[moustress]

The origins of satins in the US come from radiation experiments decades ago; I have been told that in the UK the satins have a different origin, but I don't know what that is. US satins have a tendency to have health problems because of damage to the genes that regulate digestion, blood chemistry, and immune system weaknesses on top of those. It can be hard in some parts of the US to find healthy satins if you want to breed them. It took me several years with lots of heartbreaking problems before I found a good buck, but once I found him, I was able to eliminate most of the problems.

 

[moustress]

It very well could be because of that. Many of my satins were about 25% smaller than my standard coated meeces in the first few years after I finally stared my line, but I out-crossed to larger standard meeces and now my fawn satins are among the largest meeces I have. I used to have small litters, and that is no longer the case. I used to have congenitally weak babies that would cease growing at about 2-3 weeks, look prematurely aged, and die. I rarely have that anymore; that's something that can happen in any litter of any type of mouse, especially if the parents are too young or too old. I think that meeces of the proper breeding age (3-8mo. old) provide better quality genes. One of the more disturbing things to see was fuzzies of two to three weeks of age ranging around the tank, trying to find something to eat that would satisfy the hunger, as they were unable to digest what they ate. Now I know what that is, and what to do about it, but fortunately, don't often have that problem anymore.