Lipid Panels, Longevity, and the Number Your Doctor Probably Isn't Testing

longevity Jun 11, 2026

Part of the Longevity Metrics Series: Auditing My Health as I Turn 55

My 55th birthday is June 19th. This year, for the first time, I'm auditing myself across ten longevity markers I've chosen to track. Grip strength, sleep, VO2 max, and HRV are the first four. If you've missed any of them, they're here .

Metric 5: the lipid panel. This one got complicated. In a fun(?) way.

Before I get into it, I want to be upfront about something: parts of this post took me into territory that is fast-changing and is at the genuine edge of my understanding. I used Claude to help me research and synthesize material across a rapidly evolving field. That's worth saying out loud, because as I'm sure you know, AI can misinterpret studies, miss nuance, and reflect the biases already present in the research it summarizes. But so can doctors and researchers, as we've seen time and again throughout history.

Current consensus isn't the same thing as settled truth, and I doubt we'll land on that in my lifetime.

My philosophy is to do the best we can with what we currently know, while holding it lightly enough to update when the evidence does. That's exactly why I track my lipids in the context of a lot of other things I’m tracking.

First, a Note on Language

This post uses some medical shorthand. I'll define each term the first time it appears, then use it freely. Think of this section as a quick orientation rather than a glossary.

The key terms you'll encounter:

-ApoB: a protein that counts the harmful particles in your blood, explained fully below

-Lp(a): a genetically determined cholesterol variant that most people have never been tested for but as you’ll learn, should

-TG/HDL ratio: a simple calculation from your standard panel that tells you a lot about your metabolic health

-CAC score: a CT scan that detects plaque in your coronary arteries

-and a handful of others I'll define as they come up.

The Standard Lipid Panel Isn't Enough

The first thing you should know is that the standard lipid panel is no longer considered sufficient, yet most doctors haven't caught up.

The test most people receive once a year reports four numbers: total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. This panel was designed as a population screening tool. It was built to efficiently identify people at elevated risk across a large group. It wasn't designed to tell you, specifically, what's happening in your arteries.

Let me explain why that distinction matters.

LDL cholesterol is the number most people fixate on, the one that determines whether a doctor starts talking about cholesterol-lowering medication like statins. But it measures the cholesterol content inside LDL particles, not the particles themselves, not how many of them are circulating, not how dangerous they are individually. Think of it this way: if harmful particles in your bloodstream are delivery trucks, LDL cholesterol tells you how much cargo they're carrying. It doesn't tell you how many trucks are on the road.

Two people can have identical LDL cholesterol numbers and have radically different risk profiles depending on factors the standard panel doesn't see. One person might have a small number of large, relatively harmless particles. Another might have a much larger number of small, dense particles that burrow into arterial walls more aggressively. Same number, very different story.

Total cholesterol is even less useful on its own. It can be high because your protective HDL is high, which is actually good. It can be elevated because of Lp(a), a separate harmful particle that most lipid panels don't even report. The number alone tells you almost nothing, yet a huge industry has been built around lowering this number.

The field is increasingly clear on this: the standard panel is a starting point, not an endpoint.

The Numbers That Actually Matter

ApoB: How Many Trucks Are on the Road

Apolipoprotein B, or ApoB, is a protein that sits on the surface of every harmful particle in your bloodstream: every LDL, every VLDL (a precursor to LDL), and every Lp(a) particle each carries exactly one ApoB molecule. Because of this one-to-one relationship, ApoB gives you a direct count of the total number of artery-damaging particles circulating in your blood.

This is the distinction that matters in practice. The standard panel tells you how much cholesterol those particles are carrying. ApoB counts the particles themselves. And it's the particles that embed in arterial walls and initiate plaque formation. A systematic review published in 2024 analyzing fifteen studies involving 593,354 participants found that ApoB outperformed LDL cholesterol as a cardiovascular risk predictor in nine out of nine head-to-head comparisons.

That's a fairly decisive result, yet most people have no idea what their number is. ApoB isn't included in a standard lipid panel but it's available through any major lab with a standard blood draw, no specialist required.

The National Lipid Association sets the primary prevention target for people at moderate cardiovascular risk at below 90 mg/dL, though in practice most clinicians evaluate this alongside other markers rather than as a standalone number.

