Systems Biology

The New Science of Heart Health.

Moving beyond outdated cholesterol models to address the true drivers of cardiovascular disease: metabolic dysfunction, inflammation, and endothelial health.

"It is the particles, not the cholesterol within them, that cause atherosclerosis." – Dr. Thomas Dayspring, Lipidologist

We are challenging the cholesterol status quo.

Heart disease isn't just plumbing. It’s driven by inflammation and insulin resistance.

We look beyond basic lipids to identify the root cause of cardiovascular risk.

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The Root Cause Cascade

Atherosclerosis doesn't happen overnight. It's a progressive cascade driven by underlying dysfunction. Understanding this process is the key to reversal.

1. Metabolic Dysfunction

Insulin resistance and high blood sugar create systemic stress, driving inflammation and altering lipid profiles.

2. Endothelial Damage

Inflammation damages the delicate lining of the arteries (endothelium), making them "sticky" and vulnerable.

3. Lipid Infiltration

Atherogenic particles (ApoB) breach the damaged endothelium and become trapped in the arterial wall.

4. Plaque Formation

The immune system responds to the trapped lipids, leading to chronic inflammation and the formation of atherosclerotic plaque.

The Evolution of Cardiovascular Science

Tracing the path from the simplistic diet-heart hypothesis to the modern understanding of atherosclerosis as a complex, multifactorial disease.

1958-1964

The Seven Countries Study & The Diet-Heart Hypothesis

Ancel Keys' influential study popularized the link between saturated fat and heart disease. However, methodological concerns, including the selective exclusion of countries that contradicted the hypothesis (e.g., France), biased the interpretation.[1, 2]
1968-1973

Suppressed Evidence: Minnesota Coronary Experiment (MCE)

A large, randomized controlled trial found that replacing saturated fat with vegetable oils lowered cholesterol but paradoxically increased mortality. The results remained largely unpublished for decades, delaying a critical reassessment of dietary guidelines.[3]
1990s

The Rise of the Inflammation Hypothesis

Research pioneered by Dr. Paul Ridker established chronic inflammation (measured by hs-CRP) as a key driver of atherosclerosis, independent of cholesterol levels. This marked a shift toward understanding the immune system's role in cardiovascular disease.[6, 8]
2000s

Advanced Lipid Testing & Particle Number (ApoB)

Advancements allowed for the measurement of lipoprotein particle number (ApoB) rather than just cholesterol content (LDL-C). Studies confirmed that particle count is a superior predictor of cardiovascular events.[12, 25]
2020

JACC Paradigm Shift on Saturated Fat

A landmark review in the Journal of the American College of Cardiology concluded that the evidence does not support limiting saturated fat intake to prevent cardiovascular disease, officially challenging decades of dietary guidelines.[5]

The Four Pillars of Cardiovascular Disease

Atherosclerosis is not simply a plumbing problem. It is a systemic process driven by the interplay of endothelial damage, metabolic dysfunction, lipid transport, and environmental exposures.

Endothelial Health & The Glycocalyx

The process begins with damage to the endothelial glycocalyx—the delicate, protective layer lining the arteries. High blood sugar, oxidative stress, and toxins degrade this barrier, initiating inflammation and allowing lipoproteins to breach the arterial wall.[7, 24]

Key Markers
hs-CRP, Fibrinogen, ADMA

Insulin Resistance & Metabolic Syndrome

The central driver of cardiovascular risk. Insulin resistance directly promotes hypertension, impairs nitric oxide production, drives systemic inflammation, and creates atherogenic dyslipidemia (small dense LDL particles).[10, 11]

Key Markers
Fasting Insulin, HOMA-IR, Trig/HDL Ratio

Advanced Lipidology: ApoB and Lp(a)

Risk is driven by the number of atherogenic particles (ApoB), not the cholesterol they carry (LDL-C). ApoB is superior for risk prediction.[25] Lipoprotein(a) (Lp(a)) is a critical genetic risk factor often missed in standard panels, affecting 20% of the population.[13]

Key Markers
ApoB, Lp(a), LDL-P

Environmental & Systemic Factors

The total body burden contributes significantly. Exposure to heavy metals (lead, cadmium, arsenic) is strongly linked to CVD.[14] Recent studies also identified microplastics in arterial plaques, associated with a 4.5-fold increase in cardiovascular events.[15]

Key Factors
Toxins, Gut Dysbiosis, Stress

The Diagnostic Paradigm Shift

Comparing the predictive power (Relative Risk Ratio) of conventional vs. advanced cardiovascular markers.[25]

Landmark Evidence for Reversal

Clinical trials and advanced imaging studies demonstrating that heart disease can be halted and reversed with intensive, root-cause interventions.

