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Cardiovascular disease is the leading cause of death in the European Union. It is responsible for over 42% of all deaths, roughly 10,000 people every day across the WHO European Region. [1] In Germany specifically, coronary heart disease is the single leading cause of death, with mortality rates above the European average. [2]
And yet, the standard blood test most people rely on to assess their risk, the basic lipid panel, was designed in the 1970s and hasn't fundamentally changed since. While valuable, science has now established that are important aspects what it misses, why that matters, and what you should be looking at instead.
When you get a routine cholesterol test, the lab typically reports four numbers: total cholesterol, LDL cholesterol ("bad"), HDL cholesterol ("good"), and triglycerides. These are part of Aniva's heart health panel, but they're just the starting point, not the full picture.
Here's something most people don't realize: your LDL-C number is usually not directly measured. In most labs, it's calculated using the Friedewald equation — a formula from 1972 that estimates LDL cholesterol from total cholesterol, HDL, and triglycerides. [3] The formula assumes a fixed ratio between triglycerides and VLDL cholesterol (5:1), which breaks down in people with high triglycerides, insulin resistance, or metabolic syndrome — precisely the population most at risk.
But even when LDL-C is measured directly, there's a more fundamental problem: LDL-C tells you the mass of cholesterol carried by LDL particles, not the number of particles doing the carrying. And it's the number of particles that drives atherosclerosis.
Think of lipoproteins as delivery trucks on a highway. LDL-C tells you the total weight of cargo (cholesterol) those trucks are carrying. ApoB tells you how many trucks are on the road. Two people can have the same LDL-C: the same total cargo weight, but very different numbers of particles. The person with more, smaller, cholesterol-depleted particles has more trucks hitting their arterial walls, and substantially higher cardiovascular risk. [3] But their LDL-C looks the same as someone with fewer, larger, cholesterol-enriched particles.
This is the core problem with using LDL-C as your primary measure of cardiovascular risk: it's an imperfect proxy for what actually matters.
Apolipoprotein B (ApoB) is a protein found on the surface of every atherogenic lipoprotein particle, every LDL, VLDL, IDL, and Lp(a) particle in your blood. Crucially, each particle contains exactly one ApoB molecule. [3] That makes ApoB a direct count of the total number of particles that can penetrate your arterial wall and drive plaque formation. It's not a proxy. It's not a calculation. It's a measurement.
In 2019, the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS) concluded that ApoB is a more accurate marker of cardiovascular risk than LDL-C or non-HDL cholesterol. [3] They di that based on evidence from prospective epidemiological studies, randomized clinical trials, and Mendelian randomization analyses. A comprehensive 2025 systematic review in the European Heart Journal, analyzing 15 discordance studies involving 593,354 participants, confirmed this. So, in every single study, when ApoB and LDL-C disagreed, ApoB was the better predictor of cardiovascular events. [4]
The CARDIA study followed 2,794 young adults (aged 18–30) for 25 years and found that those with high ApoB but normal LDL-C had 55% higher odds of developing coronary artery calcification, visible plaque buildup, in midlife. Those with high LDL-C but normal ApoB showed no statistically significant increase in risk. [5] Read that again: normal LDL-C did not protect people whose ApoB was elevated.
A 2025 UK Biobank analysis of over 41,000 participants went further still, finding that ApoB outperformed not just LDL-C but also LDL particle number (LDL-P) in predicting cardiovascular events — with risk elevation detectable at as little as 2% discordance. [6]
This disagreement, called discordance, is far more common than most people think. It's especially prevalent in people with metabolic syndrome, type 2 diabetes, obesity, high triglycerides, or those on statin therapy. [4] In one study, 51% of patients with metabolic syndrome had discordant LDL-C and ApoB values. [7] That means for roughly half of this high-risk group, LDL-C alone was giving either falsely reassuring or falsely alarming information.
Despite this evidence, less than 1% of insured Americans get their ApoB measured each year. [7] In Germany and most of Europe, the situation is similar: ApoB is available but almost never part of standard GP blood work.
This is exactly why Aniva includes ApoB in its heart health panel.When 51% of people with metabolic syndrome get a misleading LDL-C reading, relying on the standard lipid panel alone isn't prevention — it's guessing. Aniva tests 140+ biomarkers including ApoB, Lp(a), hs-CRP, triglycerides, and a full cardiovascular risk profile. The waitlist is free, and a full membership is just €199/year.
