The Cardio-Performance Panel
The arteries you have at sixty were built by the numbers you ran at forty.
Ten cardiovascular and metabolic markers, read against the time horizon that actually determines whether your performance holds for the decades ahead.
What This Is
The next sections walk you through the ten markers, why each one matters, and how to read your own cardiovascular risk across the decades that actually determine the outcome. If you want to read your own numbers against this same time horizon, the last section tells you how.
Before the Markers
Cardiovascular risk is measured in decades, not in single readings.
A standard cholesterol panel was designed to flag overt disease in symptomatic adults, which is a different clinical question than the one a founder in their forties actually needs answered. The annual physical asks whether you are sick today, and most years it correctly says no. The version of cardiovascular risk that matters for your next twenty-five years builds in the background during that same window, while the standard panel reads as normal.
Recent intracoronary imaging research has made this concrete. When patients on maximal lipid therapy add aggressive ApoB lowering, fibrous caps protecting existing plaques thicken by roughly 38%, dangerous lipid cores shrink by about 30%, and overall plaque volume regresses, visible inside the arteries and not just inside a risk calculator. (YELLOW-III · JACC: Cardiovascular Imaging · 2025)
The Miami Heart Study put 2,359 asymptomatic adults aged 40 to 65 through CT angiography. Nearly half, 49%, already had coronary plaque, and even among those with a calcium score of zero, often treated as the all-clear, about 1 in 6 had it too. Half of the people told they were fine had disease building in their arteries without a single symptom. The standard panel did not see it because it was not designed to look that far ahead. (Miami Heart Study · JACC: Cardiovascular Imaging · 2022)
The Time Horizon
Your real risk window opens decades before the first symptom.
Atherosclerosis begins forming in the arterial wall in most adults by their late twenties, accumulates without you noticing across the next two to three decades, and only becomes a clinical event sometime in the fifties or sixties. Standard cardiovascular risk calculators read only the final ten-year window.
Silent Onset
arterial wall begins building plaque
28
avg. age
Asymptomatic Accumulation
2–3 decades of silent build
40–50
avg. age
Clinical Event
heart attack, stroke, or first symptom
50–70
avg. age
Standard cardiovascular risk calculators read only the final ten-year window
This is why the panel that follows looks the way it does. We are measuring earlier, measuring more, and targeting lower, because the time horizon we care about is not the next ten years of disease risk but the next thirty years of how you actually perform.
A Quick Reference for Your Own Numbers
Two questions, two panels.
The standard panel and the Second Prime panel are calibrated to answer fundamentally different questions about your biology, which is why the same person can read normal on one and elevated on the other.
Standard Panel
LDL Cholesterol (LDL-C)
Threshold flagged: ≥ 160 mg/dL
Reads: cholesterol cargo, single snapshot
Question answered: are you sick today
Second Prime Panel
ApoB + 9 supporting markers
Second Prime target: ≤ 60 mg/dL, ideal 40 mg/dL
Reads: particles, inflammation, insulin, hidden accelerants
Question answered: will you be performing at the highest level a decade from now
If your last physical showed an LDL-C in the normal range and no other red flags, the panel that follows is the conversation you have not been offered yet. It does not contradict your physical. It answers a different question.
The question we ask: does this number allow full health and performance a decade from now?
Who finds this panel
Most people who find this are in one of three situations.
01
You have been told everything looks fine, but something feels off. Energy, recovery, performance. The standard panel says normal. You are not convinced.
02
You have a family history of heart disease and you want to know your actual trajectory, not a risk calculator built for the average 65-year-old.
03
You are already dialing in training, sleep, and nutrition, and you want to know whether your cardiovascular biology is keeping up with the demands you are placing on it.
If any of those feel accurate, the ten markers below were built to answer your specific question.
The Second Prime System
Two buckets. One system.
Second Prime reads your biology through two lenses at once. The Health Foundation reads against decline, disease, and death, organized as the Four Horsemen plus Two Accelerators. The Performance Blueprint reads the same biology against how you actually function, covering functional longevity, visible stressors, hidden stressors, and recovery. The full equation is simple: Health × Performance = Performance Longevity.
