Serment d’Hippocrate

Le serment d’Hippocrate est un serment traditionnellement prêté par les médecins en Occident avant de commencer à exercer. Le texte original de ce serment, probablement rédigé au IVe siècle av. J.-C., appartient aux textes de la Collection hippocratique, traditionnellement attribués au médecin grec Hippocrate. Le serment d’Hippocrate peut être considéré comme le principe de base de la déontologie médicale.

Lire plus ici: https://fr.wikipedia.org/wiki/Serment_d’Hippocrate

The Hippocratic Oath for scientists: https://en.wikipedia.org/wiki/Hippocratic_Oath_for_scientists

Publicités

Ce n’est pas inoffensif.

ProhibitionSign2  No-pase  Roadsign-no-entry

On ne peut pas vous greffer un autre cerveau.

Le pot n’est pas inoffensif pour les ados
Mise à jour le mardi 27 août 2013 à 20 h 18 HAE

Source: http://www.radio-canada.ca/nouvelles/science/2013/08/27/002-adolescents.shtml

Le cannabis, première drogue associée aux psychoses
8 février 2014 | Isabelle Paré
http://dependancemontreal.ca/actualites/le-cannabis-premiere-drogue-associee-aux-psychoses

Le cannabis multiplie par 2 le risque de cancer du testicule: http://www.sudinfo.be/519208/article/actualite/sante/2012-09-11/le-cannabis-multiplie-par-2-le-risque-de-cancer-du-testicule

Risque accru d’accident vasculaire cérébral et consommation de marijuana – Adverse health effects of marijuana use – Higher risk of stroke:

In their article, Volkow et al. (June 5 issue)1 state that marijuana may have adverse health effects, particularly on the vulnerable brains of young people. Potential mechanisms underlying the effect of marijuana on the cerebrovascular system are indeed complex, although a temporal relationship between the use of marijuana (natural or synthetic) and stroke in young people has recently been described.2,3 Simultaneously, the presence of multifocal intracranial arterial vasoconstriction was observed, which was reversible in some cases after cessation of cannabis exposure.3 Thus, stroke, which is still underdiagnosed, may potentially play a role in neuronal damage related to marijuana use, even in young people without cardiovascular risk factors. Furthermore, tetrahydrocannabinol (THC), a major component of cannabis, has been shown experimentally to impair the function of the mitochondrial respiratory chain and to increase the production of reactive oxygen species in the brain.4 Both of these processes are key events during stroke,5 suggesting that THC may also increase a patient’s vulnerability to stroke. In the ongoing shift toward marijuana legalization, physicians should probably inform marijuana users, whether they are using it for recreational purposes or therapeutic indications, about the risk of stroke with potential severe disability: http://www.nejm.org/doi/full/10.1056/NEJMc1407928

Alcool et Cannabis : le foie parle à vos ados: http://www.professeur-joyeux.com/cannabis-le-foie-parle-vos-ados/

The Deadly Health Risk Most Pot Smokers Don’t Know About  –  New research shows that marijuana doubles the risk of stroke—and not in older people: http://www.takepart.com/article/2013/02/15/pot-linked-risk-stroke?cmpid=tp-internal-taboola

High Potency Cannabis Affects Corpus Callosum (CC) Microstructural Organization:

Conclusions: Frequent use of high-potency cannabis significantly affects callosal microstructure, regardless of the presence of a psychotic disorder. Given the increased availability and use of high potency preparations in Europe, raising awareness about some of their detrimental effects is an important avenue to pursue. http://www.sciencedirect.com/science/article/pii/S0924933815302340

Proportion of patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study:

Findings

Between May 1, 2005, and May 31, 2011, we obtained data from 410 patients with first-episode psychosis and 370 population controls. The risk of individuals having a psychotic disorder showed a roughly three-times increase in users of skunk-like cannabis compared with those who never used cannabis (adjusted odds ratio [OR] 2·92, 95% CI 1·52–3·45, p=0·001). Use of skunk-like cannabis every day conferred the highest risk of psychotic disorders compared with no use of cannabis (adjusted OR 5·4, 95% CI 2·81–11·31, p=0·002). The population attributable fraction of first-episode psychosis for skunk use for our geographical area was 24% (95% CI 17–31), possibly because of the high prevalence of use of high-potency cannabis (218 [53%] of 410 patients) in our study:

http://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366%2814%2900117-5/abstract

download pdf: http://www.thelancet.com/pdfs/journals/lanpsy/PIIS2215-0366%2814%2900117-5.pdf

download images ppt: www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(14)00117-5/ppt

