Cholesterol and Heart Disease: What the Evidence Shows

Why We Actually Need Cholesterol

(And How the Body Handles It)

Cholesterol is not a waste product. It is a fundamental structural molecule required for life.

Every cell in your body depends on cholesterol to exist, function and renew itself. Cholesterol typically makes up 30–40% of the lipid content of cell membranes, where it provides strength, flexibility and stability. Without adequate cholesterol, cell membranes become fragile and dysfunctional, impairing repair, signalling and cell division.

This requirement extends beyond the outer cell membrane to essential internal structures, including mitochondria, where membrane integrity is critical for normal energy production.

Because tissues such as blood vessels, immune cells, the liver and the nervous system are constantly renewing and adapting, cholesterol production and handling must be precisely regulated.

When this system functions properly, cholesterol supports cellular resilience and repair. When it becomes damaged, particularly through oxidative stress, inflammation or metabolic dysfunction, the problem is not cholesterol itself, but the loss of structural integrity and signalling control within the system that handles it.

LDL - A Transport System, Not a Villain

Because cholesterol is a fat, it cannot circulate freely in the bloodstream. The body solved this problem elegantly.

Your liver produces cholesterol based on need, then packages it into transport particles called lipoproteins. These particles, often simplistically labelled “LDL”, deliver cholesterol to tissues, then return to the liver to be refilled and recycled.

This delivery system evolved over millions of years. It is adaptive, regulated and efficient.

LDL particles are not harmful by design. Problems arise when lipoproteins become damaged or oxidised, most often in the presence of:

• Chronic inflammation

• Oxidative stress

• Insulin resistance and metabolic dysfunction

This raises an important and often overlooked question:

If cholesterol synthesis and transport are artificially disrupted, do we fully understand the long-term biological consequences, especially when cholesterol synthesis is tightly linked to many essential cellular pathways?

That question deserves thoughtful consideration.

Why LDL-C Alone Doesn’t Tell the Whole Story

If cholesterol is essential, and damage, not quantity, is the issue, then focusing solely on LDL-C becomes biologically questionable.

In fact, large datasets consistently show that around 75% of people who suffer heart attacks have LDL-C within “normal” ranges.

This suggests either:

• “Normal” LDL-C ranges are poor predictors of cardiovascular events, or

• LDL-C itself has limited direct relevance to the true causes of heart attacks and strokes

Decades of research now point to the real drivers of acute cardiovascular events:

• Inflammation within vessel walls

• Oxidative stress

• Small dense LDL particles that become oxidised

• Endothelial injury

• Clot formation, which ultimately blocks blood flow

Lowering LDL-C does not directly address these upstream biological processes, which may explain why statins reduce events modestly in some groups, yet fail to eliminate cardiovascular risk.

Triglycerides - The Overlooked Risk Factor

Triglycerides are a distinct lipid class with independent relevance to cardiovascular risk.

Key points supported by research:

• Elevated triglycerides are strongly associated with insulin resistance and metabolic dysfunction

• High triglycerides promote formation of small dense LDL, which oxidises more easily

• People can have “normal” LDL-C but remain at high risk due to elevated triglycerides

Markers such as:

• Triglycerides

• HDL

• Triglyceride:HDL ratio

• Remnant cholesterol

often provide a more meaningful picture of risk than LDL-C alone.

Thrombosis and Plaque Instability - The Real Cause of Heart Attacks

Heart attacks and strokes occur when a blood clot forms on a vulnerable plaque, abruptly blocking an artery.

A detailed review published in the Journal of Internal Medicine explains that acute cardiovascular events arise from:

• Plaque instability

• Endothelial injury

• Immune activation

• Lipid accumulation

• Thrombus (clot) formation

not cholesterol levels alone.

If inflammation, oxidative stress, endothelial damage and platelet activation drive acute events, the logical question becomes:

Can we safely influence these upstream processes rather than focusing narrowly on LDL-C?

Tocotrienols, Platelets and Vascular Protection

Tocotrienols, particularly annatto-sourced delta and gamma tocotrienols (T3), have demonstrated multiple cardioprotective properties in experimental and emerging human research, including:

• Antioxidant activity, protecting LDL particles from oxidation

• Anti-inflammatory effects, supporting healthier vessel walls

• Antiplatelet activity, reducing platelet aggregation in experimental models

Geranylgeraniol (GG), a naturally occurring isoprenoid, supports cellular and metabolic pathways linked to:

• Vascular integrity

• Mitochondrial function

• Lipid handling and cellular resilience

Together, annatto-derived T3 and GG act upstream, supporting the biological systems that actually determine cardiovascular risk, rather than simply lowering a cholesterol number.

Statins vs Biological Systems Thinking

Statins primarily reduce LDL-C by inhibiting cholesterol synthesis. They do not directly address:

• Oxidative damage

• Platelet biology

• Triglyceride-rich lipoproteins

• Endothelial dysfunction

This does not mean statins are always inappropriate, but it does mean they address only part of the problem.

A systems-based approach asks a broader, more important question:

Are we protecting the biology that prevents plaque rupture and clot formation?

Questions Worth Asking Your Doctor

When discussing statins, supplements and cardiovascular risk, informed questions matter.

If told “vitamin E doesn’t help”:

• Which form?

• Alpha-tocopherol or tocotrienols?

• Which outcomes were measured?

If told “supplements don’t work”:

• Which supplements?

• At what doses?

• Based on which studies?

If prescribed a statin:

• Are inflammation, oxidation and clot risk being addressed?

• How are triglycerides and metabolic markers monitored?

Good medicine starts with good questions.

What Does This All Mean?

Several conclusions are now difficult to ignore:

• Heart disease is not a cholesterol problem alone

• Most heart attacks occur in people with “normal” LDL-C

• Acute events are clot-driven

• Inflammation, oxidative stress and lipid instability are central

• Statins target only one pathway

• Annatto-sourced T3 and GG support multiple upstream mechanisms

This science exists, yet many people are never taught it.

Practical, Evidence-Informed Takeaways

✔ Be informed, not frightened
✔ Look beyond LDL-C
✔ Address inflammation, oxidation and triglycerides
✔ Consider upstream nutritional support
✔ Take ownership of your health decisions

You don’t need to reject conventional medicine, but you do need to understand the biology behind the advice you’re given.

Final Take-Home Message

Heart disease is not a cholesterol issue.
It is a biological systems issue.

Strategies that protect antioxidant defences, stabilise lipids, support vascular health and maintain healthy clotting address the true drivers of cardiovascular events.

Annatto-sourced tocotrienols (T3) and geranylgeraniol (GG) offer a scientifically grounded, biologically rational way to support these upstream mechanisms, safely, naturally and proactively.

The best health decisions are not made from fear.
They are made from understanding.