1/10 People often tell me to “look at the statin trials” sponsored by the pharmaceutical industry. Personally, I prefer to start with the mechanism of action of statins. When you do that, the scale of the claims being made begins to look implausible, which raises serious /2 2/10 questions about how those trial results were produced.
As has long been observed, individuals who are overly confident in their theories are not only less likely to make genuine discoveries, but they also tend to be poor observers. Their interpretations are shaped by /3

1/8 What the LDL is going on ? "Because the presence of coronary artery disease can be associated with the proportion of small, dense LDL, we analysed the effect of statins on small, dense LDL subfractions in people without coronary artery disease. /2 2/8 Unexpectedly, in the analysis, the proportion of small, dense LDL was significantly higher in patients treated with statins. Moreover, there were no differences in CRP, plasma fibrinogen, HOMA–IR,BMI, or metabolic syndrome between the statin and control groups. /3

1/11 If you went to a doctor with a broken leg and he started putting a cast on your arm, you’d question it immediately. Yet something similar is happening in how we approach heart disease. /2 2/11 Statins block the mevalonate pathway, a fundamental biological process involved in more than just cholesterol production. This pathway is essential for cellular energy, hormone synthesis, and repair mechanisms. /3

1/13 We live in a post-truth era where single biomarkers are taken out of context and used to construct incomplete, and often misleading, narratives. ApoB is one of the clearest examples of this. /2 2/13 Measuring ApoB in isolation is fundamentally misleading, because while it reflects the number of atherogenic particles, it tells us nothing about the protective role of ApoA1-containing lipoproteins. It is the ApoB/ApoA1 ratio that truly matters, as it captures /3

1/6 This comes from the statin toxicity document (). Its real purpose ? To steer patients away from cheap, generic statins toward newer, more expensive cholesterol-lowering drugs./2ahajournals.org/doi/10.1161/CI… 2/6 Ironically, in trying to downplay generic statins, they shot themselves in the foot by laying out in meticulous detail how statins harm every cell and organ in the body.
Statins inhibit HMG-CoA reductase, blocking the mevalonate pathway. /3

1/7 LDL is not just a cargo carrier. In its native form, it’s protective, carrying essential lipids and antioxidants like CoQ10, helping cells function and supporting vascular health. The danger doesn’t come from LDL itself. /2 2/7 It comes from how we damage LDL, and what happens to it in the body. High blood sugar, processed fats, seed oils, and chronic oxidative stress can modify LDL, making it more prone to damage. But infection is another potent trigger. /3

1/13 Statins don’t “lower cholesterol.” They cripple the mevalonate pathway, the body’s core engine for energy, repair, and longevity.
What follows is the science Big Pharma left out:
/2 2/13 The pathway
The enzyme HMG‑CoA reductase doesn’t merely make cholesterol; it governs the entire mevalonate‑isoprenoid cascade, the pipeline that produces:
Cholesterol (for membranes & hormones),
CoQ10 (mitochondrial respiration),
Dolichols (cell‑surface signalling),
/3

1/8 A study from the Essen group in Germany compared normal-dose Atorvastatin (10 mg/day) with high-dose Atorvastatin (80 mg/day)

Over one year, patients were followed for the progression of coronary artery calcification using electron-beam computed tomography. /2 2/8 Despite lowering LDL from 109 mg/dL to 87 mg/dL, there was no difference in the progression of calcified coronary atherosclerosis. Reductions in hsCRP and fibrinogen were similar between the low- and high-dose groups, indicating that 80 mg provided no measurable /3

1/6 The brain is nearly 60% fat. The fattiest organ in the body.
Glial cells rely on mevalonate to produce cholesterol, which is especially abundant in brain tissue. To maintain and repair myelin, these cells must rapidly replicate. /2 2/6 You cannot suppress cholesterol with a statin and expect optimal myelin repair.
Statins lower cholesterol by blocking the mevalonate pathway. In doing so, they also reduce production of key compounds like isopentenyl adenine, which is essential for DNA replication. /3

1/8 The cholesterol story is a lie we’ve been fed for decades.
We are told LDL cholesterol is the enemy. Lower it, and heart attacks vanish. That’s the official script. It’s comforting. It’s simple, and it’s dead wrong. /2 2/8 Arteries do not spontaneously “clog” because of LDL. Healthy arteries don’t get infiltrated by cholesterol. Plaque doesn’t form in a vacuum. What actually drives atherosclerosis is endothelial damage, inflammation, oxidative stress, metabolic chaos. That damage is driven /3

1/10 Statins are sold as 'anti-inflammatory' drugs that lower inflammation, but the science shows they're far more likely to trigger inflammation through apoptosis (cell killing), and mitochondria-damaging mechanisms.
Time to dispel the myth. /2

https://twitter.com/ClausCarlsen1/status/2022239096610193675

2/10 This is how statins trigger inflammation:
CoQ10 depletion leads to mitochondrial dysfunction, massive ROS production, oxidative stress, and cell death which drive inflammation.