Bucket 01 · Health Foundation
Horseman
Cardiovascular
Heart disease, stroke
Horseman
Metabolic
Diabetes, fatty liver
Horseman
Neurological
Cognitive decline
Horseman
Immune
Cancer, autoimmune
Two Accelerators
Inflammatory load
Toxic load
Bucket 02 · Performance Blueprint
Performance
Physical
Grip strength, leg strength, VO2 max, movement, skeletal muscle, fat mass
Performance
Internal
Gut health, micronutrients, inflammation, hormone profile, immune function, toxic load
Performance
Environment
Sleep, nutrition, hydration, emotional health, body composition, lifestyle
Performance
Recovery
CO2 tolerance, body armour, physical and mental commitment, efficiency rating
This guide covers the cardiovascular slice of the Health Foundation. The full Second Prime assessment maps all four Horsemen, both Accelerators, and the complete Performance Blueprint, covering 1,000+ data points across both buckets.
The Two Accelerators
Why clean numbers can still carry double the risk.
The Four Horsemen tell which environment is breaking down. The Two Accelerators tell how fast it is breaking down. They are the reason two people with identical cardiovascular panels carry very different real-world risk.
Two Founders, Same ApoB
Founder A
ApoB 75 · hs-CRP 0.4 · GGT 14
1.0× risk
baseline trajectory
Founder B
ApoB 75 · hs-CRP 2.8 · GGT 42
~2.0× risk
accelerated trajectory
Same ApoB. Different inflammatory and toxic load. The accelerators multiply the underlying risk both carry.
Accelerator 01
Inflammatory load
Chronic inflammation turns quiet plaque into the inflamed kind that ruptures. Elevated hs-CRP roughly doubles cardiovascular event risk at any given ApoB level.
READ BY · hs-CRP (marker 04)
Accelerator 02
Toxic load
Liver-detoxification stress and accumulated toxin burden amplify cardiovascular and metabolic dysfunction in the background. Elevated GGT tracks this signal long before standard liver panels flag a problem.
READ BY · GGT (marker 08)
The accelerators are the multiplier most standard physicals never measure.
Know where you stand
Want to know where your own numbers land on this map?
A focused 30-minute call. Bring whatever labs you already have, and Andrew will show you where the standard panel stopped looking.
Book a Consult →These ten markers are a focused slice of the 1,000+ data points we run on every founder. A full Second Prime assessment maps you across all four Horsemen and both Accelerators, where cardiovascular risk reads alongside metabolic, neurological, immune, inflammatory, and toxic signals.
Cardiovascular
Four markers that predict the actual event.
ApoB· Apolipoprotein B
ApoB is a direct count of the particles that drive plaque into your arterial wall, and it is the single best predictor of cardiovascular events we currently have. Standard panels measure the cholesterol cargo those particles carry, while ApoB counts the particles themselves. The two numbers can disagree, and when they do, ApoB is the one that matches what is actually happening inside the artery.
Target ≤ 60 mg/dL · Second Prime target 40 mg/dLLp(a)· Lipoprotein little-a
Lp(a) is a genetic risk multiplier set at birth that does not respond to diet, exercise, or statins, and roughly one in five adults carries an elevated level without ever knowing. We run it once in your life because the result changes how aggressively we target your ApoB and how we structure the rest of your protocol.
ApoB / ApoA-1 Ratio
The ratio of ApoB to ApoA-1 is the strongest predictor of ischemic stroke that clinical research has identified, yet most annual physicals never run ApoA-1, so the ratio cannot be calculated from your standard results. We pair these two readings so you see both your risk concentration and your protective capacity in the same view.
hs-CRP· High-sensitivity C-reactive protein
hs-CRP measures the systemic inflammation that turns quiet plaque into the inflamed kind that ruptures, which is the actual mechanism behind most heart attacks. We run it alongside ApoB so we can see both the particles and the fire, because either reading on its own gives an incomplete picture of where your real risk sits today.
The Risk Horizon Argument
Low risk today. High risk in a decade. Every year in the “normal” zone still compounds.
