Walk into any primary care office in Overland Park or Kansas City and you’ll hear the same narrative about heart disease:

“Your cholesterol is a little high. Let’s watch it.”
“Your LDL isn’t terrible.”
“Your HDL is good, so you’re protected.”

This framing is not just incomplete—it’s outdated.

If you care about longevity, long-term cardiovascular prevention, and lowering your lifetime probability of a heart attack or stroke, you need to understand ApoB, Lp(a), and the true pathophysiology of atherosclerosis. Without this foundation, discussions about diet, supplements, statins, or “natural alternatives” become guesswork.

At EvoHealth Functional Medicine, we use the same mechanistic, quantitative framework popularized by Peter Attia and other longevity physicians:
identify the causal drivers, diagnose risk early, and treat aggressively long before symptoms appear.

Because here is the truth:

Heart disease is not caused by “high cholesterol.”
It is caused by ApoB-containing lipoproteins entering and becoming retained in the arterial wall.
Everything else—LDL-C, HDL, triglycerides—is secondary.

Understanding this biology allows us to intelligently evaluate where pharmacology, nutrition, and evidence-based natural statin alternatives fit into a complete prevention strategy.

The Real Etiology of Atherosclerosis — A Particle Disease, Not a Cholesterol Disease

Atherosclerosis begins the moment an ApoB-containing lipoprotein—LDL, VLDL remnants, IDL, or Lp(a)—crosses the endothelium and becomes trapped in the subendothelial space. Once retained, the particle oxidizes, triggers inflammatory signaling, attracts macrophages, and initiates plaque formation.

The crucial point:
Each atherogenic particle carries exactly one ApoB molecule.

This means:

• ApoB = particle count

• Particle count = risk

• More particles = more opportunities to enter the artery

LDL-C can be misleading because it reflects the mass of cholesterol, not the number of particles. Many patients with “normal LDL” have high ApoB, which explains why people with normal cholesterol still develop heart disease.

Lp(a) is an even more potent risk factor—an LDL particle grafted to an apolipoprotein(a) tail, making it both atherogenic and pro-thrombotic. It is genetically set and minimally responsive to lifestyle. For many patients in the Kansas City region who discover they have “high Lp(a),” this explains family histories of early cardiovascular disease.

This biology sets the stage for understanding which therapies actually matter—and which supplements are useful adjuncts versus placebos.

Where Natural Statin Alternatives Fit Into the Biology of ApoB

With the rise of functional medicine and longevity practices nationwide, including here in Overland Park, patients routinely ask:

“Can I lower ApoB naturally without a statin?”

The correct answer is nuanced—not binary.

Natural compounds can modulate ApoB-driven risk, but only if they influence the same causal pathways:

Monacolin K (Red Yeast Rice)

Mechanistically identical to lovastatin.
It inhibits HMG-CoA reductase, upregulates LDL receptors, and reduces ApoB-containing particles.

• LDL-C reduction: ~20-30%

• ApoB reduction: ~15-25%

• Most “pharmacologic” nutraceutical available

• Best evidence base among natural options

But because monacolin K is a statin, it carries the same biological considerations—potential liver enzyme changes, myalgias, and drug interactions.

Berberine HCl

Acts on hepatic metabolism, AMPK signaling, and PCSK9 expression.
Its effect is weaker but mechanistically real.

• ApoB reduction: ~5-10%

• LDL-C reduction: ~5-15%

• Major effects on insulin resistance and triglycerides

• Useful in metabolic syndrome and mixed dyslipidemia

This is not a statin replacement—but a metabolic therapy.

Niacin (Vitamin B3)

Decreases hepatic VLDL synthesis and reduces LDL particle secretion.
Most importantly:

• Lp(a) reduction: 20-30%

• ApoB: ~10%

• TG: 15-30%

Niacin remains one of the only accessible therapies that meaningfully lowers Lp(a), though it must be used cautiously and selectively.

Where Pharmaceuticals Belong — The Time and Place for Statins and PCSK9 Inhibitors

Despite the effectiveness of certain natural agents, there are clear thresholds where pharmaceuticals are not optional—they’re lifesaving.

Pharmacology is indicated when:

• ApoB is significantly elevated

• There is established ASCVD

• A patient has multiple risk enhancers (diabetes, hypertension, smoking, strong family history)

• Lp(a) is very high and ApoB also elevated

• There is evidence of plaque on coronary calcium or CT angiography

• Lifestyle and nutraceutical therapy fail to achieve target ApoB reductions

Why pharmaceuticals dominate in high-risk disease

• Moderate-intensity statins: 30-50% ApoB reduction

• High-intensity statins: 50-60%+ reduction

• PCSK9 inhibitors: 50-60% ApoB reduction + 25-30% Lp(a)

Natural therapies simply cannot compete at this magnitude.

The correct framework is not “natural vs pharmaceutical.”
It is: Use the gentlest intervention capable of achieving the ApoB reduction required by the patient’s risk level.

EvoHealth’s Precision Approach: Combined Pathophysiology + Targeted Therapy

At EvoHealth Functional Medicine in Overland Park and Kansas City, we take a data-first, risk-driven approach that mirrors the best preventive cardiology and longevity practices:

1. Identify the primary driver: ApoB, Lp(a), insulin resistance, inflammation.

2. Map the causal pathways: LDL receptor activity, hepatic cholesterol synthesis, PCSK9 levels.

3. Match the intervention to the biology:

   • Red yeast rice if mild ApoB elevation in primary prevention

   • Berberine for combined metabolic dysfunction

   • Niacin when Lp(a) is high and no pharmacologic options are available

   • Statins/PCSK9 inhibitors when risk demands pharmacologic force

4. Track outcomes longitudinally: ApoB, NMR lipoproteins, Lp(a), hs-CRP, fasting insulin.

This is not supplement-based care.
It is mechanistically precise risk reduction with the gentlest effective tools.

Take the Next Step Toward True Cardiovascular Prevention

If your goal is to reduce your lifetime risk of heart attack, stroke, and metabolic disease—not just “watch your cholesterol”—you need a precision strategy that targets ApoB, Lp(a), metabolic dysfunction, and early plaque biology long before symptoms appear.

At EvoHealth Functional Medicine in Overland Park, we use the same quantitative, mechanistic framework employed by leading longevity physicians:

• Advanced lipid, ApoB, and Lp(a) testing

• Early identification of subclinical atherosclerosis

• Precision nutrition and metabolic optimization

• Evidence-based natural therapies when appropriate

• Pharmacologic intervention when risk demands stronger suppression

• Clear, trackable biomarkers and structured longitudinal follow-up

If you want a cardiovascular prevention plan built around your actual physiology rather than generic cholesterol targets, schedule a consultation with EvoHealth.

EvoHealth Functional Medicine
13801 Metcalf Ave, Suite 205
Overland Park, KS 66223

(913) 404 2193