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It's time people spoke the truth.
Reproductive and Perinatal EffectsBasic science research outstrips clinical research in the complex area of the role endocannabinoids play in all aspects of human reproduction and the impact of exogenous cannabinoids (i.e., the THC and other cannabinoid compounds in marijuana) on reproductive physiology. Animal studies have demonstrated the existence of CB1 receptors, endogenous cannabinoid ligands and the degradation by fatty acid amide hydrolase (FAAH) in sperm, eggs, and preimplantation embryos (Schuel 2006). Studies have found a critical balance between anandamide synthesis and its degradation by FAAH in mouse embryos and oviducts necessary for normal embryo development, oviductal transport, implantation and pregnancy (Wang, Guo et al. 2004; Wang, Xie et al. 2006). As a result, marijuana and THC have been shown in animal models to effect multiple aspects of reproductive physiology, including secretion of gonadotrphic hormones by the pituitary and sex steroids by the gonands, sperm production and capacitation, ovulation, fertilization, early embryonic devepoment, implantation, placental functions, fetal growth, number of pregnancies carried to term, lactation, suckling behavior by newborns and growth of malignant breast and prostate cells (Schuel 2006). The clinical implications of these basic science findings for human reproduction remains unclear despite the fact that animal studies show that exogenous THC can swamp endogenous anadamide signaling systems, thereby affecting multiple physiological processes.
The question of marijuana and birth defects perfectly illustrates the disparity between basic science and clinical research. The California Teratogen Information Service (CTIS) fact sheet on marijuana and pregnancy reports that the frequency of birth defects was not increased in the babies of 1246 women who reported occasionally smoking marijuana during pregnancy (CTIS). However, mutations in lymphocyte are increased in cord blood of infants exposed to THC in utero and surveys have found an increase in specific birth defects, including ventricular septal defect, in offspring of marijuana smokers (Ammenheuser, Berenson et al. 1998; Forrester and Merz 2007). As with use of all drugs during pregnancy, caution is advised even in the face of inconclusive evidence.
Many of the compounds in smoked marijuana readily cross the placenta, where the growing fetus absorbs them, and pass into breast milk, where nursing infants ingest them. Because it is not ethical to give pregnant or nursing women marijuana, most of the studies in this area have followed groups of women who have been identified as smoking marijuana during those risk periods. Interpretation of these studies is limited by confounding valiables such as the fact that pregnant marijuana users are also more likely to use other illicit drugs, tobacco, alcohol, and less likely to receive antenatal care. Nonetheless, studies show that marijuana use during pregnancy or breast feeding is linked with the following outcomes: Low birth weight; developmental delay; and behavioral problems (Fergusson, Horwood et al. 2002). Are these short term or long term effects? Monitoring these effects over time suggests that some of these effects may persist throughout a child's development, and that early exposure to marijuana is associated with behavioral problems at age 10 (Goldschmidt, Richardson et al. 2004), and an increased risk of marijuana use at age 14(Day, Goldschmidt et al. 2006). Altogether, the effects of marijuana on child development appear to be subtle but significant, particularly given what is known about the importance of the early years as a critical period for establishing a foundation for growth and function throughout the rest of life.
The question of marijuana and birth defects perfectly illustrates the disparity between basic science and clinical research. The California Teratogen Information Service (CTIS) fact sheet on marijuana and pregnancy reports that the frequency of birth defects was not increased in the babies of 1246 women who reported occasionally smoking marijuana during pregnancy (CTIS). However, mutations in lymphocyte are increased in cord blood of infants exposed to THC in utero and surveys have found an increase in specific birth defects, including ventricular septal defect, in offspring of marijuana smokers (Ammenheuser, Berenson et al. 1998; Forrester and Merz 2007). As with use of all drugs during pregnancy, caution is advised even in the face of inconclusive evidence.
Many of the compounds in smoked marijuana readily cross the placenta, where the growing fetus absorbs them, and pass into breast milk, where nursing infants ingest them. Because it is not ethical to give pregnant or nursing women marijuana, most of the studies in this area have followed groups of women who have been identified as smoking marijuana during those risk periods. Interpretation of these studies is limited by confounding valiables such as the fact that pregnant marijuana users are also more likely to use other illicit drugs, tobacco, alcohol, and less likely to receive antenatal care. Nonetheless, studies show that marijuana use during pregnancy or breast feeding is linked with the following outcomes: Low birth weight; developmental delay; and behavioral problems (Fergusson, Horwood et al. 2002). Are these short term or long term effects? Monitoring these effects over time suggests that some of these effects may persist throughout a child's development, and that early exposure to marijuana is associated with behavioral problems at age 10 (Goldschmidt, Richardson et al. 2004), and an increased risk of marijuana use at age 14(Day, Goldschmidt et al. 2006). Altogether, the effects of marijuana on child development appear to be subtle but significant, particularly given what is known about the importance of the early years as a critical period for establishing a foundation for growth and function throughout the rest of life.
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