The Great Cholesterol Con

1. The cholesterol hypothesis is fundamentally flawed

A raised cholesterol level does not cause heart disease.

Flawed foundations. The cholesterol hypothesis, which proposes that high cholesterol levels cause heart disease, is built on shaky scientific ground. Despite decades of research, there is little evidence supporting a causal link between cholesterol levels and heart disease risk. In fact, many studies contradict this hypothesis:

• Low cholesterol levels are associated with increased mortality in older adults
• Women with higher cholesterol levels often have lower rates of heart disease
• Many populations with high cholesterol levels have low rates of heart disease (e.g. France, Switzerland)
• Cholesterol levels don't predict heart disease risk in most age groups

Lipid confusion. Much of the confusion stems from conflating cholesterol with lipoproteins like LDL and HDL. Cholesterol itself doesn't float freely in the bloodstream - it's carried by lipoproteins. The idea of "good" and "bad" cholesterol is overly simplistic and misleading. LDL and HDL play complex roles in lipid transport and metabolism that can't be reduced to "good" or "bad."

2. Diet has little impact on heart disease risk

Eat whatever you like (Diet has nothing to do with heart disease)

Dietary guidelines debunked. Despite decades of dietary recommendations focused on reducing saturated fat and cholesterol intake, there is little evidence that diet significantly impacts heart disease risk. Major studies and historical data contradict the diet-heart hypothesis:

• Reducing saturated fat intake has not been shown to reduce heart disease in clinical trials
• Many populations with high saturated fat intake have low rates of heart disease
• Attempts to link specific foods or nutrients to heart disease have produced inconsistent results

Failed interventions. Large-scale dietary interventions aimed at reducing heart disease through diet modification have largely failed to show significant benefits. The human body tightly regulates cholesterol levels regardless of dietary intake. Focusing on diet as a primary means of preventing heart disease has likely been misguided and ineffective.

3. Statins provide minimal benefit for most people

Statins do not save lives in women.

Overhyped benefits. While statins can reduce cardiovascular events in high-risk individuals, their benefits have been greatly exaggerated for most people. The absolute risk reduction from taking statins is often quite small:

• For people without pre-existing heart disease, statins do not reduce overall mortality
• Women show no mortality benefit from taking statins at any risk level
• The number needed to treat to prevent one cardiovascular event is often over 100
• Any benefits are likely due to anti-inflammatory effects rather than cholesterol lowering

Overlooked harms. The potential side effects and harms of statins are often downplayed. These can include muscle pain, cognitive issues, and increased diabetes risk. Given the minimal benefits for many people, the risk-benefit profile of statins is questionable for primary prevention in low-risk individuals.

4. Stress and social factors are key drivers of heart disease

The most deadly long-term stressor that can affect entire populations is something that I define as 'social dislocation'

Beyond traditional risk factors. While conventional wisdom focuses on factors like cholesterol, blood pressure, and smoking, evidence suggests psychosocial stress plays a major role in heart disease development. Chronic stress can lead to physiological changes that damage the cardiovascular system over time.

Social determinants of health. Population-level social factors strongly predict heart disease rates:

• Social isolation and lack of community support increase heart disease risk
• Low socioeconomic status is associated with higher rates of heart disease
• Major social disruptions (e.g. forced relocation, cultural upheaval) precede rises in heart disease
• Racism and discrimination create chronic stress that damages cardiovascular health

Understanding these social and psychological factors is crucial for developing effective heart disease prevention strategies beyond traditional risk factor modification.

5. The HPA axis links stress to cardiovascular damage

HPA-axis dysfunction ties together a whole series of apparently disparate factors known to cause heart disease.

Stress response physiology. The hypothalamic-pituitary-adrenal (HPA) axis is the body's primary stress response system. Chronic activation of this system due to ongoing psychosocial stress can lead to dysfunction and dysregulation of cortisol and other stress hormones. This HPA axis dysfunction appears to be a key mechanism linking chronic stress to cardiovascular damage.

Metabolic disruption. HPA axis dysfunction can cause a cascade of metabolic changes that promote atherosclerosis:

• Insulin resistance and blood sugar dysregulation
• Increased visceral fat deposition
• Elevated inflammatory markers
• Alterations in blood lipids and clotting factors
• Endothelial dysfunction

These metabolic disturbances create an environment conducive to arterial damage and plaque formation, independent of traditional risk factors like LDL cholesterol levels.

6. Blood clotting factors play a crucial role in atherosclerosis

Plaques start life as small areas of damage to the endothelium, which are normally healed by the body's natural repair mechanisms – thrombus formation and endothelial re-growth.

Clotting cascade. The formation and growth of atherosclerotic plaques appears to be intimately linked to blood clotting processes. Damage to the arterial lining triggers clot formation as a repair mechanism. In some cases, these clots become incorporated into the artery wall, forming the basis of a plaque.

Thrombosis risk. Factors that promote blood clotting or impair clot breakdown may accelerate plaque growth:

• Elevated fibrinogen levels
• High levels of clotting factors like PAI-1 and von Willebrand factor
• Increased platelet reactivity
• Impaired fibrinolysis (clot breakdown)

Many effective cardiovascular treatments, including statins, aspirin, and omega-3 fatty acids, have anti-thrombotic effects. This suggests modulating clotting processes may be a key mechanism for preventing and treating heart disease.

7. Population-level social disruption predicts heart disease rates

Fifteen or twenty years earlier they had suffered, proportionally, the greatest forced relocation in the history of Europe.

Historical patterns. Major social upheavals often precede dramatic increases in heart disease rates by 15-20 years. Examples include:

• Forced relocation of 400,000 Finns from Karelia in 1948, followed by Finland having the world's highest heart disease rates in the 1960s
• Massive urban renewal and relocation programs in Glasgow in the 1950s-60s, followed by Scotland having the world's highest heart disease rates in the 1970s-80s
• Social and economic turmoil in Eastern Europe after WWII and the fall of communism, followed by skyrocketing heart disease rates

Community disruption. These population-level stressors appear to work by disrupting social networks, community cohesion, and cultural continuity. The resulting chronic stress and loss of social support create an environment conducive to widespread cardiovascular damage.

8. The medical establishment resists challenging prevailing theories

My theory is that Keys was so stung by this event that he left the Geneva meeting intent on gathering the definitive evidence to establish or refute the Diet-Heart theory.

Entrenched paradigms. The medical and scientific establishment often fiercely resists challenges to prevailing theories, even in the face of contradictory evidence. The cholesterol hypothesis has become so entrenched that contrary data is often ignored or explained away rather than prompting a reevaluation of the theory.

Conflicts of interest. Financial ties between researchers, medical organizations, and pharmaceutical companies create conflicts of interest that can bias research and clinical guidelines. This is particularly evident in the promotion of statins and cholesterol-lowering strategies:

• Many guideline writers have financial ties to statin manufacturers
• Negative statin trials often go unpublished or underreported
• Critical perspectives on cholesterol are often marginalized

Paradigm shift needed. Overcoming these entrenched ideas will require a major paradigm shift in how we conceptualize and approach heart disease prevention. This shift must prioritize addressing psychosocial factors and social determinants of health over the current focus on individual-level risk factors and pharmaceutical interventions.

Last updated: April 6, 2025