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  1. Last 7 days
    1. Jak obniżyć CHOLESTEROL? Dieta, suplementy czy statyny? — lipidolog Magdalena Kaczan

      Summary of "How to Lower Cholesterol? Diet, Supplements, or Statins?"

      Guest: Magdalena Kaczan (Lipidologist)

      The video provides an extensive overview of cholesterol management, the mechanism of atherosclerosis, and the roles of lifestyle, genetics, and medication in cardiovascular health.

      1. Understanding Cholesterol and Lipoproteins

      • The Nature of Cholesterol: Cholesterol is an essential fatty substance required for building cell membranes and producing hormones [00:02:55].
      • The Role of Lipoproteins: Since cholesterol is a fat, it cannot travel alone in the blood. It is carried by "packages" called lipoproteins. The most problematic ones contain Apolipoprotein B (ApoB), which allows them to penetrate arterial walls [00:04:30].
      • LDL vs. HDL: * LDL (Low-Density Lipoprotein): Often called "bad" cholesterol. High levels are a primary driver of plaque buildup [00:05:31].
        • HDL (High-Density Lipoprotein): Generally "good" as it transports cholesterol back to the liver, though it can become dysfunctional in some cases [00:06:04].
      • The Importance of ApoB: ApoB is increasingly seen as a more accurate marker than LDL alone because it counts the total number of atherogenic (plaque-forming) particles [00:32:09].

      2. The Process of Atherosclerosis

      • Infiltration: Lipoproteins (like LDL) enter the arterial wall (intima) through a process called transcytosis [00:07:45].
      • Oxidation and Inflammation: Once inside the wall, LDL particles oxidize. The immune system views them as intruders; macrophages "eat" them and turn into "foam cells," triggering chronic inflammation [00:08:13].
      • Plaque Formation: Over time, a "lipid core" forms, surrounded by a fibrous cap. If this plaque ruptures, a blood clot forms, which can lead to a heart attack or stroke [00:13:07].

      3. Risk Factors and Individual Norms

      • Personalized Norms: There is no single "normal" cholesterol level. Targets depend on an individual's 10-year cardiovascular risk (based on age, smoking, blood pressure, etc.) [00:20:01].
      • Lipoprotein(a) [Lp(a)]: This is a genetically determined, highly aggressive form of LDL. It acts as an "accelerator" for heart disease and should be tested at least once in a lifetime, as it isn't lowered by traditional diet or exercise [00:36:10].
      • Metabolic Factors: High triglycerides, insulin resistance, and obesity significantly worsen the quality of LDL particles, making them smaller, denser, and more dangerous [00:28:22].

      4. Dietary Strategies

      • Saturated Fats: High intake of animal fats (butter, lard, fatty meats) and certain plant fats (coconut/palm oil) increases LDL levels [00:43:04].
      • The Power of Fiber: Soluble fiber (found in oats, legumes, and psyllium) binds bile acids in the gut, preventing the reabsorption of cholesterol [00:45:24].
      • Plant-Based Fats: Replacing saturated fats with polyunsaturated and monounsaturated fats (olive oil, nuts, fatty fish) is a primary dietary intervention [00:44:46].
      • Carbohydrates and Triglycerides: Excess simple sugars and alcohol are the main drivers of high triglycerides [00:47:48].

      5. Pharmacological Treatment (Statins)

      • Safety Profile: Statins are described as some of the safest drugs in cardiology [00:01:08].
      • Beyond Lowering LDL: Statins do more than lower cholesterol; they have "pleiotropic" effects, meaning they stabilize existing plaques and reduce systemic inflammation [00:56:33].
      • Side Effects and the "Nocebo" Effect: * Muscle pain occurs in about 9% of patients in clinical trials, but many subjective complaints are due to the nocebo effect (expecting side effects because of negative publicity) [01:03:06].
        • True statin intolerance is rare; switching to a different type or dose of statin often resolves issues [01:01:15].
      • Liver Impact: Serious liver damage is extremely rare (1 in 100,000). Minor elevations in liver enzymes are usually temporary as the liver adapts [01:04:05].

