« Drogues et Expériences/Marijuana & dérivés » : différence entre les versions
Contenu supprimé Contenu ajouté
m Révocation des modifications de 213.49.172.87 (retour à la précédente version de 80.11.237.172) |
→Effets physiologiques : correction lien |
||
Ligne 1 :
{{Traduction}}
[[Image:Marijuana.jpg|right|250px|thumb|Un plant de [[cannabis]].]]
[[Image:Trichome-close-up.jpg|right|thumb|250px|Micro shot of mature glandular trichome]]
Il existe aujourd'hui une quantité substantielle de [[propagande]], fausse science, et [[désinformation]] au sujet du cannabis; à la fois des partisans du cannabis et de ses opposants. Existent également des contraintes légales et politiques sur la recherche liée au cannabis.
Bien que de nombreuses études contradictoires impliquant le cannabis, certains effets [[santé|sanitaires]] sur le corps et le mental ont été déterminés. Cet article utilise une diversité de sources crédibles, essentiellement des articles venant de [[Revue médicale|revues médicale]] internationales à [[comité de lecture]] mais aussi de rapports scientifiques, de textbooks, sites web et magazines, pour établir une vue d'ensemble clairement documentée (références/bibliographie) associé à l'usage du cannabis .
== Contraintes légal et politiques sur la recherche ==
Dans beaucoup d'États, la [[science expérimentale]] souffre de restrictions légales. Donc, le cannabis serait souvent difficilement étudiable dans le domaine de la recherche médicale, parce que les échantillons ne peuvent pas être obtenus légalement, sans l'accord du gouvernement de l'État.
Le phénomène de curiosité scientifique légitime entrant en conflit avec le gouvernement ''(et son agenda)'' a été récemment illustré aux [[États-Unis d'Amérique]] par le clash entre Multidisciplinary Association for Psychedelic Studies (MAPS), un groupe de recherche indépendant, contre le National Institute on Drug Abuse (NIDA), une agence fédérale des États-Unis d'Amérique chargé de l'utilisation de la science pour étudier la toxicomanie. Le NIDA fonctionnant grandement sous le contrôle général de l'Office of National Drug Control Policy (ONDCP), un bureau de la Maison Blanche responsable pour la coordination directe de tous les aspects légaux, législatifs, scientifiques, sociaux et politiques du contrôle policier fédéral de stupéfiants.
Le cannabis qui est disponible pour des recherches aux États-Unis d'Amérique est cultivé à l'Université du Mississippi et uniquement contrôlé par le NIDA, qui a même un pouvoir de veto sur la [[Food and Drug Administration]] (FDA) pour définir les protocoles acceptables/acceptés. Depuis [[1942]], année où le cannabis disparu de la [[pharmacopée]] états-unienne, et où son usage médical fut prohibé, il n'existe aucune histoire légale (du point de vue de la loi fédérale) de projet de production de cannabis financé par des fonds privés. Le résultat est que le nombre de recherches sur le sujet fut très limité, vu que ceux-ci doivent utiliser le produit produit par le NIDA, qui a été allégé pour être moins puissant, et est donc d'une qualité différente . <ref>''Lyle E. Craker, Ph.D. v. U.S. Drug Enforcement Administration'', Docket No. 05-16, 8 mai 2006, 8-27 [http://www.maps.org/mmj/dea_maps_final_briefs_5.8.06.pdf PDF]</ref>
MAPS, en conjonction avec le professeur [[Lyle Craker]], PhD, le directeur du '' Medicinal Plant Program'' de l'Université du Massachusetts à Amherst, proposa de fournir de cannabis cultivé indépendamment d'une qualité ciblée pour la recherche pour des études de recherches approuvées par la FDA et se heurta à l'adversité du NIDA, de l' ONDCP, et du [[Drug Enforcement Administration]] (DEA). Ce projet, et d'autres de ce type, n'auraient, d'après la wikipedia anglophone pratiquement aucune chance, sur un terrain légal dominé par le concept guerre contre les drogues.
Cependant, dans d'autres États tel que le [[Royaume-Uni]], une licence pour cultiver la marijuana n'est pratiquement qu'une affaire de bureaucratie, de même longueur que pour d'autres sujets botaniques ou scientifiques. ''Hence the phrase "controlled drug.'' Dans de tels États, beaucoup d'essais ''(tests)'' ont été pratiqués, dans des buts variés. Plus récemment, plusieurs fumeurs habitués/dépendants ont été invités à participer à des essais variés par des entreprises médicales britanniques dans le but de permettre au gouvernement du royaume de déterminer l'influence du cannabis sur la conduite d'un véhicule motorisé.
== [[Pharmacologie]] ==
=== Effets biochimiques ===
[[Image:THC-skeletal.png|thumb|right|250px|[[Formule développée plane]] du [[Tetrahydrocannabinol|Δ9-tetrahydrocannabinol]].]]