Statins deplete GGPP & FPP leading to impaired protein prenylation (e.g., RhoA/Rac1), which /3

1/7 “Statins stabilise plaque,” they say… 🤔😂
It always makes me pause when I hear:
“My doctor told me I need statins to stabilise my plaque.”
Let’s look at what was actually published in Toxicological Sciences (via Oxford University Press):
/2 2/7 “Dysfunction of Vascular Smooth Muscle and Vascular Remodeling by Simvastatin.”
The study examined the effects of Simvastatin on vascular smooth muscle.
Not cholesterol levels.
Not plaque size.
Vascular smooth muscle itself.
/3

1/5 If someone thinks sending me more statin studies/ trial data will change my mind, let’s be clear - the quality of the data matters far more than the quantity.
It’s why Michel de Logeril, a cardiologist with decades of experience, didn’t just skim the major statin trials /2

https://twitter.com/MSerdikoff/status/2021552687628865595

2/5 he dissected them in detail in his book "Cholesterol and Statins Sham Science and Bad Medicine".
He doesn’t just disagree with the conclusions, he argues that many of the foundational trials are fatally flawed in design, interpretation, or reporting, which undermines the /3

1/7 No one can deny that statins do exactly what they are designed to do. That is: to suppress cholesterol production and reduce measurable blood serum levels. The question is, rather, at what price do they accomplish this feat, and for what ultimate purpose ? /7 2/7 With the National Cholesterol Education Program Guidelines having been designed by "experts" on the payroll of statin drug manufacturers, requiring ultra-low levels to obtain a strictly theoretical and numerical definition of "health," statin drugs are guaranteed to /7

1/10 It's often claimed that statins are "merely HMG-CoA reductase inhibitors." This is not true. Statins also dramatically elevate reductase levels. In a 1984 Merck paper, they reported that higher statin doses trigger more reductase production to compensate /2 2/10 for blocking mevalonate synthesis - essentially a desperate cellular workaround. Merck even photographed the resulting structural damage to cells. The question: Is this a toxic effect of Lovastatin? Yes, it is unequivocally toxic. It is not normal for cells to churn /3

1/11 You don’t get to shut down a core human metabolic pathway and call it “extremely safe.”
Yet that’s exactly how statins are being marketed to the public.
The BBC says there’s little to worry about.
Let’s look at what the drug actually does. /2 2/11 Statins inhibit HMG-CoA reductase, the gatekeeper enzyme of the mevalonate pathway.
This pathway does far more than make cholesterol.
It also produces:
• CoQ10 (mitochondrial energy)
• Farnesyl pyrophosphate (FPP)
• Geranylgeranyl pyrophosphate (GGPP) /3

1/5 Statins have years of 'manipulated' trial data. If in doubt read "Cholesterol and Statins. Sham science and bad medicine" by Cardiologist Michel de Logeril. Using statins to Inhibit HMG-CoA reductase blocks the entire mevalonate pathway, not just cholesterol. /2

https://twitter.com/drterrysimpson/status/2018500847186117033

2/ This depletes:

FPP and GGPP, impairing prenylation of GTPases like RhoA/Rac/Ras/Rab - disrupted cytoskeletal integrity, signaling, vesicle trafficking, and increased myocyte apoptosis risk (key in statin myopathy).
/3

1/8 Cholesterol is a key component of the structure and function of all cell membranes, including skeletal muscles. Increased sensitivity of skeletal muscle to HMG-CoA reductase inhibition via (Statins) can lead to a reduction in the cholesterol content in skeletal muscle /2 2/8 cell membranes, rendering them unstable and altering fluidity and excitability of ion channels. This can modulate the function of sodium, potassium, and chloride channels, leading to muscle damage and myopathy /3

1/5 I appreciate Nick’s post on statin mitochondrial toxicity. I began researching statins in 2008. It was a tough journey. Little independent research existed. After reviewing hundreds of docs & talking to statin users, I discovered statin toxicity is what makes them "work."
/2

https://twitter.com/nicknorwitz/status/1972986242724667823

2/5 In 2011, I opened @holmanm to raise awareness
of statin toxicity. Now here's the irony. A few years ago, Nick left a scathing comment on one of my posts, claiming I spread misinformation & sent a threatening DM demanding I remove it. Times have changed Nick.
/3

1/5 Animals keep eating until their protein requirements are fully satisfied, so a diet short on protein naturally triggers overeating. This is why the most effective strategy to turn around Metabolic Syndrome centers on increasing protein intake while scaling back on /2 2/5 carbohydrates.
This way of eating does wonders for stabilizing hunger hormones.. It also awakens mitochondria, encouraging them to release energy as heat, while building lean muscle mass, revving up metabolism, and fortifying bone strength. /3

1/10 Polypharmacy: Taking multiple drugs can turn a health goal into a nightmare. Instead of fixing root issues like high insulin, inflammation, or infection, one drug leads to another drug being prescribed, worsening your condition. /2 2/10 Here's an example. Pregabalin is commonly prescribed for statin-induced muscle pain.
Statins: The Wrong Target ? Statins are prescribed to lower cholesterol, but the real culprits in heart disease are hyperinsulinemia, inflammation, and infection, not cholesterol.
/3