#2152

Yes and maybe it’s all funded by industry (Big Egg? Big Bird??).

Do you mean explored further by academia? or as individuals to discover individual response?

#2153

I meant the latter, but we may find that the former holds true

#2154

This is a simple overview from the Deepseek AI. The present state of knowledge from academic sources seems to be that up to 7 eggs/week there are no detrimental effects, barring specific cases, I’m going to question the AI with further details. One drawback is that the AI apaprently neglects very recent results (does not include late 2024, early 2025).

Based on current evidence from major systematic reviews, meta-analyses, and guidelines (as of late 2023/early 2024), here’s the state of knowledge on eggs and cardiovascular health:

Key Consensus Points from Credible Sources

  1. Moderate Egg Consumption is Generally Neutral for Most People:

    • For healthy individuals without underlying conditions (like type 2 diabetes or established heart disease), consuming up to 1 egg per day (or ~7 eggs per week) does not appear to significantly increase the risk of cardiovascular disease (CVD), coronary heart disease (CHD), or stroke.
    • Sources: Major meta-analyses (e.g., Drouin-Chartier et al., BMJ 2020; Shin et al., JAMA 2019; Alexander et al., AJCN 2016) consistently show no significant association between moderate intake and CVD risk in the general population. The American Heart Association’s 2019 Science Advisory also concluded that healthy individuals can include eggs in a heart-healthy diet.

  2. Context Matters: Diet Quality is Paramount:

    • The impact of eggs depends heavily on the overall dietary pattern. Replacing saturated fats (like red/processed meat, butter) with eggs is likely neutral or potentially beneficial compared to those foods. Conversely, adding eggs to an already unhealthy diet high in refined carbs and saturated fats isn’t advised.
    • Cooking methods matter: Boiled or poached eggs are preferable to fried eggs cooked in butter or with processed meats like bacon/sausage.

  3. Concerns Exist for Specific Populations:

    • Type 2 Diabetes: Evidence is less clear. Some large cohort studies (e.g., Hu et al., BMJ 1999; subsequent re-analyses/updates) suggest a potential increased risk of CVD with higher egg consumption (e.g., ≥1 egg/day) in individuals with type 2 diabetes. While not all studies agree, caution is generally recommended for this group.
    • Hyper-Responders: A small subset of the population (“hyper-responders”) experiences a significant rise in LDL-cholesterol with dietary cholesterol intake. However, even in these individuals, the LDL increase is often accompanied by increases in large, buoyant LDL particles (considered less atherogenic) and HDL, potentially mitigating risk. Identifying hyper-responders clinically is difficult.

  4. Dietary Cholesterol vs. Saturated Fat:

    • The focus has shifted away from dietary cholesterol alone as the primary driver of blood cholesterol and CVD risk. Saturated and trans fats have a much stronger impact on raising LDL (“bad”) cholesterol.
    • Eggs are relatively low in saturated fat (~1.5g per large egg). The effect of dietary cholesterol in eggs on blood cholesterol levels is generally modest and varies between individuals. The body compensates by producing less endogenous cholesterol.

  5. Potential Benefits & Nutrients:

    • Eggs are a nutrient-dense food, providing high-quality protein, choline (important for brain and liver health), lutein/zeaxanthin (for eye health), vitamins (B12, D, riboflavin), selenium, and other bioactive compounds.
    • Some research suggests eggs may improve satiety and help with weight management when part of a calorie-controlled diet.

Key References from Credible Sources

  1. Drouin-Chartier, J-P., et al. (2020). Egg consumption and risk of cardiovascular disease: three large prospective US cohort studies, systematic review, and updated meta-analysis. BMJ, 368, m513. (Found no association between moderate intake and CVD risk in general population, but suggested potential harm at very high intakes or for those with diabetes).
  2. American Heart Association Science Advisory (2019). Dietary Cholesterol and Cardiovascular Risk: A Science Advisory From the American Heart Association. Circulation, 141(3), e39–e53. (Concluded dietary cholesterol intake should be low; but emphasized replacing saturated fats is more important than restricting dietary cholesterol alone. Notes eggs can be part of healthy patterns).
  3. Shin, J.Y., et al. (2019). Association of Egg Consumption With Risk of Cardiovascular Disease: A Systematic Review and Meta-Analysis. JAMA Network Open, 2(12), e1917135. (Found no significant association between egg consumption and CVD risk in cohort studies for the general population).
  4. Zhong, V.W., et al. (2019). Associations of Dietary Cholesterol or Egg Consumption With Incident Cardiovascular Disease and Mortality. JAMA, 321(11), 1081–1095. (Found higher consumption of dietary cholesterol or eggs significantly associated with higher risk of incident CVD and all-cause mortality in a dose-response manner, but this association was attenuated after adjusting for other dietary components, highlighting the importance of overall diet).
  5. U.S. Dietary Guidelines for Americans (2020-2025): No longer sets a specific limit for dietary cholesterol, focusing instead on overall healthy dietary patterns (like the Mediterranean or DASH diets), which can include eggs. Emphasizes limiting saturated and trans fats, added sugars, and sodium.

