Re: Why is (LONG POST)

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Posted by A. C. Highfield on July 01, 2000 at 01:42:43:

In Reply to: Re: Why is posted by EJ on June 30, 2000 at 23:46:12:

: This kind of response is totally worthless. It eludes to an explaination without giving one.

That's because detailed explanations cannot be given in a few lines. Forums like this are unsuited to posting the length of content necessary.

: If this topic is so well understood why do many vets that discusse this topic in publication begin with the disclaimer that it is not very well understood in chelonians but there are several factors that are suspect. By opening this up to DISCUSSION it might become clearer how those factors interact and those that wish to participate might actually learn something. Everytime I have opened up this discussion I have come away learning something. Usually it was from a person who has been keeping turtles/tortoises for 5 years or less because the experts say the answer is obvious and leave it at that. Not very stimulating in a DISCUSSION.

Possibly because the vets in question have not studied it sufficiently?

What follows is a succinct discussion of just one aspect of this problem - there are several other factors involved as well, some obvious, some not so (like acidosis, for example). However, the following does - hopefully - provide a fairly complete explanation of the core issue.

Classes of carapace deformity linked to diet

Carapace deformities fall into two broad classes. The first class is that observed in animals that have been reared on an all-round deficient diet; deficient in calcium, vitamins, trace elements and other essential nutrients. A typical example would be a tortoise reared on a lettuce, tomato and cucumber diet without mineral supplementation. Such animals typically manifest with classical "softshell syndrome", where the bones of the plastron and carapace remain pliable long after they would normally have hardened. Some degree of "pyramiding" or "lumpiness" is present, but typically not to a gross degree. The pelvic area of the carapace is typically depressed, and there may be concurrent problems with feeding due to the bones of the jaw being similarly affected (Cooper and Jackson, 1981, Mader, 1996, Wallach, 1971). On dissection, the bony tissue is fibrous, porous, fractures easily and is many times thicker than normal (Highfield, 1990). Keratin thickness is normal, however and abnormal urea levels are atypical. Serum urea levels, if anything, tend to be at the lower end of normal deviation. Growth rates are not artificially accelerated, but rather tend to be inhibited (Highfield, unpublished data). The aetiology of this class of deformity is identical to that seen in all other animals where calcium deficient diets are provided (Robbins, 1983) and in green iguanas and other herbivorous lizards raised on similarly calcium and or vitamin D3 deficient dietary regimes (Donoghue, S. in Mader, 1996). The problem can be prevented by providing adequate levels of dietary calcium, by ensuring that the Ca to P ratio is within the correct range, and by providing adequate levels of vitamin D3 either by exposure to UV-B or via oral supplementation (Highfield, in preparation). It should be stressed that even on a generally grossly deficient and restricted diet such as that described above, normal bone growth can be achieved if supplementation with calcium, magnesium and other bone-building minerals is provided in conjunction with a source of vitamin D3 (Highfield, pers. obs.). It is notable that in nature, many tortoise species actively seek out additional sources of calcium, including sun-bleached bones and mineral rich soils (Schulkin, 1995, Esque and Peters, 1994). The present author has observed Testudo graeca graeca in Morocco and Testudo kleinmanni in Egypt both out and consume vacated snail shells which are plentiful in such arid environments.

The second class of carapace deformity occurs in conjunction with high protein diets and consequent accelerated growth rates. The underlying cause is the same, however. The high growth rates dramatically increase demand for calcium and other bon-building trace elements and if these are not present in adequate quantity a state of deficiency will quickly occur, as bone deposition outstrips available materials. In response, the bony tissue becomes porous, fibrous and thickened. It also needs to be stressed that absolute high protein intake can and does have a direct effect upon the animal's ability to absorb calcium even when it is present in the diet in adequate quantities (Holford, 1997, Robbins,1983.). Furthermore, high protein intakes promote high rates of keratin growth (Robbins, op. cit.) and this results not only in a visible overgrowth of beak and nail material, but also in a considerable thickening of the outer (keratin) layer of the carapace. Typically, such animals manifest a melanistic appearance due to the darker, thicker layer of keratin overlying the intermediate membrane and underlying bony structures. Where keratin growth exceeds the rate of exponential growth of underlying bone, physical stresses are created that further tend to create distortion and abnormal patterns of growth (Highfield, unpublished data). One additional and little realized side-effect of unnaturally high rates of keratin growth and consequent melanization is that the tortoises' thermoregulatory abilities are severely impacted. The darkened carapace absorbs more radiant heat than would occur following normal growth and coloration (Highfield, 1999) and this affects both a) permissible activity levels in high temperatures and b) elevates the average body temperature with further dramatic consequences for microbial fermentation and overall digestive efficiency (Lichtenbelt, 1992). Although not directly relevant to the topic of carapace deformity and bone development, it is also very important to note that herbivores raised on high protein diets have dramatically reduced life expectancy due to premature renal failure and very high incidences of articular and visceral gout and bladder calculi of uric acid origin (Donoghue, S. in Mader, 1996, Highfield, 1990, 1996, 1999, MacArthur, 1996). There is a direct and absolute correlation between protein intake and uric acid generation (Schmidt-Nielsen, 1990). Commercial tortoise foods and vitamin or mineral supplements that include separate amino acids (e.g., lysine, leucine, trytophan or arginine, etc.) are best avoided as these have been associated with liver and kidney damage, gout, and calcium loss in human patients studied (Nantow and Heslin, 1997).

