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http://www.bmj.com/content/348/bmj.g3244/rr/702087
It continues to amaze me that so few look to the pharmacologic mechanisms of statins to understand how it leads to an increased risk of diabetes, thus showing why statins have fundamental problems and offering potential real alternatives to these toxic drugs for multiple health endpoints.
It is known by pharmaceutical researchers that inhibition of endogenously made quinones such as ubiquinone or menaquinone-4 occur with statins, with the more lipophilic statins causing more inhibition than those that are less lipophilic, which partially may explain the various seeming conflicting results when statins are considered. Not only dose, but lipophilicity is a factor in how statins behave and what havoc they may create, as well as the nutritional status of the individual...thus, these multiple confounders lead to mis-steps regarding statins.
Occasionally, it is suggested that statin users take a supplemental CoQ10 to offset this inhibition, but it looks like the inhibition of menaquinone-4 biosynthesis via statins may be even more disruptive to many processes and pathways than inhibition of CoQ10, yet this remains off the typical radar. (1,2)
In fact, the tissues where statin side effects occur tend to be those tissues where MK-4 is a relatively high level storage form of menaquinone: brain, muscles, beta cells of pancreas, kidneys, etc. These stores of MK-4 are created via the enzyme UBIAD1 (also known as TERE1) which is found widely in tissues throughout the body and which appears to be impaired via statins as well as other Rx drugs and also an aberrant form of dietary fat, dihydrophylloquinone, biomarked by trans fatty acids since it is created when high phylloquinone oils such as soy and canola are hydrogenated. We inhibit MK-4 biosynthesis from some Rx drugs and via foods high in trans fatty acids.
The seeming benefit of statins in inflammation inhibition are via suppression of activation of NFkB. In fact, it increasingly appears that this inflammation suppression is what leads to improved outcomes for those who have suffered a cardiovascular event instead of reduction of cholesterol, also synthesized via the same enzyme as MK-4. BUT vitamin K2, the menaquinones, ALSO suppresses NFkB activation and this needs to be considered much more as a way to optimize cardiovascular health. (3)
Rather than try to justify statins and their benefits v risks, why do we not look at how vitamin K works, how it converts into MK-4, and how to optimize this? It truly appears that vitamin K is directly involved in cardiovascular risk (4, 5) as well as cancer, osteoporosis, and DIABETES. (6, 7)
Until a long chain menaquinone drug is created, our current system precludes really looking at the benefits of increased vitamin K intake, especially of long chain menaquinones, due to financial incentives to only look to drugs and this has coincided with a loss of old-fashioned foods that happen to be high in long chain menaquinones such as organ meats or fermented foods.
Among the various footnotes, many common chronic diseases are mentioned including osteoporosis, diabetes, CVD, cancer. It is no coincidence that they tend to be concomitant: they share the same etiological insufficiencies of vitamin K and vitamin K actions. We need to look much more closely at vitamin K of all forms instead of drugs such as statins, et al for health optimization.
Micki Jacobs
It continues to amaze me that so few look to the pharmacologic mechanisms of statins to understand how it leads to an increased risk of diabetes, thus showing why statins have fundamental problems and offering potential real alternatives to these toxic drugs for multiple health endpoints.
It is known by pharmaceutical researchers that inhibition of endogenously made quinones such as ubiquinone or menaquinone-4 occur with statins, with the more lipophilic statins causing more inhibition than those that are less lipophilic, which partially may explain the various seeming conflicting results when statins are considered. Not only dose, but lipophilicity is a factor in how statins behave and what havoc they may create, as well as the nutritional status of the individual...thus, these multiple confounders lead to mis-steps regarding statins.
Occasionally, it is suggested that statin users take a supplemental CoQ10 to offset this inhibition, but it looks like the inhibition of menaquinone-4 biosynthesis via statins may be even more disruptive to many processes and pathways than inhibition of CoQ10, yet this remains off the typical radar. (1,2)
In fact, the tissues where statin side effects occur tend to be those tissues where MK-4 is a relatively high level storage form of menaquinone: brain, muscles, beta cells of pancreas, kidneys, etc. These stores of MK-4 are created via the enzyme UBIAD1 (also known as TERE1) which is found widely in tissues throughout the body and which appears to be impaired via statins as well as other Rx drugs and also an aberrant form of dietary fat, dihydrophylloquinone, biomarked by trans fatty acids since it is created when high phylloquinone oils such as soy and canola are hydrogenated. We inhibit MK-4 biosynthesis from some Rx drugs and via foods high in trans fatty acids.
The seeming benefit of statins in inflammation inhibition are via suppression of activation of NFkB. In fact, it increasingly appears that this inflammation suppression is what leads to improved outcomes for those who have suffered a cardiovascular event instead of reduction of cholesterol, also synthesized via the same enzyme as MK-4. BUT vitamin K2, the menaquinones, ALSO suppresses NFkB activation and this needs to be considered much more as a way to optimize cardiovascular health. (3)
Rather than try to justify statins and their benefits v risks, why do we not look at how vitamin K works, how it converts into MK-4, and how to optimize this? It truly appears that vitamin K is directly involved in cardiovascular risk (4, 5) as well as cancer, osteoporosis, and DIABETES. (6, 7)
Until a long chain menaquinone drug is created, our current system precludes really looking at the benefits of increased vitamin K intake, especially of long chain menaquinones, due to financial incentives to only look to drugs and this has coincided with a loss of old-fashioned foods that happen to be high in long chain menaquinones such as organ meats or fermented foods.
Among the various footnotes, many common chronic diseases are mentioned including osteoporosis, diabetes, CVD, cancer. It is no coincidence that they tend to be concomitant: they share the same etiological insufficiencies of vitamin K and vitamin K actions. We need to look much more closely at vitamin K of all forms instead of drugs such as statins, et al for health optimization.
Micki Jacobs
