Pour l'instant avec les études que jai trouvé la conclusion indique quil peut y avoir des risque que le bébé naisse avec un poids plus faible mais ils nont pas fait le lien de cause a effet.
On sait que le thc traverse le placenta mais aucune idée dea effets assuré
Le probleme est que les femmes testé ne prenait pas tous que du cannabis alors cest dure de prouver le lien cause a effet. Le mieux cest de pas en abuser comme n'importe quoi
https://www.ncbi.nlm.nih.gov/books/NBK425751/
SUMMARY:
This chapter summarizes the literature on prenatal, perinatal, and neonatal exposure to cannabis that has been published since 1999 and deemed to be of good or fair quality by the committee. Overall, there is substantial evidence of a statistical association between cannabis smoke and lower birth weight, but there is only limited, insufficient, or no evidence in support of any other health endpoint related to prenatal, perinatal, or neonatal outcomes. This may be due to a number of limitations faced by many of the research studies reviewed in this chapter, including an almost exclusive reliance on self-reporting to ascertain cannabis exposure, as is true in many areas of this report. While many studies used standardized questions regarding frequency and duration of cannabis use, others relied on data extracted from the medical record. Also, as with other portions of this report, the potency of cannabis varied across time. The lack of biological validation of self-reporting suggests caution is warranted. Moreover, dosage and timing of exposure in pregnancy is particularly important, as exposures early in pregnancy may affect organogenesis leading to birth defects, whereas later exposures are more likely to affect the growth of the fetus.
Second, even within substantial cohorts, the number of women who used cannabis exclusively was small. These sample sizes may have limited statistical power to detect many outcomes.
Third, cannabis exposure was almost exclusively through smoking and was often confounded by the use of other substances—namely, tobacco and alcohol. Although many authors relied on a variety of statistical techniques to isolate the effects of cannabis exposure, attribution of outcomes to cannabis alone was difficult. Even when cannabis is the sole exposure, it is not straightforward to attribute outcomes to THC alone versus the mode of exposure.
Finally, caution needs to be used in interpreting the numerous findings of “no association” in this chapter. Absent a pooled estimate of effect and confidence intervals, such conclusions may be based on a small number of studies, some of which may even conflict.
The committee has formed a number of research conclusions related to these health endpoints (see Box 10-1); however, it is important that each of these conclusions be interpreted within the context of the limitations discussed in the Discussion of Findings sections.