Cardiometabolic, decoded.

The honest TLDR.

Cardiovascular disease remains the leading cause of death for American women. It kills more women annually than all cancers combined. Despite that, the conversation around women's heart health still tends to default to a script — "watch your cholesterol, eat less salt, exercise" — that's a generation behind the research. The diagnostic side of that conversation is worse: most women walk out of an annual physical with a panel of four numbers that was designed in the 1980s and hasn't meaningfully evolved since.

The standard annual physical typically runs total cholesterol, LDL, HDL and triglycerides. Those numbers aren't useless. They are, however, an incomplete picture — particularly for women, whose cardiovascular risk profile diverges from men's in ways that the standard panel was never calibrated to catch. Studies on women's-specific risk markers have been accumulating for two decades. Most U.S. primary care offices haven't caught up.

The modern panel worth knowing about — and worth asking your provider about — adds five things to the standard set: ApoB (the count of atherogenic particles), Lp(a) (a genetic risk marker tested once in your life), hsCRP (vascular inflammation), fasting insulin or HbA1c (metabolic dysfunction, the most under-tested cardiovascular driver in women), and a coronary artery calcium score where clinically indicated. Each gets walked through below. None of this is a treatment plan. All of it is the conversation worth having earlier than most women are told to have it.

Why women's cardiovascular risk has been under-measured.

Some history is worth being plain about. For most of the modern era of cardiovascular research, trial cohorts were predominantly male. The landmark studies that shaped current treatment thresholds, current reference ranges, and current symptom expectations — they were largely run on men. Women were under-enrolled, often deliberately excluded, and the resulting data was generalised across sexes as if the underlying biology behaved the same way. It doesn't.

The cleanest example is symptom presentation. The classic Hollywood heart attack — crushing chest pain, left-arm radiation, clutching the chest — is the typical male presentation. Women more often present with fatigue, jaw or back pain, nausea, shortness of breath, and a vague sense of unease. Because the textbook description was calibrated to men, women presenting with the "atypical" pattern — which is in fact typical for them — have been historically more likely to be sent home from an ER, told it was anxiety, told it was reflux. This is a documented gap, not a complaint.

The other persistent oversimplification is the framing that "heart disease starts after menopause" for women. It doesn't start then. It accelerates then. Plaque begins building in the 30s. The risk that becomes statistically visible in a woman's 60s is the result of a process that has been running since her 30s and 40s — quietly, without symptoms, and without being measured. Women in their 30s and 40s deserve the same modern diagnostic panel that longevity-focused men have been asking for and getting. The case for testing earlier, not later, is straightforward: if you wait for a symptom, you have waited too long to change the trajectory cheaply.

"Plaque is a 30-year project. The standard annual physical assumes you'll notice it as a 60-year emergency."

The five markers worth understanding.

None of these are exotic. None of them require a specialist referral in most cases. All of them are available through standard labs, and several are now included by default in direct-to-consumer panels like Function Health. The case for them, in plain terms:

The first four are blood work that can be added to a standard panel for relatively modest cost. The CAC is a separate imaging study, generally a one-time conversation rather than a recurring test. Together they answer questions the standard four-number panel simply can't.

What "in range" misses — particularly for women.

U.S. labs flag results "out of range" at population statistical cutoffs. Those cutoffs are not the same as "optimal for cardiovascular longevity." They are not the same as "optimal for a 42-year-old woman entering perimenopause with a family history of early cardiac events." They are a statistical convenience, and they should be read that way.

The clearest example is ApoB. Many cardiology and longevity specialists — Peter Attia, Mark Cucuzzella, and others working in the preventive-cardiology space — argue that the population "in range" for ApoB is meaningfully looser than what the evidence supports for long-horizon risk reduction. Their argument, in plain terms, is that women particularly benefit from tighter ApoB targets than the lab default suggests, and that the relevant question isn't "am I out of range" but "am I in a range associated with the lowest long-term event risk." This is a discussion worth having with your provider, not a number we'd quote at you here. The framing matters: "in range" is a screening cutoff, not an optimisation target.

The same logic applies to Lp(a). There's currently no widely available treatment to lower Lp(a) directly — therapeutics are in late-stage trials but not yet standard of care. The argument for testing it anyway is that knowing your number changes how aggressively a thoughtful provider would manage your modifiable risk factors. A woman with high Lp(a) and moderately elevated ApoB is a different conversation from a woman with low Lp(a) and the same ApoB. The standard panel can't see that distinction.

HDL is the third area where the conventional reading is increasingly out of step with the research. The old framing — "higher HDL is better, that's the good cholesterol" — has been substantially complicated by the past decade of data. Newer research suggests it's the functionality of HDL particles, not the quantity, that matters for cardiovascular protection. Very high HDL in women is no longer reassuring on its own. It's another input into a fuller picture, not a green light.

The evidence on all of this has moved. Many specialists argue for tighter targets and more nuanced interpretation than a standard primary care panel typically applies. Worth discussing with your provider directly — particularly if your provider's read of your results is "everything looks normal, see you next year."

When in life this becomes more important.

The honest answer is "earlier than most women are told." A more useful answer breaks it down by decade.