Invited Commentary: The Association Between Marijuana Use and Male Reproductive Health:

The current report provides important information for patients and providers regarding the negative association of marijuana use on semen quality. Although the benefit of marijuana cessation on recovery is uncertain, further study on the impact of marijuana use on male reproductive health is warranted as more states explore marijuana legalization. http://aje.oxfordjournals.org/content/182/6/482.short

CB1 cannabinoid receptor stimulation during adolescence impairs the maturation of GABA function in the adult rat prefrontal cortex:

http://www.ncbi.nlm.nih.gov/pubmed/24589887

Long-term effects of cannabis on brain structure:

We provide evidence that regular cannabis use is associated with gray matter volume reduction in the medial temporal cortex, temporal pole, parahippocampal gyrus, insula, and orbitofrontal cortex; these regions are rich in cannabinoid CB1 receptors and functionally associated with motivational, emotional, and affective processing.

The effects of cannabis on memory function in users with and without a psychotic disorder: findings from a combined meta-analysis:

Conclusions: These results suggest that cannabis use is associated with a significant domain-specific impairment in memory in healthy individuals but not in cannabis-using patients, suggesting that they may represent a less developmentally impaired subgroup of psychotic patients. http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=9947919&fileId=S0033291715001646

Interaction between DRD2 and AKT1 genetic variations on risk of psychosis in cannabis users: a case–control study:

http://www.nature.com/articles/npjschz201525?WT.mc_id=GOP_SCHZ_1507_201525

Adolescent brain maturation, the endogenous cannabinoid system and the neurobiology of cannabis-induced schizophreniahttp://www.ncbi.nlm.nih.gov/pubmed/20624444

Regional brain abnormalities associated with long-term heavy cannabis use: http://www.ncbi.nlm.nih.gov/pubmed/18519827

March 2015 – Further human evidence for striatal dopamine release induced by administration of ∆9-tetrahydrocannabinol (THC): selectivity to limbic striatum:

Conclusions: In the largest data set of healthy participants so far, we provide evidence for a modest increase in human striatal dopamine transmission after administration of THC compared to other drugs of abuse. This finding suggests limited involvement of the endocannabinoid system in regulating human striatal dopamine release and thereby challenges the hypothesis that an increase in striatal dopamine levels after cannabis use is the primary biological mechanism underlying the associated higher risk of schizophrenia. http://link.springer.com/article/10.1007/s00213-015-3915-0

Effect of long-term cannabis use on axonal fibre connectivity: http://www.ncbi.nlm.nih.gov/pubmed/22669080

The Impact of Cannabis Use on the Dosage of Antipsychotic Drugs in Patients Admitted on the Psychiatric Ward at the University Hospital of the West Indies:

This study provides preliminary evidence that cannabis users diagnosed with a psychotic disorder may require larger doses of medication to effect eradication of symptoms compared to non-cannabis users diagnosed with a psychotic disorder.  http://www.mona.uwi.edu/wimjopen/sites/default/files/wimjopen/article_pdfs/Thomas%20et%20al–Cannabis%20Use%20on%20Dosage%20of%20Antipsychotic%20Drugs.pdf

Altered cerebral blood flow and neurocognitive correlates in adolescent cannabis users: http://www.ncbi.nlm.nih.gov/pubmed/22395430

Telling true from false: cannabis users show increased susceptibility to false memories:  These findings indicate that cannabis users have an increased susceptibility to memory distortions even when abstinent and drug-free, suggesting a long-lasting compromise of memory and cognitive control mechanisms involved in reality monitoring. http://www.nature.com/mp/journal/v20/n6/abs/mp201536a.html

Cannabis smoke can be a major risk factor for early-age laryngeal cancer—a molecular signaling-based approach:  This study provides evidence for a direct association between cannabis smoking and increased risk of laryngeal cancer. Higher expression of the EGFR cascade in cannabis smokers revealed that cannabis smoking may be a major cause for the early onset of aggressive laryngeal cancer. http://link.springer.com/article/10.1007/s13277-015-3279-4

Quand est-ce que le plus important du neuro-développement de la matière grise est complété?  À 25 ans!

When is significant gray matter neurodevelopment complete ?  At age 25 !!!!!!!!

