Vitamin K2, CoQ10, "High" Cholesterol, and Schnyder Corneal Dystrophy

This is a new discovery, quietly making its way through the internet of knowledge in 2016, but probably no less profound than Brown and Goldstein's uncovering active LDL feedback and control mechanisms.  This is more contemporary evidence that those wonk heads who honestly think they have put an end to new discovery are usually wrong.  While ascorbate is important to prevent the damage that apo(a) repairs, it is not the only thing you need to prevent atherosclerosis.  Huge amounts of ascorbate can cover for a UBIAD1 deficiency as I will explain later on here, but probably you will never recover what you could gain by augmenting the loss-of-function from not having enough menaquinone-4 vitamin K2..and CoQ10.

UBIAD1, the vitamin K2 generating enzyme, is necessary in its un-mutated form to chaperone HMG CoA reductase as a steric protease inhibitor.  When encountering geranylgeraniol in the mevalonate pathway, UBIAD1 dissociates from the reductase, removing the steric hindrance to proteolysis and then the reductase is degraded, and cholesterol synthesis goes down.

The prenyltransferase UBIAD1 is the target of geranylgeraniol in degradation of HMG CoA reductase.

When the UBIAD1 enzyme is mutated, it does not dissociate from the mevalonate pathway enzyme and it does not degrade and so over-functions in constitutive cholesterol synthesis.

Not only this, but mutated UBIAD1 can be rescued by the administration of its gene product, menaquinone-4, a molecular species of Vitamin K2, making this a very solvable problem for people if they understand what it is they have.  If they do not understand what they have, they will get Schnyder Corneal Dystrophy and eventual coronary and renal calcifications if not also calcium deposits in all the arterial bifurcations and curvatures.

Role of UBIAD1 in Intracellular Cholesterol Metabolism and Vascular Cell Calcification

Looks like someone already beat me to the punch here:

Vitamin K2 biosynthetic enzyme, UBIAD1 is essential for embryonic development of mice.

So there is a bonafide conjunction, not coincidental or supplemental, but an essential conjoining of function between HMG CoA reductase, UBIAD1, cholesterol levels, and prevention of vascular calcification.  Not having K2 or CoQ10 will raise intracellular cholesterol levels directly at the enzymatic level, not at a degradation or accumulation aspect.

As I speculated, massive doses of vitamin C can cover some of the defects of a UBIAD1 defect by virtue of it being an electron donor and labile redox molecule, but won't fully rescue the UBIAD1 defect.  "In COQ2 mutant fibroblasts, increased superoxide anion production and oxidative stress-induced cell death were normalized by all supplements."

Treatment of CoQ10 Deficient Fibroblasts with Ubiquinone, CoQ Analogs, and Vitamin C: Time- and Compound-Dependent Effects

Of these compounds, you make CoQ10 until age 20 when the enzymatic synthesis starts to run down (sad but true) until age 80 when the synthesis levels are very low to nil.  Vitamin K is needed in the micrograms quantity per day, qualifying it as a classical "MICRO" nutrient.  I will argue that ascorbate IS NOT a micronutrient but a millinutrient.  For some bubble headed quackademic to claim that you can get by on micrograms of ascorbate is not paying attention and will cause a massacre by scurvy.  Leave it to a quack (mal) nutritionist to have only two blunt categories:  Macro and micronutrients, ignoring millinutrients.  It is like a person saying there is only 2 hours in a day when there are 12 or spring and winter, forgetting summer and autumn.  Nobody ever makes vitamin C, so if you had to supplement only 1 out of 3 things, I would most definitely choose vitamin C.