How do I lower my risk of atherosclerotic cardiovascular disease?

Our read is that early intervention is crucial, with half of all heart attacks and strokes occurring before age 60, and a 35-year-old can be informed of a 30% chance of infarct or stroke before age 65 to understand risk and the impact of early intervention, according to Peter Attia.

Our read is that genetic instruments strongly infer a causal relationship between Lp(a) and atherosclerotic cardiovascular diseases, with elevated Lp(a) associated with a hazard ratio of approximately 2 to 4 for atherosclerosis, depending on the concentration, as noted by Peter Attia.

Our read is that pharmacologically reducing apoB to infantile levels of 30-40 mg/dL in adults may be beneficial, according to Peter Attia, and physically active, healthy, non-overweight, and non-smoking individuals may not need to worry about protein intake causing atherosclerosis, as stated by Rhonda Patrick.

• 01Women can experience myocardial infarction events during their menopausal years (Peter Attia, 1x).
• 02Elevated Lp(a) is associated with a hazard ratio of approximately 2 to 4 for atherosclerosis, depending on the concentration (Peter Attia, 2x).
• 03Increasing polyunsaturated fatty acids while decreasing saturated fat increased oxidized LDL and Lp(a) in a study (Paul Saladino, 2x).
• 04Bob Harper had a heart attack due to high lipoprotein(a) levels (Paul Saladino, 1x).
• 05Half of all heart attacks and strokes occur before the age of 60 (Peter Attia, 1x).
• 06A 35-year-old can be informed of a 30% chance of infarct or stroke before age 65 to understand risk and the impact of early intervention (Peter Attia, 1x).
• 07In adults aged 50+ who developed shingles, prior vaccination was linked to a 21% lower risk of Major Adverse Cardiovascular Events (Bryan Johnson, 1x).
• 08A combination of high LDL, high HDL, and low triglycerides represents a favorable cardiovascular risk profile, with the exception of high LDL (Paul Saladino, 1x).
• 09Pharmacologically reducing apoB to infantile levels of 30-40 mg/dL in adults may be beneficial (Peter Attia, 1x).
• 10Physically active, healthy, non-overweight, and non-smoking individuals may not need to worry about protein intake causing atherosclerosis (Rhonda Patrick, 1x).
• 11Hyperinsulinemia negatively impacts LDL receptor function and related proteins, altering LDL particle levels (Peter Attia, 1x).
• 12Genetic instruments strongly infer a causal relationship between Lp(a) and atherosclerotic cardiovascular diseases (Peter Attia, 3x).
• 13A large increase in LDL cholesterol and LDL particle count on a carnivore diet raises concerns about long-term cardiovascular risk (Peter Attia, 1x).
• 14Lipoprotein(a) [LP(a)] levels of 13.1 require attention due to increased cardiovascular risk (Paul Saladino, 1x).

Our read is that cardiovascular disease risk prediction models should focus on 30-year or lifetime risk rather than the common 10-year risk, according to Peter Attia. Paul Saladino questions the assertion that LDL alone is sufficient to initiate atherosclerosis and notes that the oxidized LDL test may not be a valuable marker. Peter Attia also points out that some individuals believe LDL is causally related to atherosclerotic cardiovascular disease only in the context of metabolic illness. Paul Saladino cautions against relying on the 'weight of the evidence' in meta-analyses that include poorly done studies and suggests the pharmaceutical industry may exaggerate benefits. Peter Attia states that measuring the cholesterol content of Lp(a) particles is not informative for estimating risk and that HDL cholesterol is considered a less relevant metric. Rhonda Patrick notes that standard laboratory reference ranges for ApoB are not ideal for clinical management. Andrew Huberman believes not screening 20-year-olds for Lp(a) is a missed opportunity. Paul Saladino also claims that consuming seed oils or excess polyunsaturated fats can lower apoB and LDL-C but increase LP(a) and oxidized LDL, thereby increasing cardiovascular risk.

Our read is that the verdict would change if new evidence emerged challenging the causal link between Lp(a) and atherosclerotic cardiovascular disease, or if studies demonstrated that pharmacologically reducing apoB to very low levels was not beneficial or had significant adverse effects. Additionally, if new risk prediction models or biomarkers were identified that were more accurate and actionable than those currently discussed, it would alter the approach to risk reduction.