Statins damage muscles by increasing endotoxin/LPS absorption and inhibiting glucose metabolism
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Statin drugs that lower cholesterol are perhaps the most widely prescribed medications globally. Despite their effectiveness at lowering cholesterol, the evidence that they actually decrease rusk of future heart disease (CVD) or ameliorate already existing one is very slim. In addition, evidence has emerged over the years that statins have severe side effects, including increased risk of muscle damage, and even some evidence of them causing the lethal Amyotrophic Lateral Sclerosis (ALS) condition. While all of those risks have been vehemently disputes by Big Pharma, the evidence of statin risks is stubborn and continues to accumulate. One of the plausible mechanisms through which statins may be causing muscle issues is the fact that statin inhibit the synthesis of the crucial mitochondrial electorn carries Coenzyme Q10 (CoQ10). Animals depleted of CoQ10 reliably develop severe mayopathies, including cardiomyopathy, and usually die if the CoQ10 depletion is severe enough. However, statins have also been implicated in increasing chronic inflammation and so far there has been no plausible mechanism of action proposed for this side effect of statins. The study below offers one plausible explanation. Namely, it found that statins increased endotoxin absorption into the bloodstream, and that (aside from PUFA and its metabolites) is probably the main endogenous pathway for creating systemic inflammation. In addition, statins were found to inhibit glucose metabolism, which is known to both cause inflammation de-novo also synergize with endotoxin to further increase the inflammatory burden posed by endotoxni alone. If the study findings below are confirmed by other studies, it would mean that statins may be one of the most dangerous classes of drugs, considering the vital systemic effects of endotoxn and glucose oxidation, affecting every tissue/organ and not just muscles. But even if we limit ourselves to muscle damage, even now it is mighty ironic that statins are prescribed to protect the heart, which is a muscle itself, when in reality statins can severely damage muscles through endotoxin/inflammation and metabolic inhibition by interfering with glucose oxidation.
https://doi.org/10.1126/sciadv.adz3612
https://www.verywellhealth.com/statins-may-contribute-to-muscle-weakness-12010808
“…Healthcare providers prescribe statins to manage cholesterol levels. However, muscle pain and weakness can be side effects.1 In a 2026 study, researchers may have revealed the biological mechanism underlying this drug’s effects on muscles.2”
“…To investigate why statins might cause side effects, researchers used a clinical model of the low-level damage they cause. They found that statins can introduce lipopolysaccharide (LPS), a component of bacteria, which can trigger an immune response in some people, making them more susceptible to statin-related myopathy (muscle damage). “We discovered that statins cause a type of metabolic danger, which lowers the ability to use sugar in muscle cells,” Jonathan Schertzer, PhD, one of the study’s authors and professor of biochemistry and biochemical sciences at McMaster University, told Verywell. “This activates a very specific immune response that promotes muscle damage directly within muscle cells.” The study also showed that the muscle side effects might be separate from statins’ cholesterol-lowering effects. “Importantly, we found that the pathway to muscle side effects was completely separate from the cholesterol-lowering benefits of statins,” said Schertzer.”
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Endotoxins from using statins? I wonder what the mechanism is. Are statins also antibacterial? As endotoxins are what is left after bacteria is killed.
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Yes, statins possess antibacterial properties, so in principle they will introduce LPS by helping the white blood cells to kill bacteria. But it's a strange wording, so I don't understand what he means either.
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@yerrag That should reduce LPS in the long term, so i think it's unlikely to be the mechanism
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I have to rephrase for you to understand my question.
Why would statin usage cause endotoxins to increase?
How does ststin usage cause increase in endotoxins? Another way of asking is to to replace the how with asking what is the mechanism involved.
You merely accepted without question that stating usage will increase endoroxins. I ask why and how.
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@yerrag
All i have said is that it would unlikely to be coming from any possible antibacterial effect, don't see the need for the patronizing reply.
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