Do I Actually Need to Take a Statin?
There is currently an unopened box of statins traveling around the world with me.
SHIMA in Japan - A sandwich that definitely was not good for my cholesterol, but totally worth it :)
A doctor prescribed them. Every decent primary-care or concierge doctor who sees my bloodwork asks some version of: why are you not already taking this?
They have a point.
My latest numbers (tested regularly via Function Health, you can order here):
Total cholesterol: 309 mg/dL
LDL-C: 180
ApoB: 128
LDL particle number: 2,013
Non-HDL cholesterol: 195
Those aren’t numbers I can explain away as a slightly enthusiastic laboratory reference range.
And yet, I haven’t opened the box.
Which is slightly absurd because I fundamentally believe in early intervention. The whole premise of longevity medicine is that if you can see risk developing decades before disease, why wait?
Apparently, unless the intervention is a pill I might have to take for the next 50 years. And the subject in question is me.
Disclaimer: Should you take the statin? I don’t know. I’m not a doctor. But I’ve been thinking about cholesterol much longer than I’ve been thinking about longevity, because it’s been a family conversation around our table for as long as I can remember. This is not medical advice. It’s the personal journey of someone trying to understand the science, think through the trade-offs, and build a framework for making a decision. Your risk, biology and treatment options may look very different, so you should always make these decisions with a doctor who knows your history.
I’ve had high cholesterol since I was 15
My mom kept every blood test in a folder, printed on paper, because mothers apparently understood longitudinal health records before healthcare did.
My cholesterol was already over 250 when I was around 15.
Doctors noticed. They cared. But I was young, so nobody did much about it.
Twenty years later, I find myself wondering: if I were 15 today, would the recommendation be different?
Possibly.
For children with familial hypercholesterolemia, long-term follow-up suggests that starting statins in childhood can meaningfully slow the development of atherosclerosis and reduce cardiovascular events later in life. That doesn’t mean every teenager with cholesterol above 200 needs a statin.
It does mean that “you’re young, therefore we can ignore it” is increasingly hard to defend when the underlying risk is genuinely high.
And mine certainly looks familial.
My mom’s has high cholesterol. My father has it and takes a very low dose of a statin. There is stroke history on his side - and family history for this matters.
Then there is my grandmother.
She is 94, extremely sharp, independent, doesn’t take a statin, and has had total cholesterol somewhere around 350–400 for as long as I can remember discussing it.
She is an absolutely terrible scientific study.
She is also a very effective reason to wonder whether a number tells the whole story.
First lesson: “high cholesterol” is almost a useless sentence
The 309 is the number that looks terrifying on my Function dashboard.
It isn’t actually the number I care about most.
What matters more is what is transporting that cholesterol around.
My simplified version:
LDL-C = how much cholesterol is being carried inside LDL particles.
ApoB = a proxy for the number of atherogenic particles circulating.
LDL-P = another measurement of particle number.
Lp(a) = a largely genetically determined lipoprotein-associated risk factor.
HDL-C = cholesterol carried in HDL particles. Calling it simply “good cholesterol” is increasingly unhelpful.
My ApoB of 128 and LDL-P of 2,013 are what make it harder for me to wave away my LDL.
A large body of genetic, observational and randomized-treatment evidence supports ApoB-containing lipoproteins as causal drivers of atherosclerotic cardiovascular disease. The basic issue is cumulative exposure: more atherogenic particles circulating for more years creates more opportunity for those particles to enter the arterial wall.
Being young doesn’t eliminate that problem. In some ways, it makes the duration part more relevant.
But everything else looks pretty good
This is where I think many women get confused.
My panel also says:
HDL: 114
Triglycerides: 54
Lp(a): 13
hs-CRP: 0.2
A1c: 5.0%
LDL pattern: A
If I were using the cholesterol vocabulary most of us grew up with, I might say: yes, my bad cholesterol is high, but look at all this excellent good cholesterol.
Unfortunately, biology isn’t that tidy.
Very high HDL does not appear to simply cancel the cardiovascular risk associated with elevated ApoB-containing particles. And “good cholesterol” has become one of those health phrases that survives because it is convenient, not because it accurately describes the physiology.
Cholesterol itself isn’t bad. We need it for cell membranes, steroid hormones, bile acids and normal human function.
The problem is where it is being carried, how many atherogenic particles are circulating, and for how long.
What about healthy women with high cholesterol?
This is the part I keep hearing anecdotally.