[[Image:THV structure.png|right|thumb|250px|[[Tétrahydrocannabivarine]]]]
[[Image:CBN structure.png|right|thumb|250px|[[Cannabinol]]]]
La substance psychoactive la plus importante ''(prevalent)'' dans le [[cannabis]] est le [[Tetrahydrocannabinol|delta-9-tetrahydrocannabinol]] (couramment noté Δ<sup>9</sup>-THC, ou parfois THC). Sur les deux dernières décennies (NDT : traduite en 2006), le contenu moyen en THC dans la marijuana vendue dans les territoires d' [[Amérique du Nord]] aurait augmenté d'au moins environ 1% à 3-4%. Les plants sélectionnés et clonés peuvent conduire à des taux de 15% THC. <ref name="Kalant">''Principles of Medical Pharmacology'', 6th edition, H.K. Kalant & W.H.E. Roschlau, 1998, pages=373-375}}</ref> Un autre [[cannabinoïde]] psychoactif présent dans le ''Cannabis sativa'' est le [[tétrahydrocannabivarine]] (THCV), mais il ne se trouve qu'en faibles quantités. En addition, existent des composés similaires contenus dans la marijuana qui n'exhibent aucune réponse psychoactive mais sont nécessaires pour fonctionner: [[Cannabidiol]] (CBD), un [[isomère]] du THC; [[Cannabinol]] (CBN), un produit de l'[[oxydation]] du THC; [[Cannabivarine]] (CBV), un [[analogue]] du CBN avec une différente chaîne, [[Cannabidivarine]] (CBDV), un analogue du CBD avec une chaîne différente, aet l'[[acide cannabinolique]]. La manière dont ces autres composés interagissent avec le THC n'est pas complètement comprise, mais des études cliniques proposent l'hypothèse que le CBD agit comme force de compensation pour réguler le ''strength'' de l'agent psychoactif THC. Un rapport anecdotique et non concluant affirme que la marijuana avec des ratios relativement élevés de THC:CBD risquerait moins d'induire de l'[[anxiété]] que de la marijuana avec de faibles ratios THC:CBD. <ref name="joy">''Marijuana and Medicine: Assessing The Science Base'', J.E. Joy, S. J. Watson, Jr., and J.A. Benson, Jr, United States National Academy of Sciences, 1999, http://books.nap.edu/html/marimed/</ref> On pense également que le CBD pourrait réguler le métabolisme du corps du THC en inactivant le [[cytochrome P450]], une classe importante d' enzymes qui métabolise les drogues. Des expériences dans lesquelles les souris ont été traitées avec du CBD puis avec du THC ont montré que le traitement CBD été associé avec une augmentation substantielle dans les concentrations de THC dans le cerveau ''(et ses principaux métabolites)'', le plus vraisemblablement parce qu'il réduit le taux de nettoyage du THC dans le corps. <ref name="joy" /> Des composés cofacteurs du cannabis ont également été reliés à une baisse de la [[température corporelle]], modulant le fonctionnement immunitaire, et la protection des cellules. L'[[huile essentielle]] de cannabis contient également beaucoup de [[terpénoïdes|terpenoid]] aromatiques, qui peuvent agir en synergie avec les cannabinoïdes pour produire leurs propres effets. Le THC se convertit rapidement en [[11-hydroxy-THC]], qui est également pharmacologiquement actif, tant et si bien que l'effet de la drogue dépasse les niveaux de THC mesurables dans le sang. <ref name="Kalant" />
En [[1990]], la découverte de recepteurs aux cannabinoïdes situés à travers le [[cerveau]] et le corps, ainsi qu'un cannabinoïde endogène [[neurotransmetteur]]s comme l'[[anandamide]] (un matériel [[lipide|lipidique]] dérivé [[ligand]] de l'[[acide arachidonique]]), suggère que l'utilisation de marijuana affecte le cerveau de la même manière que '' a naturally occurring brain chemical''. Les cannabinoïdes usuellement contiennent un anneau ''1,1'-di-methyl-pyrane'', ''a variedly derivatized [[aromatic ring]] and a variedly [[saturation (chimie)|unsaturated]] [[Cyclohexane|cyclohexyl]] ring'' et leurs précurseurs chimiques immédiats, constituant une famille d'environ 60 composés bi-cyclic et tri-cyclic. Comme la plupart des autres processus neurologiques, les effets de la marijuana sur le cerveau suivent le protocole standard de signal transduction, le système électrochimique d'envoi de signaux à travers les [[neurone]]s pour une réponse biologique. On sait maintenant que des récepteurs cannabinoides apparaissent dans des formes similaires dans la plupart des [[vertébré]]s et [[invertébré]]s et ont une longue histoire d'évolution de 500 millions d'années. Le fait que ces récepteurs ont été conservés tout ces temps semble indiquer qu'ils doivent avoir un rôle basique important dans la physiologie animale. Les cannabinoides recepteurs réduisent l'activité [[adénylate-cyclase]], inhibent les [[canaux ioniques]], et désinhibent [[potassium channel|K<sup>+</sup><sub>A</sub> channels]]. Deux types de ''cannabinoides recepteurs'' existent (CB1 et CB2).
Le récepteur CB1 se trouve principalement dans le cerveau et mlitige les effets [[psychologique]]s du THC. Le récepteur CB2 se trouve de manière plus abondante dans les cellules du [[système immunitaire]]. Les cannabinoïdes agissent comme des immunomodulators sur les récepteurs CB2, signifiant qu'ils augmentent certaines réponses immunitaires et en diminuent d'autres. Par exemple, les cannabinoïdes nonpsychotrophic peuvent être utilisés comme [[anti-inflammatoire]] très efficace. <ref name="joy" /> L'affinité des cannabinoïdes pour correspondre ''(bind)'' à chacun des deux récepteurs est la même, ''with only a slight increase observed with the plant-derived compound CBD binding to CB2 receptors more frequently''. Les cannabinoïdes semblent avoir un rôle dans le contrôle par le cerveau du [[locomotion|mouvement]] et de la [[mémoire]], ainsi que de la modulation de la souffrance ''(pain)'' naturelles. ''It is clear that cannabinoïdes can affect pain transmission and, specifically, that cannabinoïdes interact with the brain's natural [[opioid]] system acting as a [[dopamine]] [[agonist]]''. <ref name="abadinsky">''Drugs: An Introduction'', 5th edition, H. Abadinsky, 2004, pages=62-77; 160-166</ref> ''This is an important physiological pathway for the medical treatment of pain. ''
''The cannabinoid receptor is a typical member of the largest known family of receptors called a [[G protein-coupled receptor]]. A signature of this type of receptor is the distinct pattern of how the receptor molecule spans la [[Membrane (biologie)|membrane cellulaire]] seven times. The location of cannabinoid receptors exists on la membrane cellulaire, and both outside ([[extracellulaire|extracellularly]]) and inside ([[intracellulaire|intracellularly]]) la membrane cellulaire. CB1 receptors, the bigger of the two, are extraordinarily abundant in the brain: 10 times more plentiful que les [[Récepteur opiacé|récepteurs mu]], responsables des effets de la [[morphine]]. Les récepteurs CB2 sont structurellement différents (the [[homology (biology)|homology]] between the two subtypes of receptors is 44%), found only on cells of the immune system, and seems to function similarly to its CB1 counterpart. CB2 receptors are most commonly prevalent on [[B-cells]], des [[Cellule tueuse naturelle|cellules tueuses naturelles]], et des [[monocytes]], but can also be found on [[polymorphonuclear neurtrophil cells]], [[Cytotoxic T cell|T8 cells]], and [[T helper cell|T4 cells]]. Dans les [[Tonsille|amygdales]] les récepteurs CB2 appear to be restricted to [[Lymphocyte B|lymphocytes B]]-enriched areas. ''
Cannabis also contains a related class of compound: the [[Cannaflavine]]s. These compounds have been suggested to contribute certain effects of cannabis, such as [[analgesique|analgesia]] and anti-inflammatory properties, and are considerably more effective than [[aspirine]]. Cannaflavins usually contain a 1,4-pyrone ring fused to a variedly derivatized aromatic ring and linked to a 2nd variedly derivatized aromatic ring and include for example the non-psychoactive Cannflavin A and B.