[…]The largest lessons the scientific community can share are that we need to 1) invest resources to delay the onset of cannabis use past the sensitive period of significant neuromaturation (i.e., close to age 25), 2) increase resources for prevention, screening, and early intervention for regular cannabis users (especially targeting youth), and 3) invest in more research regarding the impact of cannabis content and dosage on addiction risk and neurocognition (i.e., following-up on preliminary evidence that higher levels of CBD and limiting THC content may reduce public health impact of cannabis use). In order to optimize neuronal development and reduce the prevalence of cannabis use disorders, empirically validated interventions aimed at lowering and preventing cannabis use in youth need to be consistently implemented to minimize the impact of regular cannabis use on the developing brain[…] …read more http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4084860/

Genetic and environmental contributions to cannabis dependence in a national young adult twin sample:

[…]There was consistent evidence that genetic risk factors are important determinants of risk of cannabis dependence among men. However, it remains uncertain whether there are genetic influences on liability to cannabis dependence among women.[…]  http://www.ncbi.nlm.nih.gov/pubmed/11871371

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:

RESULTS:  A functional polymorphism in the catechol-O-methyltransferase (COMT) gene moderated the influence of adolescent cannabis use on developing adult psychosis. Carriers of the COMT valine158 allele were most likely to exhibit psychotic symptoms and to develop schizophreniform disorder if they used cannabis. Cannabis use had no such adverse influence on individuals with two copies of the methionine allele.

CONCLUSIONS: These findings provide evidence of a gene x environment interaction and suggest that a role of some susceptibility genes is to influence vulnerability to environmental pathogens: http://www.ncbi.nlm.nih.gov/pubmed/15866551

Cannabis, COMT and psychotic experiences:

[…] In sensitivity analyses we observed highly variable evidence of interaction, whereby psychotomimetic effects of cannabis were greater in methionine homozygotes under some scenarios, but in valine homozygotes under others.

CONCLUSIONS: Cannabis increases risk of psychosis irrespective of underlying COMT genotypes. These findings argue against the widely held belief that the relative risk of developing psychosis following use of cannabis is dependent upon variation within COMT. The public health message about the potential increase in risk of psychotic disorders following cannabis use should not be tempered by reports that this harm is subgroup specific in the absence of robust evidence of replication.[…]  http://bjp.rcpsych.org/content/199/5/380.long

Interaction between COMT haplotypes and cannabis in schizophrenia: a case-only study in two samples from Spain:  http://www.ncbi.nlm.nih.gov/pubmed/21310591

Can Cannabis Cause Psychosis?  by Michaels, Timothy I BA; Novakovic, Vladan MD:  

This article provides a brief review of evidence that support cannabis use as a risk factor in the complex etiology of psychotic illness. http://journals.lww.com/clinicalneuropharm/Abstract/2015/03000/Can_Cannabis_Cause_Psychosis_.8.aspx

Family-based analysis of genetic variation underlying psychosis-inducing effects of cannabis: sibling analysis and proband follow-up:  http://www.ncbi.nlm.nih.gov/pubmed/21041608

Association Between Cannabis and Psychosis: Epidemiologic Evidence:

[…]Overall, evidence from epidemiologic studies provides strong enough evidence to warrant a public health message that cannabis use can increase the risk of psychotic disorders. However, further studies are required to determine the magnitude of this effect, to determine the effect of different strains of cannabis on risk, and to identify high-risk groups particularly susceptible to the effects of cannabis on psychosis. […] http://www.sciencedirect.com/science/article/pii/S0006322315006472

[…] We showed that a substantial number of people with first episode psychosis used cannabis and that its use was associated with increased likelihood of hospital admission and number of days spent in hospital. These associations were partly mediated by an increase in number of unique antipsychotic medications prescribed. These findings suggest that cannabis might reduce response to conventional antipsychotic treatment and highlight the importance of strategies to reduce its use.[…] http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2815%2960394-4/abstract

Role of Blonanserin in Cannabis-induced Psychosis:

[…]While several antipsychotic drugs have already been proven beneficial in the treatment of cannabis-induced psychosis, almost all of them have troublesome side effects and even some of them, like Risperidone has actually been found to increase craving for cannabis in some patients, as available literature suggests.[…] http://www.sciencedirect.com/science/article/pii/S092493381530643X

