Search PubMedSearch

PubMed · 9825947

Does thalidomide cause second generation birth defects?

Abstract

The proposed association between thalidomide and second generation birth defects is an improbable hypotheses which lacks, so far, any credible scientific foundation. However, the media have chosen to give it extensive coverage. So much so that even the hard-headed scientist may start wondering if there is anything in it. However, there is no reason to suppose that people with birth defects caused by exposure to thalidomide during embryonic life have any greater or lesser chance of producing children with birth defects. This appears to be the case in practice. The question could be reworded to, 'Can thalidomide be responsible for identical, or similar, birth defects in 2 generations of the same family?' For such a phenomenon to be possible, a mechanism must be proposed and there appear to be only 2 possible candidates. The first is that the defects in the parent, originating during embryonic life, have somehow been transmitted to the next generation. The second is that thalidomide is a mutagen as well as a teratogen. The first mechanism can be excluded, since Lamarckism has long since been abandoned by scientists. The hypothesis that thalidomide is a mutagen and might be responsible for birth defects in the children of thalidomide-damaged people is without any scientific foundation. Birth defects appear to be no more common amongst the children of thalidomide-affected parents than in the general population. It is important that thalidomide-affected adults are firmly reassured on this point. Most of them have now completed their own families, but they may still worry about their grandchildren. Therefore, unless and until further supportive evidence is reported by a separate and independent source, the answer to the question, 'Can thalidomide cause second generation defects?' is a very definite 'No.'

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D Smithells. 1998. Does thalidomide cause second generation birth defects?. https://doi.org/10.2165/00002018-199819050-00001

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Delayed 5-HT release in the developing cortex of microencephalic rats.

Postnatal changes in the fiber distribution and release of 5-HT in the somatosensory cortex (Sm) of methylazoxymethanol acetate (MAM)-induced microencephalic rats were studied. A transient accumulation of serotonergic fibers was observed in the Sm of the control and MAM rats in the first 2 weeks following birth. However, the density of serotonergic fibers was higher in the MAM rats than in the controls, and the distribution pattern of serotonergic fibers was more extensive in the MAM rats. The microdialysis indicated a high basal level and a delayed K+ -evoked 5-HT release in the Sm of MAM rats on postnatal day 10. The present results suggest morphological and functional alterations of serotonergic fibers in the Sm of MAM rats during the critical period of cortical formation.

Abnormalities, Drug-Induced

Disruption of androgen-regulated male reproductive development by di(n-butyl) phthalate during late gestation in rats is different from flutamide.

Gestational and lactational exposure to di(n-butyl) phthalate (DBP) at >/=250 mg/kg/day disrupts male rat reproductive development and function. Although this indicates an antiandrogenic mechanism, DBP and its biologically active metabolite do not interact with the androgen receptor (AR) in vitro. In the present study, we compared the effects of DBP and the antiandrogen flutamide using a shorter exposure during the prenatal period of male sexual differentiation in rats. Pregnant CD rats received DBP at 0, 100, 250, or 500 mg/kg/day po (n = 10) or flutamide at 100 mg/kg/day po (n = 5) from Gestation Days 12 to 21. In F1 males, DBP (500 mg/kg/day) and flutamide caused hypospadias; cryptorchidism; agenesis of the prostate, epididymis, and vas deferens; degeneration of the seminiferous epithelium; and interstitial cell hyperplasia of the testis. Flutamide and DBP (250 and 500 mg/kg/day) also produced retained thoracic nipples and decreased anogenital distance. Interstitial cell adenoma occurred at 500 mg DBP/kg/day in two males. The only effect seen at 100 mg DBP/kg/day was delayed preputial separation. In contrast to flutamide, DBP caused a low incidence of prostate agenesis and hypospadias with no vaginal pouch. The low incidence of DBP-induced intraabdominal testes contrasted with the high incidence of inguinal testes seen with flutamide. Thus prenatal male sexual differentiation is a sensitive period for the reproductive toxicity of DBP. A no observed adverse effect level was not established and the lowest observed (adverse) effect level was 100 mg/kg/day. Flutamide and DBP disrupted the androgen signaling necessary for male sexual differentiation but with a different pattern of antiandrogenic effects. DBP is an example of an environmental antiandrogen that disrupts androgen-regulated male sexual differentiation without interacting directly with the AR, as does flutamide.

Abnormalities, Drug-Induced

Chemical hair treatments and adverse pregnancy outcome among Black women in central North Carolina.

Several studies suggest that toxic chemicals in hair products may be absorbed through the scalp in sufficient amounts to increase the risks of adverse health effects in women or their infants. This case-control study of 525 Black women from three counties in North Carolina who had delivered a singleton, liveborn infant examined whether exposure to chemicals used in hair straightening and curling increased the odds that the infant was preterm or low birth weight. Cases consisted of 188 preterm and 156 low birth weight births (for 123 women, their infant was both low birth weight and preterm). Controls were 304 women who delivered term and normal birth weight infants. Women who used a chemical hair straightener at any time during pregnancy or within 3 months prior to conception had an adjusted odds ratios (OR) of 0.7 (95% confidence interval (CI) 0.4-1.1) for preterm birth and 0.6 (95% CI 0.4-1.1) for low birth weight. Exposure to chemical curl products was also not associated with preterm delivery (adjusted OR = 0.9, 95% CI 0.5-1.8) or low birth weight (adjusted OR = 1.0, 95% CI 0.5-1.9). Despite this failure to find an association, continued search for risk factors to which Black women are uniquely exposed is warranted.

Abnormalities, Drug-Induced