Not sure if this means anything, but birth defects resulting from maternal thalidomide ingestion occur when the medication is taken between days 20 and 34 of gestation. (More here - https://academic.oup.com/toxsci/article/122/1/1/1672454?login=false). Some key aspect of cell differentiation could take place that contributes to a higher "value". Or perhaps the body is more malleable (in terms of affecting epigenetic markers, imprinting of mother's environment on the child, etc) prior to this point that is desirable.
There is evidence to support all the hypotheses for the mechanisms of action of thalidomide limb teratogenicity: (1) oxidative stress/damage, (2) DNA intercalation, (3) inhibition of angiogenesis, and (4) CRBN binding, although the use in some experiments of very high concentrations of thalidomide raises questions about more clinically relevant exposure levels. The proposed mechanisms are not mutually exclusive. It is quite possible that several of the proposed mechanisms are working in parallel or synergistically to result in the hallmark thalidomide-associated limb anomalies.
I believe it may be referring to organ trafficking.
Not sure if this means anything, but birth defects resulting from maternal thalidomide ingestion occur when the medication is taken between days 20 and 34 of gestation. (More here - https://academic.oup.com/toxsci/article/122/1/1/1672454?login=false). Some key aspect of cell differentiation could take place that contributes to a higher "value". Or perhaps the body is more malleable (in terms of affecting epigenetic markers, imprinting of mother's environment on the child, etc) prior to this point that is desirable.
Also from this article, it looks like there is significant physiological development during that time period >> https://embryology.med.unsw.edu.au/embryology/index.php/Timeline_human_development#Introduction
Possible mechanisms of action from sci article>>
There is evidence to support all the hypotheses for the mechanisms of action of thalidomide limb teratogenicity: (1) oxidative stress/damage, (2) DNA intercalation, (3) inhibition of angiogenesis, and (4) CRBN binding, although the use in some experiments of very high concentrations of thalidomide raises questions about more clinically relevant exposure levels. The proposed mechanisms are not mutually exclusive. It is quite possible that several of the proposed mechanisms are working in parallel or synergistically to result in the hallmark thalidomide-associated limb anomalies.