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: : This kind of response is totally worthless. It eludes to an explaination without giving one. : That's because detailed explanations cannot be given in a few lines. Forums like this are unsuited to posting the length of content necessary. : : If this topic is so well understood why do many vets that discusse this topic in publication begin with the disclaimer that it is not very well understood in chelonians but there are several factors that are suspect. By opening this up to DISCUSSION it might become clearer how those factors interact and those that wish to participate might actually learn something. Everytime I have opened up this discussion I have come away learning something. Usually it was from a person who has been keeping turtles/tortoises for 5 years or less because the experts say the answer is obvious and leave it at that. Not very stimulating in a DISCUSSION. : Possibly because the vets in question have not studied it sufficiently? : What follows is a succinct discussion of just one aspect of this problem - there are several other factors involved as well, some obvious, some not so (like acidosis, for example). However, the following does - hopefully - provide a fairly complete explanation of the core issue. : Classes of carapace deformity linked to diet : Carapace deformities fall into two broad classes. The first class is that observed in animals that have been reared on an all-round deficient diet; deficient in calcium, vitamins, trace elements and other essential nutrients. A typical example would be a tortoise reared on a lettuce, tomato and cucumber diet without mineral supplementation. Such animals typically manifest with classical "softshell syndrome", where the bones of the plastron and carapace remain pliable long after they would normally have hardened. Some degree of "pyramiding" or "lumpiness" is present, but typically not to a gross degree. The pelvic area of the carapace is typically depressed, and there may be concurrent problems with feeding due to the bones of the jaw being similarly affected (Cooper and Jackson, 1981, Mader, 1996, Wallach, 1971). On dissection, the bony tissue is fibrous, porous, fractures easily and is many times thicker than normal (Highfield, 1990). Keratin thickness is normal, however and abnormal urea levels are atypical. Serum urea levels, if anything, tend to be at the lower end of normal deviation. Growth rates are not artificially accelerated, but rather tend to be inhibited (Highfield, unpublished data). The aetiology of this class of deformity is identical to that seen in all other animals where calcium deficient diets are provided (Robbins, 1983) and in green iguanas and other herbivorous lizards raised on similarly calcium and or vitamin D3 deficient dietary regimes (Donoghue, S. in Mader, 1996). The problem can be prevented by providing adequate levels of dietary calcium, by ensuring that the Ca to P ratio is within the correct range, and by providing adequate levels of vitamin D3 either by exposure to UV-B or via oral supplementation (Highfield, in preparation). It should be stressed that even on a generally grossly deficient and restricted diet such as that described above, normal bone growth can be achieved if supplementation with calcium, magnesium and other bone-building minerals is provided in conjunction with a source of vitamin D3 (Highfield, pers. obs.). It is notable that in nature, many tortoise species actively seek out additional sources of calcium, including sun-bleached bones and mineral rich soils (Schulkin, 1995, Esque and Peters, 1994). The present author has observed Testudo graeca graeca in Morocco and Testudo kleinmanni in Egypt both out and consume vacated snail shells which are plentiful in such arid environments. : The second class of carapace deformity occurs in conjunction with high protein diets and consequent accelerated growth rates. The underlying cause is the same, however. The high growth rates dramatically increase demand for calcium and other bon-building trace elements and if these are not present in adequate quantity a state of deficiency will quickly occur, as bone deposition outstrips available materials. In response, the bony tissue becomes porous, fibrous and thickened. It also needs to be stressed that absolute high protein intake can and does have a direct effect upon the animal's ability to absorb calcium even when it is present in the diet in adequate quantities (Holford, 1997, Robbins,1983.). Furthermore, high protein intakes promote high rates of keratin growth (Robbins, op. cit.) and this results not only in a visible overgrowth of beak and nail material, but also in a considerable thickening of the outer (keratin) layer of the carapace. Typically, such animals manifest a melanistic appearance due to the darker, thicker layer of keratin overlying the intermediate membrane and underlying bony structures. Where keratin growth exceeds the rate of exponential growth of underlying bone, physical stresses are created that further tend to create distortion and abnormal patterns of growth (Highfield, unpublished data). One additional and little realized side-effect of unnaturally high rates of keratin growth and consequent melanization is that the tortoises' thermoregulatory abilities are severely impacted. The darkened carapace absorbs more radiant heat than would occur following normal growth and coloration (Highfield, 1999) and this affects both a) permissible activity levels in high temperatures and b) elevates the average body temperature with further dramatic consequences for microbial fermentation and overall digestive efficiency (Lichtenbelt, 1992). Although not directly relevant to the topic of carapace deformity and bone development, it is also very important to note that herbivores raised on high protein diets have dramatically reduced life expectancy due to premature renal failure and very high incidences of articular and visceral gout and bladder calculi of uric acid origin (Donoghue, S. in Mader, 1996, Highfield, 1990, 1996, 1999, MacArthur, 1996). There is a direct and absolute correlation between protein intake and uric acid generation (Schmidt-Nielsen, 1990). Commercial tortoise foods and vitamin or mineral supplements that include separate amino acids (e.g., lysine, leucine, trytophan or arginine, etc.) are best avoided as these have been associated with liver and kidney damage, gout, and calcium loss in human patients studied (Nantow and Heslin, 1997).

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