📈 The Great Midlife Cholesterol Conundrum

I’ll be honest. Cholesterol feels like the bane of my existence sometimes. It tends to run high in my family, and mine has never been low. But when I hit the menopause transition, it took on a life of its own, shooting up about 30 points and with a few biomarkers going from yellow/borderline straight into the red. 

But my picture is also hella complicated–and I know it is for many of you, too, because I hear from you. Breaking it down: my total cholesterol is high; my LDL cholesterol is borderline high; my ApoB is high; my Lp(a) is low; my triglycerides are low; my HDL is very high; my TG/HDL-C ratio is excellent, and my total cholesterol to HDL ratio is also excellent. In short, I’ve got a good metabolic profile with a genuinely elevated particle count riding on top of it. 

As I’ve discussed on a podcast 2 years ago, in attempts to understand what impact this was having on my arteries (where it matters), I went to have a Cleerly-enabled coronary computed tomography angiography (CCTA), which uses AI-enabled software to help characterize coronary plaque composition and cardiovascular disease risk. My coronary CT angiogram (this is a full Cleerly plaque analysis, not just a calcium score) found Stage 1 atherosclerosis — the mildest detectable category on a 0-3 scale — with only 1.6% percent atheroma volume (PAV) overall. For context, Cleerly's own staging framework defines Stage 1 as >0-5% PAV, so I’m sitting near the very low end of even the mildest band.

That’s great. But I still don’t like those elevated numbers, especially the ApoB, which counts the actual number of atherogenic (artery-clogging) particles circulating in your blood. So, as I’ve also discussed, I’ve worked with my doctor to try some stuff. For a while I took a supplement with phytosterols and berberine, which lower LDL primarily by blocking cholesterol absorption in your gut. It worked like a charm–dropping my LDL by 30 points…until it stopped working. Turns out your liver constantly monitors your cholesterol levels. When it senses a sudden drop because your gut is absorbing less, your liver may try to keep things balanced by increasing its own internal production of cholesterol to make up for the loss. That was me. 🙋🏻‍♀️

Same thing happened with red yeast rice, even though it works on a different mechanism. Red yeast rice successfully blocks the liver's cholesterol production. However, if you are genetically a "hyper-absorber" of cholesterol (again, 🙋🏻‍♀️), your body will notice the drop in blood levels and respond by cranking up its absorption of dietary cholesterol from your digestive tract to compensate. Yay.

Menopause, of course, makes this all worse. Estrogen helps your liver clear LDL cholesterol out of your blood. As estrogen declines through the menopause transition, that clearance slows down, and cholesterol backs up. A large cohort study tracking women through menopause found that LDL, total cholesterol, and ApoB start climbing roughly five years before your final period, and about 40% of women worldwide are dealing with dyslipidemia — abnormal cholesterol or triglyceride levels — by midlife. Some women see it happen fast: one study found total and LDL cholesterol jumped about 7% in a single year during the premenopause-to-postmenopause transition.

So if your numbers seemed to shoot up out of nowhere, you're not imagining it, and you're definitely not alone…I’m right there with you.

Why I’m not just shrugging it off

Though right now my real risk appears low, I’m not just shrugging it off because both of my parents have had heart attacks (later in life, and there was smoking and other elements involved, but still). After consulting with my doc, who works with athletic women in our demographic, I’ve been making some more adjustments to my diet–specifically eating more complex carbohydrates.

Very high HDL (mine is 102) and very low triglycerides (mine are 45) paired with elevated LDL/ApoB is a recognized pattern, sometimes called the "lean mass hyper-responder" profile in the research literature — it shows up disproportionately in lean, metabolically fit people, and gets notably more pronounced on lower-carbohydrate eating patterns. To be clear, I don’t intentionally restrict carbs, but I also have a history of just not getting enough and accidentally wading into low energy availability territory. So it’s worth a shot.

I’m also going to look at getting another scan next year. Imaging research has found that arterial plaque builds up roughly twice as fast in postmenopausal women as in similarly aged men — even among women already on statins (which I’m not…yet), so I want to stay on top of screening.

Other levers to pull

If you’re in the same frustrating lipid boat as me, there are other evidence-backed levers you can pull (along with exercise, which I know you’re already doing):

Diet. A new randomized crossover trial in Nature Communications shows a whole-food, plant-based diet dropped LDL by nearly 18% compared to a standard diet — in just four weeks. Worth knowing: that study was done in adults with a genetic cholesterol disorder (familial hypercholesterolemia), not midlife women broadly. But it's a strong illustration of how powerful diet can be on LDL, and the effect held regardless of sex. It lines up with what a broader meta-analysis of vegetarian and vegan diets across the general population also found: consistent, meaningful LDL and ApoB reductions. You don't have to go fully plant-based to benefit — shifting your plate in that direction, more legumes and fiber, less saturated fat, may move the needle.

Hormone therapy. Menopause hormone therapy is not a primary treatment for cholesterol. However, some women have found estrogen can decrease LDL cholesterol and increase "good" HDL cholesterol. But it's not a sure thing (and didn't budge mine). Also worth noting: the pill and the patch don't behave the same way. A January 2026 meta-analysis found oral estrogen raises HDL more than the patch — but also raises triglycerides more, with no real difference between the two on LDL. One update for today's regimens specifically: micronized progesterone, now the standard pairing with estradiol, doesn't blunt those lipid benefits the way the older synthetic progestins used in past trials did.

Statins. A new JAMA analysis examined the 2026 national cholesterol guidelines and determined a lot more folks should be recommended statin therapy. In fact, an estimated 21.5 million more US adults are now statin-eligible, and women ages 50 to 59 saw the single biggest jump in new eligibility — over a quarter of that age group. Statins reduce heart attack and stroke risk by about 20% in women, and women have historically been under-screened and undertreated with them.

The main concern with women in our audience is statin-related muscle pain. The good news is there are options if you experience it. According to the Cleveland Clinic, lipophilic statins (meaning they passively diffuse into the muscle) like atorvastatin (Lipitor®), simvastatin (Zocor®), and fluvastatin (Lescol®) may be more likely to cause muscle aches, while hydrophilic statins like rosuvastatin (Crestor®) and pravastatin (Pravachol®) may cause fewer. Worth flagging: the evidence for that distinction is actually mixed — a large 2021 cohort study of 15+ million patients found no consistent muscle-risk advantage for hydrophilic statins at equivalent doses. Still, switching statin type is a low-risk thing to try, and each woman responds differently.

If my current approach falls short, this may be my next route. Stay tuned.