La nature de la marijuana, ses propriétés [[liposoluble|de solubilité dans les graisses]], conduisent à une longue demi-vie d'élimination en comparaison à d'autres drogues récréatives. La molécule THC, et les composés relatifs, sont généralement détectable dans les tests de drogues jusqu'à environ un mois après consommation. Cette détection est possible parce que des [[métabolite]]s non psychoactifs du THC sont stockés pour de longues périodes de temps dans les cellules de graisse, et cette substance a une très faible solubilité dans l'eau. ''It is this slow and steady removal from the body that is linked with usually mild or nonexistent withdrawal symptoms after single or occasional use of the drug. Le taux d'élimination des métabolites est légèrement plus élevé chez les grands usagers en raison de la tolérance, et indique une plus grande possibilité de sypmtômes de sévrage à l'arrêt de la consommation arrêt de l'emploi habituel. ''
Le [[LD50]] de THC est 1270 mg/kg (rats mâles), 730 mg/kg (rats femelles) oral dans huile sésame, et 42 mg/kg (rats) par inhalation. <ref>http://www.erowid.org/plants/cannabis/cannabis.shtml</ref>
=== Effets physiologiques ===
Certains des effets de la consommation de marijuana incluent l'augmentation du [[rythme cardiaque]], sécheresse de la bouche, rougeures occulaires'' (congestion of the [[Conjunctiva|conjunctival]] [[blood vessel]]s)'', une réduction de la pression intra-oculaire, un disfonctionnement modéré des [[facultés motrices]] et de la [[concentration]], et augmente la [[faim]]. Lors d'une [[électroencéphalographie]] on observe des persistance d'[[onde alpha]] de [[fréquence]] légèrement plus basse que la normale. <ref name="Kalant" /> Le cannabis produit également beaucoup d'effets [[Subjectivité|subjectifs]] , tels que une plus grande jouissance du goût de la nourriture et des arômes et une jouissance avancée de la [[musique]] et de la comédie. A plus hautes doses, le cannabis peut provoquer des distortions marquées des perceptions du [[temps]] et de l'[[espace]], de la [[proprioception]], ainsi que des [[hallucination]]s auditives et/ou visuelles (ressemblant à un rêve éveillé), '' [[ataxie]] from selective impairment of [[polysynaptic reflex]]es'', et de [[depersonnalisation]]. La marijuana plus communément soulage les tensions et provoque des effets [[euphorie|euphoriques]]. Une liste plus complète de ses effets est disponible à: [[Cannabis#Cannabis thérapeutique|cannabis]].
Les [[cerveau|aires cérébrales]] à forte densité de recepteurs cannabinoïdes correspondent aux effets [[comportement humain|comportementaux]] produits par les cannabinoïdes. ''Brain regions in which cannabinoid receptors are very abundant are: the [[basal ganglia]], associated with movement control; the [[cerebellum]], associated with body movement coordination; the [[hippocampe (cerveau)|hippocampe]], associated with [[learning]], memory, and [[stress (medicine)|stress]] control; the [[cerebral cortex]], associated with higher cognitive functions; and the [[nucleus accumbens]], regarded as the reward center of the brain. Other regions where cannabinoid receptors are moderately concentrated are: the [[hypothalamus]], mediating body housekeeping functions; the [[amygdala]], associated with emotional responses and [[fear]]s; the [[spinal cord]], associated with peripheral sensations like pain; the [[brain stem]], associated with [[sleep]], [[arousal]], and motor control; and the [[Solitary nucleus|nucleus of the solitary tract]], associated with visceral sensations like [[nausea]] and [[vomiting]]. <ref>''Pharmacology of Cannabinoid CB1 and CB2 Receptors'', R.G. Pertwee, Pharmacology and Therapeutics, 1997, 129-180, volume=74</ref>
Most notably, the two areas of motor control and memory are where the effects of marijuana are directly and irrefutably evident. Les cannabinoïdes, selon la [[dose]], inhibent la transmission of neural signals through the basal ganglia and cerebellum. At lower doses, canabinoids seem to stimulate locomotion while greater doses inhibit it, most commonly manifested by lack of steadiness (body sway and hand steadiness) in motor tasks that require a lot of attention. Other brain regions, like the cortex, the cerebellum, and the neural pathway from cortex to [[striatum]], are also involved in the control of movement and contain abundant cannabinoïde receptors, indicating their possible involvement as well.''
''One of the primary effects of marijuana sur les humains is the disruption de la [[mémoire à court terme]], which is consistent with the abundance of CB1 receptors on the hippocampe. The effects of THC at these receptor sites produce what is called a "temporary hippocampal lesion." <ref name="joy" /> As a result of this lesion, several neurotransmitters like [[acetylcholine]], [[norepinephrine]], and [[glutamate]], are released that trigger a major decrease in neuronal activity in the hippocampe and its inputs. In the end, this procedure leads to the blocking of cellular processes that are associated with memory formation. There is no scientific evidence to suggest that these effects are permanent, and normal neurological functionality is eventually regained, usually as the drug is metabolized.''
''The total duration of cannabis intoxication when smoked is about 1 to 4 [[heure]]s. A study of ten healthy male volunteers who resided in a residential research facility sought to examine both acute and residual subjective, physiologic, and performance effects of smoking marijuana cigarettes. On three separate days, subjects smoked one NIDA marijuana cigarette containing either 0%, 1.8%, or 3.6% THC, documenting subjective, physiologic, and performance measures prior to smoking, five times following smoking on that day, and three times on the following morning. Subjects reported robust subjective effects following both active doses of marijuana, which returned to baseline levels within 3.5 hours. Heart rate increased and the [[pupil|puplilary light reflex]] decreased following active dose administration with return to baseline on that day. Additionally, marijuana smoking acutely produced decrements in smooth pursuit eye tracking. Although robust acute effects of marijuana were found on subjective and physiological measures, no effects were evident the day following administration, indicating that the residual effects of smoking a single marijuana cigarette are minimal. <ref>''Acute and residual effects of marijuana in humans'', R.V Fant, S.J. Heishman, E.B. Bunker, W.B Pickworth, Pharmacology, Biochemistry, and Behavior, Aug 1998, volume=60, pages=777-84</ref>''
La recherche animale a montré que le potentiel de dépendance psychologiqie cannabinoïde existe, et inclut des symptômes '' mild withdrawal'' . Bien que n'étant pas aussi sévère que les dépendances à l'[[boisson alcoolisé|alcool]], [[héroïne]], ou la [[cocaïne]], la [[marijuana]] ''withdrawal'' est usuellement caractérisée par des [[insomnie]]s, ''restlessness'', perte d' [[appétit]], [[irritabilité]], [[angoisse]], ''increased muscle activity (jerkiness), and aggression after sudden cessation of chronic use as a result of [[physiological tolerance]].'' ''Prolonged marijuana use produces both [[pharmacokinetic]] changes (how the drug is absorbed, distributed, metabolized, and excreted) and [[Pharmacodynamie|pharmacodynamic]] changes (how the drug interacts with target cells) to the body. These changes require the user to consume higher doses of the drug to achieve a common desirable effect, and reinforce the body’s metabolic systems for synthesizing and eliminating the drug more efficiently.'' <ref name="joy" />
Preliminary research, published in the [[avril 2006]] issue of the ''Journal of Consulting and Clinical Psychology'', indicates that cannabis addiction can be offset by a combination of [[Cognitive therapy|cognitive-behavioral therapy]] and motivational incentives. Participants in the study (previously diagnosed with marijuana dependence) received either vouchers as incentives to stay drug free, cognitive-behavioral therapy, or both over a 14-week period. At the end of 3 months, 43 percent of those who received both treatments were no longer using marijuana, compared with 40 percent of the voucher group, and 30 percent of the therapy group. At the end of a 12-month follow-up, 37 percent of those who got both treatments remained abstinent, compared with 17 percent of the voucher group, and 23 percent of the therapy group. <ref>{{''Combination of Cognitive-Behavioral Therapy and Motivational Incentives Enhance Treatment for Marijuana Addiction'', National Institutes of Health, April 1, 2006, http://www.nih.gov/news/pr/apr2006/nida-01.htm</ref>