5.1 30s — establish a baseline

The case for measuring ApoB and Lp(a) at least once in your 30s is straightforward. Lp(a) is essentially stable across your life — the sooner you know it, the longer your runway to act on the information. ApoB measured in your 30s gives you a baseline against which to read the changes that will come in your 40s and 50s. You don't need to retest annually at this stage in most cases. You do want the number on file.

5.2 40s + perimenopause — re-test annually

This is where the lipid picture starts moving. Declining estradiol — which begins well before the cessation of periods — changes how the body handles lipids. ApoB tends to rise. Visceral fat distribution shifts. Insulin sensitivity tends to drop. The 40s are the decade where the difference between "I'll deal with this later" and "I'll deal with this now" compounds. Annual re-testing of the modern panel, plus a real conversation about the perimenopause connection, becomes worth the time.

5.3 50s + post-menopause — CAC conversation

Cardiovascular risk in women accelerates measurably after menopause. The estrogen-protective effect winds down. This is the decade where the coronary artery calcium conversation becomes most relevant — particularly if blood markers have been creeping upward, if there's family history, or if any of the earlier markers have flagged. A CAC score in your 50s gives you and your clinician a much clearer picture of whether plaque is already there, and how aggressively to act on it.

5.4 Family history of early cardiac events — test earlier

"Early" generally means before 55 in male first-degree relatives, before 65 in female first-degree relatives. If you have that history, the timeline above shifts forward. Baseline measurement in your late 20s isn't unreasonable. Annual measurement starting in your 30s isn't unreasonable. A CAC conversation in your 40s rather than 50s isn't unreasonable. Family history doesn't determine outcome — but it determines how loud the case is for measuring early.

Lifestyle levers backed by actual evidence.

None of these replace measurement, and none of them are a substitute for a real clinical conversation when the numbers warrant it. They are the levers that the evidence consistently supports, ranked roughly by how robust the evidence is for women specifically.

Resistance training — the strongest evidence base for women over 35

If there's a single lever with the most robust evidence for cardiometabolic health in women over 35, it's resistance training. The benefits run through multiple pathways at once — improved insulin sensitivity, preserved lean mass through perimenopause and beyond, improved lipid handling, better blood pressure regulation, and a meaningful contribution to bone density. Two to three sessions a week with real intensity and real recovery between them outperforms five mediocre sessions. The under-rated point: resistance training matters more in women's 40s and 50s than it does in their 20s, precisely because the metabolic environment is harder to maintain by default.

Sleep duration and quality — particularly through perimenopause

The evidence linking chronically short or fragmented sleep to elevated cardiovascular risk has grown sharper over the past decade. The mechanism runs through blood pressure regulation, inflammatory markers (including hsCRP), insulin sensitivity, and cortisol patterning. The complication for women: perimenopause routinely fragments sleep — the 3 a.m. wake-up, the night sweats, the lighter overall sleep architecture. Protecting sleep through that window is harder and arguably more important than at any earlier stage.

Dietary saturated fat — where the evidence has genuinely gone back and forth

This is the area worth being honest about. The mid-20th-century framing that all saturated fat is uniformly cardiovascular-harmful has been substantially complicated. The current preponderance of evidence still supports moderating saturated fat intake — particularly from highly processed sources — but the categorical "saturated fat is bad" framing of the 1990s has not held up. Dietary patterns matter more than individual nutrients. Mediterranean and similar whole-food patterns continue to have the strongest evidence base for cardiovascular outcomes in women. We won't pretend the literature has been clean on this one. It hasn't.

Alcohol — the evidence has reversed

The old "one glass of red wine a day is cardioprotective" finding has not survived rigorous re-analysis. More recent and better-designed studies suggest the protective effect was largely a confounding artefact — the people who drank moderately also had other healthier behaviours, and the moderate-drinking effect attached to those, not to the alcohol. The current evidence base trends toward: less is better, none is better still, and the cardiovascular case for "moderate" drinking has weakened substantially. Particularly relevant for women through perimenopause, where alcohol also fragments sleep, raises overnight heart rate, and exacerbates the metabolic shifts that are already underway.

Stress and cortisol patterns

Chronic stress is a real cardiovascular contributor — not in the hand-wavy way the wellness conversation sometimes implies, but through measurable elevations in cortisol, blood pressure, inflammatory markers and insulin resistance. The intervention evidence is messier than the association evidence. What is reasonably clear: practices that down-regulate the stress response — adequate sleep, regular movement, deliberate decompression, social connection — track with better cardiovascular markers over time. "Just relax" is not useful advice. "Build a daily structure that lowers your baseline stress load" is.

When to escalate to a clinician.

Heme is an editorial layer, not a clinic. The bloodwork conversation is a starting point — it gives your clinician a more useful picture than the standard panel produces. There are specific situations where escalating sooner rather than later is genuinely warranted.

To be clear: any new chest pressure, severe shortness of breath, jaw pain or sudden unexplained fatigue with associated symptoms warrants urgent care, not a future appointment. The female-pattern presentation is real, and it has historically been under-recognised. If something feels seriously wrong, treat it that way.

These aren't a script. Your clinician will steer the conversation where it's most useful given your specific history. They are a starting point that tends to widen the panel, sharpen the interpretation, and produce a clearer plan than the default annual physical usually yields.