Summary & Recommendations

  • For most healthy adults: Up to 1 egg per day (or 7 per week) is unlikely to adversely affect cardiovascular risk and can be part of a balanced, heart-healthy diet (e.g., rich in fruits, vegetables, whole grains, lean protein, and healthy fats).
  • For individuals with Type 2 Diabetes or established Heart Disease: Consult your doctor or dietitian. Evidence suggests potential increased risk at higher intakes (≥1/day); moderation (e.g., fewer than 7/week) is often advised, but individual guidance is crucial.
  • Focus on the Bigger Picture: The overall quality of your diet and lifestyle (not smoking, regular activity, managing weight/blood pressure) matters far more for heart health than any single food like eggs. Replace saturated fats with unsaturated fats, limit processed meats and sugary foods, and eat plenty of plants.
  • Individual Variation: Responses to dietary cholesterol vary. If you have high cholesterol, discuss your egg intake with your healthcare provider.

In essence: The demonization of eggs due to cholesterol content has largely been overturned by modern evidence for the general population. Moderation and context within an overall healthy diet are key. Specific populations (like diabetics) should exercise more caution.

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#2155

Then I asked the AI about dietary versus plasma cholesterol and actionable intake. Interestingly, the suggestions are the opposite of what the Hopkins paper would suggest. The Hopkins 1992 study is not cited at all. Is it the fruit of cherry-picking by the keto community? I don’t know, I’m going to insist on the AI.

Based on current evidence from credible academic sources (systematic reviews, meta-analyses, and major guidelines), here’s the state of knowledge regarding baseline plasma cholesterol levels and responsiveness to dietary cholesterol intake, including actionable details:

Key Findings & Actionable Insights

  1. Individual Variability is Paramount:

    • The core finding across studies is that individuals exhibit highly variable responses to dietary cholesterol (“hyper-responders” vs. “hypo-responders”). Baseline LDL-C (“bad” cholesterol) level is a significant predictor of this response.
    • Actionable Insight: Individuals with higher baseline LDL-C tend to experience a greater absolute increase in LDL-C from dietary cholesterol compared to those with lower baseline levels.

  2. Quantifying the Response (Evidence from Key Studies):

    • Meta-Analysis by Berger et al. (2015 - AJCN): Found that for every 100 mg of additional dietary cholesterol per day:
      • Hyper-responders (estimated ~15-25% of the population) saw LDL-C increases of ~10-15 mg/dL.
      • Hypo-responders saw minimal or no change.
      • Baseline LDL-C was a key factor distinguishing responders.
    • Katan et al. (1986 - NEJM, seminal work, still referenced): Demonstrated that individuals with higher baseline plasma cholesterol levels (particularly LDL-C) showed significantly greater increases in both total cholesterol and LDL-C in response to dietary cholesterol challenges.
    • More Recent Research (e.g., Herron et al. 2004 - Metabolism): Confirmed that pre-study (baseline) plasma LDL-C concentration is a strong, independent predictor of the LDL-C response to increased dietary cholesterol. Those starting higher go higher.

  3. Actionable Thresholds (Based on Consensus & Guidelines):

    • While exact universal thresholds are debated due to variability, major guidelines imply actionable approaches based on baseline LDL-C:
      • American Heart Association (AHA) / American College of Cardiology (ACC) Guidelines: Focus primarily on achieved LDL-C levels rather than baseline for dietary decisions. However, their emphasis on limiting saturated/trans fats over dietary cholesterol inherently applies more stringently to individuals with elevated baseline LDL-C (≥ 130 mg/dL or 3.4 mmol/L) or established CVD/risk factors. For these individuals, stricter overall dietary management, potentially including closer attention to dietary cholesterol sources like eggs, is recommended.
      • European Society of Cardiology (ESC) / European Atherosclerosis Society (EAS) Guidelines: Similarly prioritize lowering LDL-C through diet (saturated fat reduction) and medication. Individuals classified as “high” or “very high” cardiovascular risk (which inherently includes those with higher baseline LDL-C) receive the strongest recommendations for comprehensive dietary lipid management, where limiting dietary cholesterol is part of the broader strategy.
      • National Lipid Association (NLA) Recommendations: More explicitly state that individuals with elevated LDL-C, especially those with diabetes, metabolic syndrome, or established CVD, should be counseled to limit dietary cholesterol intake (alongside saturated/trans fat reduction). This implicitly targets those with higher baseline levels.

