ShiningPlain

has anybody ever smoked any of these?

Ben Stiller is being lined up to star in a new Ghostbusters movie. The comic actor is wanted by movie bosses to appear in the long-awaited third instalment of the popular '80s series by the film's director Harold Ramis.Ramis admits he is keen for Stiller to join Dan Aykroyd and Rick Moranis, who both starred in the original movies opposite Bill Murray, in the sequel Ghostbusters In Hell because he is a "huge fan" of his work.Aykroyd is also writing the script for the film which will see the paranormal investigators transported to a parallel dimension from New York. environments. But what worked so well about the first two films was how it was all so mundane."When the Ghostbusters step out of this portal, it looks just like New York but it's hell. No cars are moving and all the drivers are swearing at each other in different foreign languages. All the worst things about modern urban life - just magnified."It is not yet known if Murray will reprise his role as Dr Peter Venkman in the new movie or whether Sigourney Weaver will appear again as his love interest, Dana Barrett. Full article: http://www.tonight.co.za/index.php?fArticleId=2985700

happy now?

you never know. and i wasn't talking about them anyway.

good job on proving me wrong about the study there.

well thanks master civil. i'm really glad that you took the time to make that very illustrated reply. and no they weren't... those were different questions. and if the full study was so referred, how come i didn't see you referring it? could it be that all you ever told me to do was re-read the study?!

nah i haven't mescalito. and i agree in a way when you say that study's mean shit... all of the tokers i know that don't have psychosis have had a good upbringing, and don't appear to have that fucked up gene. all of the stoners i know that do have psychosis haven't had a good upbringing, and/or have that fucked up gene.

oh well now i've finally bloody seen the full study! Limitations of the study It was not possible to perform an adjusted analysis of the effects of amphetamines, cocaine, and opiates, mainly because of the small number of drivers positive for these substances. This highlight, however, that these drugs are not a major issue in France at the moment (2003). Psychoactive medical drugs were only sought in the case of positive blood testing. No further study of this confounding effect was possible. good. Methods Study population and drug detection process We included all fatal crashes resulting in immediate death (including pedestrian fatalities) in the study. All the drivers involved were taken as soon as possible to the hospital, under the control of the police, for compulsory urine testing to detect four major drug families (cannabis, amphetamines, opiates, and cocaine). If the test was positive or impossible a blood sample was taken. This information was associated with the blood alcohol concentration in the police reports. These reports provided 10 748 drivers who had had full tests for drugs and alcohol. We considered urinary screening for drugs as positive above a concentration of 1000 ng/ml of urine for amphetamines, 300 ng/ml for cocaine and opiates, and 50 ng/ml of acid tetrahydrocannabinol for cannabis.We considered blood tests for drugs (using gas chromatography-mass spectrometry) positive above a concentration of 50 ng/ml for amphetamines and cocaine, 20 ng/ml for opiates, and 1 ng/ml of 9 tetrahydrocannabinol for cannabis. We considered drivers negative if their urine tests were negative or their blood concentrations below these thresholds. However, during the analyses of dose and effect, we no longer considered non-null below threshold concentrations as “negative.” not so good. The particular problem with cannabis is that it stays in a person's system for up to 30 hours but its effects wear off within a few hours. http://cannabisnews.com/news/thread6717.shtml

spin doctors. amulte - i assume it's a good assumption then. you degrade me by always stating the obvious like i'm blind to it, even if i've wrote it myself. you haven't proved that they're inconclusive facts. you don't know what the people that lie about it have to gain?! well keeping it illegal of course! keeping people away from the best medicine for mind, body, and soul; and possibly making more money from keeping masses of people wanting materialism instead of enlightenment. torsten - you're just happy with the mystery because you already have your beliefs. i on the otherhand need solid facts. okay, now i understand that there were passengers in the cars. great. but guess what, the article didn't mention it! it doesn't say whether there were users of other drugs in the study... they failed to say that cannabis and alcohol were the main causes of "fatal crashes". i think speeding and tiredness would be the main causes of fatal crashes. and what are you saying, that the people that died with low-levels of thc in them don't have any excuses, but the straight people do? if so, what are all of them? it can't be too many things right? "i didn't want to run over the cat in the road."... "i wasn't looking."... etc. it doesn't tell us exactly, and that's what i'm talking about. it doesn't tell us how much more people were killed from the higher doses, and how much more damage was done to their cars than the others etc. it shouldn't be claiming that cannabis almost doubles the risk of fatal crashes then should it. and it appears that you're forgetting the tests that had thousands of members and were totally objective. what paragraph that says methods?? haven't i read the complete article or something? all they have at the link is the exact same thing you posted. i don't see it saying at all there were blood tests. all i see it saying is that there was a "blood concentration of cannabis". this can be picked up with urine tests, you see? it seems more important to publish a study that straight people can understand. and i haven't smoked any cannabis for 2 months! it isn't my fault that i have naturally shit short-term memory. i'm gonna take a memory course if that makes you feel better. i don't see why you should be so concerned though, because the only thing i forgot was that there were passengers in the cars. anyway, i think we're just trying to prove different points.