RCT

Ornish Lifestyle Heart Trial

First randomized trial to show regression of coronary atherosclerosis through lifestyle changes alone (no lipid-lowering drugs).
82% of the experimental group experienced regression of arterial blockages after 1 year.
Ornish D, et al. The Lancet. 1990;336(8708):129-133.[21]
Secondary Prevention

Lyon Diet Heart Study

A Mediterranean-style diet resulted in a 50-70% reduction in recurrent cardiovascular events compared to a standard low-fat diet.
Benefits occurred despite similar cholesterol levels between the groups, highlighting non-lipid pathways.
de Lorgeril M, et al. Circulation. 1999;99(6):779-785.[22]
Meta-Analysis

ApoB Superiority Confirmed

Analysis of 233,455 subjects confirmed ApoB as the most potent lipid marker of cardiovascular risk, superior to LDL-C.
When ApoB and LDL-C are discordant (common in metabolic syndrome), ApoB is the accurate predictor.
Sniderman AD, et al. Circ Cardiovasc Qual Outcomes. 2011;4(3):337-345.[25]
Imaging Innovation

AI-Enhanced CCTA Analysis

Direct visualization and quantification of all plaque types, including soft, vulnerable plaques missed by calcium scoring.
Enables precise tracking of disease progression or regression in response to therapy.
Choi AD, et al. JACC Cardiovasc Imaging. 2022;15(3):508-520.[18]

The 3 Billion Beats Difference

From reactive management to proactive reversal: How we leverage advanced diagnostics and root-cause medicine.

Conventional Approach

Stress tests that miss early-stage, non-obstructive plaques.
Calcium scores blind to soft, rupture-prone lesions.
Reliance on LDL-C, ignoring the crucial ApoB particle count.
Ignoring Lp(a) genetic risk in 20% of the population.
Statins as the primary tool, offering limited absolute risk reduction in primary prevention.[19]

Our Evidence-Based Approach

CCTA with AI analysis—visualize and quantify every plaque type.
Quantify vulnerable, high-risk plaque characteristics.
Comprehensive lipid panel: ApoB, Lp(a), oxidized LDL, and particle size.
Deep dive into insulin resistance and inflammatory markers.
Addressing root causes (metabolism, inflammation, environment) for disease reversal.

The Future of Personalized Heart Health.

Our AI platform analyzes 100+ root-cause labs and wearable data to map out your personalized journey.

Our AI platform is launching soon. Be the first to know:

Scientific References

  1. Ravnskov U, et al. The Lipid–Heart Hypothesis and the Keys Equation... Nutrients. 2022; 14(19):4147.
  2. Kromhout D. Seven Countries Study. In: Encyclopedia of Food and Health. Academic Press; 2016.
  3. Ramsden CE, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ. 2016;353:i1246.
  4. Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death... BMJ. 2013;346:e8707.
  5. Astrup A, et al. Saturated Fats and Health: A Reassessment... JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;76(7):844-857.
  6. Libby P, Ridker PM, Hansson GK. Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol. 2009;54(23):2129-2138.
  7. Ushiyama A, et al. Vascular Endothelial Glycocalyx as a Mechanism of Vascular Endothelial Dysfunction and Atherosclerosis. Int J Mol Sci. 2022;23(23):14881.
  8. Ridker PM. Inflammation and atherosclerosis... N Engl J Med. 2001;344(25):1959-1961.
  9. Gao S, Liu J. Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases. Front Cardiovasc Med. 2022;9:961032.
  10. Laakso M. Insulin Resistance and Coronary Heart Disease in Nondiabetic Individuals. Arterioscler Thromb Vasc Biol. 2019;39(6):e147-e155.
  11. di Pino A, DeFronzo RA. Insulin Resistance and Atherosclerosis... Endocr Rev. 2019;40(6):1447-1467.
  12. Cromwell WC, et al. LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study. J Clin Lipidol. 2007;1(6):583-592.
  13. Tsimikas S. A Test in Context: Lipoprotein(a)... J Am Coll Cardiol. 2017;69(6):692-711.
  14. Bhatnagar A, et al. Contaminant Metals as Cardiovascular Risk Factors: A Scientific Statement From the American Heart Association. J Am Heart Assoc. 2023;12(15):e029822.
  15. Marfella R, et al. Microplastics and Nanoplastics in Atheromas and Cardiovascular Events. N Engl J Med. 2024;390(10):900-910.
  16. Trøseid M, et al. Gut-derived low-grade endotoxaemia, atherothrombosis and cardiovascular disease. Nat Rev Cardiol. 2020;17(3):123-132.
  17. Cohen S, et al. State of the Art Review: Psychological Stress and Cardiovascular Disease. JAMA. 2015;314(24):2664-2675.
  18. Choi AD, et al. Advances in Artificial Intelligence-Assisted Coronary Computed Tomographic Angiography... JACC Cardiovasc Imaging. 2022;15(3):508-520.
  19. TheNNT.com. Statins for Heart Disease Prevention (Without Prior Heart Disease). Accessed August 2025.
  20. Davignon J. Pleiotropic effects of statins. Circulation. 2004;109(23 Suppl 1):III39-43.
  21. Ornish D, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280(23):2001-2007.
  22. de Lorgeril M, et al. Mediterranean diet... final report of the Lyon Diet Heart Study. Circulation. 1999;99(6):779-785.
  23. Reitsma S, et al. The endothelial glycocalyx: composition, functions, and visualization. Pflugers Arch. 2007;454(3):345-59.
  24. Sniderman AD, et al. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes. 2011;4(3):337-345.