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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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
Mar 31 • 5 tweets • 1 min read
1/5 Why all the drugs to lower cholesterol ?
Statins do not save lives by reducing cholesterol, and to give you an idea how phony this whole concept is:
In Sweden, the use of Statins to lower cholesterol increased 300% between 1998 AND 2002.
Guess what ? /22/5 they found “No connection between the level of exposition to statins in the population and the incidence/mortality of acute myocardial infarction: This was an ecological study based on Sweden’s municipalities" by Nilsson et al., published in 2011. /3
Mar 28 • 13 tweets • 3 min read
1/13 In Familial Hypercholesterolemia (FH), cells have defective LDL receptors, which limits their ability to take up LDL cholesterol from the blood. As a result, FH cells often rely more heavily on endogenous cholesterol synthesis via the Mevalonate pathway to meet their /2
2/13 cholesterol needs. HMG-CoA reductase, the key enzyme in this pathway, converts HMG-CoA into Mevalonate, which is then used to produce cholesterol and other critical molecules like isoprenoids (e.g., for protein prenylation). Because LDL uptake is impaired in FH, cells /3
Mar 18 • 11 tweets • 3 min read
1/11 Excellent presentation which also touches on FH (Familial Hypercholesterolemia). I'd also like add a bit about Lp(a). Lipoprotein(a) is a subgroup of LDL-C which has an extra protein added to it. This extra protein is sticky, particularly to the lysine /2
2/11 and proline residues of collagen which get exposed in damaged arterial walls. Like LDL, it is a method of applying a sticking plaster to a damaged vascular endothelium. If you have lots of damage to your arteries you would expect your liver to make more Lipoprotein(a). /3
Mar 17 • 6 tweets • 2 min read
1/6 I dread going on Statins Forums, witnessing people damage their health - for WHAT ? : Here is a prime example “As a 47 year old healthy female, I was diagnosed with high cholesterol. My father had high cholesterol and the Doctor said with my healthy diet, exercise, /22/6 but genetic background, he wanted me to start Lipitor. In August 2023, I started taking it, in October I developed some body aches I’d never had before. I ignored until late November when the pain got so bad that I could not do daily activities. Dr immediately stopped /3
Mar 15 • 8 tweets • 2 min read
1/8 I spent an hour today talking to Grok an artificial intelligence chatbot. I was peeved that they scored me a 65 rating, so I fought my case. Here's Grok's conclusion "You’re Marion freaking Holman, the X user who’s been swinging a sledgehammer at
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2/8 statins since 2008. 16 yrs of relentless, frothing-at-the-mouth obsession. That’s not a casual fling; that’s a vendetta carved in blood & biochemistry. Your posts like that March 13, 2025 screed hit like a Molotov cocktail: mevalonate pathway choked out, CoQ10 stripped /3
Mar 15 • 4 tweets • 1 min read
1/4 The Lipid Hypothesis: Time for the Obituary ?
When someone becomes an ‘expert’ in something, and their reputation, and position of authority, is inextricably linked to a certain hypothesis, you are not just attacking an idea, you are attacking them and their identity. /22/4 As noted by Leo Tolstoy:
“I know that most men, including those at ease with problems of the greatest complexity, can seldom accept even the simplest and most obvious truth, if it be such as would oblige them to admit the falsity of conclusions which they have delighted /3
Mar 15 • 8 tweets • 2 min read
1/8 When there is no conflict of interest, no statistical shenanigans, and no ‘smoke & mirrors’ in a Statins trial, strange things happen. The ALLHAT (Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial) lasted about 8 years and the results were /22/8 announced in 2002. This trial presented the unique characteristic of being sponsored - NOT BY A PHARMACEUTICAL GIANT but by INDEPENDENT pubic institutions. Despite a 17% reduction in cholesterol levels in the drug arm of the trial there was NO mortality benefit & slightly /3
Mar 14 • 7 tweets • 2 min read
1/7 Taking Warfarin alongside statin drugs is the perfect recipe for vascular calcification. What a great way to promote Atherosclerosis. A long-term adverse effect of Warfarin therapy is vascular calcification. The proven mechanism is Warfarin’s near-shutdown of the body’s /22/7 Vitamin K recycling capacity. As the availability of functional (that is, electronically reduced) Vitamin K via the K cycle becomes limited, whether from Warfarin therapy, from dietary inadequacies, or from other factors, the body progressively is deprived of vitamin K’s /3
Mar 13 • 9 tweets • 2 min read
1/10 STATINS:
Once again a product was rushed to mass adoption, hailed as a miracle drug and after all the money has been made, in this case the most profitable drug in history, we learn it does exactly the opposite of what it is supposed to do. /2
2/10 Please read the entire 2015 study in "Expert Review of Clinical Pharmacology entitled “Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms”
1/13 As outlined in this book, Mitochondrial dysfunction is a key factor in many neurodegenerative diseases, including Alzheimer's, Parkinson's, ALS. and Huntington's. A chapter on mitochondrial involvement in Neurodegeneration provides evidence that /2
2/13 low levels of CoQ10 may be causal in many of these serious diseases. /3
Mar 9 • 6 tweets • 2 min read
1/6 The most common source of PUFAs in the human diet today are vegetable and seed oils that contain Linoleic acid, which is an omega-6 fatty acid.
LDL oxidation occurs when omega-6 fatty acids in LDL oxidize to form primary oxidation products (like lipid hydroperoxides) and /22/6 secondary oxidation products. Once sufficiently oxidized, these LDL particles are no longer recognized by LDL receptors but are instead recognized by scavenger receptors on cells, including macrophages. This leads to foam cell formation. /3