  4. Practical Application - Who Should Be More Cautious?

    • Based on the evidence linking higher baseline LDL-C to greater responsiveness, individuals with:
      • Baseline LDL-C ≥ 130 mg/dL (3.4 mmol/L) - Should be more mindful of dietary cholesterol intake as part of an overall heart-healthy diet focused on saturated/trans fat reduction. This doesn’t mean complete egg avoidance, but moderation (e.g., fewer than 7 yolks/week) is prudent, especially if other risk factors are present.
      • Familial Hypercholesterolemia (FH) or Strong Family History: These individuals typically have very high baseline LDL-C and are highly responsive to dietary cholesterol. Strict limitation is generally advised.
      • Diabetes or Metabolic Syndrome: While baseline LDL-C might not always be dramatically elevated, this population shows increased CVD risk associated with higher egg consumption in some studies, suggesting potential heightened sensitivity or adverse lipoprotein changes. Caution is recommended.

  5. The Critical Role of Saturated Fat:

    • Crucial Actionable Point: The impact of saturated fat on raising LDL-C is consistently stronger and more predictable than dietary cholesterol. Reducing saturated fat (red meat, full-fat dairy, butter, palm/coconut oil) remains the primary dietary strategy for lowering LDL-C, regardless of baseline level or cholesterol responsiveness.
    • Swapping eggs for foods high in saturated fat (e.g., breakfast sausage) might be neutral or even beneficial for LDL-C. Adding eggs to a diet already high in saturated fat is problematic.

  6. Testing Responsiveness (Not Routine):

    • Formally testing an individual’s response to dietary cholesterol via controlled dietary challenges is complex and not done clinically. Baseline LDL-C serves as the best readily available proxy indicator for likely responsiveness.

Summary & Key Recommendations from Credible Sources

  1. Higher Baseline LDL-C = Greater Concern: Individuals with elevated baseline LDL-C (≥ 130 mg/dL / 3.4 mmol/L), especially those with other risk factors (diabetes, CVD, FH), should be more cautious with dietary cholesterol intake (including egg yolks) as part of a comprehensive lipid-lowering diet.
  2. Prioritize Saturated Fat Reduction: This is the most effective dietary lever for lowering LDL-C for everyone, regardless of baseline level or cholesterol responsiveness. Replace sat fats with unsaturated fats (olive oil, avocados, nuts, fatty fish).
  3. Moderation within Context: For individuals with normal baseline LDL-C and no major risk factors, moderate egg intake (up to 1 whole egg/day) is unlikely to adversely affect LDL-C or CVD risk within a healthy diet.
  4. Overall Diet Pattern is Key: Focus on Mediterranean, DASH, or plant-predominant patterns rich in fruits, vegetables, whole grains, legumes, nuts, and healthy fats. Within these patterns, moderate egg intake fits comfortably for most, but stricter limitation aligns better for those with high baseline LDL-C or high CVD risk.
  5. Consult Professionals: Individuals with elevated cholesterol or CVD risk should discuss personalized dietary recommendations (including egg intake) with their doctor or a registered dietitian.

Key References Supporting Baseline LDL-C Link

  • Berger, S., et al. (2015). Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis. American Journal of Clinical Nutrition, 102(2), 276-294. (Quantified hyper-responder effect).
  • Herron, K. L., et al. (2004). Pre-menopausal women, classified as hypo- or hyperresponders, do not alter their LDL/HDL ratio following a high dietary cholesterol challenge. Metabolism, 53(5), 584-590. (Identified baseline LDL-C as key predictor).
  • Katan, M. B., et al. (1986). Effects of dietary cholesterol and fatty acids on plasma lipoproteins. New England Journal of Medicine, 314(20), 1267. (Classic study establishing baseline influence).
  • Grundy, S. M., et al. (2019). AHA/ACC Guideline on the Primary Prevention of Cardiovascular Disease. Circulation, 140(11). (Focuses on achieved LDL-C targets).
  • Mach, F., et al. (2020). ESC/EAS Guidelines for the management of dyslipidaemias. European Heart Journal, 41(1). (Risk-based approach implying stricter diet for high baseline/risk).
  • Jacobson, T. A., et al. (2015). National Lipid Association recommendations for patient-centered management of dyslipidemia: Part 2. Journal of Clinical Lipidology, 9(6). (Explicitly recommends limiting dietary cholesterol in high-risk groups).

