Heart Disease: My Personal Approach to Prevention
Heart disease doesn’t start with a heart attack.
It starts decades earlier.
Plaque builds slowly.
Arteries narrow quietly.
Nothing feels wrong—until it does.
And when it shows up, it’s often too late.
That’s the part that doesn’t get talked about enough.
Because the first symptom of heart disease is frequently:
👉 the event itself
For me, this isn’t theoretical.
Nearly every man in my family had a heart attack before 50.
That changes how you think.
It forces you to stop asking:
👉 “Am I healthy right now?”
And start asking:
👉 “What’s happening beneath the surface?”
That shift is what led me to build a prevention strategy—not based on guesswork, but on data, risk, and long-term thinking.
The Real Problem: “Normal” Isn’t Good Enough
Traditional healthcare is built around detection.
You get your labs.
They fall within the “normal” range.
You’re told everything looks fine.
But “normal” is based on population averages.
And the average person:
Develops cardiovascular disease
Is metabolically unhealthy
Experiences decline long before death
So being “normal” often means:
👉 being on the same trajectory
That’s not a useful benchmark.
For heart disease prevention, the goal isn’t normal.
👉 It’s optimal—and personalized.
What Drives Heart Disease
At a high level, heart disease is driven by one core process:
👉 Atherosclerosis — the buildup of plaque in your arteries
That process is influenced by:
Lipoproteins (especially ApoB-containing particles)
Inflammation
Metabolic health
Genetics
Time
Time is the multiplier.
You don’t get heart disease overnight.
You get it from:
👉 years of exposure to risk
Which means:
👉 prevention has to start early
The Foundation: Biomarkers That Matter
A lot of people still focus on basic cholesterol.
LDL. HDL. Total cholesterol.
That’s a starting point—but it’s incomplete.
The marker I care about most:
ApoB (Apolipoprotein B)
ApoB measures the number of atherogenic particles in your blood.
Each of these particles:
Can enter the arterial wall
Can contribute to plaque formation
More particles = more opportunities for damage.
This is why ApoB is a better predictor than LDL alone.
My Target:
👉 ~65 mg/dL or lower
That’s not a standard “normal” range.
That’s a prevention target.
And the difference matters.
Lipoprotein(a): The Genetic Wildcard
Lp(a) is a different kind of risk.
Largely genetic
Not easily modified (yet)
Strong independent driver of cardiovascular disease
If Lp(a) is elevated:
👉 your baseline risk is higher
Which means:
👉 your ApoB target should likely be lower
This is where personalization becomes critical.
A1C and Metabolic Health
Heart disease isn’t just about lipids.
Metabolic dysfunction plays a major role.
Even mild insulin resistance:
Increases inflammation
Accelerates plaque development
Raises overall risk
That’s why I track:
👉 A1C quarterly
The goal:
Stay well below pre-diabetic range
Maintain metabolic flexibility
Because once metabolic health declines:
👉 everything gets harder to control
Genetics: Context, Not Destiny
Genetic testing can reveal:
Predisposition to heart disease
Variants that impact lipid metabolism
Risk patterns that aren’t visible in labs alone
But genetics aren’t the outcome.
They’re the starting point.
👉 They tell you how aggressive you need to be
The Missing Layer: Cardiac Imaging
Biomarkers tell you about risk.
Imaging tells you what’s already happening.
This is one of the biggest gaps in traditional care.
You can have:
“Normal” cholesterol
No symptoms
A clean bill of health
And still have plaque.
I’ve seen it happen.
Calcium Score (CAC)
A CAC scan measures:
👉 calcified plaque in the arteries
It’s:
Fast
Relatively low cost
Highly predictive
A score of 0:
👉 reassuring in the short term
Any detectable calcium:
👉 changes the conversation
CT Angiography (CCTA)
This goes deeper.
It shows:
Calcified plaque
Soft plaque (often more dangerous)
Blood flow dynamics
This is how you catch:
👉 disease before it becomes an event
CIMT (Carotid Intima-Media Thickness)
A non-invasive ultrasound that measures:
👉 thickness of artery walls
No radiation.
Useful for:
Tracking vascular aging
Monitoring progression over time
A Real Example: Why Imaging Matters
One of our clients:
Ate well
Exercised regularly
Had normal labs
By conventional standards:
👉 low risk
We recommended imaging anyway.
The result:
👉 significant arterial blockage
No symptoms.
No warning signs.
That’s the reality of heart disease.
And that’s why imaging is part of the strategy.
Lifestyle Still Drives the Outcome
Testing and imaging guide decisions.
But lifestyle determines execution.
This is where consistency matters.
VO₂ Max: Your Cardiovascular Capacity
Cardiorespiratory fitness is one of the strongest predictors of:
Longevity
Cardiovascular health
Resilience
My target:
👉 VO₂ max > 50
Not because it looks good on paper.
Because it creates a buffer:
👉 against decline over time
Body Composition: The Real Lever
Weight is a weak signal.
What matters:
Muscle mass
Visceral fat
My target:
👉 <1 lb of visceral fat (ideally closer to 0.5)
Why?
Because visceral fat:
Drives inflammation
Impairs metabolic health
Increases cardiovascular risk
This is where DEXA becomes critical.
Exercise: Structured, Not Random
The goal isn’t “working out.”
It’s:
👉 training with intent
For me:
Strength training
Cardio
~5 days per week
Not extreme.
Just consistent.
Alcohol, Smoking, and the Obvious
Some things don’t need nuance.
Smoking: eliminate
Alcohol: minimize
I’ve landed at:
👉 ~1 drink per month
Not because of a rule.
Because the data (sleep, recovery, energy) made the decision obvious.
The Strategy: How It All Fits Together
This isn’t about doing everything.
It’s about doing the right things in the right order.
Here’s the framework:
1. Establish Your Baseline
Bloodwork (ApoB, A1C, Lp(a))
Body composition
VO₂ max
2. Assess Risk
Family history
Genetics
Metabolic health
3. Add Imaging (When Appropriate)
CAC
CCTA
CIMT
4. Build a Plan
Lifestyle adjustments
Nutritional strategy
Training program
5. Re-test and Adjust
Quarterly or biannual
Based on data—not guesswork
The Bigger Shift: From Reactive to Preventive
Heart disease isn’t inevitable.
But it is predictable.
And in many cases:
👉 preventable
The problem isn’t lack of knowledge.
It’s lack of:
Measurement
Personalization
Follow-through
A prevention strategy isn’t complicated.
It just requires:
👉 consistency over time
Heart disease isn’t something you wait to treat.
It’s something you prevent—years before symptoms appear.
At Longevity Health, we combine advanced diagnostics, imaging, and physician-led guidance to build a personalized strategy based on your actual risk—not population averages.
Because the goal isn’t just to live longer.
👉 It’s to remove your biggest risk before it becomes your reality.
Book a consult and let’s build your own prevention strategy.