576: Your Doctor Is Wrong About Cholesterol & Heart Disease! | Dr. Malcolm Kendrick
Dec 26, 2023
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Dr. Malcolm Kendrick, a General Practitioner and bestselling author, challenges the cholesterol hypothesis and discusses the role of saturated fat and LDL cholesterol in heart disease. He explains the anatomy of plaque in arteries, the importance of protecting the glycocalyx, and the real causes of heart disease. Kendrick also shares practical tips to repair the endothelium and highlights the flawed understanding of LDL cholesterol and heart disease.
Contrary to popular belief, LDL does not damage endothelial cells or directly contribute to plaque formation.
Lp(a), a form of LDL with an additional protein attached, plays a role in blocking damaged areas in blood vessels.
Plaque is not simply composed of LDL or cholesterol; it contains a variety of components, including fiber, red blood cells, white blood cells, and more.
Deep dives
The Flaws in the Cholesterol Hypothesis
The cholesterol hypothesis suggests that an elevated blood level of LDL cholesterol causes heart disease. This podcast episode challenges this hypothesis, pointing out the flaws in the current understanding. Firstly, saturated fat does not raise LDL levels, as there is no direct pathway for this to occur. Furthermore, LDL does not haphazardly pass through the endothelial cells lining the arteries and cause plaque formation. The focus on LDL in heart disease is misguided, as there is no identified mechanism of action by which it can damage endothelial cells or contribute to plaque formation. The anatomy of plaque also reveals that it is not solely composed of LDL or cholesterol, but contains various components such as fiber, red blood cells, white blood cells, and more. Additionally, the episode discusses the existence of Lp(a), an evil twin of LDL that has an additional protein attached. Lp(a) is attracted to damaged areas in blood vessels and plays a role in blocking them, but its exact function is not fully understood.
Debunking the Notion of LDL Damage
Contrary to popular belief, LDL does not damage endothelial cells or directly contribute to plaque formation. The body has highly effective mechanisms, such as the tight junctions formed by endothelial cells and the protective glyco-calix layer, to prevent LDL from passing through and causing damage. Endothelial cells have tight junctions that create a barrier to the passage of substances, including LDL. The glyco-calix layer further protects the endothelial cells and prevents blood clot formation. The notion that LDL can damage or penetrate endothelial cells lacks evidence and does not align with the body's intricate control systems.
Unveiling the Role of LPA
Lp(a), a form of LDL with an additional protein attached, plays a role in blocking damaged areas in blood vessels. When blood vessel lining is damaged, Lp(a) is attracted to the site and binds to the damaged area, contributing to the blockage. The exact function of Lp(a) is not fully understood, with mainstream medicine still exploring its purpose. However, it is clear that Lp(a) has different characteristics compared to LDL and plays a role in responding to vascular damage.
The Complexity of Plaque Composition
Plaque is not simply composed of LDL or cholesterol. It contains a variety of components, including fiber, red blood cells, white blood cells, and more. While LDL and cholesterol are present within plaque, they are only a small part of the overall composition. Plaque formation is a complex process involving multiple factors, and a singular focus on LDL does not fully capture the intricacies behind plaque formation.
The Thrombogenic Hypothesis: Exploring the Role of Blood Clotting in Heart Disease
The Thrombogenic Hypothesis suggests that blood clotting plays a significant role in the development of heart disease. When the endothelium (lining) of arteries is damaged, the body triggers the formation of a blood clot to repair the area. Elevated levels of LPA (lipoprotein A) act as a "sticking plaster" on the damaged artery walls, making it difficult to remove the clot. The enzyme plasmin is responsible for breaking down the fibrin in blood clots, but LPA inhibits the activation of plasmin. Studies have found that LPA is present in plaques along with LDL, indicating that LDL is not the sole cause of heart disease. Plaques are believed to be blood clots in various stages of breakdown and change. The Thrombogenic Hypothesis suggests that repeated episodes of blood clotting in specific areas lead to plaque growth, which can eventually rupture and cause heart attacks or strokes. Factors such as smoking, high blood sugar levels, and cocaine use can damage the endothelium and contribute to the formation of blood clots. Strategies to enhance endothelial health include adopting a low-carbohydrate diet, getting regular sunshine, and reducing negative stress and strain on the body.
Enhancing Endothelial Health and Preventing Heart Disease
To enhance endothelial health and minimize the risk of heart disease, several strategies can be implemented. These include maintaining healthy blood sugar levels through intermittent fasting or reducing carbohydrate consumption. Regular exposure to sunshine can stimulate the release of nitric oxide, lower blood pressure, and protect blood vessels. Consuming certain proteins like chondroitin sulfate may strengthen the glycocalyx, a protective layer on endothelial cells. Additionally, managing stress levels and cultivating positive social relationships are essential for cardiovascular health. By addressing individual risk factors and optimizing endothelial function, the likelihood of heart disease can be reduced.
Dr. Malcolm Kendrick is a General Practitioner and bestselling author.
He is now well worn around the edges, from battling the cholesterol hypothesis. This hypotheses states that an elevated blood level of LDL cholesterol causes heart disease.
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