En [[1998]] , un rapport gouvernemental français commissionné par le secrétaire d'État à la santé, [[Bernard Kouchner]], et dirigé par Dr. Pierre-Bernard Roques, classa les drogues d'après leur addictivité et [[neurotoxicité]]. Il plaça héroïne, cocaïne et alcool dans les catégories les plus addictives et les plus mortelles ; [[benzodiazépine]], [[hallucinogène]]s et tabac dans la catégorie intermédiaire, et le cannabis dans la dernière. Le rapport établit que ''«Addiction to cannabis does not involve neurotoxicity such as it was defined in chapter 3 by neuroanatomical, neurochemical and behavioral criteria. Thus, former results suggesting anatomic changes in the brain of chronic cannabis users, measured par [[tomographie]], were not confirmed by the accurate modern [[Magnetic resonance imaging|neuro-imaging techniques]]. Moreover, morphological impairment of the [[hippocampe (cerveau)|hippocampe]] [which plays a part in memory and navigation] of rat after administration of very high doses of THC (Langfield et al., 1988) was not shown (Slikker et al., 1992).»'' Le secrétaire d'État, [[Bernard Kouchner]] en conclut que : ''«Scientifical facts show that, for cannabis, no neurotoxicité is demonstrated, to the contrary of alcool et cocaïne.»'' <ref>''1998 [[INSERM]]-[[Centre national de la recherche scientifique|CNRS]] report, directed by Pr. Bernard Roques'' and commissionned by Health Secretary of State [[Bernard Kouchner]] [http://www.chanvre-info.ch/info/en/Hemp-is-less-toxic-than-alcohol-or.html] [http://translate.google.com/translate?sourceid=navclient-menuext&hl=en&u=http%3A%2F%2Fwww%2Elesverts%2Efr%2Farticle%2Ephp3%3Fid%5Farticle%3D2092] [http://www.circ.ch/chanvretherap/extraits_du_rapport_roques.htm] [http://www.esculape.com/politique/alcooldrogue.html]</ref>
=== Effets sur la [[reproductive system|reproduction]] ===
Il a été montré que l' administration de hautes doses de THC aux animaux abaisse leur niveau de sérum [[testostérone]], affecte la production de [[sperme]], la motility, la viability, et affecte le cycle d' [[ovulation]], et réduit la sortie de [[Gonadotrope|gonadotropic hormones]]. Ceci est modéré par des rapports contradictoires selon lesquels la tolérance pourrait se développer à ces effets . <ref name="Kalant" /> <ref>''Adverse Effects of Cannabis'', W. Hall, N. Solowij, [[The Lancet]], Nov 1998, pages= 1611-6, volume=352</ref> D'après le [[1997]] [[Merck Manual of Diagnosis and Therapy]], les effets sur la fertilité dus à la consommation de cannabis seraient incertain.
La recherche a montré que le sperme humain contient des récepteurs qui sont stimulés par des substances comme la THC et d'autres produits chimiques du cannabis. Des tests ont montré que le sperme exposé à de haut niveaux de THC commencent à se mouvoir de manière anormale, et sont moins capable de s'attacher à un œuf de manière à le [[fertilisation|fertiliser]]. <ref>''Evidence that anandamide-signaling regulates human sperm functions required for fertilization, H. Schuel et al., Molecular Reproduction and Development, Sep 2002, volume=63, issue=3, pages=376-387, http://www3.interscience.wiley.com/cgi-bin/fulltext/98517201/PDFSTART</ref> While many men who use cannabis have fathered children, certain men at risk for infertility may be more susceptible to reproductive complications.
La Marijuana utilisée durant la grossesse, dans certains cas, a été relié à des [[low birth weight]] mais le lien entre cannabis et les complications de naissance est questionné par la '' [[communauté scientifique]]. ''Many studies about toxicomanie during pregnancy are self-administered by the applicants and not always [[anonymous]]. The [[social stigma|stigma]] of using illicit drugs while pregnant discourages honest reporting and can invalidate the results. Studies show that femmes qui consomment du cannabis while they are pregnant may also be likely to consume [[éthanol|alcool]], [[tabac]], or other [[illicit drugs]], which makes it difficult to deduce scientific facts about just marijuana use from statistical results. Very few large, well-controlled [[epidemiological]] studies have taken place to understand the connection of marijuana use and pregnancy. One for example, by Zuckerman and colleagues, included a large sample of women with a substantial prevalence of marijuana use that was verified by [[urinalysis|urine analysis]] and no increased [[probabilité]] of birth defects was found dans l'[[échantillon (statistiques)|échantillon]]. Opposed to [[syndrome d’alcoolisation fœtale]], similar type facial features and related symptoms are not associated with prenatal marijuana exposure. <ref>''Analysis of facial shape in children gestationally exposed to marijuana, alcohol, and/or cocaine'', S.J. Astley, S.K. Clarren, R.E. Little, P.D. Sampson, J.R. Daling, Pediatrics, Jan 1992, volume=89, pages=67-77</ref> THC passes into the [[breast milk]] and may affect a breastfed [[infant]]. <ref>{''The Merck Manual of Medical Information (Home Edition)'', R. Berkow MD et al., 1997, pages=449</ref>''
''A study of the development of 59 [[Jamaican]] children, one-half of the sample's [[mother]]s used marijuana during pregnacy, was research de la naissance à 5 ans. Pregnant non-using mothers were paired with cannabis users who matched [[ageing|age]], parity, and [[socioeconomic]] status. Testing was done at 1, 3, and 30 days of age with the Brazelton Neonatal Behavioral Assessment Scales, and at ages 4 and 5 years with the McCarthy Scales of Children's Abilities test. Data was also collected from the child's home environment and temperament, as well as standardized tests. The results over the entire reseach period showed no significant differences in development testing outcomes between using and non-using mothers. At 30 days of age, however, the children of marijuana-using mothers had higher scores on autonomic stability and reflexes. <ref>''Five-year follow-up of rural Jamaican children whose mothers used marijuana during pregnancy'', J.S. Hayes, R. Lampart, M.C. Dreher, L. Morgan, West Indian Medical Journal, Sept 1991, volume=40, pages=120-3</ref> The absence of any differences between the exposed on nonexposed groups in the early neonatal period suggest that the better scores of exposed neonates at 1 month are traceable to the cultural positioning and social and economic characteristics of mothers using marijuana that select for the use of marijuana but also promote [[infant|neonatal]] development. <ref>Prenatal Marijuana Exposure and Neonatal Outcomes in Jamaica: An Ethnographic Study, M.C. Dreher, K. Nugent, R. Hudgins, Pediatrics, Feb 1994, volume= 93, pages= 254-260</ref>''
==
===Effets comportementaux===
It is sometimes observed, and generally stéréotyped, that systematic changes in a person’s [[lifestyle]], [[ambition]]s, [[motivation]], et [[personnalité]] happen when a young person starts smoking marijuana. In fact, in many situations when people are asked to describe the personality traits of a marijuana user, they will most likely portray a person of [[apathy]] or loss of effectiveness: a person with diminished capacity or willingness to carry out complex long-term plans, endure frustration, concentrate for long periods, follow routines, or even successfully master new material. <ref>''Amotivational Syndrome'', W.A. McKim, Drugs and Behavior, 1993, pages=229-230</ref>
The term "[[amotivational syndrome]]" is often applied to young individuals who have changed from clean, assertive, upwardly mobile achievers into the sort of person just described, with marijuana as the culprit. The syndrome, comme d'autres phénomènes [[corrélation|corrélés]] pose la [[Paradoxe de l'œuf et de la poule|question de l'œuf et de la poule ]]; marijuana use can just as easily be seen as the result of such a personality shift as it can be the cause of it. Regardless, studies to raise this and other questions, like the prevalence of such "syndrome" in the population, and proving a biological or psychological connection of the "syndrome" to substance use, have not happened. Instead, a political tug of war has ensued with each point of view claiming their own scientific research as evidence.
