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==Cognitive performance and psychiatric conditions== ==Cognitive performance and psychiatric conditions==
A 2012 ] found although it was difficult to draw firm conclusions, there was some evidence that prenatal exposure to certain substances, especially marijuana and cocaine, was associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence".<ref>{{cite journal |author=Irner TB |title=Substance exposure in utero and developmental consequences in adolescence: a systematic review |journal=Child Neuropsychol |volume=18 |issue=6 |pages=521–49 |year=2012 |pmid=22114955 |doi=10.1080/09297049.2011.628309 }}</ref> A 2011 review said that cannabis use during the prenatal developmental phase was a factor in disruption in gene regulation, making offspring potentially vulnerable to addiction and psychiatric conditions, but a "lack of molecular investigations in the human brain as well as the limited knowledge regarding their long-term impact significantly hinders insights about the neurobiology underlying risk for psychiatric disorders".<ref name=Morris >{{cite journal |author=Morris CV, DiNieri JA, Szutorisz H, Hurd YL |title=Molecular mechanisms of maternal cannabis and cigarette use on human neurodevelopment |journal=Eur. J. Neurosci. |volume=34 |issue=10 |pages=1574–83 |year=2011 |month=November |pmid=22103415 |pmc=3226730 |doi=10.1111/j.1460-9568.2011.07884.x}}</ref> Although it is difficult to draw firm conclusions, there is some evidence that prenatal exposure to certain substances, especially marijuana and cocaine, are associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence".<ref>{{cite journal |author=Irner TB |title=Substance exposure in utero and developmental consequences in adolescence: a systematic review |journal=Child Neuropsychol |volume=18 |issue=6 |pages=521–49 |year=2012 |pmid=22114955 |doi=10.1080/09297049.2011.628309 |type=Review}}</ref> Cannabis use during the prenatal developmental phase is a factor in disruption in gene regulation, making offspring potentially vulnerable to addiction and psychiatric conditions, but a "lack of molecular investigations in the human brain as well as the limited knowledge regarding their long-term impact significantly hinders insights about the neurobiology underlying risk for psychiatric disorders".<ref name=Morris >{{cite journal |author=Morris CV, DiNieri JA, Szutorisz H, Hurd YL |title=Molecular mechanisms of maternal cannabis and cigarette use on human neurodevelopment |journal=Eur. J. Neurosci. |volume=34 |issue=10 |pages=1574–83 |year=2011 |month=November |pmid=22103415 |pmc=3226730 |doi=10.1111/j.1460-9568.2011.07884.x|type=Review}}</ref>


A 2011 review of rodent studies by Campolongo ''et al'' found:<ref name= Campolongo2011>{{cite journal |author=Campolongo P, Trezza V, Ratano P, Palmery M, Cuomo V |title=Developmental consequences of perinatal cannabis exposure: behavioral and neuroendocrine effects in adult rodents |journal=Psychopharmacology (Berl.) |volume=214 |issue=1 |pages=5–15 |year=2011 |month=March |pmid=20556598 |pmc=3045519 |doi=10.1007/s00213-010-1892-x}}</ref><blockquote>There is increasing evidence from animal studies showing that cannabinoid drugs ... induce enduring neurobehavioral abnormalities in the exposed offspring ... clinical studies report hyperactivity, cognitive impairments and altered emotionality in humans exposed in utero to cannabis. ... Conversely, although animal models allow to A 2011 review of rodent studies by Campolongo ''et al'' found:<ref name= Campolongo2011>{{cite journal |author=Campolongo P, Trezza V, Ratano P, Palmery M, Cuomo V |title=Developmental consequences of perinatal cannabis exposure: behavioral and neuroendocrine effects in adult rodents |journal=Psychopharmacology (Berl.) |volume=214 |issue=1 |pages=5–15 |year=2011 |month=March |pmid=20556598 |pmc=3045519 |doi=10.1007/s00213-010-1892-x|type=Review}}</ref><blockquote>There is increasing evidence from animal studies showing that cannabinoid drugs ... induce enduring neurobehavioral abnormalities in the exposed offspring ... clinical studies report hyperactivity, cognitive impairments and altered emotionality in humans exposed in utero to cannabis. ... Conversely, although animal models allow to control for several confounding factors associated with human studies, they do not take into account environmental and social factors that could influence the long-term neurobehavioral effects of maternal cannabis exposure.<ref name=Campolongo2011/></blockquote>
control for several confounding factors associated with human studies, they do not take into account environmental and social factors that could influence the long-term neurobehavioral effects of maternal cannabis exposure.<ref name=Campolongo2011/></blockquote>


