Why is it so difficult to establish the healthiest level for Vitamin D forms?

Scientists have discovered over 30 forms or metabolites for various vitamin D generated compounds. While it might be assumed that nature would take the proper course for these breakdown D elements and keep them in balance, that is definitely not the case, just like with estrogen. Many altered genes are involved in Vitamin D metabolism. There is perhaps as much as 5% of the human gene genome that is regulated by and involved with vitamin D hormone form. 

Some of these cascading compounds built as vitamin D breaks down are involved in immune functions and such disease processes as infection fighting and even numerous cancers. Nature also provided that some of these elements would be the limiting factor to speed the destruction and elimination of the active hormone form of vitamin D called calcitriol, 1,25(OH)2D3, plus the storage D form listed as 25-OHD. Nature often uses a downstream produced element as an indicator that the preceding nutrient has done it's job and it is now time to destroy that element form and limit further actions. Calcitriol lasts only hours in the body while 25-OHD up to 15 days, and some vitamin D precursors for months, especially if stored in fat cells. This fat storage aspect is why larger people need to consume slightly greater amounts of vitamin D compared to underweight or regular weight people to get the same blood level increases. 

Then remember, many vitamin D forms react and turn on vitamin D receptor sites on cell walls, even on cancer cells. Add to this process that about half of the vitamin D forms can attach to Vitamin D Binding Protein which acts as a time release mechanism for the various vitamin D forms. When attached, they are evidently not available for biological actions at that moment, according to one theory that explains quite a few observed actions unexplainable without this theory. Are you beginning to see how complex an issue it is to arrive at proper dosages?

A study looked at holding people at different D levels over the winter months when levels typically drop from less sun activity. Amounts needed to hold were between 600 IUs to 1600 IUs. The exact healthy level of vitamin D as 25-OHD is still a matter of debate. But, it is probably somewhere between 25-35 ng/mL or 65 to 85 nmol/L. To convert ng to nmol, multiple ng by 2.5. Plus remember, the 2 forms 25-OHD and 1,25(OH)2D are not exactly equally connected. As on goes up, the other does not automatically follow. You can have one high and the other low, or vice versa.

Many disease states also generate differences in these levels to compound the issue. Cancer cells develop a mechanism, an enzyme,  to speed the breakdown and elimination of 1,25(OH)2D, the calcitriol hormone form, and prevent calcitonin, the 25-OHD storage form, from producing more hormone D. 1,25(OH)2D has anti-cancer properties and has been used for this purpose, but because it also increases calcium uptake, this eventually leads to a negative side effect. Analogs of calcitriol were developed to try to mitigate this calcium increasing effect.

Many enzymes are involved in the Vitamin D compound breakdown forms. These enzymes are one area that controls how vitamin D compounds are produced, plus how they function and regulate each other.

WRAP UP 

Scientists like to look at just single aspects of a nutrient to produce effects in only one area like vitamin D on bone health. But vitamin D also impacts immune system aspects, especially on cancers, and blood sugar regulation. It also works synergistically with many other nutrients and hormones to build and maintain strong bones. All of these areas need to be evaluated together to arrive at the proper dosage level for vitamin D. And, unfortunately, sometimes there are different ideal dosage levels for different functions requiring an average or priority decision depending upon which area of influence is vital to the individual's current state of health. And remember to add to these facts that vitamin D hormone form increases calcium absorption, not to build bones but to maintain a proper level of calcium in blood plasma. This is necessary for muscles to contract, nerves to fire, and for various other vital metabolic processes. The fact that this process involves bone health is really more of a side show for vitamin D. article 

Let this concept soak in for a moment. Your body uses vitamin D to maintain blood levels of calcium, and increased bone density is just one possible side show response of this action. Plus, since this increased bone density is really just a temporary calcium storage solution, when the high amount of dietary calcium intake is reduced or stopped, the increased bone density will return to previous levels before the increased calcium intake started.

Because many Health Professionals fail to grasp this concept, their recommendations for the proper supplement dosage of vitamin D and calcium can be counter to long term bone health. While it looks logical to keep a high intake of dietary calcium to continually maintain this forced storage action of higher bone density, future bone building processes are getting compromised. Literally, the bone building cells are overworking and wear out or age* faster than the bone tearing down cells. The balance between tear down and rebuild is critical for bone health. Without enough healthy bone building cells, the bone repair process allows the bone tearing down cells to continue clearing out older bone areas scheduled for repair, but the rebuild process is too slow. Holes develop in bones that weaken their structure, and they eventually fracture. Here is another mechanism that also plays a critical role in bone tearing down cell controls. article

While the preceding process explanation has been greatly simplified, it gives a clear idea of a failed appreciation for human physiology. Bones are designed to last a lifetime.

* Yes, many body cells age similar to the way humans age. They get old and are no longer as vital at performing living functions. A Researcher tested the average age of bone building cells in people with osteoporosis versus those without. The results showed older bone building cells in those with osteoporosis. The question this raises, what ages bone building cells faster in some people?