Government studies often point to statistical data accumulated by methods like the National Household Survey on Drug Abuse (NHSDA), the Monitoring the Future study (MTF), and the Arrestee Drug Abuse Monitoring (ADAM) program, which claim lower [[grade point average|school averages]] and higher [[dropout]] rates among users than nonusers, even though these differences are very small and may be exaggerated by the stigma attached to students who use the drug. However, the major contributor to a lack of credibility in these studies, is that in many cases, like with NHSDA and MTF, these surveys are usually self-administered and may or may not be anonymous. The likeliness of over or under representing data definitely undermines the effectiveness of these instruments. <ref name="abadinsky" /> The MTF study is conducted anonymously, but only seeks information from a sample of people who have been arrested for drug-related offenses. Clearly, the case can easily be made that socially deviant behavior will be found more frequently in individuals of the criminal justice system compared to those in the general population, including non users. In response, independent studies of college students have shown that there was no difference in grade point average, and achievement, between marijuana users and nonusers, but the users had a little more difficulty deciding on career goals, and a smaller number were seeking advanced professional degrees. <ref>''Marihuana and Psychosocial Adjustment'', N.Q. Brill, R.L. Christie, Archives of General Psychiatry, 1974, volume= 31, pages= 713-719</ref> Laboratory studies of the relationship between motivation and marijuana outside of the classroom, where volunteers worked on operant tasks for a wage representing a working world model, also fail to distinguish a noticeable difference between users and non users. <ref>''The Effects of Marihuana Use on Human Operant Behavior: Individual Data'', H.H. Mendelson, J.C. Kuehnle, I. Greenberg; N.K. Mello, Pharmacology of Marihuana, publisher=Academic Press, 1976, volume= 2, pages= 643-653</ref>
====Gateway drug hypothesis====
The [[gateway drug]] hypothesis asserts that the use of cannabis ultimately leads to the use of [[hard drug|harder drugs]]. For the most part, it was commonly thought that cannabis gateways to other drugs because de facteurs [[sociologie|sociaux]]. For example, la [[criminalisation]] du cannabis dans de nombreux pays associates its users with [[crime organisé]] promoting the [[illegal drug trade]].
According to [[neurologist]] [[Jim van Os]], some scientists believe that there is also a physiological component to the gateway drug effect. He states there is "overwhelming evidence that nobody in the brain's developmental stage – under the age of 21 – should use cannabis." <ref>Gaia Vince, ''Why teenagers should steer clear of cannabis'', NewScientist.com, July 5, 2006, http://www.newscientist.com/article/dn9488-why-teenagers-should-steer-clear-of-cannabis.html</ref>
A July 2006 study by Ellgren et al. <ref>''Adolescent Cannabis Exposure Alters Opiate Intake and Opioid Limbic Neuronal Populations in Adult Rats'',Maria Ellgren, Sabrina M Spano & Yasmin L Hurd, Neuropsychopharmacology, July 5, 2006, http://www.nature.com/npp/journal/vaop/ncurrent/full/1301127a.html</ref> strictly tested [[lab rat]]s for the biological mechanism of the gateway drug effect. The study administered 6 "[[Adolescence|teenage]]" (28 and 49 days old) rats delta-9-tetrahydrocannabinol, and 6 were the [[Scientific control|control]]. One week after the first part was completed, [[catheters]] were inserted in the [[jugular vein]] of all of the adult rats and they were able to self-administer themselves [[héroïne]] by pushing a lever. The study found that initially both groups behaved the same and began to self-administer héroïne frequently, but then stabilized at different levels. The rats that had previously been administered THC consumed about 1,5 fois more héroïne than those that had not. Because many cannabinoid receptors interact with the [[opioid]] system, the study found that adolescent cannabis use overstimulates and alters the pleasure and reward structures of the brain, thus increasing the already high risk of addiction for people who start to use [[héroïne]]. [[Psychopharmacologie|Psychopharmacologist]] Ian Stolerman, from [[King's College London]], finds the biological cannabis gateway drug effect "somewhat preliminary", and states "it's too early to say there's a consensus, but a small number of studies like this suggest that there is a physiological basis for this effect." Other drugs, he notes, such as cocaïnee and [[amphetamines]] are involved in another brain pathway called the [[dopaminergic system]]. Cells in that system also interact with THC receptors and could be modified by cannabis exposure. <ref>Michael Hopkin, ''Rats taking cannabis get taste for heroin'', [[Nature (journal)|Nature]], date=July 5, 2006, http://www.nature.com/news/2006/060703/full/060703-9.html</ref> Cannabinoid receptors are 10 fois more prevalent in the brain que les [[récepteur opiacé|récepteurs opiacés]]. Selon le Dr. Hurd, un des responsables de cette étude, deux autres drogues qui stimulent aussi les cellules opiacées, et pourraient donc aussi provoquer un effet gateway, ce sont la [[nicotine]] et l'[[Boisson alcoolisée|alcool]].
