Why K2 stops your arteries clogging up with calcium

Imagine being offered a heart related drug with the promise of reducing heart attacks/CVA and thus death, but it increases your arterial calcification.

Would it seem to be something of an oxymoron?

Well, our old friend statins are once again trying to gaslight the whole world into believing your liver just cannot stop making those naughty lipoproteins carrying around fat, which we call cholesterol.

Sure, we need them to create all our steroid hormones, from testosterone and progesterone to cortisol to aldosterone.

And OK, it might make vitamin D a life-saving hormone, woefully low in the general population.

But apart from that, what has cholesterol ever done for us?

So, the big pharma companies decided back in the 1980’s that they were no longer happy treating sick patients. They want healthy ones too, for “preventive medicine”.

So, we have written about statins before on muscle pain:



Perhaps you’d like to know just how preventative these preventative drugs are (hint its wayyyy less than you think).


But now we have clear data that statins actually increase calcification in your arteries.

This study compared statins users against control groups both with and without existing heart issues.

Note CACS stands for Coronary Calcification Arterial Score, dark blocks are no statins, grey blocks are statin users.

Whether you have known CVD or are looking for prevention, it still increases calcification in your arteries.

The mechanism is the blocking of a vitamin K2-dependent protein called osteocalcin which, when carboxylated, binds calcium.

Thus, if you leave it UN-carboxylated, your calcium disappears into your soft tissues.

Thus, ucOC is un-carboxylated osteocalcin, a functional marker of low K2 status.

In reality, we knew this was an issue, but this confirms the whole thing.

But how it happens is key, and can we get around this issue with patients who want or need to stay on statins?

The key vitamin K2 molecule in all this is MK4.

This is a special molecule missing from 99% of all supplements in favour of its longer-chain (and cheaper) cousin MK7.

MK4 is found in the breast milk of every mammal, hence why we get it in high-quality dairy.

The only form of K2 to cross the placenta is MK4.

Think about it, if every mammal on the planet uses MK4, not MK7, to nourish its young, it must be special.

So special, in fact, that all other forms of K2 and even K1 can be converted into MK4.

And herein lies the issue with statins.

It is statins that inhibit the enzyme that converts K1, the form found in plants, into MK4, the K2 form found only in animals and dairy (sorry vegans).

So, by inhibiting the enzyme, your MK4 levels drop, and you get higher un-carboxylated osteocalcin, and your calcium disappears into your arteries.

FYI – the enzyme is MAGNESIUM dependent, and remember 20-40% of the population is below optimal.

In our clinical population, the rates are much higher.

Double jeopardy.

So then, what to do?

Well, fear not, because I have spent months on end sitting in my office reading the literature as it pertains to the neuro-mechanical system, we added MK4 to our vitamin D/K2 sublingual, 100 mcg.

Remember, all roads lead to MK4, even the supplement companies’ favourite cheaper form of K2 converts to MK4.

It is effectively a slow release form of MK4, but we don’t know how well everyone converts it.

But we do know that the vast majority of osteoporosis and fracture studies using K2, use MK4.

And I mean the VAST majority.

Plus MK4 boosts sex hormones and may play a role in cancer.