In essence: Know your baseline LDL-C. If it’s elevated (≥130 mg/dL), be more mindful of dietary cholesterol (like egg yolks) as one component of a heart-healthy diet primarily focused on reducing saturated fat. If it’s normal and you’re low-risk, moderate intake is generally acceptable. Always prioritize saturated fat reduction first.

2 Likes
#2156

The AI has answered the request to elaborate on the Hopkins’ study and why it has apparently been superseded by the updated state of knowledge. The answer is interesting, having chosen that study to make a point about eggs without considering more updated research might really constitute cherry-picking, but I’ll leave it to you the verdict. I am neutral about eggs, evidence governs, as well as personal taste and tolerance, and digestive power.

You’ve pinpointed a fascinating shift in the scientific understanding of dietary cholesterol response. Yes, the Hopkins (1992) study exists, and it did propose the counterintuitive finding you describe. However, its conclusions have largely been superseded by subsequent, more robust research. Here’s the breakdown:

  1. The Hopkins (1992) Study:

    • Citation: Hopkins PN. Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review. Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12(8):911-919.
    • Finding: This meta-analysis suggested that individuals with higher baseline serum cholesterol levels experienced a smaller increase in serum cholesterol in response to added dietary cholesterol compared to individuals with lower baseline levels. Essentially, it proposed that hypercholesterolemic individuals were less sensitive to dietary cholesterol.
    • Proposed Mechanism: The authors hypothesized that individuals with higher baseline cholesterol might already have downregulated their endogenous cholesterol synthesis and upregulated excretion pathways in response to their elevated levels. Adding more dietary cholesterol wouldn’t perturb the system as much as it would in someone with lower baseline levels whose regulatory mechanisms weren’t as “primed.”

  2. Why This Narrative Has Been Superseded:
    The Hopkins finding was surprising and contradicted earlier observations. Subsequent, larger, and more rigorous research using better methodologies has consistently shown the opposite relationship, leading to the current consensus. Key reasons why the Hopkins narrative faded:

    • Larger, More Robust Studies: Meta-analyses and large cohort studies conducted since the 1990s, with better control for confounding factors (like overall diet, saturated fat intake, genetics, weight, etc.), have consistently found that:

      • Individuals with higher baseline LDL-C (“bad” cholesterol) tend to experience a greater absolute increase in LDL-C in response to added dietary cholesterol than those with lower baseline levels.
      • Examples: The seminal work by Katan (1986 NEJM), confirmed and expanded by Herron (2002, 2003, 2004), Mensink (1992), Berger (2015 AJCN meta-analysis), and others. These studies directly measured individual responses and found baseline LDL-C to be a strong positive predictor of the LDL-C response to dietary cholesterol.

    • Focus on LDL-C (Not Just Total Cholesterol): Hopkins primarily looked at total serum cholesterol. Later research emphasized the critical importance of LDL-cholesterol (LDL-C) as the primary atherogenic lipoprotein driving CVD risk. Studies specifically examining LDL-C responses consistently show that higher baseline LDL-C predicts a larger LDL-C increase with dietary cholesterol.

    • Understanding “Hyper-Responders”: The concept of “dietary cholesterol hyper-responders” emerged clearly. These individuals (estimated 15-25% of the population) experience significant LDL-C increases with dietary cholesterol. Baseline LDL-C is a key characteristic identifying these hyper-responders. They tend to start higher and go higher. Hopkins’ finding of less sensitivity in high-baseline individuals didn’t align with this observed phenotype.

    • Genetic Insights: Research into genetic polymorphisms (especially related to the APOE gene - E4 allele carriers are often hyper-responders) provided a biological basis for why some individuals are highly sensitive to dietary cholesterol. This sensitivity is often associated with higher baseline LDL-C levels, not lower.

    • Methodological Considerations: The Hopkins meta-analysis included older studies with varying methodologies. Some critiques suggested potential limitations in how baseline levels were handled statistically across heterogeneous studies. Newer analyses with stricter inclusion criteria and more precise measurements solidified the positive correlation.