===Co-occurrence of mental illness===
Scientific studies have correlated a change in [[mental health]] with cannabis use for young people. Particularly, studies have shown that a risk does exist in some individuals to develop symptoms of [[psychosis]] <ref>''Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people'', Cécile Henquet, Lydia Krabbendam, Janneke Spauwen, Charles Kaplan, Roselind Lieb, Hans-Ulrich Wittchen and Jim van Os, British Medical Journal, Dec 2004, volume= 330, issue= 11</ref> and [[anxiety]] <ref>''Cannabis use and mental health in young people: cohort study'', G C Patton, Carolyn Coffey, J B Carlin, Louisa Degenhardt, Micheal Lynskey and Wayne Hall, British Medical Journal, 2005, volume=325, pages=1195</ref>. The risk was found to be directly related to high dosage and frequency of use, early age of introduction to the drug, and was especially pronounced for those with a predisposition for mental illness. These results have been questioned as being biased by failing to account for medicinal versus recreational usage: <ref>''Decreased depression in marijuana users'', T.F. Denson, M. Earleywine, Addictive Behaviors, June 20, 2005, http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VC9-4GFCR48-5&_user=10&_coverDate=06%2F20%2F2005&_rdoc=1&_fmt=summary&_orig=browse&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7dac506ad701a12cddfe8dd713f77138</ref> It could be a causal relationship, or it could be that people who are susceptible to mental problems tend to smoke cannabis, or it could be connected to the criminalization of cannabis. Another important question is whether the observed symptoms of mental illness are actually connected to development of a permanent [[mental disorder]]. Cannabis may trigger latent conditions, or be part of a complex coordination of causes of mental illness, referred to as the [[diathesis-stress model]] in [[psychology]]. People with developed psychological disorders often tend to [[self-medicate]] their symptoms with cannabis as well, although one study has claimed that those with a predisposition for psychose did not show an increase in likelihood of cannabis use four years later. There has not currently been enough scientific study of the drug's effects to come to a definite conclusion.
====Similitude des symptômes====
There is a classification of psychosis within the [[DSM-IV]] called 'psychose cannabique' which is very rare. In susceptible individuals, ingestion of sufficient quantities of the drug can trigger an acute psychotic event. It should be noted that the extent of a subject's experience with cannabis is a strong factor determining susceptability.
A Yale research study notes that subjects administered pure delta-9-THC induced transient symptoms which resemble those of schizophrenia "ranging from suspiciousness and delusions to impairments in memory and attention". There were no side effects in the study participants one, three, and six months after the study. <ref>''Study Finds Cannabis Triggers Transient Schizophrenia-Like Symptoms'', J. Weaver, Yale News Release, 14 June 2004, http://www.yale.edu/opa/newsr/04-06-14-01.all.html</ref>
====Correlation studies====
Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It might be a component cause, part of a complex constellation of factors leading to psychosis, or it might be a correlation without forward causality at all. Similar correlations can be drawn between cannabis usage and [[cancer]], for instance, because those who suffer from cancer may be more likely to use cannabis due to the pain relief it provides.
A review of the evidence by Louise Arsenault, et al en [[2004]] reports that on an individual level, cannabis use confers an overall twofold increase in the relative risk of later [[schizophrénie]]. This same research also states that « There is little dispute that cannabis intoxication can lead to acute transient psychotic episodes in some individuals ». The study synthesizes the results of several studies into a statistical model. <ref>''Causal association between cannabis and psychosis: examination of the evidence'', L. Arseneault et al., The British Journal of Psychiatry, 2004, volume=184, pages= 110-117, http://bjp.rcpsych.org/cgi/content/full/184/2/110</ref>
A landmark study, in [[1987]], of 50,000 [[Swedish Army]] conscripts, found that those who admitted at age 18 to having taken cannabis à plus de 50 occasions, were six times more likely to develop [[schizophrénie]] in the following 15 years. In fact, [[psychosis]] cases were restricted to patients requiring a hospital admission. These findings have not been replicated in another population based sample. <ref>''Cannabis and Schizophrenia: A Longitudinal Study of Swedish Conscripts'' , S. Andreasson et al., The Lancet, 1987, volume= 2, pages=1483-1486</ref> As the study did not control for symptoms preexisting onset of cannabis use, the study does not resolve the ''correlation versus causality'' question but has fueled a major debate within the scientific community.
A [[2005]] study found that "the onset of schizotypal symptoms generally precedes the onset of cannabis use. The findings do not support a causal link between cannabis use and schizotypal traits". <ref>''Symptoms of schizotypy precede cannabis use'', J. Schiffman et al., Psychiatry Research, volume= 134, issue=1, 30 March 2005, pages= 37-42, http://www.journals.elsevierhealth.com/periodicals/psy/article/PIIS0165178105000284/abstract</ref> It should be noted that a [[schizotypal personality disorder]] is a [[personality disorder]] different from [[schizophrenia]], which is a [[mood disorder]].
Research based on the [[Dunedin Multidisciplinary Health and Development Study]] has found that those who begin regular use of cannabis in early adolescence (from age 15, [[median]] 25 days per year by age 18) and also fit a certain [[genetics|genetic]] profile (specifically, the Val/Val variant of the [[COMT|COMT gene]]) are five times more likely to develop psychotic illnesses than individuals with differing [[genotypes]], or those who do not use cannabis. <ref>''Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study'', Louise Arseneault, Mary Cannon, Richie Poulton, Robin Murray, Avshalom Caspi, Terrie E Moffitt, British Medical Journal, 23 November 2002, http://bmj.bmjjournals.com/cgi/reprint/325/7374/1212.pdf</ref> <ref>''Moderation of the Effect of Adolescent-Onset Cannabis Use on Adult Psychosis by a Functional Polymorphism in the catechol-O-Methyltransferase Gene:Longitudinal Evidence of a Gene X Environment Interaction'', Avshalom Caspi, Terrie E. Moffitt, Mary Cannon, Joseph McClay, Robin Murray, HonaLee Harrington, Alan Taylor, Louise Arseneault, Ben Williams, Antony Braithwaite, Richie Poulton, and Ian W. Craig, Society of Biological Psychiatry, 18 January 2005, http://www.ukcia.org/research/COMTgene.pdf</ref> The study was noted for it having controlled for preexisting symptoms, but is open to the criticism that it cannot control for late adolescent onset of psychotic illness. Also, the study was on a cohort population, so there is no way to correlate a change in the ''rate'' of adolescent use with a change in the ''rate'' of incidence of schizophenia in the study population. These points undermine its value in resolving the ''correlation versus causality'' question.
== Smoking ==
The process most popularly used to ingest cannabis is smoking, and for this reason most research has evaluated health effects from this method of ingestion. Other methods of ingestion may have lower or higher health risks, as the case may be. See section on réduction des risques below pour plus d'information sur les autres méthodes d'ingestion.