      6. Supplements and "Nutraceuticals"

      • Supplements vs. Medication: Supplements like berberine or red yeast rice (monacolin K) are not substitutes for medication in high-risk patients (e.g., those who have already had a heart attack) [01:09:46].
      • Red Yeast Rice: Contains monacolin K, which is chemically identical to lovastatin. While "natural," it can still cause the same side effects as prescription statins [01:11:14].
      • Coenzyme Q10: While statins can lower CoQ10 levels, clinical studies do not definitively show that supplementing it reduces muscle pain [01:06:19].

      7. Key Takeaways for Longevity

      • Start Early: Prevention is more effective than treating advanced disease.
      • Test Extensively: Go beyond a basic lipid panel; request ApoB and Lp(a) tests [01:13:05].
      • Continuity: Lifestyle changes and medications are long-term commitments. If you stop the intervention, the risk levels typically return to their baseline [01:14:11].
  2. Oct 2025
    1. Zjadł 720 jajek w miesiąc! Efekt? Nikt się tego nie spodziewał

      Based on YT video I Ate 720 Eggs in 1 Month. Here's What Happened to my Cholesterol:

      • Nick Norwitz, a Harvard medical student with a doctorate in human cerebral metabolism, ate 720 eggs in one month, averaging 24 eggs per day, to test the effects on his cholesterol levels.
      • Contrary to popular belief that eggs increase bad cholesterol (LDL), his LDL cholesterol dropped during the experiment. It decreased by 2% in the first two weeks and then by an additional 18% in the next two weeks.
      • The high cholesterol intake (about 133,000 mg from eggs) did not raise his blood cholesterol. This was explained by a hormone called cholesin, released when cholesterol binds to receptors in the gut, which signals the liver to reduce cholesterol production, maintaining balance in the body.
      • During the last two weeks, he also increased carbohydrate intake slightly, which further helped reduce LDL levels, possibly in combination with other dietary elements like fruits.
      • The experiment challenges the long-held medical advice limiting egg consumption due to cholesterol concerns, suggesting that dietary cholesterol may not significantly impact blood cholesterol levels in healthy individuals.
      • Norwitz documented his experiment publicly on YouTube, sparking discussions on nutrition and metabolism and encouraging re-evaluation of egg consumption guidelines.
      • Eggs are a veritable treasure trove of nutrients: harmful vitamins A, D, E, and K, harmful B vitamins, calcium, phosphorus, iron, sodium, and potassium. However, even such a valuable product should not replace other essential nutrients.
  3. Oct 2023
  4. Nov 2021
  5. Oct 2020
  6. Mar 2017
    1. Findings In a meta-regression analysis of 49 clinical trials with 312 175 participants, each 1-mmol/L (38.7-mg/dL) reduction in LDL-C level was associated with a relative risk (RR) of major vascular events of 0.77 (95% CI, 0.71-0.84; P < .001) for statins and 0.75 (95% CI, 0.66-0.86; P = .002) for established nonstatin interventions that act primarily via upregulation of LDL receptor expression.Meaning These data suggest statins and nonstatin therapies that act through upregulation of LDL receptor expression are associated with similar cardiovascular risk reduction per decrease in LDL-C. The clinical value of adding specific nonstatin interventions to lower LDL-C to background statin therapy should be confirmed in appropriately powered clinical trials.
    1. In addition, the vast majority of animal studies have shown that oral administration of PS reduces the progression atherosclerosis. However, it has been recently suggested that an increase in PS plasma concentrations may increase CV risk. Evidence to support this hypothesis come mainly from observations in sitosterolemic patients who hyperabsorb PS and cholesterol and display very high levels of PS, which may be associated with a premature atherosclerosis. Some epidemiological studies in non-sitosterolemic subjects have shown a positive correlation between PS plasma levels and coronary heart disease. However, these are observational studies and some of them present major methodological bias. In addition, recent studies with a larger number of subjects have indicated, either an absence or a negative relationship between PS and the incidence of CV disease.