Cannabis in pregnancy

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Cannabis consumption in pregnancy might be associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits.[1] The American Congress of Obstetricians and Gynecologists recommended that cannabis use be stopped before and during pregnancy,[2] Cannabis is the most commonly used illicit substance among pregnant women.[3]

Although it is difficult to draw firm conclusions, there is some evidence that prenatal exposure to marijuana may be associated with deficits in language, attention, cognitive performance, and delinquent behaviors.[4] THC exposure in rats during the prenatal developmental phase may cause epigenetic changes in gene expression, but there is limited knowledge about the risk for psychiatric disorders because of ethical barriers to studying the developing human brain.[5] While animal studies cannot take into account factors that could influence the effects of cannabis on human maternal exposure, such as environmental and social factors,[6] a 2011 review of rodent studies by Campolongo et al. said there was "... increasing evidence from animal studies showing that cannabinoid drugs ... induce enduring neurobehavioral abnormalities in the exposed offspring ..."[6] Campolongo et al. added that "clinical studies report hyperactivity, cognitive impairments and altered emotionality in humans exposed in utero to cannabis".[6] Martin et al. investigated recent trends in substance abuse treatment admissions for cannabis use in pregnancy in the US, based on Treatment Episodes Data Set (TEDS) from 1992 to 2012, and discovered that, while the proportion of treatment admissions for pregnant women was stable (about 4%), the admissions for women who were pregnant and reported any marijuana use grew from 29% to 43%.[7] A 2015 review found that cannabis use by pregnant mothers impaired brain maturation in their children, and that it also predisposed their children to neurodevelopmental disorders.[8]

Endocannabinoid system[edit]

The role of the endocannabinoid system (ECS) in female fertility has long been suspected and studied.[9] Most studies through 2013 linking development of the fetus and cannabis show effects of consumption during the gestational period, but abnormalities in the endocannabinoid system during the phase of placental development are also linked with problems in pregnancy.[1] According to Sun and Dey (2012), endocannabinoid signaling plays a role in "female reproductive events, including preimplantation embryo development, oviductal embryo transport, embryo implantation, placentation, and parturition".[9] Karusu et al (2011) said that a "clear correlation ... in the actual reproductive tissues of miscarrying versus healthy women has yet to be established. However, the adverse effects of marijuana smoke and THC on reproductive functions point to processes that are modulated by ECS."[10]

Keimpema and colleagues (2011) said, "Prenatal cannabis exposure can lead to growth defects during formation of the nervous system"; "[c]annabis impacts the formation and functions of neuronal circuitries by targeting cannabinoid receptors ... By indiscriminately prolonging the "switched-on" period of cannabinoid receptors, cannabis can hijack endocannabinoid signals to evoke molecular rearrangements, leading to the erroneous wiring of neuronal networks".[11] A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as they may interact with the endocannabinoid system.[1][12]

See also[edit]

References[edit]

  1. ^ a b c Fonseca BM, Correia-da-Silva G, Almada M, Costa MA, Teixeira NA (2013). "The Endocannabinoid System in the Postimplantation Period: A Role during Decidualization and Placentation". Int J Endocrinol (Review). 2013: 510540. doi:10.1155/2013/510540. PMC 3818851Freely accessible. PMID 24228028. 
  2. ^ Committee on Obstetric Practice (July 2015). "Committee Opinion No. 637: Marijuana Use During Pregnancy and Lactation". Obstetrics & Gynecology. 126 (1): 234–238. doi:10.1097/01.AOG.0000467192.89321.a6. 
  3. ^ Neurol, Future. "Lasting impacts of prenatal cannabis exposure and the role of endogenous cannabinoids in the developing brain". NCBI. Future Neurol. Retrieved 28 July 2017. 
  4. ^ Irner TB (2012). "Substance exposure in utero and developmental consequences in adolescence: a systematic review". Child Neuropsychol (Review). 18 (6): 521–49. doi:10.1080/09297049.2011.628309. PMID 22114955. 
  5. ^ Morris CV, DiNieri JA, Szutorisz H, Hurd YL (November 2011). "Molecular mechanisms of maternal cannabis and cigarette use on human neurodevelopment". Eur. J. Neurosci. (Review). 34 (10): 1574–83. doi:10.1111/j.1460-9568.2011.07884.x. PMC 3226730Freely accessible. PMID 22103415. 
  6. ^ a b c Campolongo P, Trezza V, Ratano P, Palmery M, Cuomo V (March 2011). "Developmental consequences of perinatal cannabis exposure: behavioral and neuroendocrine effects in adult rodents". Psychopharmacology (Review). 214 (1): 5–15. doi:10.1007/s00213-010-1892-x. PMC 3045519Freely accessible. PMID 20556598. 
  7. ^ Martin CE, Longinaker N, Mark K, Chisolm MS, Terplan M (March 2015). "Recent trends in treatment admissions for marijuana use during pregnancy". Journal of Addiction Medicine. 9 (2): 99–104. doi:10.1097/ADM.0000000000000095. PMID 25525944. 
  8. ^ Alpár, A; Di Marzo, V; Harkany, T (25 September 2015). "At the Tip of an Iceberg: Prenatal Marijuana and Its Possible Relation to Neuropsychiatric Outcome in the Offspring". Biological Psychiatry. 79: e33–e45. doi:10.1016/j.biopsych.2015.09.009. PMID 26549491. 
  9. ^ a b Sun X, Dey SK (May 2012). "Endocannabinoid signaling in female reproduction". ACS Chem Neurosci (Review). 3 (5): 349–55. doi:10.1021/cn300014e. PMC 3382454Freely accessible. PMID 22860202. 
  10. ^ Karasu T, Marczylo TH, Maccarrone M, Konje JC (2011). "The role of sex steroid hormones, cytokines and the endocannabinoid system in female fertility". Hum. Reprod. Update (Review). 17 (3): 347–61. doi:10.1093/humupd/dmq058. PMID 21227997. 
  11. ^ Keimpema E, Mackie K, Harkany T (September 2011). "Molecular model of cannabis sensitivity in developing neuronal circuits". Trends Pharmacol. Sci. (Review). 32 (9): 551–61. doi:10.1016/j.tips.2011.05.004. PMC 3159827Freely accessible. PMID 21757242. 
  12. ^ Copeland, Jan; Gerber, Saul; Swift, Wendy (2006). Evidence-based answers to cannabis questions: a review of the literature. Canberra: Australian National Council on Drugs. ISBN 978-1-877018-12-1. [page needed]

Further reading[edit]

  • Behnke M, Smith VC (March 2013). "Prenatal substance abuse: short- and long-term effects on the exposed fetus". Pediatrics (Review). 131 (3): e1009–24. doi:10.1542/peds.2012-3931. PMID 23439891. 
  • Hoell I, Havemann-Reinecke U (October 2011). "[Pregnant opioid addicted patients and additional drug intake. Part I. Toxic effects and therapeutic consequences]". Med Monatsschr Pharm (Review) (in German). 34 (10): 363–74; quiz 375–6. PMID 22010420. 
  • Huizink AC (April 2012). "Prenatal substance use, prenatal stress and offspring behavioural outcomes: considerations for future studies". Nord J Psychiatry (Review). 66 (2): 115–22. doi:10.3109/08039488.2011.641586. PMID 22242892. 
  • Jutras-Aswad D, DiNieri JA, Harkany T, Hurd YL (October 2009). "Neurobiological consequences of maternal cannabis on human fetal development and its neuropsychiatric outcome". Eur Arch Psychiatry Clin Neurosci (Review). 259 (7): 395–412. doi:10.1007/s00406-009-0027-z. PMID 19568685.