=== Different and fewer risks than tabac ===
Le tabagisme has well-established risks such as [[bronchitis]], [[cough]]ing, overproduction of [[mucus]], and [[wheezing]]. Similar risks for smoking cannabis related to airway [[inflammation]] have been suggested in a study of healthy cannabis users who exhibited similar early characteristics to [[tabagisme]]. <ref>{{''Airway Inflammation in Young Marijuana and Tobacco Smokers'', M.D. Roth et al., American Journal of Respiratory and Critical Care Medicine, volume=157, issue= 3, March 1998, pages= 928-937, http://ajrccm.atsjournals.org/cgi/content/full/157/3/928</ref>
The effects of tabac and cannabis smoking differ, however, as they affect different parts of the [[respiratory tract]]: whereas le tabac tends to penetrate to the smaller, peripheral passageways of the [[poumon]]s, cannabis tends to concentrate on the larger, central passageways. One consequence of this est que le cannabis, contrairement au tabac, ne semble pas provoquer d'[[emphysème]]. De même, contrairement à celui du tabac, l'usage régulier de cannabis ne semble pas non plus provoquer de [[maladie pulmonaire obstructive chronique]]. <ref>''Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age'', D.P. Tashkin et al., Am. J. Respir. Crit. Care Med., volume= 155, Jan 1997, pages=141-148, http://ajrccm.atsjournals.org/cgi/gca?SEARCHID=1127855512481_8334&AUTHOR1=Tashkin%252C%2BD&FULLTEXT=Marijuana&JOURNALCODE=&FIRSTINDEX=0&hits=10&RESULTFORMAT=&gca=155%2F1%2F141&sendit=Get+All+Checked+Abstract%28s%29</ref> Researchers have speculated on potential side effects from the fact that cannabis burns at a higher temperature than tabac.
It is important to note that in some cases, a cannabis user may encounter commercial tabac in [[Spliff|joints]] (popular in [[Europe]]), added tabac with hash in [[chillum]] ([[Inde]]), or cannabis rolled in tabac leaves, which would expose the user to the additional risks of tabac, though nothing on the same order as regular tobacco use.
=== Potency matters ===
By analogy avec le tabagisme, an [[National Institute on Drug Abuse|NIDA]]-funded study sought to establish a risk to respiratory health by analysing the contents of cannabis smoke, observe inhalation volume of cannabis smokers, and infer risks such as blood [[carboxyhemoglobin]] levels from this. <ref>''Pulmonary hazards of smoking marijuana as compared with tobacco'', T.C. Wu et al., New England Journal of Medicine, volume= 318, 11 Feb 1988, 347-351http://content.nejm.org/cgi/content/abstract/318/6/347</ref>
The methodological difficulty, however, was that all the subjects were both tabagisme and cannabis smokers, smoking ultra-low-potency (0,004 % et 1,24 %) NIDA-provided cannabis. Typical potency is closer to 7-15%. Like a listener turning up a radio until he can hear it, un fumeur de cannabis will regulate the dose by smoking until the desired effect is felt, which in ultra-low-potency cannabis translates into much greater volume of inhaled smoke, and so abnormally high blood carboxyhemoglobin levels. Typical levels would therefore be much lower than the study found. These problems notwithstanding, this is a primary study cited by NIDA in this regard.
=== Risque de cancer ===
Cannabis smoke contains numerous compounds known to cause cancer <ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16054989&query_hl=3&itool=pubmed_docsum],[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=1253890&query_hl=3&itool=pubmed_docsum]</ref><ref>[http://www.norml.org/pdf_files/NORML_Cannabis_Smoke_Cancer.pdf]</ref>. Surprisingly, however, scientific studies have failed to show higher cancer rates in cannabis smokers. A study published in 2006 <ref>''Pot Smoking Not Linked to Lung Cancer'' , 23 mai 2006, http://www.webmd.com/content/article/122/114805.htm<br/>[http://sciencenow.sciencemag.org/cgi/content/full/2006/523/3 ScienceNOW]<br/> [http://www.drugwarrant.net/wiki/tiki-index.php?page=Marijuana_and_Cancer Abstract]</ref> on a large population sample (1,200 people with lung, neck, or head cancer, and a matching group of 1,040 sans cancer) failed to positively correlate un risque de [[cancer du poumon]], in fact the results indicated a slight ''negative'' correlation between long and short-term cannabis use and cancer, suggesting a possible therapeutic effect. This followed an even larger [[1997]] study <ref>''Marijuana use and cancer incidence (California, United States)'', S. Sidney, Cancer Causes and Control, volume=8, issue=5, Sep 1997, pages= 722-728, http://www.springerlink.com/link.asp?id=l221477720240752</ref> examining the records of 64,855 Kaiser patients, which also found no positive correlation between cannabis use and cancer. It has been noted, separately, that [[THC]], a dilative agent, may help cleanse the lungs by dilating the bronchia, and could actively reduce the instance of tumors. <ref>''Antitumor Effects of THC'', J. Huff & P. Chan, Environmental Health Perspectives, volume= 108, issue=10, Oct 2000, pages=A442-3, http://ehp.niehs.nih.gov/docs/2000/108-10/correspondence.html#thc</ref> Additionally, a study by Rosenblatt et al. found no association between marijuana use and the development of head and neck squamous cell carcinoma. <ref>''Marijuana Use and Risk of Oral Squamous Cell Carcinoma'', K.A. Rosenblatt et al., Cancer Research, volume= 64, 1 June 2004, pages=4049-4054, http://cancerres.aacrjournals.org/cgi/content/full/64/11/4049</ref>
Although la [[cancérogène|cancérogènicité]] du tabac is thought to be caused mainly by tar, it has been suggested that it could be the result of radioactive substances present in tabac soils <ref>{{''Cancer risk in relation to radioactivity in tobacco'', G.F. Kilthau, Radiologic Technology, volume=67, issue=3, Jan-Feb 1996, http://galenet.galegroup.com/servlet/HWRC/hits?index1=RN&tcit=0_1_0_0_0&rlt=2&origSearch=true&t=RK&s=11&r=d&items=0&secondary=false&n=10&l=d&sgPhrase=true&c=1&bucket=per&text1=A19101062&docNum=A19101062&locID=nysl_me_weillmdc}}</ref>. This problem does not pertain to cannabis, the vast majority of which is grown in wild, organic, or hydroponic conditions.
=== Attempts at réduction des risques ===
The health consequences of cannabis use may vary depending on method of use. Proposed alternatives include:
* filtered cigarettes
* [[bong]]s (specialized pipes filtering smoke through water)
* vaporizeurs (devices for extracting THC without combusting the cannabis)
* eating ("[[space cake]]s")
* high potency cannabis
Comme la fumée de tabac, la fumé de marijuana contient tars which are riches en [[polycyclic aromatic hydrocarbons]], [[cancérogène]]s which are a prime culprit in smoking-related cancers. However, cannabinoïdes themselves are not carcinogenic. An obvious way to protect smokers' health is therefore to minimize the content of smoke tars relative to cannabinoïdes.