CHEMICALS STAY IN YOUR BODY FROM ONE HOUR TO A LIFETIME. The length of time any drug (illicit or prescribed) stays in your system will vary. The time depends on on your physiological makeup (e.g., your physical height, weight, your amount of body fat, your age, current state of health, whether or not you exercise mildly - aggressively - not at all.). One should consider whether or not one is currently undergoing any degree of stress (i.e., your "state of mind") at the time you ingest drugs can play a part as well. Other considerations include your "frequency" of use (1x per day? 3 - 5x per day?), the "quantity" of drug you used each time, and the "length of time" (days? weeks? months?) of your consistent drug-use prior to your drug test. Even the quality ("potency") of the drug you ingest determines "how long" the drug is detectable in your system when your urine is analyzed (tested) at the lab. Amount and Frequency of Use: Single, isolated, small doses are generally detectable at a lower boundary. Chronic and long-term use typically result in detection periods near or at the upper boundary. http://www.alwaystestclean.com/how_long.htm HOW DRUG TESTS WORK. Basically there is little difference between a blood drug test, a urine drug test or a saliva drug test. The tests all look for very small concentrations of contaminates, called metabolites, that can be used to determine which specific products have been used. The body naturally stores metabolites in the fatty cells and fast growing cells in your body. These metabolites leach out into the blood over time and are expelled mostly through the urinary tract. Metabolites stay in the fat for different periods of time causing you to fail a drug test many weeks or months in the future. Your fat content, activity level and your metabolism all have a major impact on how long chemicals can be detected in your system. Being your hair is a fast growing tissue it also stores metabolites. This is why a hair follicle drug test can detect metabolites for an extended period of time. Trace amounts of drug metabolites become entrapped in the core of the hair as it grows out from the body. These metabolite residues cannot be washed, bleached or flushed out of the hair follicles and are stable over a long period of time. An analysis of the hair fiber will produce an accurate drug history for about 90 - 120 days. It takes approximately 5 days for drugs to show up in a person's hair. As a side note, any hair can be used for a hair follicle test, This means under arm hair or even pubic hair. Shaving your head is not effective. Root Clean will cause you to pass your drug test for up to 8 hours after use. Companies mostly test for drugs in the urine and not the blood because the urine test is much cheaper with similar accuracy. Saliva drug tests are very cheap and less reliable so its use if somewhat limited. Hair follicle tests are the most accurate and enduring, but are very expensive and usually must be sent out to an independent laboratory for analysis. http://www.alwaystestclean.com/blood_drug_test.htm

i'm defensive because cannabis is the most beneficial plant in history, yet also the most attacked and lied about "thing" in history. that aswell as the fact that people such as torsten keep putting this study before my experiences and facts, yet never proving that the study is correct; or that my experiences or facts are incorrect. EVERYONE, re-read this study... now, do you really believe it proves that cannabis almost doubles the risk of fatal crashes? i don't want to sound cynical or something, but i just honestly, unbiasedly can't see that it proves cannabis doubles the risk of fatal crashes. this is what i've critically taken from it: - it doesn't say how many (if any) of the people in these fatal crashes died. "i mean i believe some of the people did, but that's not the point." - it doesn't say if all of the people with thc in them died from their fatal crashes. - it doesn't say whether the people with thc in them had any other drug (besides alcohol of course) in them. - it doesn't mention that most of the people that had fatal crashes were cannabis-free. - it doesn't tell us how much more of a danger there is when the thc levels rise. - it doesn't note that epidemiological studies are not always trustworthy. - it doesn't say how long after the crashes the drug tests occurred. - it doesn't actually say whether the drug tests were blood tests or not. ah well, at least it gave the percentage of people who had BOTH alcohol and cannabis in them. i give it credit for that. personally, if i was serious about warning people of driving dangers, i would try my best to prove that there was a danger.