If ApoB is the most underused marker in cardiovascular prevention, lipoprotein(a), written as Lp(a) and pronounced "L-P-little-a", is the most underappreciated.
Lp(a) is an LDL-like particle with a unique addition: a large, genetically variable protein called apolipoprotein(a) that's covalently bonded to the ApoB100 molecule. This gives Lp(a) a triple threat profile: it's pro-atherogenic (drives plaque), pro-inflammatory (fuels arterial wall damage), and anti-fibrinolytic (inhibits clot breakdown). [8] In other words, it doesn't just build plaque — it makes existing plaque more dangerous.
Approximately 20% of the global population, roughly 1.5 billion people, has elevated Lp(a) levels (≥50 mg/dL or ≥100 nmol/L). [8] [9] And here's the part that makes Lp(a) fundamentally different from every other lipid marker: your Lp(a) level is 70–90% genetically determined. [8] Diet doesn't change it. Exercise doesn't change it. Statins don't lower it, and in some cases may slightly raise it. [10]
Lp(a) levels remain relatively stable throughout life in men, while in women they tend to rise after menopause. [10] Because it's predominantly a genetic trait, a single measurement in adulthood can inform risk assessment for a lifetime. Which is why both the AHA and the ESC now recommend that every adult get Lp(a) tested at least once. [9]
There are currently no approved pharmaceutical therapies that specifically target Lp(a) lowering. [8] Several RNA-based drugs (including muvalaplin, olpasiran, and lepodisiran) are in late-stage clinical trials at the time of writing this (early 2026), and early results are promising, but they're not yet available. In Germany, lipoprotein apheresis is available for patients with progressive coronary artery disease and severely elevated Lp(a), with over 1,500 patients receiving this treatment (compared to fewer than 50 in the United States). [11]
So why test for something you can't directly treat? Because knowing your Lp(a) level fundamentally changes how you manage everything else. A person with an Lp(a) of 80 nmol/L needs a much lower LDL-C (and ApoB) target than someone with an Lp(a) of 10 nmol/L. Elevated Lp(a) is an independent risk factor, meaning it adds risk on top of whatever your other numbers say. Ignoring it because you can't treat it directly is like ignoring a family history of heart disease because you can't change your DNA.
There's one more technical detail that matters clinically: the cholesterol inside Lp(a) particles is included in your LDL-C measurement. [9] If your Lp(a) is high, a meaningful portion of what your lab reports as "LDL cholesterol" is actually Lp(a)-cholesterol, which responds differently to treatment and carries different risk implications. Without knowing your Lp(a), you can't accurately interpret your LDL-C.
Your standard lipid panel already contains two numbers that, when combined as a ratio, function as a surprisingly accurate surrogate marker for insulin resistance — and most doctors never calculate it.
A 2024 systematic review in Biomedicines analyzed 32 studies spanning 20 years, involving 49,782 participants across multiple ethnicities, and confirmed: the triglyceride-to-HDL cholesterol ratio (TG/HDL) is a valid, cost-free proxy for insulin resistance, the metabolic dysfunction that underlies type 2 diabetes, fatty liver, and a major portion of cardiovascular risk. [12] Average cutoffs indicating insulin resistance were a TG/HDL ratio above 2.53 for women and above 2.8 for men (in Caucasian populations).
A UK Biobank genome-wide association study used TG/HDL as a surrogate for insulin resistance in 382,129 individuals and identified 251 genetic loci. 62 of which were specifically associated with insulin resistance rather than triglycerides or HDL alone. [13]
The insight for practical purposes: if your triglycerides are 150 mg/dL and your HDL is 45 mg/dL, your TG/HDL ratio is 3.3, above the threshold, and a signal that merits further investigation with fasting insulin or HOMA-IR. Aniva calculates this ratio automatically in your results dashboard, alongside the raw lipid values and your full metabolic panel.
Standard lipid panels report triglycerides as a single number. But triglycerides travel inside particles such as VLDL, IDL, and chylomicron remnants. The cholesterol carried by these particles is called remnant cholesterol. Recent research, including a 2024 European Heart Journal analysis, has demonstrated that remnant cholesterol independently predicts cardiovascular events and may carry risk comparable to LDL on a per-particle basis. [14] Standard panels capture total triglycerides but do not quantify remnant cholesterol directly.
