Today, I have an article for you on vitamin K.
It is from Sol Orwell.
Sol has created an amazing guide on supplements.
In Sol’s guide, the Supplement Goals Reference Guide he highlights the research out there when it relates to supplements and what the research says about supplements and their effect on conditions.
Sol knows that I focus on injury and pain. He felt people needed to know more about vitamin K because most people don’t.
Rick Kaselj, MS
What is Vitamin K?
Vitamin K is a fat soluble vitamin which can come in a few forms: K1 (known as phylloquinone and exclusive to plants) and K2 (which is actually a collection of molecules known as menaquinones which is designated as MK and their size indicated by the number that follows; examples being MK-4 and MK-7). It is surprisingly non-toxic for a fat soluble vitamin, and similar to vitamin D it appears to have a gap between the recommended daily intake and its optimal intake.
All the above molecules work via something called the ‘vitamin K cycle,’ which is how these molecules exert the benefits of vitamin K.
How does Vitamin K work?
How vitamin K works is a bit indirect. Vitamins tend to either work as a ‘cofactor’ of sorts (associating with an enzyme to optimize its function) or they work directly on receptors to start signalling through the cell (like hormones and vitamin D). Vitamin K is in the former, but works on a particular class of proteins known as ‘Vitamin K dependent proteins.’
Proteins of this class have a little residue (glutamate residue) that is modified by vitamin K (gamma-carboxylated) and when it is modified the protein is switched from an ‘inactive’ state to an ‘active’ state. The vitamin K cycle (mentioned previously) is the cycle that activates these proteins with vitamin K.
Increasing dietary vitamin K will increase activity of these proteins up until a certain point (which is dependent on the protein in question), and the proteins involved in blood clotting are pretty much maximally activated at around 100mcg of dietary vitamin K intake (and thus where the RDI comes from).
Recently, however, some other proteins such as an important one known as osteocalcin have been noted to be maximally activated at 1,000mcg (1mg) dietary intake; so between 100mcg and 1,000mcg is a dose-dependent increase in osteocalcin activity and its benefits.
How does this benefit heart health?
There is a process known as soft tissue calcification, which is a process where soft tissue (ie. not bone) have calcium deposited onto them forming bone-like surfaces. This can occur in most soft tissue including arteries, and when calcification of arteries occur it is known as ‘stiff arteries’ (since the calcium deposits reduce how flexible the arteries can be).
Although it isn’t necessarily atherogenic (plaque forming), the stiffness of arteries is known to be a large risk factor for cardiovascular disease and death from it. Interestingly, the main side-effects of vitamin D overdoses are an increase in arterial calcification.
The protein known as osteocalcin (the vitamin K dependent protein maximized at around 1,000mcg dietary intake) is a negative regulator of arterial calcification; in other words, it works to prevent how much calcium is deposited on arteries and slowly removes calcium from the arteries as well. This results in a preservation of arterial flexibility and prevents (somewhat) the increased risk from stiffness from occurring.
This is relatively interesting since there are many herbs or supplements that reduce the risk for cardiovascular disease but they tend to work via reducing triglycerides or cholesterol, blood pressure, or plaque buildup (atherosclerosis); the reduction in calcium buildup is not a common mechanism.
How does this benefit bone health?
Two cell types in bone tissue are osteoclasts and osteblasts, the former of which mediates bone breakdown (to supply the body with vital minerals) and the latter is the opposite and supports bone formation. In many states of bone loss such as osteopenia, the activity of osteoclasts is significantly larger than the activity of osteoblasts.
Vitamin D is known to increase the activity of osteoblasts (to support bone growth) but also proliferates osteoclasts; Vitamin K (or more specifically, its proteins of which include osteocalcin) inhibit the ability of Vitamin D to proliferate osteoclasts but don’t interfere with the beneficial effects of Vitamin D. Although vitamin K itself is beneficial, it is more commonly called a ‘synergist’ of vitamin D.
Due to this reason, vitamin D and vitamin K (as well as some minerals such as calcium and magnesium) are commonly all supplemented together for bone health.
When looking at human trials, this tends to manifest itself as a reduced fracture rate of bones. Vitamin K seems to strengthen the bones, but does not seem to reliably increase bone mineral density (possibly since it increases bone size as well as mineral content, keeping density somewhat consistent).
If you would like more information on The Supplement Goals Reference Guide, click here: