The TRUTH about Statins, formerly @holmanm
Info is provided for educational purposes only & should not be considered as medical advice. (NO DM's please)
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May 16 • 6 tweets • 2 min read
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)
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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
May 11 • 6 tweets • 2 min read
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 /22/6 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
May 8 • 8 tweets • 2 min read
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 /22/8 but prioritize profits over lives.
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/3ahajournals.org/doi/10.1161/CI…
May 6 • 7 tweets • 1 min read
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.
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May 5 • 9 tweets • 2 min read
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.
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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
May 5 • 8 tweets • 2 min read
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 /22/8 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
May 2 • 5 tweets • 1 min read
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.
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May 1 • 9 tweets • 2 min read
1/9 Lovastatin, Lipitor, and their Mevalonate Blockade:
Have you ever wondered how statins gained FDA approval ?
A lie by omission.
Lovastatin (1987) & Lipitor (1996) were FDA-approved statins to lower cholesterol. Merck & Pfizer didn’t disclose /22/9 the fact that statins blocked the Mevalonate Pathway. This omission is indefensible. Here’s why: Both drugs inhibit HMG-CoA reductase, reducing cholesterol while also depleting vital biochemicals necessary for cell survival : farnesyl pyrophosphate, /3
Apr 29 • 9 tweets • 2 min read
1/8 Are Statins Contributing to Rising CVD Rates in the USA and UK ?
Over 80M people in the USA and 30M in the UK use cholesterol-lowering drugs, mainly statins, to reduce heart disease risk. But CVD rates are still climbing, and statins’ "direct effects" like pre-diabetes, /22/8 heart failure, muscle damage, and autoimmune issues be playing a role.
In the USA, CDC data shows CVD deaths rose from 836,546 in 2015 to 928,741 in 2022. A 10% increase.
In the UK, BHF reports CVD deaths increased from 159,000 in 2018 to 170,000 in 2023, /3
Apr 29 • 7 tweets • 2 min read
1/7 Statins can cause Rhabdomyolysis which involves the rapid breakdown of skeletal muscle, releasing myoglobin and other intracellular contents into the bloodstream. When this happens, the onset of muscle damage can be swift, especially in the presence of risk factors like /2
2/7 high doses, drug interactions (e.g., with CYP3A4 inhibitors), or other underlying health conditions.
Timeline of Rhabdomyolysis Onset: Symptoms like muscle pain, weakness, and dark urine (from myoglobinuria) are a red flag./3
Apr 27 • 7 tweets • 2 min read
1/6 Rethinking Heart Disease: Is LDL Really the Villain ?
High LDL cholesterol is often blamed for heart disease, but here’s the twist: people with low LDL also have heart attacks. Why ? Because the real drivers of atherosclerosis are: insulin resistance, chronic /22/6 inflammation and infections.
Here’s what’s happening:
Insulin resistance (often tied to high blood sugar) damages blood vessels and promotes plaque buildup, Plaque accumulation can occur regardless of high or low LDL levels, with various factors contributing to /3
Apr 14 • 9 tweets • 2 min read
1/9 LDL is crucial for damage repair and immune response, and Trump’s “way too low” LDL from Crestor/Ezetimibe does not improve heart health, it merely creates an illusion of progress. Insulin resistance and inflammation are the true drivers of heart disease. /2
2/9 There’s no hard proof Trump’s doctors were influenced to inflate his heart health, but circumstantial factors, political pressure, selective reporting, and a history of shaped narratives make it a reasonable suspicion. Low triglycerides and “excellent” claims /3
Apr 14 • 14 tweets • 3 min read
1/14 UNMASKING STATIN TRIALS: How Big Pharma Tips the Scales:
Statins are a pharmaceutical juggernaut, prescribed to millions to lower cholesterol and prevent heart disease. Their dominance rests on clinical trials touted as gold-standard evidence. /2
2/14 Yet, as Cardiologist Michel de Lorgeril argues in his book "Cholesterol & Statins: Sham Science & Bad Medicine (2014)", these trials often employ tactics that inflate benefits and obscure risks, undermining trust in the results. From selective recruitment to statistical /3
Apr 13 • 8 tweets • 2 min read
1/8 Ditch the lipid test, check insulin - get the real heart risk scoop !