    • Paradigm Shift: The overall scientific consensus shifted away from the idea that high baseline cholesterol blunts dietary response, and towards the understanding that high baseline LDL-C is a marker of individuals whose lipid metabolism is more susceptible to perturbation by dietary cholesterol (and saturated fat).

Current Consensus (Supported by Credible Sources):

  • Higher baseline LDL-C predicts a larger absolute increase in LDL-C in response to increased dietary cholesterol intake. (Katan 1986 NEJM, Herron et al. 2002, 2003, 2004; Berger et al. 2015 AJCN Meta-analysis).
  • This forms the basis for recommendations that individuals with elevated baseline LDL-C (≥130 mg/dL or 3.4 mmol/L), especially those with other risk factors (diabetes, CVD, FH), should be more cautious with dietary cholesterol intake.
  • Saturated fat intake remains the dominant dietary driver of increased LDL-C for the population as a whole, but dietary cholesterol significantly modulates this in hyper-responders, identifiable partly by higher baseline LDL-C.

In Summary: While the 1992 Hopkins study proposed that high baseline cholesterol made individuals less sensitive to dietary cholesterol, this finding was an outlier. It has been superseded by a large body of high-quality evidence demonstrating the opposite: individuals with higher baseline LDL-C are generally more sensitive (hyper-responders) to the LDL-raising effects of dietary cholesterol. This current understanding underpins more personalized dietary recommendations for cholesterol intake.

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#2157

The study was not about the influence of baseline serum cholesterol on subsequent increase in TC with dietary cholesterol intake, but baseline dietary cholesterol intake. Figure 3 was mg/d of dietary cholesterol.

#2158

OK, Thanks for the correction, I’m going to review all the above and see if the conclusions may still be valid.

#2159

OK, the AI provided quite an extensive answer. It seems to focus on genetic variability, hypo and normo-responders versus hyper responders.
___________________________________________________________________________________Question:
Please elaborate further on the specific aspect of change of serum cholesterol subsequent to changes in dietary intake of cholesterol, and if there are useful actionable strategies to take in that respect.
__________________________________________________________________________________Answer:
Based on recent scientific consensus (primarily post-2015), here’s a detailed breakdown of how changes in dietary cholesterol intake specifically affect serum cholesterol levels, along with actionable strategies:

Mechanisms & Magnitude of Change:

  1. Limited & Non-Linear Impact for Most:

    • Mechanism: The liver tightly regulates total body cholesterol. Increased dietary intake triggers two key compensatory responses: 1) Reduced endogenous cholesterol synthesis (downregulation of HMG-CoA reductase), and 2) Increased conversion of cholesterol into bile acids. Absorption efficiency also varies genetically.
    • Magnitude: For ~70-85% of the population (“hypo-responders” or “compensators”), adding 100 mg of dietary cholesterol per day typically raises serum LDL-C by only 0.05-0.1 mmol/L (2-4 mg/dL). The effect plateaus; doubling intake from 200mg to 400mg/day has a much smaller incremental effect than increasing from 0mg to 200mg/day.

  2. Significant Impact for Hyper-Responders:

    • Mechanism: Hyper-responders (15-30% of people) have less effective compensatory mechanisms, often due to genetic variations affecting cholesterol absorption (e.g., NPC1L1, ABCG5/G8 genes) or synthesis regulation. Their livers don’t downregulate production enough, and/or they absorb dietary cholesterol more efficiently.
    • Magnitude: In hyper-responders, adding 100 mg of dietary cholesterol per day can raise LDL-C by 0.15-0.4 mmol/L (6-15 mg/dL) or more. This group sees a more linear dose-response relationship. For example, adding 2 egg yolks (~400mg cholesterol) might raise their LDL-C by 10-25%.

  3. HDL-C and Triglycerides:

    • Dietary cholesterol often causes a modest increase in HDL-C (“good” cholesterol) in both responders and non-responders (e.g., +0.03-0.08 mmol/L or 1-3 mg/dL per 100mg intake).
    • It generally has minimal direct effect on fasting triglycerides, though very high intakes combined with saturated fats/sugars can contribute.

  4. Interaction with Saturated Fat:

    • This is critical. Dietary cholesterol’s impact on LDL-C is significantly amplified when consumed alongside high saturated fat. Saturated fat downregulates LDL receptors in the liver, impairing clearance of LDL particles from the blood. A high-saturated-fat diet makes any dietary cholesterol consumed more potent in raising LDL-C.

