That hypothesis is questionable.
This is not a hypothesis. It has been tested and verified.
It is surprising to me that no one has actually made the effort to determine exactly why it cause the birth defects it did.
Did you really believe that noone had done this?
From the BBC News Online January 25, 2001
The controversial drug Thalidomide is being used to help treat the most deadly form of lung cancer.
The drug became notorious in the 1960s when it was prescribed to pregnant women to ease morning sickness.
It was found to cause severe birth defects by limiting the blood flow to developing limbs. Many children were born limbless or with severely shortened limbs. Now scientists hope to use the blood limiting properties to help small cell lung cancer patients by starving the blood supply to tumors.
Researchers are already using Thalidomide in drugs trials to treat Kaposi's sarcoma (a type of cancer involving blood vessels in the skin) and brain cancer.
The article is MOLECULAR BASIS OF ENVIRONMENTALLY INDUCED BIRTH DEFECTS Annu. Rev. Pharmacol. Toxicol. , Vol. 42: 181-208
from their 2002 issue.
Here is their paragraph on Thalidomide:
PROPOSED MOLECULAR MECHANISMS OF KNOWN TERATOGENSThalidomide
The literature on birth defects associated with in utero exposure to thalidomide contains over two thousand citations, in keeping with the fact that this is the most infamous of all pharmaceutical teratogens (96). In spite of intensive investigation over the past forty years, the mechanism by which thalidomide disrupts normal embryogenesis remains a topic of considerable controversy. Perhaps as a result of its checkered history, a large number of hypotheses have been put forward over the years in an attempt to explain its teratogenic mechanism of action. Twenty-four different hypotheses were reviewed by Stephens, who found that 13 of the hypotheses were fundamentally incorrect (97). Of the remaining 11 hypotheses, some were supported by experimental data, albeit not sufficiently conclusive or convincing. Several other hypotheses remain to be adequately tested. The hypotheses could generally be classified into those proposing that thalidomide affects DNA replication or transcription, its impact on the synthesis and/or function of growth factors or integrins, and finally, thalidomide's effects on angiogenesis, chondrogenesis, cell death, or cellular injury.
More recently, Stephens and coworkers (96, 98) proposed a model of the thalidomide embryopathy that neatly unifies previous hypotheses and provides a biologically sensible model system that accounts for the existing biochemical data, as well as explains the molecular specificity of this teratogen. In this model system, the insulin-like growth factor-1 (IGF-1) and fibroblast growth factor-2 (FGF-2) proteins work cooperatively in order to stimulate the production of alpha-5 and beta-3 integrin subunits. These integrin subunits have been previously demonstrated to function as angiogenesis factors, promoting vascularization in the developing limb bud, as well as select embryonic structures (99, 100, 101). The IGF-I and FGF-2 genes are transcriptionally regulated by the transcription factor Sp1. Sp1 binds guanine-rich GC box elements (GGGCGG) located in the promoter regions of select target genes. In this case, the genes are IGF-I and FGF-2, as well as their receptors. Stephens & Fillmore (96) propose that binding of thalidomide to the promoter prevents subsequent Sp1 binding, thereby downregulating the transcription of the two target genes. Even a subtle downregulation of critically important genes can adversely affect the developmental processes involved in embryogenesis.
Data in support of this hypothesis include a relatively robust literature that demonstrates that IGF-I can stimulate chondrogenesis and limb development (102, 103, 104). More recently, it has also been demonstrated that thalidomide can inhibit IGF-I stimulation of limb development under experimental conditions (102). The IGF-I gene promoter lacks both TATA and CCAAT boxes and is highly guanine-rich, containing several Sp1 binding sites (105). This makes the IGF-1 gene particularly vulnerable to intercalation by thalidomide. The drug is able to oxidize DNA at position 8, which faces the major groove of the DNA molecule and may serve to facilitate intercalation at those sites. Similarly, FGFs also play significant roles in both limb development (106, 107, 108) and angiogenesis (109, 110, 111). Like the IGF-I gene, there are no TATA or CCAAT boxes on the FGF-2 promoter, but there are multiple Sp1 and early growth response protein (Egr-1) binding sites. The FGF-2 gene, then, represents another potential target of thalidomide interference in limb development.
The question of specificity of teratogenic effects can also be explained by thalidomide's proposed interaction with specific gene promoters. Clearly, the key morphological structures affected by in utero exposure to thalidomide are the limbs, ears, and eyes. As such, it is thought that the intercalation of thalidomide at guanine-rich sites in DNA is having its greatest impact at the promoter regions of genes critical to the development of these structures. Perhaps less than 9% of all gene promoters have neither a TATA nor a CCAAT box. These genes depend upon promoters with one or more GGGCGG sequences (112). Stephens & Fillmore propose that thalidomide intercalates into promoter regions that have long stretches of poly-G regions, as these are biophysically favorable sites for thalidomide binding (96). The specificity of thalidomide targets is further enhanced by the fact that since most GC regions in the Sp1 binding sites are constitutive, they would be unlikely to tolerate regulation during embryonic development (96).
Here are the Stephen's references:
Stephens TD, Fillmore BJ. 2000. Hypothesis: thalidomide embryopathy-proposed mechanism of action. Teratology 61:189–95
Stephens TD. 1988. Proposed mechanisms of action in thalidomide embryopathy. Teratology 38:229–39
Stephens TD, Bunde CJ, Fillmore BJ. 2000. Mechanism of action in thalidomide teratogenesis. Biochem. Pharmacol. 59:1489–99
Have a look.