becoming more prevalent in women after 50. Clinically, this matters because Lp(a) is largely genetically determined yet can change: pregnancy, menopause, and inflammatory states may all alter levels. A single lifetime measurement — as current guidelines in many settings suggest — may be inadequate for women moving through these transitions.

Perimenopause adds a further layer that most clinical encounters fail to address. Oestrogen is cardioprotective in multiple ways: it influences HDL/LDL particle distribution, supports endothelial function — the health of the inner lining of blood vessels — and exerts anti-inflammatory effects throughout the vasculature. As oestrogen declines, all of these protections withdraw.

Women’s cardiovascular risk rises sharply in the decade following menopause — often catching both patients and clinicians off guard, in women who had previously unremarkable lipid panels and no cardiovascular concerns.

What the research tells us about women cardiovascular risk

The Women’s Health Study — one of the most rigorous and long-running cardiovascular studies in women — followed nearly 28,000 participants for over 30 years. Key findings, presented at the European Society of Cardiology Congress 2024 and subsequently published in the New England Journal of Medicine, demonstrated that LDL cholesterol, Lp(a), and C-reactive protein (CRP) measured at midlife predict a woman’s cardiovascular risk over the subsequent three decades with striking accuracy.

Women with the highest LDL levels showed a 36% increased relative risk of cardiovascular disease over follow-up. Those with the highest Lp(a) showed a 33% increased relative risk. These are not trivial associations — and they unfold over a timeframe that standard 10-year cardiovascular risk calculators are structurally unable to capture. Which is precisely why relying on those calculators alone, for women in midlife, is clinically insufficient.

Lp(a) — lipoprotein(a) — deserves specific attention because it is both independently significant and systematically undertested. The National Lipid Association now recommends measuring Lp(a) at least once in every adult. Levels at or above 50 mg/dL place a person in the high-risk category. Despite this, a significant proportion of adults have never had the test — because Lp(a) does not appear on most standard lipid panels.

Cardiovascular specialists increasingly recognise ApoB — apolipoprotein B — as a more accurate predictor of events than LDL cholesterol alone. ApoB reflects the actual number of atherogenic particles in circulation, not the quantity of cholesterol those particles carry. Two people with identical LDL-C can have very different ApoB levels and therefore very different atherogenic burdens. For precision risk assessment, ApoB matters — and it is worth requesting explicitly.

The hormonal context that most clinical conversations miss

I want to stay with the oestrogen piece, because it is systematically underappreciated and the consequences of that underappreciation are serious.

Oestrogen has multiple direct effects on the cardiovascular system: it promotes vasodilation through nitric oxide pathways, reduces LDL oxidation — a key step in atherosclerotic plaque formation — maintains arterial elasticity, raises HDL-cholesterol, and modulates inflammatory signalling within the vessel wall.

When oestrogen declines — as it does in perimenopause, typically through the late forties and into the fifties — all of these protective effects are progressively withdrawn. The cardiovascular system, which has been operating in a broadly protective hormonal environment for decades, now has to manage without that protection. Lipid patterns change. Inflammatory markers may rise. Arterial stiffness increases. Blood pressure tends to climb.

For women who are already carrying elevated ApoB or Lp(a) — as I do — this hormonal transition adds meaningful additional cardiovascular risk on top of an already elevated baseline. The clinical response to this should be attentive and personalised, not generic. The question is not simply “should we monitor?” but “what does monitoring change, and what intervention is indicated?”

This is a conversation I have regularly with patients who have been told their lipids are “borderline” or “not quite high enough to treat” — a framing that makes sense if you are assessing a 40-year risk horizon through a 10-year lens, but is considerably less adequate when you start thinking in terms of lifetime atherogenic exposure and the physiological changes that perimenopause is about to introduce.

My own picture in full

My cardiovascular risk picture is not simply a lipid story, and it would be misleading to present it as one.

I have experienced a prolonged period of elevated cortisol — the biological residue of years of elite training, of childhood adversity, and of the significant neuroendocrine consequences of Long COVID. Cortisol, beyond its effects on metabolism and immune function, has direct cardiovascular consequences: it raises blood pressure, promotes atherogenic lipid changes, and contributes to endothelial dysfunction through inflammatory mechanisms.

I carry the imprint of early adversity in my nervous system — a shaped HPA axis baseline that has influenced my cortisol rhythms for decades. This is not unique to me. It is the biology of a very large proportion of high-achieving adults who grew up in difficult circumstances and who have — with considerable skill and discipline — created functional, successful lives, while the nervous system underneath continues to run the programme it learned early.

Long COVID has added additional complexity: inflammatory sequelae, altered autonomic function, and cardiovascular changes that researchers are only beginning to fully characterise. The post-viral literature increasingly points to lasting effects on endothelial function, microclotting, and autonomic regulation — all of which are relevant to cardiovascular risk in ways that are not captured by a lipid panel alone.

This is why I value medicine that holds complexity. That does not reduce female cardiovascular risk to a cholesterol number, or a cholesterol number to a dietary choice. That understands the hormonal, inflammatory, neuroendocrine, and genetic landscape that shapes the lipid picture and the overall cardiovascular risk profile — and responds to that whole picture with clinical precision.

The treatment gap: women are less likely to receive prevention

Women are also less likely to receive appropriate lipid-lowering treatment despite clear evidence that prevention works. That gap in care has consequences — measured in events that were preventable and in women who were reassured when they should have been investigated.

Clinicians reach for the standard 10-year risk calculator. A reassuring number comes back. The conversation ends. But that calculator was built predominantly on male data — it ignores female-specific risk factors, fails to capture lifetime atherogenic exposure, and cannot reflect the cardiovascular inflection point that perimenopause represents. The calculator is not wrong. It is simply the wrong tool for the question.

What preventive cardiovascular medicine for women should actually look like

The answer is not more of the same assessment interpreted the same way. Good preventive cardiovascular medicine for women means: advanced lipids — not just total cholesterol and LDL-C, but ApoB and Lp(a) in context; metabolic and inflammatory insight, because women cardiovascular risk is never simply a lipid story; stress physiology and recovery capacity, which carry direct cardiovascular consequences through cortisol, autonomic function, and inflammatory tone; and where appropriate, imaging — coronary artery calcium scoring or carotid intima-media thickness — rather than relying on bloodwork alone.

The additional cost of ApoB and Lp(a) testing is minimal. The additional information can fundamentally change clinical decisions and the conversations that follow.

Test earlier. Interpret more intelligently. Stop waiting for obvious disease before acting. By the time cardiovascular disease is obvious, the window for the most impactful prevention has often passed.

Fit is not the same as protected. I am a former elite athlete with raised ApoB and Lp(a), a post-COVID inflammatory history, and a shaped HPA axis from years of high-load sport and early adversity. My external presentation does not tell the cardiovascular story my biomarkers tell. Neither does that of many of the women I see in clinic.

Women deserve a more honest, more sophisticated cardiovascular conversation — one that does not reduce female risk to a cholesterol number or a cholesterol number to a dietary choice. The science to do this well already exists. The will to translate it into routine clinical practice is what we are still building.

If you are a woman in midlife who has not had a comprehensive cardiovascular assessment — including ApoB, Lp(a), hormonal markers, and inflammatory markers — this is worth prioritising. To explore how Wellgevity approaches preven