In a recent trial of statin use in diabetes, greater compliance was associated with coronary calcium progression.
Statin doctors were quick to discount the findings. But aren't statins supposed to stop atherosclerosis? In this case, whether or not the statins caused the problem, they certainly didn't prevent it.
Is there a mechanism whereby statins may increase calcium deposits in arteries?
Let's look first at another side effect of statins; "certain cognitive effects such as memory loss and confusion".
Is there one effect of statins that could account for both these results?
Statins are HMG-CoA reductase inhibitors. HMG-CoA reductase is the rate-limiting enzyme for cholesterol synthesis. Cholesterol, like most lipophilic hormones and vitamins, is a terpene derivative, or isoprenoid.
Some of the essential isoprenoid structures, such as those found in vitamins E and A, are formed in plants, but others, including Co-enzyme Q10 (ubiqionone) are formed in the cytosol from a product of the HMG-CoA reductase pathway, mevalonate.
That statins can lower ubiquinone levels is well-known and accounts for occasional serious adverse reactions.
However, ubiquinone and cholesterol are not the only HMG-CoA reductase dependent compounds essential for health.
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a) ubiquinone
b) menaquinone
the repeating isoprene group derived via HMG-CoA reductase is bracketed.
Vitamin K is present in green vegetables and vegetable oils as phyloquinone, and in fatty animal foods as menaquinone-4 (MK4), while bacteria produce menaquinone-7 (MK7).
Vitamin K1 is converted to vitamin K2 by removal of the phytyl side-chain and replacement with an isoprenoid side-chain.
When this occurs in the brain the MK4 produced is an essential co-enzyme for the synthesis of special sulfur-containing lipids called sulfatides. Low CNS sulfatide levels are associated with congnitive decline and seen in the early stages of Alzheimer's disease.
Doug Bremner states that congnitive impairment is more commonly reported with the more lipid-soluble statins, such as Zocor (simvastatin) and Lipitor (atorvastatin), which cross the blood-brain barrier, and is rarer (but still seen) with water-soluble statins such as Pravachol (pravastatin).
Vitamin K2 as menaquinone-4 (MK4) also prevents arterial calcification.
Warfarin-treated rats were fed diets containing K1, MK-4, or both. Both K1 and MK-4 are cofactors for the endoplasmic reticulum enzyme γ-glutamyl carboxylase but have a structurally different aliphatic side chain. Despite their similar in vitro cofactor activity we show that MK-4 and not K1 inhibits warfarin-induced arterial calcification.
Chris Masterjohn has long been writing about the importance of vitamin K2 on his blog at Weston A. Price.
Thus there may be a common mechanism for both calcification and memory loss; decreased conversion of vitamin K1 to MK4.
Now it may be that a diet high in animal fat and fermented dairy products will supply all the MK4 you need. But is a person being prescribed statins to lower cholesterol going to be advised to consume such a diet?
Only if the doctor knows that the saturated fat lipid hypothesis is nonsense (the sugar-and-starch lipid hypothesis is another matter entirely).
An article postulating that statins might affect bone density by lowering K2 synthesis was published by Linda L. Demer in the journal Arteriosclerosis, Thrombosis, and Vascular Biology in 2001.
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Statin doctors were quick to discount the findings. But aren't statins supposed to stop atherosclerosis? In this case, whether or not the statins caused the problem, they certainly didn't prevent it.
Is there a mechanism whereby statins may increase calcium deposits in arteries?
Let's look first at another side effect of statins; "certain cognitive effects such as memory loss and confusion".
Is there one effect of statins that could account for both these results?
Statins are HMG-CoA reductase inhibitors. HMG-CoA reductase is the rate-limiting enzyme for cholesterol synthesis. Cholesterol, like most lipophilic hormones and vitamins, is a terpene derivative, or isoprenoid.
Some of the essential isoprenoid structures, such as those found in vitamins E and A, are formed in plants, but others, including Co-enzyme Q10 (ubiqionone) are formed in the cytosol from a product of the HMG-CoA reductase pathway, mevalonate.
That statins can lower ubiquinone levels is well-known and accounts for occasional serious adverse reactions.
However, ubiquinone and cholesterol are not the only HMG-CoA reductase dependent compounds essential for health.
a) ubiquinone
b) menaquinone
the repeating isoprene group derived via HMG-CoA reductase is bracketed.
Vitamin K is present in green vegetables and vegetable oils as phyloquinone, and in fatty animal foods as menaquinone-4 (MK4), while bacteria produce menaquinone-7 (MK7).
Vitamin K1 is converted to vitamin K2 by removal of the phytyl side-chain and replacement with an isoprenoid side-chain.
When this occurs in the brain the MK4 produced is an essential co-enzyme for the synthesis of special sulfur-containing lipids called sulfatides. Low CNS sulfatide levels are associated with congnitive decline and seen in the early stages of Alzheimer's disease.
Low sulfatide content in brain myelin has been recently linked with the disruption of myelin integrity [14, 21], whereas the disruption of myelin integrity was implicated as an essential contributor to cognitive deficit [6, 7, 43, 44]. Although our findings of dietary-associated decreases in myelin sulfatides suggest a potential disruption in myelin integrity in evaluated brain regions, it is currently unknown whether such disruption would be sufficient to modify motor and cognitive functions controlled by these brain regions.
In the present study both dietary forms of vitamin K1 were converted to menaquinone-4 (MK-4) in the brain.
Doug Bremner states that congnitive impairment is more commonly reported with the more lipid-soluble statins, such as Zocor (simvastatin) and Lipitor (atorvastatin), which cross the blood-brain barrier, and is rarer (but still seen) with water-soluble statins such as Pravachol (pravastatin).
Vitamin K2 as menaquinone-4 (MK4) also prevents arterial calcification.
Warfarin-treated rats were fed diets containing K1, MK-4, or both. Both K1 and MK-4 are cofactors for the endoplasmic reticulum enzyme γ-glutamyl carboxylase but have a structurally different aliphatic side chain. Despite their similar in vitro cofactor activity we show that MK-4 and not K1 inhibits warfarin-induced arterial calcification.
Chris Masterjohn has long been writing about the importance of vitamin K2 on his blog at Weston A. Price.
Thus there may be a common mechanism for both calcification and memory loss; decreased conversion of vitamin K1 to MK4.
Now it may be that a diet high in animal fat and fermented dairy products will supply all the MK4 you need. But is a person being prescribed statins to lower cholesterol going to be advised to consume such a diet?
Only if the doctor knows that the saturated fat lipid hypothesis is nonsense (the sugar-and-starch lipid hypothesis is another matter entirely).
An article postulating that statins might affect bone density by lowering K2 synthesis was published by Linda L. Demer in the journal Arteriosclerosis, Thrombosis, and Vascular Biology in 2001.