The most obvious way to do this is to bypass smoking completely by simply eating the cannabis as "[[space cake]]s".
Another way is to increase the [[THC]] potency of the marijuana (voir also section on potency above). Assuming smokers adjust their smoke intake to the cannabinoïde dosage, the higher the concentration of cannabinoïdes, the lower the amount of tars they are likely to consume to achieve their desired effect.
Vaporisers, by heating the cannabis oils to be inhaled without combustion, almost avoid the risk altogether <ref>''Vaporizers for Medical Marijuana'', B. Mirken, AIDS Treatment News, volume= 327, 17 Sep 1999</ref>. A [[2000]] <ref>[http://www.maps.org/news-letters/v06n3/06359mj1.html study] </ref>conducted by NORML and Multidisciplinary Association for Psychedelic Studies found that the two tested vaporizers performed up to 25% better than unfiltered marihuana cigarettes in terms of tar delivery.
Surprisingly, the same study found that water pipes (bongs) and filtered cigarettes performed 30% ''worse'' than regular, unfiltered joints. The reason is that waterpipes and filters filter out more psychoactive THC than they do tars, thereby requiring users to smoke more to reach their desired effect. The study does not, however, rule out the possibility that waterpipes could have other benefits, such as filtering out harmful gases such as [[monoxyde de carbone]].
== Cannabis et conduite routière ==
ils y a plusieurs obstacles principaux pour déterminer l'effet de l'usage de cannabis sur la conduite routière : cannabis use is most common in a demographic that is already vulnerable for traffic accidents; dangerous drivers who tested positive for THC often test positive for alcohol as well; there are no figures or estimates available as a "base-line," for instance, how many cannabis users drive safely without incidents; et il existe de nombreux obstacles éthiques et légaux impeding research on this topic.
A [[2001]] study by the [[United Kingdom]] Transit Research Laboratory (TRL) specifically focuses on the effects of cannabis use on driving <ref>''Cannabis and driving: a review of the literature and commentary (No.12)'', United Kingdom Department for Transport, http://www.dft.gov.uk/stellent/groups/dft_rdsafety/documents/page/dft_rdsafety_504567.hcsp</ref>, and is one of the most recent and commonly quoted studies on the subject. The report summarizes current knowledge about the effects of cannabis on driving and accident risk based on a review of available literature published since 1994 and the effects of cannabis on laboratory based tasks.
The study identified young males, amongst whom cannabis consumption is frequent and increasing, and in whom alcohol consumption is also common, as an [[a priori]] risk group for [[Motor-vehicle collision|traffic accidents]]. This is due to driving inexperience and factors associated with youth relating to [[risk]] taking, [[Delinquent|delinquency]] and [[motivation]]. These demographic and psychosocial variables may relate to both drug use and accident risk, thereby presenting an artificial relationship between use of drugs and accident involvement.
Les effets du cannabis on laboratory-based tasks show clear impairment with respect to tracking ability, [[attention]], and other tasks depending on the dose administered. These effects however, are not as pronounced on tasks of greater ecological validity, like real driving or [[Simulateur de conduite|simulateur]] tasks. Both simulation and road trials generally find that driving behavior shortly after consumption of larger doses of cannabis results in: un style de conduite plus prudent; increased variability in lane position (and headway); and longer decision times. Whereas these results indicate a 'change' from normal conditions, they do not necessarily reflect 'impairment' in terms of performance effectiveness since few studies report increased accident risk. However, the results do suggest 'impairment' in terms of performance efficiency given that some of these behaviors may limit the available resources to cope with any additional, unexpected or high demand, events. Indeed, compensatory effort can be invoked to offset impairment in the driving task. Subjects under cannabis treatment appear to perceive that they are impaired and can compensate, for example, by not overtaking, by slowing down and by focusing their attention when they know a response will be required. This compensatory effort may be one reason for the failure to implicate cannabis consumption as an accident [[risk factor]]. However, this claim is difficult to substantiate in the absence of any substantial [[Epidemiology|epidemiological]] estimates of accident risk.
Specifically, 4-12% of accident fatalities have detected levels of cannabis. However, most studies report that the majority of fatal cases with detected levels of cannabis are compounded by alcohol.
The study estimates 11ng/ml THC as the equivalent does to the legal limit of alcohol (0.08% BAC in the UK), although cannabis effects on driving are present up to an hour after smoking but do not continue for extended periods. Alcohol alone or in combination with cannabis, increases impairment, accident rate and accident responsibility. Moreover, accident risk cannot be derived in the absence of baseline data for non-fatal cases.
Similar conclusions have been reached by studies maintained by the federal governments of [[Australie]], United Kingdom, [[Nouvelle-Zélande]] and the [[United States]] (see [http://www.scotland.gov.uk/cru/kd01/blue/druguse-15.htm here] for a list of studies). Those studies that have concluded that cannabis has a significant negative effect on driving ability generally involve the use of [[Field Sobriety Test#Field sobriety test|roadside sobriety tests]] as an indicator of reduced ability (for example, see [http://www.nida.nih.gov/NIDA_Notes/NNVol11N1/marijuana.html this NIDA report]). However, studies that employ this methodology show that a majority of subjects who tested positive for THC also tested positive for alcohol, already described as a limiting factor of validity.
== Références ==
<references />
== Voir aussi ==
===Articles connexes===
* [[Toxicomanie]]
* [[Réduction des risques]]
* [[Prohibition des drogues]]
* [[
=== Liens externes ===
*[http://cannabishq.com/forum/index.php?topic=231.0 Marijuana Myths & Facts] Health effects
*[http://www.ukcia.org/research/can-psychosis.htm Cannabis Use and Psychosis] from National Drug and Alcohol Research Centre, Australie
*[http://www.erowid.org/plants/cannabis/cannabis.shtml Marijuana Vault] at [[erowid.org]]
*[http://news.bbc.co.uk/1/hi/programmes/panorama/4109360.stm The key research on cannabis use and mental illness] at [[BBC News]]
*[http://www.nida.nih.gov/about/organization/nacda/marijuanastatement.html Provision of Marijuana and Other Compounds For Scientific Research] recommendations of The [[National Institute on Drug Abuse]] National Advisory Council
* [http://www.sciam.com/article.cfm?chanID=sa006&articleID=0008F53F-80F7-119B-80F783414B7F0000 Scientific American Magazine (décembre 2004 Issue) The Brain's Own Marijuana]
[[Catégorie:Cannabis]]
[[en:Health issues and the effects of cannabis]]
| |||