Some longevity physicians, Peter Attia most prominently, argue that the clinical targets set by guidelines aren't ambitious enough for someone genuinely optimizing for a long healthspan. The logic is straightforward: plaque builds up over a lifetime as a function of how many artery-damaging particles are in circulation multiplied by how many years they have to do damage. So even if your ApoB is below the clinical threshold, it's still contributing to accumulation. By that reasoning, the real goal isn't "below 70." It's as low as possible, which Attia puts at 20 to 30 mg/dL.

I understand that argument. I'm not following it.

Getting ApoB to 20 or 30 mg/dL almost always requires medication. Statins are the familiar option. There's also a newer class of injectable drugs called PCSK9 inhibitors that work by blocking a protein that would otherwise remove cholesterol receptors from the liver, effectively forcing the liver to clear more LDL from the blood. These drugs are impressive at lowering ApoB.

My position on them is that I'm not confident we have enough long-term data on aggressive pharmaceutical intervention to know what we're trading away.

That's not a fringe view. It's the same reasonable skepticism that should have made us slower to recommend margarine and faster to question the blanket prescription of statins for everyone over 50. The evidence base for these medications is real. The multi-decade hindsight isn't.

I also want to be clear about what I'm choosing instead: not ignorance, not indifference. I track these numbers annually. I understand my numbers. I try to stay up to date on the research, with the full expectation that current truths will be disproven soon enough. My version of lipid optimization is lifestyle-based, and by the measures that lifestyle can actually shift, my results are strong. I'll get to my numbers in a moment.

The TG/HDL Ratio: Your Metabolic Health Snapshot

This one you can calculate yourself from any standard lipid panel. Divide your fasting triglycerides by your HDL cholesterol. That single number is one of the most useful calculations in preventive cardiology, because it reflects both cardiovascular health and metabolic health simultaneously.

Here's why: high triglycerides (the "TG" in the ratio) reflect excess carbohydrate load, poor fat metabolism, and early insulin resistance. High HDL, the so-called "good" cholesterol, reflects metabolic efficiency and cardiovascular protection. The ratio captures both at once. A 2021 meta-analysis of thirteen cohort studies involving more than 207,000 participants found that the highest TG/HDL ratio group had a 43% higher risk of cardiovascular events compared to the lowest group.

Reference points: below 2.0 is optimal and reflects good metabolic health. Between 2.0 and 4.0 suggests emerging insulin resistance. Above 4.0 is the high-risk zone.

This ratio is also the clearest bridge between your lipid panel and your blood sugar health, which is why blood glucose is a Birthday Audit Metric that's coming later in this series: you need the lipid picture and the body composition picture first for it to make full sense.

Lp(a): The Hidden Risk Factor You've Probably Never Been Tested For

Lipoprotein(a), abbreviated Lp(a) and pronounced "L-P-little-a", is a variant of LDL with an additional sticky protein tail attached. That tail makes it roughly six times more artery-damaging per particle than standard LDL. It promotes blood clot formation, drives arterial inflammation, and embeds in arterial walls in ways that standard LDL doesn't.

What makes Lp(a) categorically different from every other lipid marker: research currently suggests that it's more than 90% genetically determined. Meaning diet, exercise, and most medications don't meaningfully move it -the number you have is largely the number you were born with, with one significant exception I'll come to.

Approximately 20% of the population has clinically elevated Lp(a). Most of us have never been tested, though we should all be getting this test at least once in our lifetime, so we know what our risk threshold is. Risk thresholds: below 30 mg/dL is low risk. Between 30 and 50 mg/dL is mildly elevated. Above 50 mg/dL is clinically significant, and above 90 mg/dL is considered severe by the most aggressive current frameworks.

The exception to Lp(a) being stable for life: menopause. Estrogen plays a role in how the gene responsible for Lp(a) is expressed and how quickly the body clears these particles. When estrogen declines, Lp(a) rises by approximately 17% on average. A test done before the menopause transition may not reflect where a postmenopausal woman currently stands. This connects directly to the hormones post coming later in this longevity series.

A note on statins and Lp(a) specifically: statins actually raise Lp(a) by 10 to 20% on average by activating the gene that produces it.

This is documented, underappreciated, and relevant to anyone currently on a statin who has never had their Lp(a) tested. It's one of several reasons I find the reflexive reach for statins worth questioning. For a genuinely rigorous look at the statin story, the StayCurious Metabolism newsletter covers it with more depth and intellectual honesty than I can here. I highly recommend everyone explore this newsletter.

