Vitamin A plays a valuable role in managing the body's need for vitamin K2. On a molecular level, it is precisely this misunderstood role that gave vitamin A an undeserved bad rap. Vitamin D stimulates the production of vitamin K2– dependent gla proteins, thereby increasing the body's demand for vitamin K2 and the potential to benefit from K2. That makes vitamin D a superstar because the more vitamin K2–dependent proteins you make, the more calcium you can direct into bones and away from arteries, if you have the K2 to activate those proteins. So vitamin D looks good.
Here's where things get tricky. Working together, A and D synergistically improve osteocalcin production. On its own, however, vitamin A limits the production of MGP. This sounds detrimental to heart health—and in large amounts it would be—but it effectively minimizes the body's requirements for K2. Vitamin A has a K2-sparing action; having adequate amounts of retinol reduces the demand for K2, allowing your body to get by on less menaquinone.30 When K2 is scarce, vitamin A does damage control. Of course, if this is taken to an extreme with long-term high-dose vitamin A supplementation paired with a lack of vitamin D, you will eventually see problems like lower bone density because you have spared K2 too much. As with the Three Viro Brothers, it's all about balance.
Vitamins A and K2 have an additional buddy system in which retinol complements the action of vitamin D. It is yet another realm in which the effects of vitamin A are misconstrued. Remember the seasonal variations in calcium excretion that parallel changes in arterial calcifications? Calcium plaque diminishes in late summer, while bone density is retained. Where is the extra calcium going? Down the toilet.
There is a seasonal variation in urinary calcium excretion (yes, it's been studied), and it is not what you would expect. Given that bone density loss occurs almost exclusively in winter, you might predict urinary calcium loss to be highest at this time. Instead, calcium excretion is minimal in winter months when bone density is diminishing—and when arterial calcifications are growing.31 The calcium being lost from bone is not leaving the body; it is being transferred to plaque.
In the northern hemisphere, urinary calcium peaks in August, but bone density remains stable so that lost calcium is not being leached from our skeleton. Arterial calcifications, on the other hand, diminish in the same month. What prompts the body to rid itself of calcium at this time of year? It just so happens that retinol levels also follow an annual cycle, peaking in summer.32 Curiously, although vitamin A intake is generally constant year-round, blood levels of retinol and its carrier protein are elevated in the summer. Retinol is famous for causing urinary calcium loss, an effect that has long been maligned as promoting osteoporosis. Looking at annual trends, we see that when retinol levels and calcium output are highest, bone density isn't affected. Instead, arterial calcifications shrink. Vitamin A is triggering the body to release the calcium that K2 has liberated from the arteries.
Since retinol regulates the production of K2-dependent MGP, it seems to be
at odds with the action of menaquinone. And yet, K2 content in grass-fed foods varies with the content of retinol. Why would K2 pair up with its apparent nemesis? Vitamin A promotes urinary excretion of calcium. When K2 removes calcium from arterial plaque, vitamin A disposes of it. Vitamin D promotes calcium absorption so K2 can guide it into bones and teeth. Vitamin A chaperones calcium out of the body when K2 has extracted it from soft tissue. This is the calcium cycle of life.
So exactly how much A, D and K2 do we need to keep everything in balance and keep calcium in its proper place? Since vitamin K2 does not act like a hormone and stimulate protein production, it has no toxic effects, as you know. For that reason, K2 isn't a limiting factor—it will activate as much osteocalcin and MGP as it finds. It's vitamins A and D that are the limiting factors. Since they are also the nutrients with potentially toxic effects, we need to determine our relative requirements of these vitamins. How much A do we need to optimize the benefits of and prevent potential toxicity of D and vice versa?
There is no established optimal ratio for vitamins A and D, although several have been suggested based on educated guesswork. The most intelligent analysis of this question proposes that there is not an optimal ratio of vitamins A and D per se. Rather than A and D interacting by a ratio model, they interact by a switch model whereby a minimum amount of D switches off the potentially toxic effects of A and a minimum amount of A switches off the toxicity of D.33 As long as you have some of each, then, not only are you protected but you stand to reap the biggest benefits. Vitamins A and D will work synergistically to maximize production of osteocalcin and MGP. Be sure you have plenty of menaquinone available to activate all those proteins so they don't go to waste. A diet rich in all the fat-soluble vitamins will accomplish that.
A switch model makes good sense in light of the fact that traditional diets around the world would have had a varying relative intake of these nutrients.
In regions where both seafood and sunshine are staples, vitamin D intake might be relatively high compared with A. The opposite might be true in areas where the organs of land-dwelling creatures were a mainstay. Mother Nature couldn't afford to be picky about a particular ratio of A and D; she'd be happy as long as you were getting minimum amounts of each and hopefully lots of both. This is where the wisdom of obtaining fat-soluble vitamins from food shines through. Although supplements will be necessary
to bridge the gap while dietary intake of A, D, K2 and E catches up to demand, a thoughtfully diverse diet will keep it in balance.