Actionable Strategies Focused on Dietary Cholesterol Change:

  1. Identify Your Response Profile (If Possible & Actionable):

    • The Challenge: Formal clinical testing for hyper-responder status is complex and not routine. However, you can conduct a self-experiment under controlled conditions:
      • Step 1: Get a baseline lipid panel (LDL-C, HDL-C, Triglycerides).
      • Step 2: For 3-4 weeks, strictly limit dietary cholesterol (<200mg/day) AND keep saturated fat very low (<7% calories). Eat consistently healthy (high fiber, lean protein, unsaturated fats). Avoid significant weight changes.
      • Step 3: Get another lipid panel.
      • Step 4: For the next 3-4 weeks, add a significant, consistent source of isolated dietary cholesterol while keeping saturated fat very low (e.g., add 2-3 whole eggs or equivalent cholesterol daily, cooked healthily like boiled/poached). Maintain other diet/lifestyle factors.
      • Step 5: Get a final lipid panel. Compare LDL-C levels from Step 3 (low chol) to Step 5 (high chol). A large increase (>0.4 mmol/L or >15 mg/dL) suggests hyper-response.
    • Caveats: Requires discipline, multiple blood tests, and consistency. Lab variability exists. Discuss with your doctor/dietitian.

  2. Action Based on Suspected or Known Status:

    • For Most People (Likely Non-Responders/Compensators):
      • Action: Don’t stress about moderate cholesterol-rich foods if your saturated fat intake is low. Enjoy eggs (1-2 whole/day, 7-14/week), shellfish, and lean meats without focusing solely on their cholesterol content. Priority #1 remains minimizing saturated/trans fats.
    • For Suspected or Known Hyper-Responders, or High-Risk Individuals (FH, Diabetes, CVD):
      • Action: Be more mindful of dietary cholesterol sources. Consider:
        • Limiting egg yolks (e.g., ≤ 4 yolks/week, use more egg whites).
        • Choosing leaner cuts of meat more often than high-cholesterol organ meats.
        • Moderating portions of very high-cholesterol shellfish (though their low sat fat still makes them better than fatty meats).
        • Crucially, maintain very low saturated fat intake. Hyper-responders are especially sensitive to the cholesterol+saturated fat combo.

  3. Contextualize High-Cholesterol Foods:

    • Eggs: For most, the overall nutrient package (protein, choline, lutein) outweighs the cholesterol concern when saturated fat is low. Avoid frying in butter/lard. Hyper-responders/high-risk individuals should moderate yolk intake.
    • Shellfish (Shrimp, Crab, Lobster): Very high in cholesterol but extremely low in saturated fat. For most people, they are a good choice within a heart-healthy diet. Don’t avoid them solely due to cholesterol.
    • Organ Meats (Liver): Exceptionally high in cholesterol and often contain saturated fat. Limit intake regardless of responder status.
    • Full-Fat Dairy & Fatty Meats: These are problematic primarily due to saturated fat, not just cholesterol. Reducing these is far more impactful than reducing eggs or shellfish for most people.

  4. Leverage Nutrients that Counteract Absorption/Impact:

    • Soluble Fiber: Significantly binds bile acids (made from cholesterol) in the gut, promoting excretion and forcing the liver to pull more cholesterol from the blood to make new bile. Action: Consume 10-25g soluble fiber daily (Oats, barley, psyllium, beans, lentils, apples, citrus, berries, eggplant, okra).
    • Plant Sterols/Sterols: Structurally similar to cholesterol, they compete for absorption in the gut. Action: Consider foods fortified with plant sterols/stanols (e.g., certain margarines, yogurts, juices - typically 2g/day needed for ~10% LDL-C reduction).
    • Unsaturated Fats (Especially Polyunsaturated - PUFAs): Actively lower LDL-C and improve overall lipid profile. Action: Replace saturated fats (butter, lard, fatty meat, coconut oil) with oils like soybean, corn, sunflower, safflower, canola, fatty fish, nuts, seeds.

  5. Critical Considerations for Action:

    • Saturated Fat is the Lever: Reducing saturated fat intake is the single most effective dietary action for lowering LDL-C, regardless of dietary cholesterol intake. Changing cholesterol intake without changing saturated fat has minimal benefit for most.
    • Overall Pattern is Paramount: The DASH or Mediterranean diet patterns consistently lower LDL-C because they combine low saturated fat, high fiber, healthy fats, and whole foods – not because they specifically eliminate cholesterol-rich foods.
    • Individualization is Key: There is no universal “safe” cholesterol intake number. Factors include genetics, baseline LDL-C, diabetes status, CVD history, and overall diet quality. High-risk individuals benefit from stricter limits on both saturated fat and dietary cholesterol.

In Summary:

While dietary cholesterol does raise serum LDL-C, the effect is modest and plateaus for most people due to liver compensation. A significant minority (hyper-responders) experience a stronger increase. The most powerful dietary strategy for lowering serum LDL-C is unequivocally reducing saturated and trans fat intake. Within the context of a diet low in saturated fat:

  • Most people can safely consume moderate amounts of cholesterol-rich foods like eggs and shellfish.
  • Hyper-responders and high-risk individuals should moderate their intake of specific high-cholesterol foods (like egg yolks and organ meats).
  • Always prioritize: Soluble fiber, unsaturated fats, whole foods, weight management, and exercise for optimal cholesterol management. Testing your individual response can be informative but requires careful execution. Consult a healthcare professional or registered dietitian for personalized guidance, especially if you have existing conditions or concerns.

Based on current scientific consensus (primarily post-2015), below are key academic references supporting the relationship between dietary cholesterol intake and serum cholesterol changes, along with actionable strategies. These reflect major systematic reviews, meta-analyses, and authoritative guidelines.

Core References on Dietary Cholesterol & Serum Lipids

  1. USDA Dietary Guidelines Advisory Committee (2020)
    Scientific Report of the 2020 Dietary Guidelines Advisory Committee

    • Key Finding: Concluded that dietary cholesterol is “not a nutrient of public health concern for overconsumption,” emphasizing that saturated fat has a stronger effect on LDL-C. Shifted focus to overall dietary patterns.
    • Actionable Insight: Recommends limiting saturated fat to <10% of calories and prioritizing plant-based fats, whole grains, and fiber.
    • Access: DietaryGuidelines.gov (Chapters 7, 9).

  2. American Heart Association (AHA) Science Advisory (2019)
    Carson, J.A.S. et al. “Dietary Cholesterol and Cardiovascular Risk: A Science Advisory From the American Heart Association.” Circulation. 2019.

    • Key Finding: For most people, dietary cholesterol has a modest effect on serum LDL-C. Saturated fat remains the primary dietary driver of elevated LDL-C.
    • Actionable Insight: Recommends eggs/shrimp in moderation within heart-healthy patterns (e.g., Mediterranean diet) but stricter limits for high-risk groups (e.g., diabetes, FH).
    • DOI: 10.1161/CIR.0000000000000743.

  3. Meta-Analysis: Eggs & Cardiovascular Risk (2019)
    Zhong, V.W. et al. “Associations of Dietary Cholesterol or Egg Consumption With Incident Cardiovascular Disease and Mortality.” JAMA. 2019.

    • Key Finding: Each additional 300 mg/day of dietary cholesterol increased CVD risk by 17% and all-cause mortality by 18%. However, confounding by saturated fat intake was significant.
    • Actionable Insight: Eggs should be consumed in moderation (≤1/day) in context of overall diet; avoid pairing with high-saturated-fat foods (e.g., bacon).
    • DOI: 10.1001/jama.2019.1572.

  4. Meta-Analysis: Hyper-Responders (2018)
    Soliman, G.A. “Dietary Cholesterol and the Lack of Evidence in Cardiovascular Disease.” Nutrients. 2018.

    • Key Finding: ~15–25% of people are hyper-responders to dietary cholesterol (LDL-C ↑ up to 15–25% with high intake). Genetics (APOE4, ABCG8) play a key role.
    • Actionable Insight: High-risk individuals should test responsiveness via controlled dietary challenges (e.g., low-cholesterol baseline → high-cholesterol challenge).
    • DOI: 10.3390/nu10060680.

References on Mechanisms & Compensatory Responses

  1. Cholesterol Homeostasis (2019)
    Luo, J. et al. “Cholesterol Homeostasis and Liver X Receptor (LXR) Signaling.” Current Topics in Medicinal Chemistry. 2019.

    • Key Finding: Dietary cholesterol suppresses endogenous synthesis via SREBP-2 downregulation. Hyper-responders exhibit reduced compensation.
    • DOI: 10.2174/1568026619666190125144157.

  2. Saturated Fat Amplification Effect (2010)
    Astrup, A. et al. “The Role of Reducing Intakes of Saturated Fat in the Prevention of Cardiovascular Disease.” American Journal of Clinical Nutrition. 2010.

    • Key Finding: Saturated fat reduces LDL receptor activity, amplifying LDL-C elevation from dietary cholesterol.
    • Actionable Insight: Replace saturated fats (butter, lard) with PUFAs/MUFAs (olive oil, nuts) to mitigate cholesterol absorption.
    • DOI: 10.3945/ajcn.2009.27725.