ApoB captures this risk because each VLDL and IDL particle contains an ApoB molecule, so when you measure ApoB, you're counting these dangerous remnant particles along with LDL. This is one of the key reasons ApoB outperforms LDL-C: it doesn't have a blind spot for triglyceride-rich lipoproteins.
High-sensitivity C-reactive protein (hs-CRP) measures systemic inflammation. The landmark JUPITER trial showed that statin therapy reduced cardiovascular events by 44% in people with normal LDL-C but elevated hs-CRP. Vonfirming that inflammation is a causal driver of atherosclerosis, not merely a marker of existing disease. [15]
A 2024 AHA analysis found that adults with elevated levels of all three biomarkers, Lp(a), remnant cholesterol, and hs-CRP, had nearly triple the risk of heart attack compared to those with normal levels. [15] Each marker alone showed only modest risk elevation; it was the combination that was devastating.
This is why Aniva measures hs-CRP alongside lipids, not as an afterthought. Because interpreting cholesterol numbers without knowing your inflammatory status is like reading half the sentence.
Your lipid panel has four numbers. Your actual risk has at least eight.ApoB, Lp(a), hs-CRP, triglyceride-to-HDL ratio, remnant cholesterol, these aren't exotic research markers. They're validated, guideline-recommended, and available today. Most panels just don't include them. Aniva's 140+ biomarker panel does. One draw, one clear report, one action plan.
Because ApoB measures particle number rather than cholesterol mass, it's unaffected by the postprandial triglyceride spike that distorts calculated LDL-C. [3] This means ApoB can be reliably measured in a non-fasting state. Making it not only more accurate but more convenient. The ESC explicitly states that fasting samples are not required for ApoB measurement. Yet many labs and practitioners still default to fasting protocols because their workflows were built around LDL-C.
The ESC defines ApoB targets by cardiovascular risk level:
These thresholds matter because a "normal" ApoB for a healthy 30-year-old is not normal for a 55-year-old with a family history of premature heart disease. Aniva's action plan factors in your personal risk profile — including age, family history, medications, and the full suite of cardiovascular biomarkers — to give you targets that are specific to you, not to a population average.
Statins lower LDL-C effectively. But their effect on ApoB and LDL particle number doesn't always track proportionally with LDL-C reduction. A patient who achieves their LDL-C target on a statin may still have residual risk if their ApoB remains elevated — a scenario the standard lipid panel would never detect. [4] The ESC now recommends ApoB as a more accurate index of the adequacy of lipid-lowering therapy.
The NMR lipoprotein subclass testing that some clinics offer, breaking down LDL particles into "large buoyant" and "small dense" patterns, was popular in the early 2000s. But the 2025 European Heart Journal review by Sniderman et al. makes the case clearly: if you measure ApoB and Lp(a), you get more accurate risk information than from cholesterol, triglycerides, and particle size testing combined. [4] The particle size question becomes moot when you're directly counting particles.
Heart disease is the #1 killer in the EU. The test that screens for it is from 1972.Aniva's cardiovascular panel includes ApoB, Lp(a), hs-CRP, full lipids, HbA1c, fasting glucose, and more — all in a single blood draw, with results you can actually understand. No medical jargon, no confusing PDFs. The waitlist is free, and a full year of membership is €199.
The standard lipid panel: total cholesterol, LDL-C, HDL-C, and triglycerides, is not wrong. It's rather incomplete. It measures cholesterol mass when the real driver of atherosclerosis is particle number. It misses Lp(a), an inherited risk factor affecting one in five people worldwide. It doesn't quantify remnant cholesterol or inflammation. And it uses a 50-year-old formula that breaks down in precisely the patients who need accurate results most.
The science isn't ambiguous. The 2019 ESC/EAS guidelines, the 2025 European Heart Journal systematic review, the CARDIA study, the UK Biobank analysis: they all point in the same direction: ApoB should be the primary lipid measure for cardiovascular risk assessment, and Lp(a) should be tested at least once in every adult.
At Aniva, our 140+ biomarker panel includes ApoB, Lp(a), hs-CRP, full lipid profile, metabolic markers, and the complete cardiovascular picture: because the numbers only help if you're measuring the right ones. The waitlist is free and includes a lot of useful insights like we offer here on the blog. A full year of membership, including your blood draw, clinician-reviewed action plan, and concierge support, is €199.
Medical disclaimer: This content is for informational purposes only and is not medical advice. Always discuss results with a qualified healthcare professional.