wandjina - you call me a preacher, just for getting mad when y'all ignore new things that i've brought to the table... you say i'm preaching to the converted, yet you've seen me say that i don't think this is "the converted"... YOU say that i'm just barking propaganda, yet I'M the ignorant one?... you say that I don't appear to respect other people's opinions, yet you don't make any mention of your "friends"... you say that maturity isn't just about age, yet you've told me to come back in 5 years... alot of the rest of your post is hypocritical and purely opinoinated... and you think i'm instantly going to completely respect your opinion? EDIT: ahh, FUCK! i had this other part wrote out, but just lost it then. and god knows how?! anyway, because of that shitty turn of fate, this one is going to be shorter... every view on this subject can be looked at as a reality, but the most important "reality" (or view) is always going to be the one that takes all other views into account. and believe it or not, i have looked at this topic from numerous views. it may not appear so on the forum, but i honestly don't yet have a completely open and shut case on cannabis and driving. all i know is that me and all of my stoner friends are fine when driving high, and that i've not yet read one study which would make me believe otherwise. this is one of the reasons why i've been asking for some clarity on this study! i really want to know more. i've taken interest in the study, and i've publicly noted the facts of it... all i'm waiting for now is for you guys to publicly note or refute the facts i've posted; which could possibly discredit thes study. and seriouslly, if you want me to believe in this thing, you've got to give me some concrete evidence that its findings are right.

you're a total hypocrite that is full of assumptions. - deal with that! i really wish you and others would stop dissing me all of the time for doing the simplest things. why can't i post a couple of articles without people such as you giving me shit?? why can't i be honest about something without people such as you giving me shit?? why can't i post facts about something without people such as you giving me shit?? i wasn't posting them as a threat or anything, i was just posting them to help the discussion! and please stop degrading me by telling me to do things like watch bowling for columbine! yes i've seen bowling for columbine; yes it's filled with disinformation; and yes i know that america is filled with fear! of course i know that america is filled with fear!! god, you treat me like a fucking simpleton just because i noted some facts that could discredit the first article of the thread. you didn't attempt to discredit the facts or anything (jeez, you don't even appear to have noticed them), you just hopped onto the bandwagon of calling me an immature, whining pothead. ps - maybe you just don't understand my writing style. i'm not ALWAYS talking to you lot when i go off. alot of the time i'm just talking to the people which LIE about pot for their own gain. for example, my first post: so? just sounds like more propaganda to me. it doesn't say whether these people were experienced smokers or not.. neither does it say how they got tested. we all know that thc stays in the human body for around 30 days, right? so... and it has already been proven by various studies that cannabis can make you a safer driver. this honestly just sounds like the same old story to me. how many times have "they" (government scientsists and what have you) told us now that cannabis causes many road fatalities? and how many times have they proved this? NONE; right? finding thc in many bodies of car crash victims is not a clear indicator that cannabis is causing many car crashes... and guess what? it never will be! that is totally an attack on all of the people that have LIED about the link between cannabis and psychosis. it's not meant to be an attack on torsten.

^ propaganda. don't any of you think it sucks that you have to think like torsten in order to stay here? i mean, he's the only moderator right?

get off my dick.

haha. i guess there's just some people that can handle the truth, and some people that can't.

i've already said all of this!

get off my dick. it's all relevant.

torsten hasn't answered some very important questions i've asked about this study... it appears he'd (aswell as some of you) would rather just live in a world where these questions don't matter. it also appears that torsten is stubborn when it comes to different opinions in his threads.

