Marion Holman Profile picture
May 16 6 tweets 2 min read Read on X
1/6 Great thread from @Mangan1 !
I would also add that LDL particle size matters.
Not all LDL is equal. LDL (low-density lipoprotein) carries cholesterol, but its particle size matters for heart disease risk. Small, dense LDL (sdLDL) is more atherogenic (plaque-causing)
/2
2/6 than large, fluffy LDL. sdLDL is more plaque-promoting because it’s easily oxidized and triggers inflammation. Macrophages engulf oxidized sdLDL, forming foam cells. Foam cells are a key driver in the development and progression of atherosclerosis. /3
3/6 What causes ⬆️ sdLDL ? Insulin resistance, high Triglycerides/low HDL, metabolic syndrome, & chronic infections (like oral bacteria P. gingivalis) can drive inflammation, shifting LDL toward small, dense particles.
Diets matter too. Refined carbs & inflammatory seed oils /4
4/6 (high in linoleic acid) can worsen sdLDL profiles. Poor oral health, with bacteria like P. gingivalis found in arterial plaques, adds to the risk.
Standard lipid tests miss LDL particle size. Get advanced tests like NMR lipid profiles or VAP tests for particle size and /5
5/6 number. Also, check fasting insulin for insulin resistance and CRP for inflammation.
Fight back with diet and hygiene. LCHF diets, Keto or Carnivore with whole foods, avoiding seed oils like soybean, corn oil etc., can boost large, fluffy LDL and reduce sdLDL.
/6
6/6 Manage gum health to lower infection risk, (root canals can be a reservoir for infections). Takeaway: sdLDL’s plaque-promoting potential, driven by foam cells, inflammation from seed oils, and infections like P. gingivalis, matters more than a number on your lipid profile.

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More from @Marion436842126

May 11
1/6 Are We Ignoring the Harm of Statins ?
Insanity is doing the same thing over and over, expecting a different result. Statins are linked to muscle cell apoptosis (cell death). Yet, when patients report muscle damage, doctors often just switch the statin instead of /2
2/6 questioning the drug itself. Why ?
Take this case: A patient on statins for 20+ years—Lipitor, Crestor, Repatha. Lipitor caused crippling ankle/Achilles pain. Crestor led to torn biceps (both needing surgery) and severe neck pain requiring spinal fusion./3
3/6 Repatha ? Unbearable neck pain and shortness of breath. /4 Image
Read 6 tweets
May 8
1/8 The pharmaceutical industry knows statins are toxic (see “Statin Toxicity" document) yet they keep pushing statins to lower LDL. A 2019 study in Circulation Research details how statins cause muscle damage, mitochondrial impairment, and necrosis. They KNOW the harm /2
2/8 but prioritize profits over lives.
.
/3ahajournals.org/doi/10.1161/CI…
3/8 Statin toxicity isn’t a secret. Statins deprive cells of mevalonate in muscle cell membranes, destabilizing them and causing myopathy. Studies show elevated CK levels, mitochondrial damage, and even liver enzyme spikes. /4
Read 8 tweets
May 6
1/7 Statins lower LDL, but heart disease is driven by insulin resistance & inflammation, not LDL. Let’s rethink CVD prevention./2
2/7 LDL is vital for cell repair & hormones. When insulin & inflammation are low, LDL is protective. Oxidized LDL (oxLDL) from high insulin is the real culprit in heart disease.
/3
3/7 Insulin resistance ramps up oxLDL, damaging arteries. Lower insulin by ditching sugars, processed carbs & seed oils & curb inflammation to prevent CVD. /4
Read 7 tweets
May 5
1/10 Good question ! Believe nothing, trust no one. Stay curious. When claims sound too good to be true, they often are. Trust the science, not the rhetoric:
The Statin-Ezetimibe Plaque Shrinkage Claim Raises Red Flags, and does not stand up to scientific scrutiny.
/2
2/10 Trials like ASTEROID and ZEUS claim Statins and Ezetimibe “shrink plaque” and reduce Percent Atheroma Volume (PAV), but broader evidence shows Statins increase CAC. How can plaque volume decrease while calcification rises ? /3
3/10 This contradiction challenges the idea that these drugs improve heart health.
Calcification Isn’t Benign ! It Adds to CVD Risk.
Increased CAC from Statins isn’t harmless. It stiffens arteries, increases clotting risk, raises heart failure risk, and complicates procedures /4
Read 9 tweets
May 5
1/8 Statins: CAC, Vascular smooth muscle cell apoptosis, K2-MGP, and Cellular Damage: ⬇️
Statins by lowering LDL can increase coronary artery calcificatiton. The drug industry term this "stabilizing plaque" 🙄 This paradox suggests lowering LDL isn’t the win it’s /2
2/8 made out to be. CAC progression can signal risk. Statins induce apoptosis in Vascular Smooth Muscle Cells (VSMCs) by blocking the mevalonate pathway, reducing isoprenoids needed for cell survival. Dying VSMCs release calcium-rich vesicles, adding to arterial calcification, /3
3/8 increasing CAC burden. Statins cause oxidative stress, damage cell membranes, and impair mitochondria. ROS from CoQ10 depletion and ETC inhibition promotes VSMC apoptosis and osteogenic changes, adding to CAC. This cellular damage outweighs any anti-inflammatory benefits. /4
Read 8 tweets
May 2
1/5 After 20+ yrs researching Statins, sparked by my Father's experience on Lipitor and my Uncle’s ALS diagnosis on 80mg Lipitor, I’m alarmed.
Statins, by depleting mevalonate, pose serious risks. Here’s why we need to talk./2
2/5 Statins block Mevalonate, a key pathway, causing memory loss, muscle damage, & even heart failure. My Father was hospitalized with torn ligaments, acute pancreatitis, and memory loss/dizziness. My Uncle was diagnosed with ALS after 12 months on 80mg Lipitor.
/3
3/5 Statins act as Vit K2 antagonists, increasing vascular calcification, & can drive pre-diabetes via insulin resistance. Statins are also linked to other serious conditions like Parkinson's
/4
Read 5 tweets

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