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In the following discourse I will “attempt” to tackle 1) normal chemical values of reptiles (in general terms) and general terminology, 2) how Ca is absorbed and how D3 is synthesized/acquired, 3) how nutritional secondary hyperparathyroidism and renal secondary hyperparathyroidism have to do with this, and 4) the potential for hypercalcemia and possible risks/ cosequenses for oversupplementation.
1) Terminology and general facts-
Calcium has two forms in the blood: ionized and unionized.
Ionized- biologically active (let’s say free floating in the blood- available
for use)
Unionized- bound to proteins (like albumen in the blood) or other
complexes- so, (for our discussion) not actively utilized
(Normally when calcium levels are taken, they refer to the ionized form only. Unionized levels can be calculated by using various formulas and interpretation of other values.)
Many other factors may be involved in getting a correct reading of these levels. Examples- If blood protein (like albumen) is low, there maybe a lower unionized ratio of calcium, and a higher ionized form. If the pH is high, it will decrease the ionized form. (Remember, the body is a complex, ever adjusting system and reference ranges are merely a glimpse of what is going on.)
Parathyroid hormone (PTH) maintains calcium within normal limits by affecting bone resorption, renal calcium excretion, and metablolism of vitamin D.
Calcium to phosphorus ratio- should be 2:1
(Actual reference ranges will/may vary from reptile species to specie sand
subspecies for exact calcium and phosphorus reference ranges - though ratio
between these two chemicals will roughly be 2:1)
Typical Causes of: (to be discussed in later sections)
Hypocalcemia- low serum calcium
-nutritional deficiency- prey or food with an inadequate calcium level.
-impaired absorption- calcium absorption may be impaired by phylates (like soy ingredients), oxalates (spinach), high fat pet foods, acidic foods
-nutritional imbalance- inappropriate calcium to phosphorus ratio in the food eaten.
-renal compromise (kidney’s not working)
-inadequate lighting
Clinical signs- muscle tremors, spontaneous bone fractures, inadequately
calcified eggs
Hypercalcemia- high serum calcium
-primary hyperparathyroidism- parathyroid tumor causing excess excretion of
parathyroid hormones
-oversupplementation- supplements
-nutritional imbalance-foods rich in calcium (rare)
-bone resorption- bone infection or cancer
Clinical signs- Maximal calcium tolerances are likely 3-5 times corresponding minimums. Higher intake may lead to conditioned deficiencies of trace minerals and if combined with high- fat diet, formation of calcium soaps in the digestive tract.
Hyperphosphatemia- high phosphorus
-renal disease
-hypervitaminosis D
-excessive dietary phosphorus
Clinical signs- calcification of the heart and kidney, bone resorption, and
secondary nutritional hyperparathyroidism
Hypophosphatemia- low phosphorus
-starvation
-dietary imbalance
Hypervitaminosis D (too much D3)-
Clinical signs- soft tissue calcification, depression, anorexia, PU/PD, and
weight loss.
2) How D3 is synthesized/acquired-
There are 2 primary methods for obtaining vitamin D3
1) synthesizing it from exposure to ultraviolet B radiation
2) consuming a vertebrate that synthesized the hormone through exposure of the sun.
The production of vitamin D 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 D3 important and how does it relate to calcium?
Vitamin D3 is an essential hormone that plays many different important physiologic roles. Its role in calcium metabolism is probably its most recognized function.
Vitamin D3 stimulates intestinal absorption of both calcium and phosphorus stimulating a rise in blood serum calcium and phosphorus concentrations. Without D3, ingested calcium would not be accessable to the body.
3) That pesky parathyroid-
The parathyroid is an endocrine organ that among other things regulates calcium and phosphorus in the body by turning on an off the production of parathyroid hormone (PTH). It uses various organs, tissues, bone, and a myriad of complex feed-back loops to deal with this regulation.
What we need to know about the parathyroid- If circulating serum calcium levels are low, the parathyroid turns on production of PTH and vitamin D 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 concentrations.
PTH also stimulates the kidneys to increase excretion of phosphorus without loosing the calcium. This is important because D3 increases phosphorus absorption and breakdown of bone also increases phosphorus levels.
Metabolic Bone Disease-
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 calcium in the diet or, (2) no D3 made or available, so there was no absorption of available calcium in diet. 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 excessive phosphorus.
Problem- No D3 No absorption 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 intestinally absorb calcium and phosphorus, but can’t get rid of the phosphorus.
Consequences- if mild, metabolic bone degeneration and continued distruction of the kidneys. Hyperphosphatemia unchecked will cause death.
4) How diet and supplementation have to do with any of this.
Under ideal conditions, reptiles would get
1) adequate natural light
2) a variety of food sources like their natural habitat offering all the nutrients and calories needed for growth, maintenance and reproduction.
If these conditions were met, there would be no need for UV lighting and supplementation…
That is not how it is however, so the ultimate question is how much and of what? Again, it is not that simple.
UVB lighting- If sufficient UVB lighting can be offered, this is a big step in naturally preventing MBD in an reptile housed inside. With the tubes and bulbs offered now a days, natural synthesis of D3 is the safest way of regulating calcium absorption. This assumes 1) there is adequate calcium in the diet, and 2) the bulb used is close enough for the animal to utilize and does not have significant burn out that causes less than optimal exposure to UVB.
This statement might lead an expert like Dr. Mader to suggest that supplementation may not be necessary.
Food items- Variety is more readily available these days, but still does not simulate the variety in the wild. Additionally, some of the staple feeders used are not adequate in the calcium
hosphorus ratios. (Remember should be 2:1). Crickets, mealworms and superworms are actually the opposite ratio. Pheonix worms and butter worms are good in the ratio, but too high in fat.
This ratio in staple insects may be overcome by appropriate gut loading with appropriate legumes and greens and various formulated feeds. (Certain diets high in calcium has caused gut impaction in crickets.)
Finally supplementation- The jury is still out on the amount needed and the interaction between all the minerals and supplements.
Calcium with D3- if you have adequate UVB this should not be necessary. If D3 becomes too high it 1) messes up PTH regulation and 2) will cause hypercalcemia.
How good do you feel about your UVB bulb? If your bulb is no good, or your reptile refuses to bask close enough for it to be effective, maybe D3 is for you.
Calcium without D3- if the UVB is working, the ideally the body will take only what it needs. However, excess dietary calcium by itself may inhibit the absorption of other trace minerals. Too much is still not good.
Multivitamin- This is probably a better source of complete supplementation overall BUT- if you are giving insects that have an inverse ration of Ca
, this may not be enough. Additionally, we still do not know the exact requirements for even the best research reptiles as of yet.
Summary- There is no easy answer. Try to know how the body systems work in your perspective reptile and understand that all of us are trying to work within our own varying restrictions (environmental, financial, availability, others). Shoot for a happy medium.
I find your article very interesting. It was my husbands ideal to feed them the pinkie mice. He called me into the room one day and said look at your chameleons and they were chomping down on the pinkie mice.
. Unfortunately my chameleon has MBD. I bought him on a whim and unfortunatley did not know much about these little fellows. I have learned alot though in the last few months from the forum and a breeder I ran into at the local petco. anyway, He has a deformity in his spine. He still has use of his back legs but sometimes I see him just hanging on a branch resting on his stomach with his back legs dangilin ( like a gymnast on a bar about to do a flip.) This can't be comfortable for him can it? He is healing and becoming stronger day by day though thanks to all of the helpful people on the forum and the vet. Well thanx for the info Matt.
....) As far as reptile medicine goes, I know a decent amount, but remember there are a large number of members on this forum with significantly more practical experience with various types of chams (much more than me
