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Moving beyond outdated cholesterol models to address the true drivers of cardiovascular disease: metabolic dysfunction, inflammation, and endothelial health.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

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.

What Your Doctor Hasn't Told You

The science of heart health has changed dramatically — but the standard advice hasn't caught up. Here's what the latest research actually shows, and why it matters to you.

1958-1964

Why You Were Told Fat Was the Enemy

For decades, you've been told to avoid fat to protect your heart. That advice came from a flawed 1960s study that cherry-picked data from only the countries that supported its conclusion — while ignoring those that didn't (like France, where high-fat diets coexisted with low heart disease).[1, 2]
1968-1973

The Study They Didn't Want You to See

A major clinical trial found that following the "low-fat" advice actually increased deaths — even though it lowered cholesterol. The results were so inconvenient that they were buried for decades. You were never told about this.[3]
1990s

The Real Culprit: Inflammation

Scientists discovered that chronic inflammation — not dietary fat — is what actually damages your arteries. This changes everything about how you should think about prevention. If your doctor isn't measuring your hs-CRP, they're missing a critical piece of your heart health picture.[6, 8]
2000s

Your Standard Cholesterol Test Is Missing the Point

That LDL number your doctor checks? It's counting the wrong thing. The real risk comes from the number of particles (ApoB) trying to penetrate your artery walls — and most doctors don't test for it. A study of 233,000+ people confirmed: ApoB is the superior predictor of heart attacks.[12, 25]
2020

The Guidelines Finally Caught Up

In 2020, the most prestigious cardiology journal (JACC) officially concluded: there is no good evidence that limiting saturated fat prevents heart disease. Decades of dietary advice you followed — officially challenged by the very institutions that created it.[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.
Be Part of Something Bigger

Your Health Story Could
Change Medicine.

Every lab result, every scan, every heartbeat tracked — it's not just about you. When you choose to contribute your de-identified data, you join a growing community building one of the most comprehensive longitudinal health datasets ever assembled.

100+ Biomarkers

Advanced labs, lipid panels, metabolic markers, inflammatory profiles — tracked over time.

Wearable Intelligence

Continuous heart rate, HRV, sleep, activity, and stress data woven into your health story.

Advanced Imaging

AI-enhanced CCTA scans quantifying plaque — before and after interventions.

Nutrition & Lifestyle

Food tracking, caloric analysis, exercise habits, and behavioral patterns over time.

Initial conditions. Interventions. Results. Over time.

This is how we move medicine from reactive to preventive.
From guessing to knowing.

Privacy-First. Always.

Your data contribution is 100% opt-in and fully de-identified. We never share personal health information. You choose what to share, and you can withdraw at any time. Your privacy is non-negotiable.

Corwin and our 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.