==Endocannabinoid system== ==Endocannabinoid system==
A role in female fertility has long been suspected and studied.<ref name=Sun2012/> Most studies through 2013 linking development of the fetus and cannabis show effects of consumption during the gestational period, but problems in the ] (ECS) during the phase of placental development are also linked with problems in pregnancy.<ref name=Fonseca2013/> According to Sun and Dey (2012), endocanniboid signaling plays a role in "female reproductive events, including preimplantation embryo development, oviductal embryo transport, embryo implantation, placentation, and parturition".<ref name=Sun2012 > {{cite journal |author=Sun X, Dey SK |title=Endocannabinoid signaling in female reproduction |journal=ACS Chem Neurosci |volume=3 |issue=5 |pages=349–55 |year=2012 |month=May |pmid=22860202 |pmc=3382454 |doi=10.1021/cn300014e }}</ref> 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."<ref name= Karasu2011>{{cite journal |author=Karasu T, Marczylo TH, Maccarrone M, Konje JC |title=The role of sex steroid hormones, cytokines and the endocannabinoid system in female fertility |journal=Hum. Reprod. Update |volume=17 |issue=3 |pages=347–61 |year=2011 |pmid=21227997 |doi=10.1093/humupd/dmq058 |url=http://humupd.oxfordjournals.org/content/17/3/347.long}}</ref> A role in female fertility has long been suspected and studied.<ref name=Sun2012/> Most studies through 2013 linking development of the fetus and cannabis show effects of consumption during the gestational period, but problems in the ] (ECS) during the phase of placental development are also linked with problems in pregnancy.<ref name=Fonseca2013/> According to Sun and Dey (2012), endocanniboid signaling plays a role in "female reproductive events, including preimplantation embryo development, oviductal embryo transport, embryo implantation, placentation, and parturition".<ref name=Sun2012 > {{cite journal |author=Sun X, Dey SK |title=Endocannabinoid signaling in female reproduction |journal=ACS Chem Neurosci |volume=3 |issue=5 |pages=349–55 |year=2012 |month=May |pmid=22860202 |pmc=3382454 |doi=10.1021/cn300014e }}</ref> 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."<ref name= Karasu2011>{{cite journal |author=Karasu T, Marczylo TH, Maccarrone M, Konje JC |title=The role of sex steroid hormones, cytokines and the endocannabinoid system in female fertility |journal=Hum. Reprod. Update |volume=17 |issue=3 |pages=347–61 |year=2011 |pmid=21227997 |doi=10.1093/humupd/dmq058 |url=http://humupd.oxfordjournals.org/content/17/3/347.long|type=Review}}</ref>


Keimpema and colleagues (2011) said, "Prenatal cannabis exposure can lead to growth defects during formation of the nervous system"; "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".<ref name= Keimpema2011>{{cite journal |author=Keimpema E, Mackie K, Harkany T |title=Molecular model of cannabis sensitivity in developing neuronal circuits |journal=Trends Pharmacol. Sci. |volume=32 |issue=9 |pages=551–61 |year=2011 |month=September |pmid=21757242 |pmc=3159827 |doi=10.1016/j.tips.2011.05.004}}</ref> A report prepared for the ] concluded cannabis and other ]s are contraindicated in pregnancy as they may interact with the endocannabinoid system.<ref name="Australia">{{cite book |first1=Jan |last1=Copeland |first2=Saul |last2=Gerber |first3=Wendy |last3=Swift |year=2006 |title=Evidence-based answers to cannabis questions: a review of the literature |location=Canberra |publisher=Australian National Council on Drugs |isbn=978-1-877018-12-1}}</ref><ref name=Fonseca2013>{{cite journal |author=Fonseca BM, Correia-da-Silva G, Almada M, Costa MA, Teixeira NA |title=The Endocannabinoid System in the Postimplantation Period: A Role during Decidualization and Placentation |journal=Int J Endocrinol |volume=2013 |issue= |pages=510540 |year=2013 |pmid=24228028 |pmc=3818851 |doi=10.1155/2013/510540 }}</ref> Keimpema and colleagues (2011) said, "Prenatal cannabis exposure can lead to growth defects during formation of the nervous system"; "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".<ref name= Keimpema2011>{{cite journal |author=Keimpema E, Mackie K, Harkany T |title=Molecular model of cannabis sensitivity in developing neuronal circuits |journal=Trends Pharmacol. Sci. |volume=32 |issue=9 |pages=551–61 |year=2011 |month=September |pmid=21757242 |pmc=3159827 |doi=10.1016/j.tips.2011.05.004|type=Review}}</ref> A report prepared for the ] concluded cannabis and other ]s are contraindicated in pregnancy as they may interact with the endocannabinoid system.<ref name="Australia">{{cite book |first1=Jan |last1=Copeland |first2=Saul |last2=Gerber |first3=Wendy |last3=Swift |year=2006 |title=Evidence-based answers to cannabis questions: a review of the literature |location=Canberra |publisher=Australian National Council on Drugs |isbn=978-1-877018-12-1}}</ref><ref name=Fonseca2013>{{cite journal |author=Fonseca BM, Correia-da-Silva G, Almada M, Costa MA, Teixeira NA |title=The Endocannabinoid System in the Postimplantation Period: A Role during Decidualization and Placentation |journal=Int J Endocrinol |volume=2013 |issue= |pages=510540 |year=2013 |pmid=24228028 |pmc=3818851 |doi=10.1155/2013/510540|type=Review }}</ref>