The Tests That Are Available Right Now

Understanding what to test is one thing. Knowing which tests exist, what each one actually tells you, and where to get them is another. Here's the landscape from least to most advanced.

The standard lipid panel covers total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. It's the minimum baseline, available at any lab, typically covered by insurance. Calculate your TG/HDL ratio from it. But don't stop there.

An enhanced blood panel adds ApoB and Lp(a) to the same blood draw. Both are available through Quest, LabCorp, and most major labs without a specialist referral. While you're at it, add high-sensitivity CRP (hsCRP), a blood marker that measures systemic inflammation throughout the body. Inflammation amplifies the risk from Lp(a) specifically, and knowing whether your inflammation is low or elevated meaningfully changes how to interpret your other numbers.

A coronary artery calcium score (CAC) moves from blood work to imaging. It's a CT scan of the chest that detects and quantifies calcified plaque in the coronary arteries, expressed as a number called an Agatston score. No contrast dye, minimal radiation, and it typically costs between $75 and $200. Insurance rarely covers it. A long-term study of 25,253 patients found that CAC scores predict all-cause mortality over fifteen years in people with no cardiac symptoms. A score of zero is strongly reassuring. A score of 400 or above is associated with a 20% risk of all-cause death over fifteen years.

What a CAC scan doesn't show: soft plaque. Calcification is a late-stage process. Plaque can be building in arterial walls for years before it calcifies, and a calcium scan won't detect it.

A coronary CT angiography (CCTA) is a contrast-enhanced CT scan that visualizes the coronary arteries directly, showing both calcified and soft plaque. It uses contrast dye, involves more radiation, and costs more. But it provides significantly more information. A 2025 study found that CCTA upgraded the cardiovascular risk classification in 40% of patients compared to the calcium score alone, mostly in people who had a clean calcium score but measurable soft plaque on the more detailed scan. In other words, 40% of people who would have been reassured by a clean calcium score actually had plaque that only the CCTA caught.

The practical approach: a CAC scan is the accessible, affordable first step. CCTA is the more complete picture, particularly for anyone with elevated Lp(a), a family history of early cardiovascular disease, or a calcium score that doesn't match the rest of the picture.

Here’s Where Functional Genomics Comes In

As part of this audit, I spent time with my own functional genomics analysis - a genome report that maps all of my genome - to look for specific variants in my DNA that are relevant to cardiovascular health, lipid metabolism, and other areas of health impacting these. It helped solve a riddle in my numbers, and it yet again confirmed that getting an FGA was one of the best health moves I've made.

I'm not going to go deep into why I think everyone should get an FGA here, but think of it as a layer of context underneath the lab work: it can help explain why your body responds differently than the population averages predict.

These tools exist, they're increasingly accessible, and they represent what personalized medicine is thrillingly moving towards: not one protocol for everyone, but protocols based on your precise genetics and life history. The field is still evolving, and individual variant interpretation requires significant context. But it's been a game-changer for me and many people I know to have this information. More on that in later posts.

My Numbers and What They Mean

Here's my most recent standard lipid panel, drawn non-fasting in March 2026.

Total cholesterol is 179 mg/dL, well within the optimal range. HDL is 71 mg/dL, which is high and strongly protective: above 60 is generally considered a "negative risk factor," meaning it actively works in your favor. Triglycerides are 47 mg/dL, which is currently considered very good. LDL cholesterol is 94 mg/dL, just under the conventional threshold of 100. My cholesterol-to-HDL ratio is 2.5, also considered very good.

The number that stands out most: my TG/HDL ratio is 47 divided by 71, which equals 0.66. Below 2.0 is optimal. Below 1.0 reflects near-ideal metabolic health and insulin sensitivity. Mine is 0.66. I believe that reflects years of consistent sleep and exercise, stress regulation, and genuine attention to what I eat and how I live.

The nurse practitioner at my doctor's office was annoyingly resistant to ordering my ApoB and Lp(a), (when is the medical world going to catch up?! Later this month I'll be getting more blood drawn to check hormones and will add those two to the mix) so I'm looking at those from labs done in 2023: my ApoB was 67 mg/dL. The clinical threshold for high-risk individuals is below 70, and I'm just under it. By guideline standards, that's an OK result. By the more aggressive longevity-medicine framework Attia advocates, 67 is much higher than ideal, and closing that gap typically requires medication. I've already explained why I'm not going that route. What I can say is that a 67 on someone living as I live is a different data point than a 67 on someone with a poor diet, no exercise, and high chronic stress. The lifestyle inputs matter for interpreting the output, so I'm on alert.

