Why Low Cholesterol & ApoB Levels Are Critical for Longevity | Dr. Peter Attia & Dr. Andrew Huberman

Summary

In this insightful dialogue, Peter Attia and Andrew Huberman discuss the causal relationship between smoking and lung cancer, emphasizing the importance of causality in medicine. They extend this concept to the link between ApoB (a protein in the blood) and atherosclerosis, questioning current medical practices that wait for a high risk threshold before intervention. Attia advocates for proactive treatment to modify modifiable risks, regardless of current risk levels, to prevent diseases like heart attacks and strokes.

Takeaways

• 🚭 Smoking is causally related to lung cancer, as agreed by both Peter Attia and Andrew Huberman.
• 🔍 The discussion emphasizes the importance of establishing causality in medical research and practice.
• 🛑 Peter Attia suggests that the current approach to smoking cessation is flawed, proposing a model based on risk assessment.
• 📉 Attia argues against waiting until a certain risk threshold is reached before recommending smoking cessation.
• 🚫 The analogy is made that endorsing smoking until a risk threshold is as absurd as the hypothetical scenario presented.
• 🧬 Mendelian randomizations, which use genetic variants, provide strong evidence for the causal relationship between ApoB and atherosclerosis.
• 📊 Current medical practice involves calculating a 10-year risk of MACE (major adverse cardiac events) to assess the need for treatment.
• 🤔 Attia criticizes the practice of only treating LDL or ApoB when the 10-year MACE risk is above a certain percentage.
• 💯 He advocates for modifying modifiable risks regardless of the duration of the risk tail, suggesting earlier and less aggressive treatment.
• 🩺 Attia discusses the use of CT angiograms to assess the condition of coronary arteries and determine treatment goals for ApoB levels.
• ⚠️ A high ApoB level, even without symptoms, is considered a significant red flag and an indication for potential treatment.

Q & A

What is the consensus between Peter Attia and Andrew Huberman on the causal relationship between smoking and lung cancer?

Both Peter Attia and Andrew Huberman agree that smoking is causally related to lung cancer, not just associated with it.

What does Peter Attia consider an obsession of his in the context of medicine?

Peter Attia considers causality an obsession of his in the context of medicine, as he spends most of his day thinking about it.

What is the difficulty Peter Attia points out in studying medicine with respect to human beings?

Peter Attia points out that the difficulty in studying medicine with respect to human beings is inferring causality for most things that are done.

What is the logical equivalency according to Peter Attia if smoking is causally related to lung cancer?

The logical equivalency according to Peter Attia is that smoking cessation reduces the probability of lung cancer.

What is the new philosophy around smoking cessation that Peter Attia proposes in the script?

Peter Attia proposes a philosophy where people are allowed to smoke but are assessed for lung cancer risk using a model that predicts when their 10-year risk exceeds a certain threshold, at which point they are advised to stop smoking.

What does Peter Attia consider 'idiotic' in the context of smoking and lung cancer?

Peter Attia considers it 'idiotic' to endorse smoking until a person crosses a certain threshold of risk for lung cancer, rather than advising against smoking from the start.

What is Mendelian randomization and how does it relate to the causal relationship between ApoB and atherosclerosis?

Mendelian randomization is a method that uses genetic variants as a natural experiment to determine causality. It relates to ApoB and atherosclerosis by showing a gradation of LDL or ApoB concentration from very low to very high, indicating a causal relationship.

What does Peter Attia argue is the current backwards approach in medicine regarding LDL or ApoB treatment?

Peter Attia argues that the current approach in medicine is backwards because it only considers treating LDL or ApoB when the 10-year risk of a major adverse cardiac event is above a certain threshold, rather than modifying it regardless of the risk level if it is causal and modifiable.

What is MACE and why is it significant in the context of the script?

MACE stands for Major Adverse Cardiac Event, which includes heart attack, stroke, or death resulting from these conditions. It is significant in the script as it is the metric used to assess the 10-year risk for patients, which influences the decision on LDL or ApoB treatment.

What does Peter Attia suggest regarding the treatment of ApoB levels in patients with different risk factors?

Peter Attia suggests treating ApoB levels to the 5th percentile (about 60 mg/dL) if there are no signs of disease, but to the 1st percentile (30-40 mg/dL) if there are risk factors present such as calcification, soft plaque, family history, or other significant risk factors.

How does Peter Attia view the situation of a person with ApoB levels in the low 130s?

Peter Attia views ApoB levels in the low 130s as a huge red flag, indicating a high risk that requires attention, even though causality does not guarantee the disease in every individual.