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How calcium is absorbed and how Vitamin D3 is synthesized / acquired
In order to understand the main concepts of supplementing calcium, it is important to discuss Vitamin D3 in its relation to UVB lighting.
How is Vitamin D3 synthesized / acquired?
There are 2 primary methods for obtaining vitamin D3-
a) synthesizing it from exposure to ultraviolet B radiation
b) consuming a vertebrate that synthesized the hormone through exposure of the sun.
The production of vitamin D3 occurs as a result of the photosynthetic conversion of 7-dehydrocholesterol to pre-vitamin D3 (UVB represents the range of light considered important for synthesis of D3.) Pre-vitamin D3 is converted to vitamin D3 via a temperature dependent process. At this point the hormone is transported to the liver where it is hydroxylated to 25-hydroxyvitamin D3. The kidneys serve as the site for the final conversion of the hormone to its active form 1,25-hydroxyvitamin D3 (Calcitriol).
Why is Vitamin D3 important and how does it relate to calcium?
Vitamin D3 is an essential hormone that plays many different important physiological roles. Its role in calcium metabolism is probably its most recognized function.
Vitamin D3 stimulates intestinal absorption of both calcium and phosphorus, thus causing a rise in blood serum calcium and phosphorus concentrations. Without vitamin D3, ingested calcium would not be accessible to the body.
That pesky parathyroid
The parathyroid is an endocrine organ that regulates the production of parathyroid hormone (PTH). PTH is important to this discussion because it maintains serum calcium within normal limits by affecting bone resorption, renal calcium excretion, and metabolism of vitamin D3.
What do we need to know about the parathyroid?
If circulating serum calcium levels are low, the parathyroid turns on production of PTH and in turn, vitamin D3 is secreted by the kidney. PTH stimulates osteoclastic activity (break down of bone) to put the calcium and phosphorus in the blood. Vitamin D3 stimulates the intestinal absorption of BOTH calcium and phosphorus, thus raising both serum concentrations.
PTH also stimulates the kidneys to increase excretion of phosphorus without loosing the calcium. This is important because D3 increases phosphorus absorption in the gut and PTH causes the breakdown of bone, also increasing phosphorus levels.
What do nutritional secondary hyperparathyroidism and renal secondary hyperparathyroidism have to do with this?
Most owners call all calcium deficiencies Metabolic Bone Disease (MBD). This is actually an incomplete term as there are many ways bone disease can be affected by metabolic pathways. The ones that concern us are nutritional secondary hyperparathyroidism and renal secondary hyperparathyroidism.
Nutritional secondary hyperparathyroidism (NSHP)-
NSHP is when there is an excessive production of parathyroid hormone (PTH) due to low serum calcium. Either there was 1) no available calcium in the diet, or 2) no available vitamin D3 to stimulate intestinal absorption. Regardless, no dietary calcium is absorbed into the bloodstream. Since no calcium is readily available for intestinal absorption, calcium is resorbed from the bones.
Consequences are weakening of the bones with secondary breaks and abscesses. Since calcium is also required all over the body, weakness, tremors, anorexia are also problems.
Renal secondary hyperparathyroidism (RSHP)-
RSHP is a consequence of renal disease and lost kidney function.
Remember- the kidney (among other things) was supposed to 1) synthesize D3 and 2) respond to PTH and excrete excess phosphorus.
Problem- No D3' No absorption of calcium
No D3' the parathyroid continues to stay on to stimulate production of D3. Increasing levels of PTH continue to 1) break down bone and 2) intestinally absorb calcium and phosphorus, but now can't get rid of the phosphorus because of decreased kidney function.
Consequences- if mild, metabolic bone degeneration and continued destruction of the kidneys. Hyperphosphatemia and hypercalcemia unchecked will both cause death.