==See also== ==See also==

Revision as of 03:59, 13 December 2013

Cannabis consumption in pregnancy is associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits in offspring.

Cognitive performance and psychiatric conditions

Although it is difficult to draw firm conclusions, there is some evidence that prenatal exposure to certain substances, especially marijuana and cocaine, are associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence". Cannabis use during the prenatal developmental phase is a factor in disruption in gene regulation, making offspring potentially vulnerable to addiction and psychiatric conditions, but a "lack of molecular investigations in the human brain as well as the limited knowledge regarding their long-term impact significantly hinders insights about the neurobiology underlying risk for psychiatric disorders".

A 2011 review of rodent studies by Campolongo et al found:

There is increasing evidence from animal studies showing that cannabinoid drugs ... induce enduring neurobehavioral abnormalities in the exposed offspring ... clinical studies report hyperactivity, cognitive impairments and altered emotionality in humans exposed in utero to cannabis. ... Conversely, although animal models allow to control for several confounding factors associated with human studies, they do not take into account environmental and social factors that could influence the long-term neurobehavioral effects of maternal cannabis exposure.

Endocannabinoid system

A role in female fertility has long been suspected and studied. Most studies through 2013 linking development of the fetus and cannabis show effects of consumption during the gestational period, but problems in the endocannabinoid system (ECS) during the phase of placental development are also linked with problems in pregnancy. According to Sun and Dey (2012), endocanniboid signaling plays a role in "female reproductive events, including preimplantation embryo development, oviductal embryo transport, embryo implantation, placentation, and parturition". 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."

Keimpema and colleagues (2011) said, "Prenatal cannabis exposure can lead to growth defects during formation of the nervous system"; "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". 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.

See also

References

  1. ^ 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 3818851. PMID 24228028.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  2. 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.
  3. Morris CV, DiNieri JA, Szutorisz H, Hurd YL (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 3226730. PMID 22103415. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  4. ^ Campolongo P, Trezza V, Ratano P, Palmery M, Cuomo V (2011). "Developmental consequences of perinatal cannabis exposure: behavioral and neuroendocrine effects in adult rodents". Psychopharmacology (Berl.) (Review). 214 (1): 5–15. doi:10.1007/s00213-010-1892-x. PMC 3045519. PMID 20556598. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ Sun X, Dey SK (2012). "Endocannabinoid signaling in female reproduction". ACS Chem Neurosci. 3 (5): 349–55. doi:10.1021/cn300014e. PMC 3382454. PMID 22860202. {{cite journal}}: Unknown parameter |month= ignored (help)
  6. 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. Keimpema E, Mackie K, Harkany T (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 3159827. PMID 21757242. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. 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.

Further reading

  • Hoell I, Havemann-Reinecke U (2011). "". Med Monatsschr Pharm (in German). 34 (10): 363–74, quiz 375–6. PMID 22010420. {{cite journal}}: Unknown parameter |month= ignored (help)
  • Huizink AC (2012). "Prenatal substance use, prenatal stress and offspring behavioural outcomes: considerations for future studies". Nord J Psychiatry. 66 (2): 115–22. doi:10.3109/08039488.2011.641586. PMID 22242892. {{cite journal}}: Unknown parameter |month= ignored (help)
  • Jutras-Aswad D, DiNieri JA, Harkany T, Hurd YL (2009). "Neurobiological consequences of maternal cannabis on human fetal development and its neuropsychiatric outcome". Eur Arch Psychiatry Clin Neurosci. 259 (7): 395–412. doi:10.1007/s00406-009-0027-z. PMID 19568685. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
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