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New Science Shows Statins Don’t Target the Problem
February 14, 2010
It is quite inconvenient for the statin industry, which is bilking taxpayers and insurance companies for over 20 billion dollars every year, to find out that the statins are pointed at the wrong target. This is the conclusion that is easy to reach based on a new and highly advanced way of looking at the issue of how plaque is formed in arteries1.
Current drugs to lower cholesterol, called statins, are targeted at the primary system in your liver for the synthesis of cholesterol for all needs in your body (which are many). Unfortunately, this system is central to your survival.
The new study, using advanced gene tools and proteomics, finds that it is a protein network that is shed by cholesterol-laden macrophages that alters gene function and thereby sets the stage for plaque formation. On the surface this may sound complex and it is more complicated than the overly-simplistic notion of good and bad cholesterol. However, keep in mind that modern medicine is implementing a drug therapy when in reality they have no idea how plaque is actually formed. In other words, how do they even know what they are doing?
As it turns out, macrophages in the circulation take up excess cholesterol, a fact that has been known for years. What is new is the finding that once this happens then the macrophages shed protein fragments from their cell membranes called microvesicles. These protein fragments turn out to form a network of communication that activates genes that lead to the formation of plaque. This means that targeting the basic synthesis of LDL cholesterol production is the wrong target. Targeting the behavior of macrophages and their network of proteins and consequent gene signals is a much more relevant target.
Don’t expect to hear much about this anytime soon, as drugs are not designed for this issue. However, improving the function of macrophages is within the scope of natural health and the common theme will be reducing inflammation and cleaning your blood of debris, including toxins and surplus fat (triglycerides).
Current drugs to lower cholesterol, called statins, are targeted at the primary system in your liver for the synthesis of cholesterol for all needs in your body (which are many). Unfortunately, this system is central to your survival.
The new study, using advanced gene tools and proteomics, finds that it is a protein network that is shed by cholesterol-laden macrophages that alters gene function and thereby sets the stage for plaque formation. On the surface this may sound complex and it is more complicated than the overly-simplistic notion of good and bad cholesterol. However, keep in mind that modern medicine is implementing a drug therapy when in reality they have no idea how plaque is actually formed. In other words, how do they even know what they are doing?
As it turns out, macrophages in the circulation take up excess cholesterol, a fact that has been known for years. What is new is the finding that once this happens then the macrophages shed protein fragments from their cell membranes called microvesicles. These protein fragments turn out to form a network of communication that activates genes that lead to the formation of plaque. This means that targeting the basic synthesis of LDL cholesterol production is the wrong target. Targeting the behavior of macrophages and their network of proteins and consequent gene signals is a much more relevant target.
Don’t expect to hear much about this anytime soon, as drugs are not designed for this issue. However, improving the function of macrophages is within the scope of natural health and the common theme will be reducing inflammation and cleaning your blood of debris, including toxins and surplus fat (triglycerides).
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