Also from 2023: my LDL particle type was Pattern A, meaning my LDL particles are large and buoyant rather than the small, dense Pattern B particles that embed in arterial walls more aggressively. Pattern A is the more favorable type.

My Lp(a) from 2023 was 103 mg/dL. At the time, I was told this places me in the “moderate risk” category, though today this is considered elevated. These days, above 50 mg/dL is where every major guideline considers the risk clinically significant, though exactly which tier you assign depends on which system you're using.

Lp(a) at 103 is a number that, with current knowledge and tools, can't be lifestyle-optimized away. It's largely genetic. Here's where my functional genomics report offers some context: my APOE genotype (APOE is the gene most associated with lipid metabolism) came back as E2/E4, meaning I carry one protective variant and one risk variant. The E2 variant is associated with better LDL clearance, which is consistent with my regular lipid panel. The E4 variant is associated with slower clearance of Lp(a) particles, which is likely a contributor to why my Lp(a) is elevated despite everything else looking favorable. Two alleles, working in opposite directions.

The plot thickens: at age 51, I had a coronary artery calcium score done. My doctor and I both expected a zero, given my lifestyle and my standard panel results. The score was 3. I'm not freaking out: a score of 3 is minimal and treated as functionally similar to zero by most risk calculators. But it wasn't zero. The Lp(a) of 103 is almost certainly the explanation, and the gene is the explanation for that elevated number. It's the factor that wasn't visible in the blood work alone, doing quiet work in the background. The imaging caught what the labs didn't.

I also don't have a current hsCRP (inflammation marker) in my most recent panel, which is a gap I plan to close. My last known result showed no significant inflammation, which is consistent with my lifestyle and regular diet. Also, I take omega-3 supplements regularly.

My Philosophy

I want to be transparent about the trade-offs I'm making, because I think it's part of what makes tracking useful rather than anxiety-producing.

I know that by the most aggressive longevity-medicine framework, my ApoB could be lower and my Lp(a) is a real concern. I know there are physicians who would look at my numbers and suggest pharmaceutical intervention to drive ApoB down further.

That's a legitimate position within its own framework. But it's not mine.

My skepticism of pharmaceutical intervention isn't about being anti-medicine. It's about the fact that we genuinely don't have decades of hindsight on many of these approaches that would make me confident in the trade-offs. The pattern holds: what we believed was clearly right in medicine has been revised, sometimes dramatically, more times than any of us would like. I'm not rushing to be an early adopter of an intervention I can't undo.

I'm also not willing to live a life so optimized for longevity that I've traded all present enjoyment for hypothetical future years. I know when I'm indulging, and I make sure it's worth it and that I don’t turn it into a habit. That's different from not caring. It's an informed choice.

My lifestyle is my optimization strategy.

And by the measures that lifestyle can actually move, the results are strong. Can I do “better”? Sure. But ultimately, we all have to make our personal choices when it comes to quality of life and longevity optimization. I'm hopeful that the measures I’ll be taking to improve my VO2 max will drive my ApoB down.

My Action Plan for the Next Year

Based on everything above, here's my action plan:

Retesting Lp(a) is the most important item. The 2023 result is three years old. Given that menopause raises Lp(a) by approximately 17% on average, my current number may be higher than the last reading. I'll add it to my next blood draw this month.

Adding ApoB to my next standard panel. It wasn't included in my March 2026 results. Given my favorable lipid panel numbers it's likely still in a good range, but this is a metric I want to track closely rather than assume.

Adding hsCRP to my next blood draw. Inflammation amplifies Lp(a) risk, and I want that number confirmed and on record.

Continuing omega-3 supplementation. The primary reason at this point isn't triglycerides, which are already excellent, but the inflammatory burden that rides on Lp(a) particles. The evidence that high-quality omega-3 reduces that specific kind of inflammation is reasonable and the downside is minimal, so far as we know.

Considering repeat cardiac imaging. It's been four years since my calcium score of 3. With Lp(a) elevated, checking whether that score has changed is the most direct way to see whether the Lp(a) is having any measurable effect on my arteries.

