1/8 Please don't be fooled. There is no such thing as a statin “side effect”. Statin toxicity is a direct and predictable effect of blocking mevalonate by inhibiting the enzyme HMG-CoA Reductase, which makes it. /2
2/8 Statin poisoning is a sign that certain cells cannot mutate by increasing reductase to overcome the direct cell toxic effect of the Mevalonate blockade of Statins. Pharmaceutical companies knew this back in 1980. /3
3/8 The Journal of Biochemical Chemistry reported that when HMG-CoA Reductase is inhibited by Statins, Mevalonate formation is blocked and cultured cells DIE. Every Statin user is a victim of this process. /4
4/8 Cholesterol is so vital to life that, when needed, cells almost instantly obtain it in two ways: Cells “make it” from scratch via the Mevalonate pathway Cells “take it” from the blood in ready made form /5
5/8 As well as being a fundamental building block of cell membranes, Cholesterol plays a key role in maintaining their lipid organisation and biophysical properties, and is crucial for the function of proteins located in the plasma membrane.
6/8 Importantly, Cholesterol and other Mevalonate derivatives are absolutely essential for cell cycle progression, and their deficiency blocks different steps in the cycle. Cholesterol provides support for cell membranes and is converted by cells into life-essential hormones /7
7/8 such as Testosterone, Progesterone, Aldosterone, Cortisol and Vitamin D. When it is needed there can be no time to lose. Statins inhibit this by their Mevalonate blockade. The biochemicals necessary for good health and cell survival are lost when you ingest a Statin drug.
8/8 To add insult to injury, statins elicit a striking progressive decline in skeletal muscle mitochondrial respiratory capacity. In case you'd forgotten, your heart is a muscle !
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1/5 @realDonaldTrump's Crestor and Ezetimibe have his LDL at 51 mg/dL. It looks good on paper, but is it ? Ultra-low LDL may weaken immunity, raising infection risk. His leg swelling from venous insufficiency is also concerning.
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2/5 Are statins harming his heart & arteries instead of helping ? Trump has been on Crestor since 2016, starting at 10 mg, increased to perhaps 20–40 mg in his first term, now back to 10 mg with Ezetimibe. LDL at 51 mg/dL may seem ideal, but low CoQ10 could weaken his heart /3
3/5 risking heart failure, and worsen his leg swelling. Ultra-low LDL limits immune defenses, leaving Trump vulnerable to infections. LDL supports virus-fighting cells, and 51 mg/dL is too low for robust immunity, especially with his public exposure. /4
1/4 Statins & Muscle Pain: Class Effect, Not a Side Effect: Statins are widely prescribed to lower cholesterol, but muscle pain is a class effect due to their mechanism. Statins inhibit HMG-CoA reductase, blocking cholesterol synthesis. This deprives cells of mevalonate, /2
2/4 a critical compound. Mevalonate deprivation isn’t trivial, it can damage cell mitochondria, disrupt muscle membranes, and even cause cell death. This isn’t just a “side effect” unique to one statin; it’s a class effect shared by all statins due to how they work. /3
3/4 Yet, many doctors seem unaware. When patients report muscle pain, the response is often to switch statin brands or lower the dose. This doesn’t address the root issue. Mevalonate disruption is inherent to the drug class ! Patients deserve better. /4
1/9 Chronic inflammatory diseases, such as rheumatoid arthritis, lupus, psoriasis, and infections such as periodontal disease (p.gingivalis), & HIV, are associated with an increased risk of heart disease. Patients with these disorders also have an increase in coronary artery /2
2/9 calcium measured by CT & carotid intima media thickness measured by ultrasound. WHY ?? Because inflammation & infections induce a variety of alterations in lipid metabolism that may initially DAMPEN inflammation or fight infection, but if chronic, can contribute to the /3
3/9 increased risk of Atherosclerosis. The changes in lipids and lipoproteins that occur during inflammation & infection are part of the innate immune response & therefore are likely to play an important role in PROTECTING the host. /4
1/8 One of the vital roles of Vitamin C is to act as an antioxidant to protect cellular components from free radical damage. Vitamin C has been shown to scavenge free radicals directly in the aqueous phases of cells and the circulatory system. /2
2/8 Unlike Statins, Vitamin C has been proven to protect membranes & other hydrophobic compartments from such damage. Human subjects with low Vitamin C levels have been reported to have higher amounts of lipid peroxides in plasma than do subjects with high vitamin C levels. /3
3/8 It has also been shown that Vitamin C, may act as a preventive antioxidant against metal ion–mediated LDL oxidation. Along with the reduction of sugar/seed oils in the diet there is another measure everyone can take to reduce their risk of heart disease. /4
1/5 What benefit ? 🙄 The study linking statins’ calcification effect to mortality benefits relies heavily on correlational data, oversimplifying the role of calcification. It ignores thresholds, trade-offs, and confounders, while neglecting long-term risks and contradictory /2
2/5 evidence like apoptosis or metabolic effects. The conclusion, that statins’ calcification is clearly beneficial, lacks robust support & misrepresents cardiovascular disease complexity. A stronger study would directly test the calcification hypothesis and address /3
3/5 alternative mechanisms. Statins drive coronary artery calcification by depleting CoQ10, heme A, and ATP, acting as mitochondrial toxins. They inhibit vitamin K2 and selenoprotein synthesis, increasing the risk of atherosclerosis. /4
1/4 Metabolism is how cells "breathe", We breathe air into our lungs so that oxygen is delivered to our cells for metabolism. Anything that obstructs this process "suffocates cells" and CoQ10 is as essential as oxygen.. Skeletal & heart muscle cells have a very high demand for /2
2/4 CoQ10. Muscle cell damage (myopathy) and muscle cell death (rhabdomyolysis) are the most commonly reported Statin injury. Three years after FDA approval of Lovastatin, Merck decided that statin-blockade of CoQ10 synthesis was causing Statin Myopathy. /3
3/4 Michael Brown wrote a patent for adding CoQ10 to Merck's Statins in an attempt to ameliorate statin induced myopathy. In the body of the patent he explains how CoQ10 should both prevent and cure statin induced myopathy. However CoQ10 was never added. /4