Actionable Strategy References

  1. Soluble Fiber & LDL-C Reduction (2021)
    Ho, H.V.T. et al. “Effect of Oat β-Glucan on LDL-C and Non-HDL-C: A Meta-Analysis.” European Journal of Clinical Nutrition. 2021.

    • Key Finding: 3 g/day of oat β-glucan ↓ LDL-C by 0.25 mmol/L (10 mg/dL).
    • Actionable Insight: Consume oats, barley, psyllium (e.g., 1.5 cups oatmeal/day).
    • DOI: 10.1038/s41430-020-00749-6.

  2. Plant Sterols for LDL-C Lowering (2018)
    Ras, R.T. et al. “LDL-Cholesterol Lowering Effect of Plant Sterols: A Meta-Analysis.” Journal of the American Heart Association. 2018.

    • Key Finding: 2 g/day plant sterols ↓ LDL-C by 8–10%.
    • Actionable Insight: Use sterol-fortified foods (e.g., spreads, yogurts) daily.
    • DOI: 10.1161/JAHA.117.008070.

  3. Hyper-Responder Identification (2006)
    Herron, K.L. et al. “Men Classified as Hypo- or Hyperresponders to Dietary Cholesterol Have Distinct Plasma Lipoprotein Responses.” Journal of Nutrition. 2006.

    • Key Finding: Protocol for identifying responders: 4 weeks low-cholesterol diet → 4 weeks high-cholesterol diet (e.g., 800 mg/day).
    • DOI: 10.1093/jn/136.3.823.

Key Takeaways for Action

  1. Prioritize Saturated Fat Reduction: Replace with PUFAs/MUFAs (↑ fish, nuts, olive oil).
  2. Test Responsiveness: If LDL-C >100 mg/dL, conduct a 3-step dietary challenge (low-cholesterol baseline → high-cholesterol challenge).
  3. Use LDL-C Counters:
    • Soluble fiber (≥10 g/day).
    • Plant sterols (2 g/day).
    • Avoid simultaneous saturated fat + cholesterol (e.g., eggs with bacon).
  4. High-Risk Groups: Limit dietary cholesterol to <200 mg/day if diabetic, hyper-responder, or FH.

For personalized planning, consult a registered dietitian or use tools like the NIH LDL Genetic Test (APOE status).

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#2160

Yes, the non-linear effect is interesting and relevant. That could mean a significant difference in LDL-C for many people if they had zero cholesterol intake rather than what they’re consuming now. Many studies doesn’t take into consideration baseline dietary cholesterol intake.

I think that along with my low saturated fat intake keep my apoB even drug free around ~75 mg/dl.

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#2161

I also wonder about the exact meaning of baseline intake. Monthly average? After all, the dietary intake is an impulsive signal, not a continuous one.

#2162

If you can provide reasons for this I would like to know. Thanks.

#2163

How long have you been taking Doxy 50MG and how many days per week? Anything good/bad to report?

Thanks,

#2164

I’ve been taking it daily for several years. Seems to help with dry eye… otherwise nothing to report

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#2165

I originally started taking doxycycline as part of my anti aging stack after reading the following 2017 article by M Blagosklonny.
From rapalogs to anti-aging formula | Oncotarget
50mg since I didn’t want the full antibiotic dosage, since that’s not why I use it.

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#2166

Yoooo this is my first time testing these markers. This is pretty damn good right?

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image835×315 30.9 KB

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#2167

If I’m reading this correctly, converting it to units used in the US your ApoB is 59mg/dL, and ApoA1 is 135mg/dL. Together with very low Lp(a), these are pretty stellar values. If your hsCRP and IL-6 are low too, I think you’re in a pretty good spot, assuming your trigs are not out of whack.

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#2168

hsCRP 0.7mg/L
IL-6 I have never tested.
Triglyceride 0.9 mmol/L

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#2169

Trigs also excellent (US unit conversion 35mg/dL), decent hsCRP. You’re good!

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#2170

Feels good man. From what I hear nothing we can do currently can lower Lp(a), but I wonder if something in my crazy routine did lower it? This is the first time I’ve tested it, or APOB

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#2171

Berberine + canola oil instead of EVOO decreased my apoB to around a similar level:

Continuing the discussion from Rapamycin and risk of cardiovascular disease:

But prevention of atherosclerosis has benefits to even lower levels.

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