Continuing to protect what's already working. The TG/HDL ratio of 0.66 doesn't happen without consistent inputs. Exercise, sleep, nervous system work, stress regulation, thoughtful nutrition: these are the levers I have that can actually move the proverbial needles. My panel confirms they're working. The plan is to keep working on them.

The Summary

The standard lipid panel is a starting point.

ApoB counts the artery-damaging particles your standard panel doesn't count.

Lp(a) is the most common genetically determined cardiovascular risk factor most people have never tested.

Your TG/HDL ratio tells you more about your metabolic health than your LDL number does.

A cardiac imaging test tells you something blood work can't: whether plaque is already forming.

My standard panel looks good. My metabolic markers are strong. My Lp(a) is elevated, my genetics partially explain why, a calcium score four years ago caught something my blood work wasn't showing, and my functional genomics analysis made sense of that.

The plan ahead is built around closing the information gaps and protecting what's working, without medication and without making my life smaller in the name of risk elimination.

I'm tracking because informed choice is only possible with good information. Not because I'm afraid of every number, but because I'd rather know than assume. And I’d rather make an informed choice before eating my birthday cake and enjoying some bubbly, which helps me enjoy it all the more.

Ready to understand your own body more clearly? My concierge coaching program combines your doctor’s protocol with lifestyle practices known to bring the body into balance, all while tracking so you know what’s working and what isn’t. Learn more here.

Frequently Asked Questions

What is the most important number on a lipid panel?

No single number tells the whole story, but if I had to pick one that the standard panel misses and that matters most, it's Lp(a). It's largely genetic, present in approximately 20% of the population at elevated levels, and most of those people have never been tested. ApoB is the other critical addition: it counts the actual artery-damaging particles in your blood rather than just the cholesterol they carry, and it's a stronger predictor of cardiovascular events than LDL cholesterol in the research.

What is a good TG/HDL ratio?

Below 2.0 is optimal and reflects good metabolic health and insulin sensitivity. Below 1.0 is excellent. Above 4.0 is the high-risk zone and correlates strongly with insulin resistance. You can calculate it yourself from any standard fasting lipid panel by dividing your triglyceride number by your HDL number.

Why does Lp(a) matter if you can't do anything about it with diet and exercise?

Because knowing it changes how you manage everything else. Lp(a) multiplies your overall cardiovascular risk. If your other risk factors are low (because your ApoB is low, your inflammation is low, your metabolic health is strong) the absolute additional risk from elevated Lp(a) is much smaller than if those other factors are also working against you. Knowing you have elevated Lp(a) is a reason to protect everything you can actually control, and to monitor with imaging rather than assume blood work tells the whole story.

What is a coronary artery calcium score and should I get one?

It's a CT scan that detects calcified plaque in your coronary arteries and gives it a number. No contrast dye, minimal radiation, typically $75 to $200, and rarely covered by insurance. A score of zero is strongly reassuring. Any detectable score warrants more active monitoring. If you have elevated Lp(a), a family history of early heart disease, or a lipid profile your doctor can't fully explain, it's a reasonable and accessible next step.

How does menopause affect lipid profiles?

Estrogen is cardioprotective in multiple ways: it keeps LDL lower, raises HDL, clears triglycerides more efficiently, and reduces Lp(a). When estrogen declines at menopause, all of those protective effects are compromised at once. LDL rises, HDL tends to fall, and Lp(a) increases by approximately 17% on average. This is part of why women's cardiovascular risk accelerates significantly after menopause. The hormones post in this series will go deeper into what the current evidence actually shows about hormone therapy and these specific markers.

Can diet change Lp(a)?

It’s currently largely believed that almost nothing changes Lp(a) significantly through lifestyle. It's more than 90% genetically determined. The most actionable response to elevated Lp(a) today is to optimize everything else: keep your ApoB low, keep inflammation low, protect metabolic health, and monitor with imaging. Medications specifically designed to lower Lp(a) are in clinical trials, but they're not yet approved or available outside of research settings.

What does an ApoB of 67 mean in practice?

By clinical guideline standards, it's favorable: below the 70 threshold for high-risk individuals and well below the 90 threshold for intermediate risk. By the more aggressive longevity-medicine framework, it's not optimal: proponents of that approach target 20 to 30 mg/dL, achievable primarily through medication. My choice is to maintain a healthy lifestyle, track it annually, and monitor the impact with imaging rather than pharmaceutical intervention. That's a deliberate trade-off I'm making with full knowledge of what the more aggressive position recommends.