A 2014 Diabetes Care study found Atorvastatin increased insulin resistance (measured by HOMA-IR) by ~20% in hypercholesterolemic patients after 12 weeks. The METSIM cohort (2015, Diabetologia) showed /22/8 statin users had a 24% higher risk of insulin resistance, independent of diabetes onset.
Mechanisms:
Statins reduce adiponectin, an insulin-sensitizing hormone.
By limiting isoprenoids, statins impair glucose uptake in skeletal muscle, raising fasting insulin. /3
Apr 12 • 6 tweets • 1 min read
1/6 For decades doctors have prescribed Statins in the belief that elevated LDL-cholesterol is a major risk factor for cardiovascular disease. This is a tragic error. Doctors have failed their patients because LDL cholesterol is not a “bad” molecule. /22/6 However, when LDL cholesterol becomes oxidized, it becomes an inflammatory, “damaged” molecule that is capable of causing vascular endothelial injury which may contribute to atherosclerosis and cardiovascular disease. CoQ10 is an antioxidant that is packaged /3
Apr 8 • 15 tweets • 3 min read
1/15 Doctors who prescribe statins cannot possibly give their patients informed consent if they are unaware of the true mechanism of action of the statin drug they are prescribing.
This is what an informed doctor would tell his patients:
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2/15 HMG-CoA Reductase is the rate-limiting enzyme in the mevalonate pathway, which produces cholesterol & other isoprenoids. When it is inhibited by statins, cells can’t synthesize cholesterol de novo. Normally, this triggers a compensatory response: the SREBP pathway senses /3
Apr 5 • 7 tweets • 2 min read
1/7 Statins and Fosamax (Alendronate) have an awful lot in common:
Fosamax specifically inhibits farnesyl pyrophosphate synthase (FPPS), an enzyme in the Mevalonate pathway. By inhibiting FPPS, Fosamax reduces the production of FPP and GGPP. /2
2/7 In osteoclasts. This disruption prevents the prenylation of these GTPases, which are necessary for cytoskeletal organization. As a result, osteoclasts become less active and can undergo cell death, leading to decreased bone resorption. /3
Apr 4 • 7 tweets • 1 min read
1/7 Statins increase the risk of Alzheimer's Disease by cutting isoprenoids, stressing mitochondria, weakening myelin, reducing neurosteroids, and increasing blood glucose.
Your brain needs cholesterol to build its cells, wire its circuits, insulate its cables, and patch /22/7 itself up. It’s not optional. It’s the grease that keeps the machine running.
There's another way in which statins can cause Alzheimer’s disease:
Unlike cholesterol, which dominates most tissues, Desmosterol is abundant in the brain, especially during development /3
Apr 2 • 7 tweets • 2 min read
1/7 Statins interfere with cholesterol metabolism, which is essential for maintaining tendon integrity. Tendons are primarily composed of collagen, and cholesterol is a key component of cell membranes, including those in tenocytes (tendon cells). /22/7 Reduced cholesterol availability impairs tenocyte function, leading to weakened collagen synthesis or increased degradation. Statins can downregulate matrix metalloproteinases (MMPs) or alter their balance which impair the tendon’s ability to maintain or restore its /3
Mar 31 • 14 tweets • 3 min read
1/14 Oh dear he we go again !
Inhibiting Apo(a) synthesis in the liver using siRNA therapies like Lepodisiran—dramatically lowers plasma Lp(a) levels (up to 94% in trials).
What could possibly go wrong ? 🙄
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2/14 Studies from the 1990s (e.g., Brown & Goldstein, Journal of Lipid Research, 1997) suggest Lp(a) accumulates at sites of endothelial damage, delivering cholesterol to REPAIR cell membranes or stabilize injured vessels. /3
Mar 31 • 5 tweets • 1 min read
1/5 No matter how you are eliminating cholesterol, whether through diet or drugs, you are shrinking your brain. And, if you are taking cholesterol lowering meds, you are making drug companies rich. Where do you find the highest concentration of cholesterol ?
In your brain. /22/5 The brain is cholesterol-rich because it needs vast amounts of cholesterol to function properly. Statins can cross the blood brain barrier. Lipophilic statins, more readily than hydrophilic statins. Since cholesterol is a component of cell membranes, excessive reduction /3