Psychiatric and Medical Management of Marijuana Intoxication in the Emergency Department:  […]Cannabis-induced psychotic disorder (“cannabis psychosis”) is diagnosed when psychotic symptoms persist beyond acute intoxication and may require clinical management.8 Psychiatric symptoms include paranoia, derealization, disorganized thinking, persecutory and grandiose delusions, hallucinations, and cognitive impairment. Patients pose a danger to others and themselves due to their altered sense of reality. Safe cannabis detoxification typically requires 24 hours, but sometimes longer for patients with unstable vital signs and persistent psychosis. Benzodiazepines are recommended for agitation related to stimulant intoxication – unless psychosis is present, in which case oral atypical antipsychotics are considered first-line.9

Cannabis blood levels reflect the extent and chronicity of marijuana use. A free THC level below 3ng/mL (μg/L) suggests occasional consumption (≤1 joint/week) while a concentration higher than 40ng/mL corresponds to heavy use (≥10 joints/month).10 Levels above 10ng/mL impair motor function, leading two states with legal recreational marijuana to establish the legal limit for driving at 5ng/mL.[…] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427213/

Interaction Between Functional Genetic Variation of DRD2 and Cannabis Use on Risk of Psychosis:  http://schizophreniabulletin.oxfordjournals.org/content/early/2015/03/30/schbul.sbv032.short

What has research over the past two decades revealed about the adverse health effects of recreational cannabis use?

Conclusions:The epidemiological literature in the past 20 years shows that cannabis use increases the risk of accidents and can produce dependence, and that there are consistent associations between regular cannabis use and poor psychosocial outcomes and mental health in adulthood. http://onlinelibrary.wiley.com/doi/10.1111/add.12703/full

Cannabis and the maturing brain: Role in psychosis development:  The key concern is that currently we are unable to predict which adolescents have the genetic liability for development of psychosis, and thus would be more sensitive to the effects of cannabis (medical or otherwise) on their developing brain.

http://onlinelibrary.wiley.com/doi/10.1002/cpt.102/full#cpt102-sec-0002

http://onlinelibrary.wiley.com/doi/10.1002/cpt.102/pdf

White matter fractional anisotropy over two time points in early onset schizophrenia and adolescent cannabis use disorder: A naturalistic diffusion tensor imaging study:  http://www.sciencedirect.com/science/article/pii/S0925492714002625

Cannabis use in early adolescence: Evidence of amygdala hypersensitivity to signals of threat:

[…]Cannabis experimenting teenagers exhibit greater amygdala reactivity to angry faces. Very low use of cannabis during adolescence may impact healthy emotional development.[…] […]Given the high density of cannabinoid receptors in the amygdala, our findings suggest cannabis use in early adolescence is associated with hypersensitivity to signals of threat. Hypersensitivity to negative affect in adolescence may place the subject at-risk for mood disorders in adulthood. http://www.sciencedirect.com/science/article/pii/S1878929315000857

Course of cannabis use and clinical outcome in patients with non-affective psychosis: a 3-year follow-up study: Conclusions These findings suggest that cannabis use in patients with a psychotic disorder has a long-lasting negative effect on illness outcome, particularly when persistent. Treatment should focus on discouraging cannabis use. http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=9718825&fileId=S0033291714003092

Cannabis dependence in the San Francisco Family Study: age of onset of use, DSM-IV symptoms, withdrawal, and heritability:

[…]Although a greater percentage of men met criteria for cannabis dependence, women were found to demonstrate “telescoping” as indexed by a shorter survival time from initial use to dependence as compared to men. A cannabis withdrawal syndrome was identified in users[…] :  http://www.ncbi.nlm.nih.gov/pubmed/19818563

Morte à cause d’un demi joint par jour: http://www.journaldemontreal.com/2014/01/31/gemma-moss-une-jeune-maman-de-31-ans-est-decedee-apres-avoir-fume-un-joint

http://fr.wikipedia.org/wiki/Benzopyrène

http://en.wikipedia.org/wiki/Benzo%28a%29pyrene

Marijuana in the Workplace: Guidance for Occupational Health Professionals and Employers: Joint Guidance Statement of the American Association of Occupational Health Nurses and the American College of Occupational and Environmental Medicine:  This discordance about use, regulation, and legislation places employers in the challenging position of maintaining compliance with divergent and evolving legislation, while continuing to provide a safe workplace. http://journals.lww.com/joem/Fulltext/2015/04000/Marijuana_in_the_Workplace___Guidance_for.17.aspx

Medical Marijuana Is the Cart Before the Horse?

