Vitamin D3: calcium, magnesium and vitamin K2 the hormonal effects and Madison-HannaH (MH) effects the other pathway- a better explanation? 4/7

So, these three areas-kidneys, small intestines and skeletal bones are where calcium comes into or leaves the blood, think of them as gateways. Then there are I believe three states to these gateways, either activated-fast, active-slow or passive.

The active form of vitamin D3 acts on these areas in both the activate-fast and in the active-slow modes. In the active-fast to rapidly increase the blood level of calcium, calcium carbonate and other bases (to neutralize acids). This occurs in the activate-fast state by a non-genomic route. In two of three areas, the kidneys and small intestine, there can also be passive absorption of calcium.

Surprisingly despite the deficient state most people are of vitamin D3, this rapid system works well. As even at an extremely low blood levels of vitamin D3, when needed, there is enough of the blood form of vitamin D3 to produce adequate amounts of the active form to initiate the activated-fast state in these cells.  

Then the active form of vitamin D3 by interacting with the VDR in the cell walls of special cells located in the kidneys, small intestine and skeletal bone. In the small intestine for example this will result in active absorption of calcium from its contents.

This of course requires there to be calcium in the food or liquids ingested (eaten or drank) by the individual. Particularly if malnourished there isn’t enough calcium in the food or liquids ingested. Fortunately for most of us there is adequate calcium.

Then in the kidney, when the body sees a need to rapidly increase the blood calcium levels the active form of vitamin D3 acts to turn on the active-fast state in special cells there. These cells then go from passive to active-fast state in the absorption of calcium.

Prior and particularly at low blood levels of vitamin D3, calcium is passively reabsorbed. The following is a scientific explanation of how these special cells in the kidneys work. Though similar cells probably function in the small intestine and osteoclasts/osteoblast.

“A cytosolic vitamin D-dependent calcium binding protein (calbindin-D) sequesters calcium, which allows more calcium to enter the cell and more efficient diffusion of calcium across the cell. The ATP-dependent plasma membrane Ca2+ pump in the basolateral membrane pumps calcium out of the distal tubule cells into plasma.”1 The above I copied and pasted as I could not write it clearer.

In fact, in many the overriding of this system may be how they are developing osteoporosis. As 20% of people are suffering from what is called hypercalciuria-excess calcium in the urine. Defined as 250-300 mgs of calcium lost in your urine over a 24 hour period. A test called a 24 hour urine collection can be done to check for this. 2

This condition is caused by acidic urine, low vitamin D, K, magnesium or high intake of salt, acidic beverages-soda, or sugar. Many other causes like diabetes and thyroid disease to name a few. 2,3,4,5 Thus calcium, far from sitting in some insidious corner of our body if anything we are prone, regardless of vitamin D3 level, to lose it. The kidney, if functioning well, act mainly as a way to dump excess calcium. Which of course is not wise if rapidly trying to raise your blood level of it.

Then finally in the skeletal bones which acts as the bodies calcium bank and is critical in the active-fast state to supply the calcium and calcium carbonate when large quantities are needed quickly. Here the special cells are called osteoclast and osteblast.

Osteoclast break down and osteoblasts build up skeletal bone. There is a substance called bone fluid that osteoclasts and immature osteoblasts create. They both -have parathyroid hormone receptors (PHR) that respond to increased levels of parathyroid hormone (PTH) by increasing the amount of calcium in the blood. 6 More on PTH later.

This frees up calcium carbonate, phosphorus and other substances. Our bones are constantly being what is called remodeled. Which is the repairing of damaged bone and reorganizing the bone structure to meet the bodies demands.

For example, when you start a new exercise program you put unique stresses and strains on your bones the osteoclasts help your bones to be able tolerate that. Also, when we have a sudden need for calcium carbonate and calcium such as strenuous exercise with the build up of lactic acid.

It is critical our bodies maintain a neutral Ph. The lactic acid causes the blood to become more acidic which our bodies up to a point can tolerate but after that if not corrected it can reduce our bodies ability to function and if this persists long enough and severe enough can lead to death.

1. Johnson JA, Kumar R. Vitamin D and renal calcium transport. Curr Opin Nephrol Hypertens. 1994 Jul; 3(4):424-9.
2. Asplin JR, Donahue S, Kinder J, Coe FL. Urine calcium excretion predicts bone loss in idiopathic hypercalciuria. Kidney Int 2006; 70:1463–1467
3. Girón-Prieto MS, Cano-García M, Poyatos-Andújar A, et al. The value of hypercalciuria in patients with osteopenia versus osteoporosis. Urolithiasis August 2016. DOI: 10.1007/s00240-016-0909-2
4. Giannini S, Nobile M, Dalle Carbonare L, et al. Hypercalciuria is common and important finding and postmenopausal women with osteoporosis. Eur J Endocrinol 2003; 149:209–213.
5. Caudarella R, Vescini F, Buffa A, et al., Bone mass loss in calcium stone disease: focus on hypercalciuria and metabolic factors. J Nephrol. 2003 Mar-Apr; 16(2):260-6.
6. Teitelbaum SL, “Bone resorption by osteoclasts”. Science 2000; 289(5484): 1504-8.

*The information posted above is for educational purposes only. Always check with your doctor before initiating any changes in your medical treatment. If you do not, then The Two-Minute Health Fact, Dr. Judson Somerville, nor The Optimal Dose is responsible!