The risk zones in the chart below are not fixed horizontal lines; they are diagonal. They descend over time because the same ApoB level carries progressively more risk as prior exposure accumulates. An ApoB of 90 mg/dL sits in the low-risk zone at 36. By 46 that same number has crossed into high risk, not because the number changed, but because a decade of arterial exposure has already compounded behind it.
Standard care acts at 50, after 14 years of compounding. It drops ApoB to 60 mg/dL, which slows the rate of accumulation. But the risk already built from 36 to 50 does not reverse. The orange line flattens; it does not fall. At 65 it ends in the moderate-risk zone, not the low-risk zone.
The Second Prime standard: being in the “normal” zone is not acceptable if that normal zone still accumulates long-term damage. We target ApoB at 40 mg/dL from age 38, the number that keeps the trajectory below the descending risk boundary for the next 30 years, not just today.
No intervention
Stays at 90 mg/dL, risk climbs steeply into high zone
Standard care at 50
Drops at 50, slows but stays in high-risk zone
Second Prime from 38
Drops at 38, stays in low-risk zone throughout
Risk zones
Same ApoB carries more risk as prior exposure compounds
HIGH RISK
38%
Lifetime ASCVD risk at 65
No intervention
HIGH RISK
33%
Slows accumulation but remains in high-risk zone
Standard care at 50
LOW RISK
12%
Fundamentally different trajectory
Second Prime from 38
Ference et al., European Heart Journal (2017) · Sniderman et al., JAMA Cardiology (2018) · Illustrative model, not individual clinical predictions
The time horizon changes everything.
Standard cardiovascular risk calculators use a 10-year window. At 38, a 10-year risk calculation returns a low number, so nothing is done. A 2018 JAMA Cardiology paper by Allan Sniderman showed what happens when you extend that window to 30 years: the number of patients who need to be treated to save one life drops from 33–130 down to less than 7. The same person. The same ApoB. A different time horizon, and a completely different clinical decision.
The YELLOW-III trial adds the mechanism: aggressive ApoB reduction causes fibrous caps to thicken by ~38% and lipid cores to shrink by ~30%, structural changes inside the artery wall that no risk calculator can see. Every year spent above 70 mg/dL is a year of plaque biology that cannot be reversed.
“The earlier in life LDL-C is lowered, the greater the reduction in lifetime risk of ASCVD.”
Sources: 2022 ESC/EAS Dyslipidaemia Guidelines · Ference et al., European Heart Journal (2017) · Sniderman et al., JAMA Cardiology (2018) · YELLOW-III trial · Chart = illustrative model, not individual clinical predictions
Metabolic
Where cardiovascular risk compounds unseen.
Fasting Insulin· with HOMA-IR
Fasting insulin is the earliest signal of insulin resistance, often elevated for years before fasting glucose moves a single point. Your annual physical tests glucose almost exclusively, which means the metabolic problem builds in the background while your labs continue to read normal. HOMA-IR combines both readings into a single number we can track over time.
HOMA-IR target < 1.0Triglyceride / HDL Ratio
The ratio of triglycerides to HDL is one of the strongest predictors of heart disease in the clinical literature, and it doubles as a clear window into how well your metabolism is actually performing. We use it as a fast metabolic health check that supports the more detailed insulin work.
Target ratio < 2.0HbA1c· with Fasting Glucose
HbA1c and fasting glucose only tell the full story when read against the insulin context above, because together they reveal how your metabolism is actually performing rather than how it appears on a single-marker readout. Run in isolation they tend to miss the early stages of metabolic drift.
Hidden Accelerants
The markers that compound everything else in the background.
GGT· Gamma-Glutamyl Transferase
GGT is a sensitive liver-stress marker that standard labs only flag above 65, even though we treat anything above 20 as a signal worth investigating because elevations track closely with inflammation, alcohol load, and metabolic stress.
Homocysteine
Homocysteine is an independent cardiovascular risk factor that roughly doubles in impact when you carry an MTHFR variant, information that no panel can give you unless homocysteine is on it. The test is inexpensive enough that it belongs on any panel claiming to read long-term risk.
