Genetic and environmental factors are traditionally seen as the sole causes
of congenital anomalies. In this paper we introduce a third possible cause,
namely random “manufacturing” discrepancies with respect to design'' values. A clear way to demonstrate the existence of this component is to shut’’ the
two others and to see whether or not there is remaining variability. Perfect
clones raised under well controlled laboratory conditions fulfill the
conditions for such a test. Carried out for four different species, the test
reveals a variability remainder of the order of 10%-20% in terms of coefficient
of variation. As an example, the CV of the volume of E.coli bacteria
immediately after binary fission is of the order of 10%. In short,
``manufacturing’’ discrepancies occur randomly, even when no harmful mutation
or environmental factors are involved. Not surprisingly, there is a strong
connection between congenital defects and infant mortality. In the wake of
birth there is a gradual elimination of defective units and this screening
accounts for the post-natal fall of infant mortality. Apart from this trend,
post-natal death rates also have humps and peaks associated with various
inabilities and defects.\qL In short, infant mortality rates convert the
case-by-case and mostly qualitative problem of congenital malformations into a
global quantitative effect which, so to say, summarizes and registers what goes
wrong in the embryonic phase. Based on the natural assumption that for simple
organisms (e.g. rotifers) the manufacturing processes are shorter than for more
complex organisms (e.g. mammals), fewer congenital anomalies are expected.
Somehow, this feature should be visible on the infant mortality rate. How this
conjecture can be tested is outlined in our conclusion.

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