Joe,
Let me give you just one example that is commonly recognized by everyone in the herp industry: The cornsnake.
I breed corns, and I have NEVER seen a cornsnake detrimentally affected by albinism in ANY way. I've never seen an amel, snow, butter, or any other albinistic corn that was born with any noticeable defect of the eye, and I have never noticed them to be less hearty than any other cornsnake morph.
I have never seen a one-eyed amel, but I have seen several anerythristics and normals with one eye. I'm sure they're out there, but I've never seen an amel one. I've seen kinked amels, but never at a rate that was any different than in other morphs.
Does that prove that amelanism is a "good" gene to have floating around in other species? Not at all, but it tells me that the concept of amelanism being a "bad" gene in all reptiles is simply not 100% accurate. There is no way that a healthy amel corn is any less able to thrive than a healthy normal in captivity. Of course, in the wild, the coloration has great disadvantages, but, if I'm not mistaken, the first amelanistic corn hets were produced from an adult male amel cornsnake that was wild caught. That snake seemd to have survived his coloration "defect" just fine.
Now, let me just say that amels have been the most inbred of the morphs of other species, in my opinion, because they have been the ONLY morph in many species until very recently. So, in order to produce as many of them as they could, SOME breeders have undoubtedly inbred them over several generations. That being the case, ANY genetic defect that could be found in the population as a whole would statistically be more and more certain to come out of hiding in the amelanistic inbred animals than anywhere else. Not because of the amelanism, but because of the rampant inbreeding that brought the amelanism out in so many animals so quickly.
If amelanism is really in a cause and effect relationship with these noted deformities, whay are not more amels affected than we currently find? I mean, all amels lack melanin, because it is the genetic effect of the DNA. If deformities are genetically tied to amelanism, why aren't all amels affected? Why are the amels in the species in which (until recently) there were fewer known morphs those that are the most often affected by these deformities? Surely, if amelanism were a danger to all herps, shouldn't corns be affected as well? I, like you, am not at all meaning to be argumentative, but I just think mre evidence of an actual cause and effect relationship needs to be shown here.
There is a latin phrase with which you may be already familiar: post hoc, ergo propter hoc. It means literally, "after this, therefore, because of this." In other words, just because one genetic anomaly shows up in later proximity to another one does not mean that the first (amelanism) CAUSED the latter (the deformities). It may very well be the case that amelanism has all of these dreadful effects in herp species other than cornsnakes, but it is equally possible that the tremendous inbreeding to produce amels in those species (which has not had to take place in corns for decades) could have been the actual cause of bringing out those deformities and the fact that they were found in amels is only coincidental, being brought on by the fact that it was to obtain more amels that caused the inbreeding to take place.
That's all probably as clear as mud, but I don't know how else to put into words, what I'm trying to say. I am not refuting anything you all are saying about amelanism in herps (except for the case of corns, where I see no disadvatnges to the animals' health conditions). I am just suggesting that we make certain it is the amel gene that is the true culprit and not the breeding practices of some breeders looking for more amels too quickly. That's all.
