I hope a dietary physiologist is out there to help answer your question because it is definitely worth getting more on it.
And yes, I can see you point, but it seems to me that this is an inescapable conclusion to the facts at hand. As far as diet and venom action is concerned, the action of the venom components on the prey during immobilization seems to me to mainly prepare it for digestion. Neurotoxins are the shock-troops that block nerve signals to muscles, with the end result that not only is the prey’s mobility compromised, so too is its capacity to biochemically defend itself from other invading toxins. The proteolytic enzymes (proteases) digest proteins. Hyaluronidase depolymerises hyluronic acid resulting in the breakdown of the sticky gel between cells and so enhances the rapid breakdown of normal cellular tissue. Phospholypase attacks fatty acid residues and facilitates the breakdown of nerve tissue. The effect on the breakdown of blood through clotting or anti-clotting inclusions is well-known. Once the prey hits the stomach its just a mopping-up operation really.
As I’m sure you would know, venoms are mixtures that contain extremely complex biological compounds and the extent of this complexity is still unresolved. Similarly the variation and biological functions of such components are still not fully known. Venom structure may even vary among geographically separate populations of the same species, reflecting differences in prey type availability and/or the length of time of each population’s isolation. In some species there may be seasonal variation in venom toxicity (ie structure) and in others apparently not. Venom structure may even vary between males and females, and particularly ontogenetically. Despite this variation, the common thread is that diet and venom have co-evolved. So, venom plays a significant, if not the main, role in digestion of prey and this is a direct result of what is already known about the structure and function of venom itself. But there are other strange inclusions in snake venom that are almost totally unknown – such as retroviruses. What the hell is their function? The precautionary principle should be adopted in regards to the removal of venom glands just simply because we do not know for certain what the physiological consequences of such removals may have. Just the inclusion of specific retroviruses within snake toxins should be grounds for caution, because of their propensity for mutation when exposed to new conditions.

But just to finally comment on a few of your points….

“The injection of venom into prey starts the digestion process which actually kills the prey.”

Yes and no. Quite often prey is swallowed in an immobile or paralysed state, but it is still quite alive. If not before, death may occur soon after arrival in the stomach. Much of the action of venom on tissue depends upon the animal being alive for as long as the functional nature of the components allow. The need to promptly secure prey often results in the event of swallowing preceding the event of death.

“Indeed, the venom is digestive enzymes.”
Yes and no. Venoms per say are not just digestive enzymes, but I agree that many venom toxins are enzymes, although the majority are proteins.

“I can see a benefit to this but not that important as non-venomous snakes have no problem with digestion.”

So-called non-venomous snakes do in fact possess complex enzymatic secretions that are analogous to the venoms of other snake families, and these it would seem are primarily used in prey digestion. So yes they have no problems with digestion because their secretory systems are not being gouged out. This could in fact be a warning to be cautious about labelling some species as non-venomous simply because they lack conventional venom apparatus as Dr Fry has suggested.

“Also, pre-killed prey given to venomous snakes do not appear to cause any digestion problems, nor "dietary implications". “

Well that sure appears to be the case on the surface. However, I would suggest that all the balls are up in the air at the moment on the effects of diet on the well-being of an organism. You see, a big fat disease-free snake in a box doesn’t necessarily mean that its development has not been damaged by its diet. I mean to say, just take behaviour. The world’s classrooms are full of healthy looking kids that are just plain psychotic because of one sort of dietary problem or another – and I suspect that some of our collections have cages full of snakes that may be similarly exhibiting behavioural abnormalities that could easily be corrected by diet. We live with such change every day, but that doesn’t mean that it is inconsequential. Such diet-induced abnormalities may be reflected by changes in simple diel cycles or even in seasonal cycles of particular captives and this could easily have long-term reproductive consequences – I’ve lost count of the times that I have heard something like…“they look great, but why didn’t they breed this year?” To be sure, some dietary-induced behavioural changes may be very subtle and only discernable by the keenest eye – such as a more lethargic state or even a more active state that can’t be explained by the prevailing physical conditions. Many field Herps would also be familiar with how much quieter some species are in captivity when compared with their counterparts in the wild state and this difference in behaviour might in part be explained by changes to their diet. Although I am more familiar with field behaviour, I should say that I have kept a lot of snakes in captivity and in my opinion what they eat can affect how they act. I think snake diet has become just another symbol of the fast-food times that we live in. Snakes that are lizard-eaters are quickly converted to mammal-eaters more through the imperatives of human convenience than through the natural needs of the snake. That’s my opinion – I just like it as natural as possible. Whether this is good or bad would lead to thousands of opinions one way or the other I am sure. I won’t bother with the potential long-term problems of abnormal diet such as those that may be reflected genotypically through reduction in fitness to combat disease.

“Also, venomoid snakes seem to be living long healthy lives.”

Well, I am not so sure about that. Presumably this type of “surgery” is usually carried out once the snake has reached maturity. A “long-life” after such surgery might be more of a consequence of the snake’s condition PRIOR to surgery than after it. In any case, how much do we really know about the life span of reptiles – in particular venomous snakes? I believe that most of Australia’s species of large Elapids may attain ages in the wild in excess of 20 years as the norm. In one case in the western part of Sydney I observed the same adult Pseudonaja textilis repeatedly over 25 years until the site was destroyed for a factory complex. And this snake was no where near the known potential maximum size that has been recorded for this species. It is not inconceivable that Elapids may have life spans far exceeding the brief period since this “venomoid” business started. So, I rather doubt that such snakes are “living long healthy lives”.

Best Regards

Richard Wells

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