Deepak Cyril D’Souza, MBBS, MD1,2,3; Mohini Ranganathan, MD1,2,3

In conclusion, if the states’ initiative to legalize medical marijuana is merely a veiled step toward allowing access to recreational marijuana, then the medical community should be left out of the process, and instead marijuana should be decriminalized. Conversely, if the goal is to make marijuana available for medical purposes, then it is unclear why the approval process should be different from that used for other medications. Evidence justifying marijuana use for various medical conditions will require the conduct of adequately powered, double-blind, randomized, placebo/active controlled clinical trials to test its short- and long-term efficacy and safety. The federal government and states should support medical marijuana research. Since medical marijuana is not a life-saving intervention, it may be prudent to wait before widely adopting its use until high-quality evidence is available to guide the development of a rational approval process. Perhaps it is time to place the horse back in front of the cart. http://jama.jamanetwork.com/article.aspx?articleID=2338230

At the tip of an iceberg: prenatal marijuana and its possible relation to neuropsychiatric outcome in the offspring:  This review combines data from human and experimental studies to show that long-term and heavy cannabis use during pregnancy can impair brain maturation and predispose the offspring to neurodevelopmental disorders. http://www.sciencedirect.com/science/article/pii/S0006322315007696

GABA Deficits Enhance the Psychotomimetic Effects of Δ9-THC: http://www.nature.com/npp/journal/v40/n8/full/npp201558a.html

Delta-9-tetrahydrocannabinol, neural oscillations above 20 Hz and induced acute psychosis:  http://link.springer.com/article/10.1007/s00213-014-3684-1

These findings add to a growing literature suggesting some overlap between the acute effects of cannabinoids and the behavioral and psychophysiological alterations observed in psychotic disorders. http://www.nature.com/npp/journal/v40/n9/full/npp201553a.html

Brain volume in male patients with recent onset schizophrenia with and without cannabis use disorders: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409437/

[18F]MK-9470 PET measurement of cannabinoid CB1 receptor availability in chronic cannabis users: http://onlinelibrary.wiley.com/doi/10.1111/adb.12116/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=

The Relationship Between Catechol-O-Methyltransferase Gene Val158Met (COMT) Polymorphism and Premorbid Cannabis Use in Turkish Male Patients with Schizophrenia:  The findings from this study confirm the association between COMT Val158 Met polymorphism and pre-morbid cannabis use in causing schizophrenia. http://iv.iiarjournals.org/content/29/1/129.short

Gross morphological brain changes with chronic, heavy cannabis use:  These findings indicate that chronic cannabis use has a selective and detrimental impact on the morphology of the mediotemporal lobe. http://bjp.rcpsych.org/content/206/1/77.short

Age-Dependent Effects of Cannabinoids on Neurophysiological, Emotional, and Motivational States:  Cannabis sativa preparations are among the illicit drugs most commonly used by young people, including pregnant women. The endocannabinoid (eCB) system, which is involved in the regulation of emotional and motivational homeostasis, synaptic plasticity and cognitive functions, also plays a critical role in diverse phases of brain development. Both perinatal and periadolescent periods are critical for brain eCB system development. Thus, interference of endocannabinoid signalling by cannabis exposure may contribute to explain the enduring negative impact of cannabis on neurodevelopmental processes and the resulting psycho-physio-pathological consequences. In the present chapter we describe and discuss published data dealing with the long-term neurobehavioural effects of cannabis exposure during the prenatal and adolescent periods. http://link.springer.com/chapter/10.1007/978-1-4939-2294-9_11

Epigenetic Regulation of Immunological Alterations Following Prenatal Exposure to Marijuana Cannabinoids and its Long Term Consequences in Offspring:  http://link.springer.com/article/10.1007/s11481-015-9586-0

Marijuana, phytocannabinoids, the endocannabinoid system, and male fertility: http://link.springer.com/article/10.1007/s10815-015-0553-8

Cannabis consumption before surgery may be associated with increased tolerance of anesthetic drugs: A case report:

http://www.ijcasereportsandimages.com/archive/2015/007-2015-ijcri/CR-10534-07-2015-richtig/ijcri-1053407201534-richtig.pdf

Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood:  http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2015/6/ehp.1408577.acco.pdf

Non-Smoker Exposure to Secondhand Cannabis Smoke. I. Urine Screening and Confirmation Results:   http://jat.oxfordjournals.org/content/39/1/1.short

Et les risques pour la santé de toute source de fûmée: https://vosrisques.wordpress.com/2015/07/10/la-fumee-tue-point/