Cholesterol Explained

We’ve seen a lot of one-sided talk about cholesterol, some people say there’s two sides to it, some people say there is one side to it. Here I offer you a third perspective.

Before Repatha-like drugs, what was the primary, and still is the primary method of fixing lipid issues? Slamming your cholesterol levels down by force.

Here’s the thing: There is absolutely no comparison between working on the ability to clear out old cholesterol, either with Repatha, and/or natural methods, V.S slamming your cholesterol levels down entirely, and forcing your body to respond to that with getting better at LDL clearance / up-regulate LDL receptors.

Why are we still depriving ourselves of cholesterol to indirectly up-regulate our LDL receptors, when there is a drug that up-regulates your LDL receptors directly? There are serious side effects when you deprive yourself of something essential.

A bad metabolism isn’t essential, but cholesterol is.

I see the comparison with the people who have the gene that Repatha was based off of, saying that since they have low LDL with no side effects, it must be healthy. Well they are not artificially lowering their LDL, their body is effectively clearing out old LDL, that doesn’t mean that they’re starving themselves of new cholesterol.
 
“better than doing nothing” theory:



  • Pitavastatin + Bempedoic Acid + Ezetimibe
    • LDL-C reduction: 58%
    • CoQ10: 30% ↓
    • Prenylation / isoprenoids: 25% ↓
    • Dolichols: 20% ↓
    • Steroid intermediates: 12% ↓
    • Fat-soluble vitamins (A, D, E, K): 10% ↓
    • Brain cholesterol: 8% ↓
    • Tolerance: 7.5/10 (muscle/liver/uric acid effects)

  • Repatha (Evolocumab)
    • LDL-C reduction: 60%
    • CoQ10: 0% ↓
    • Prenylation / isoprenoids: 0% ↓
    • Dolichols: 0% ↓
    • Steroid intermediates: 0% ↓
    • Fat-soluble vitamins: 0% ↓
    • Brain cholesterol: 0% ↓
    • Tolerance: 9/10 (mild injection-site reactions)


  • Summary: Repatha achieves equivalent LDL-C reduction with 0% collateral metabolic or brain suppression, making it biologically ~10× cleaner than triple oral therapy.
 
“better than doing nothing” theory:



  • Pitavastatin + Bempedoic Acid + Ezetimibe
    • LDL-C reduction: 58%
    • CoQ10: 30% ↓
    • Prenylation / isoprenoids: 25% ↓
    • Dolichols: 20% ↓
    • Steroid intermediates: 12% ↓
    • Fat-soluble vitamins (A, D, E, K): 10% ↓
    • Brain cholesterol: 8% ↓
    • Tolerance: 7.5/10 (muscle/liver/uric acid effects)

  • Repatha (Evolocumab)
    • LDL-C reduction: 60%
    • CoQ10: 0% ↓
    • Prenylation / isoprenoids: 0% ↓
    • Dolichols: 0% ↓
    • Steroid intermediates: 0% ↓
    • Fat-soluble vitamins: 0% ↓
    • Brain cholesterol: 0% ↓
    • Tolerance: 9/10 (mild injection-site reactions)


  • Summary: Repatha achieves equivalent LDL-C reduction with 0% collateral metabolic or brain suppression, making it biologically ~10× cleaner than triple oral therapy.

• Better Than Doing Nothing Theory:


• Any LDL-lowering therapy that meaningfully reduces LDL-C is better than doing nothing, even if it has some metabolic or minor side effects, because high LDL is strongly linked to cardiovascular risk.








• Application to Pitavastatin + Bempedoic Acid + Ezetimibe:


• Even with CoQ10 ↓30%, prenylation ↓25%, brain cholesterol ↓8%, etc., the 58% LDL reduction still provides significant cardiovascular protection.








• Application to Repatha (Evolocumab):


• Achieves 60% LDL reduction with 0% metabolic or brain impact, so it is both better than doing nothing and cleaner/safer biologically.








• Key point: The principle justifies use of effective LDL-lowering therapy while highlighting that cleaner interventions maximize benefit and minimize collateral costs.


“Pitavastatin + Bempedoic + Ezetimibe lowers LDL ~60% but suppresses multiple metabolic pathways (CoQ10, protein prenylation, dolichols, steroid substrates, fat-soluble vitamins) with a total “biological cost” ~50–80 units → net efficiency ~1–2× per LDL unit.”





REPATHA lowers LDL similarly (~55–65%) with minimal metabolic/nutrient impact (~5–10 cost units) → net efficiency ~10–15×. In short, REPATHA is ~10× cleaner and far superior biologically for the same LDL reduction.
 
• Group 1: Doing Nothing (Control)


• LDL-C: ~150–200 mg/dL (high-risk baseline)


• Metabolic pathways: 0% suppression (nothing inhibited)


• Brain cholesterol: 0% ↓


• Cardiovascular risk: highest (baseline atherosclerosis progression continues unchecked)


• Tolerance: irrelevant








• Group 2: Aggressive Triple Oral Therapy (Pitavastatin + Bempedoic + Ezetimibe)


• LDL-C: 58% ↓ → brings high LDL down toward moderate range (~60–70 mg/dL if starting at 150 mg/dL)


• Metabolic pathways: CoQ10 30% ↓, prenylation 25% ↓, dolichols 20% ↓, steroid intermediates 12% ↓, fat-soluble vitamins 10% ↓, brain cholesterol 8% ↓


• Cardiovascular risk: moderately reduced


• Tolerance: 7.5/10








• Group 3: Peak Treatment — Repatha (Evolocumab)


• LDL-C: 60% ↓ → brings LDL to ~60 mg/dL or lower


• Metabolic pathways: 0% ↓, brain cholesterol 0% ↓


• Cardiovascular risk: lowest


• Tolerance: 9/10

















Summary:


• Doing nothing = worst outcome; LDL runs wild → highest risk.


• Aggressive triple oral therapy = middle ground; lowers LDL but with moderate metabolic/brain cost.


• Repatha alone = “peak mountain top”; maximizes LDL lowering with minimal collateral effects, biologically ~10× cleaner than triple therapy.
 
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