Target < 8 µmol/LOxidative Stress· with Cellular Age
Oxidative stress and cellular age measure the gap between your chronological age and how old your biology is actually performing, which gives us the single most reliable signal for whether the other nine markers are moving in the right direction over time.
Measured Outcomes
The numbers that change when the system is right.
These are average outcomes across our client base. Individual results depend on starting point, protocol adherence, and biological factors.
↓ Biological Age
−12 years
Average reduction in epigenetic biological age
↑ Free Testosterone
+40%
Average increase within 6 months
↓ Insulin Resistance
−35%
HOMA-IR reduction, primary driver of metabolic decline
↓ Mortality Risk
5×
Lower all-cause mortality: elite vs. low VO₂ Max
↓ Body Fat
−10%
Average reduction in 6 months without losing lean mass
↓ Inflammatory Markers
−52%
hs-CRP reduction, leading marker of systemic inflammation
Results shown with client permission. Individual outcomes depend on starting point, protocol adherence, and biological factors. These are not typical results.
What Changes
From where you are now, to where you should be operating.
Exhausted after 8 hours of sleep
Brain fog slowing every decision
Body composition that doesn't reflect your effort
Recovery takes 3–4 days after training
Energy crashes every afternoon
“Normal” lab results with no real answers
Too depleted to be fully present at home
Experimenting randomly, nothing sticking
Wake up sharp, before the alarm
Razor-sharp focus, faster and clearer decisions
Leanest since your athletic years
Recovered in 24 hours, training harder than ever
Sustained energy from morning to night
Biomarkers read for what's optimal and a clear, personalized roadmap
Fully present with your family every single night
A system that runs itself, zero decision fatigue
Client results
From the people who've done it.
“My cardiologist had been watching my ApoB and Lp(a) for three years. Nothing moved it. Six months here did.”
CEO, Logistics
Case #006 · Age 52
“Honestly, I came in skeptical. I'd done bloodwork a dozen times. Andrew found things in week one that nobody had ever flagged.”
Founder, Tech
Case #002 · Age 44
“I had a cardiologist, a trainer, a nutritionist. None of them talked to each other. I was the one connecting the dots.”
Executive, Asset Mgmt
Case #011 · Age 46
“I've sent three people to Andrew already. I don't do that unless something actually worked.”
Mark D.
Investment Banking · Age 47
“I kept telling myself the brain fog was just stress. It wasn't stress. Three months in and I'm sharper.”
David K.
Partner, Law · Age 48
“My wife actually said something to me about two months in. More present, more patient, actually there.”
Brian W.
Operator, Govt Contracting · Age 52
Why Second Prime
A complete system, start to finish.
Second Prime runs the full loop: deep testing, root-cause reads, and a team that runs the plan with you.
| Capability | Second Prime | Lab-Only Testing | Functional Medicine |
|---|---|---|---|
| 1,000+ biomarker assessment | ✓ | ✗ | PARTIAL |
| Interpreted for what's optimal (not just 'normal') | ✓ | ✗ | PARTIAL |
| Root cause identification | ✓ | ✗ | ✓ |
| Ongoing coaching & protocol integration | ✓ | ✗ | ✗ |
| Executive context & lifestyle integration | ✓ | ✗ | ✗ |
| Performance focus (not disease management) | ✓ | ✗ | ✗ |
| Ongoing improvement & real-time adjustment | ✓ | ✗ | ✗ |
| Medical oversight (TRT / HRT / peptides) | ✓ | ✗ | PARTIAL |
The person their kids brag about at 65.
That's the 65 we build toward.
What Happens Next
If you want to read your own numbers against this same time horizon, the next step is a conversation.
A focused 30-minute call where Andrew walks you through your numbers, maps every red flag to the markers in this guide, and shows you exactly what the standard panel missed.
This is for people who intend to stay in the room at seventy, who want to be sharp, capable, and fully present not just for the next few months but for the decades ahead, and who understand that the numbers you run today are the body you live in tomorrow.
Book a Consult →
Andrew Martin
Founder, Second Prime · Biologist
I help founders and executives find what their annual physical misses, then build the plan that keeps them in their prime.