So if cholesterol is not the problem, why are doctors so gung ho on prescribing statins to reduce cholesterol?
Statins are Antibiotics…is THAT the Pleiotropic Effect?
Statins have pleiotropic effects, ie the ability to reduce heart disease
risk and CV death via an unknown mechanism, certainly beyond the LDL
cholesterol lowering that they can achieve. Researches have known for
quite some time about these beneficial effects of HMG-CoA reductase
inhibitors (also known as “statins,” such as atorvastatin and
rosuvastatin), however the physiology behind this phenomenon remains
unclear. The answer as to why statins have these pleiotropic effects is
largely unknown, but let me throw out an interesting theory and you form
your own opinion.
To kill the surrounding bacteria so they do not invade the fungi’s space, allowing the Penicillium citrinum species to grow and spread more easily ... survival of the fittest!
Then, what is the role of mevastatin in this fungus? According to researchers, it is the exact same: To block the cholesterol synthesis in the invading bacteria and other fungi, acting like an antibiotic.
Think about this, as well: We know it takes decades for atherosclerotic plaques to form, and it is an inflammatory process. We know that the early use of statins immediately during an ACS significantly reduces mortality according to multiple clinical trials, including PROVE IT-TIMI 22 and the MIRACL trial. This benefit is thought to be from acute plaque stabilization, decreased thrombogenicity and decreased inflammation that occurs immediately after statin administration.
How does this make any sense if the only thing statins do is reduce LDL cholesterol levels through inhibition of HMG-CoA reductase? How should that short-term administration improve long-term mortality, considering the chronic nature of atherosclerosis? Why do these beneficial effects occur? Why is inflammation dramatically reduced so quickly? Again, maybe statins are antibiotics!
Quite an intriguing theory, that statins are antibiotics and kill the pathogenic cause of atherosclerosis, isn’t it? Well, of course I was not the first person to think that perhaps the process of atherosclerosis occurs from an infection. The organisms that have been implicated in contributing to atherosclerosis include Chlamydia pneumoniae (now actually called Chlamydophila pneumoniae), cytomegalovirus (CMV) and Helicobacter pylori. Here are a look at some studies that test this theory.
Interesting side note: Mevastatin caused liver tumors and severe muscle problems in animal studies, and therefore was never brought to market (although it is one of the naturally occurring statins in red yeast rice extract, which millions take ... not good).
Statins are antibiotics that kill the undiscovered organism responsible for the entire process of atherosclerosis.
Lets look at some facts first. Many don’t know that the first statin, mevastatin, was discovered in 1971 in the fungus Penicillium citrinum. As the name implies, this is the same fungus from which the first antibiotic penicillin was found. What was the role of penicillin in this fungus, you ask?To kill the surrounding bacteria so they do not invade the fungi’s space, allowing the Penicillium citrinum species to grow and spread more easily ... survival of the fittest!
Then, what is the role of mevastatin in this fungus? According to researchers, it is the exact same: To block the cholesterol synthesis in the invading bacteria and other fungi, acting like an antibiotic.
Think about this, as well: We know it takes decades for atherosclerotic plaques to form, and it is an inflammatory process. We know that the early use of statins immediately during an ACS significantly reduces mortality according to multiple clinical trials, including PROVE IT-TIMI 22 and the MIRACL trial. This benefit is thought to be from acute plaque stabilization, decreased thrombogenicity and decreased inflammation that occurs immediately after statin administration.
How does this make any sense if the only thing statins do is reduce LDL cholesterol levels through inhibition of HMG-CoA reductase? How should that short-term administration improve long-term mortality, considering the chronic nature of atherosclerosis? Why do these beneficial effects occur? Why is inflammation dramatically reduced so quickly? Again, maybe statins are antibiotics!
Quite an intriguing theory, that statins are antibiotics and kill the pathogenic cause of atherosclerosis, isn’t it? Well, of course I was not the first person to think that perhaps the process of atherosclerosis occurs from an infection. The organisms that have been implicated in contributing to atherosclerosis include Chlamydia pneumoniae (now actually called Chlamydophila pneumoniae), cytomegalovirus (CMV) and Helicobacter pylori. Here are a look at some studies that test this theory.
Interesting side note: Mevastatin caused liver tumors and severe muscle problems in animal studies, and therefore was never brought to market (although it is one of the naturally occurring statins in red yeast rice extract, which millions take ... not good).
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