The key research Panorama's "Cannabis: what teenagers need to know" explored the latest scientific research on the effects of cannabis on the human mind. In particular, the growing evidence of links between cannabis and psychotic illness in young people. What follows is a guide to the main theories and research in this field. Four hypotheses have been proposed about the relationship between cannabis use and mental health: * The first, the causal hypothesis, suggests that heavy cannabis use can cause mental disorders such as psychosis. * Second, the dormant hypothesis argues that cannabis use may precipitate a mental disorder that was previously dormant in individuals prone to mental health disorders. * Third, the common cause hypothesis states that mental illness and cannabis use may simply occur together as a result of common variables, such as unemployment, family difficulties and other drug use. * The fourth is the self-medication hypothesis, that people use cannabis after experiencing signs of a mental health disorder in order to alleviate symptoms. Until recently the consensus amongst the scientific community was that the fourth hypothesis which stated that people suffering from psychosis or schizophrenia used cannabis to alleviate some of the symptoms they were experiencing was the most likely explanation. However the new research is generating more interest in the first hypothesis; namely that cannabis use itself can cause psychosis. This research is based on studies where large numbers of people are followed through a process of questionnaires over ten to twenty years. The conclusions drawn from these statistical analyses have shown that there is an association between cannabis use by adolescents who are predisposed to mental health problems and later mental health problems. The publication of a Swedish study in 1987 was the first to suggest a link between cannabis and long-term mental health problems. The records of all the young men who had done national service in the Swedish army in 1969 and 1970 - 50,087 in total, representing about 97 per cent of the male population aged 18 to 20, were analysed. The research team then examined each man's medical history up to the mid-1980s. They found that those who had smoked cannabis before being called up were six times as likely to end up in hospital with schizophrenia as non-users. This, the team concluded, provided clear evidence that smoking cannabis was a risk factor for psychosis. However critics pointed out methodological flaws which severely undermined the conclusions drawn. However the findings led others to examine the link with new studies that were better designed to avoid the mistakes of the Swedish study. One of the new studies from New Zealand found that those who had smoked cannabis three times or more before the age of 15 were much more likely to suffer symptoms of schizophrenia by the time they were 26. The team, which included Professor Murray, concluded that there is a vulnerable minority of teenagers for whom cannabis is harmful. "We're not saying that cannabis is the major cause of schizophrenia but it's a risk factor." A re-analysis of an original Swedish study from the 1980s also found similar results. Last year Dutch researcher Prof Jim van Os and his team published the results of following a group of nearly 2500 14 to 24-year-olds living in and around Munich, Germany, over four years. After correcting for all the additional factors they could think of, they found that smoking cannabis as an adolescent moderately raised the risk of developing signs of psychosis later on, from 16 per cent to 25 per cent. However when they focused on individuals who were known to be susceptible to psychosis - those who were showing signs of disturbed thought processes by age 11 - they found a much stronger link. Susceptible individuals who avoided cannabis had a 25 per cent chance of developing psychosis. Susceptible individuals who smoked it had a 50 per cent risk. And the more cannabis they smoked, and the earlier they smoked it, the worse the outcome. Criticisms of the link theory The big criticism of research on any link between cannabis and psychosis has been that its not clear whether the symptoms are caused by cannabis use or whether people who are likely to develop psychotic symptoms happen also to be more likely to be attracted to cannabis. David Fergusson (New Zealand - Christchurch 25-year study group) took all confounding factors into account and found: a clear increase in rates of psychotic symptoms after the start of regular use, with daily users of cannabis having rates that were over 150% those of non users. His findings clearly show cause and effect from cannabis to psychosis not other way round. However, critics of the new research point out that other factors which can also cause mental health issues cannot always be adequately accounted for and that they may serve to lessen the power of the association between cannabis and mental health that these studies revealed. They also point out that such epidemiological studies are notoriously bad at proving cause and effect. Apart from the problem of identifying all the potential other factors the critics say that many of the conclusions are based on very small statistical differences. They point to one of the studies, which followed over 700 people, where the number of people who had smoked cannabis three times by the age of 15 was only 29. Of those 29 only three went on to develop psychosis. The critics also point out that if cannabis really was causing schizophrenia then there should bean increased incidence to match the rise in teenage consumption of cannabis. However in 2003 researchers at the University of New South Wales in Sydney found that, despite a steep rise in cannabis use among Australian teenagers over the past 30 years, there had been no rise in the prevalence of schizophrenia. However most recently researchers involved in the New Zealand study have found that there might genetic factors at work as well. The team led by Dr Avshalom Caspi, re-analysed the data, this time looking at the genetic makeup of their subjects. They investigated a gene called COMT, is involved with the breaking down of key brain chemical called dopamine. Dopamine is thought to be involved in psychosis- people with psychosis have increased dopamine in one area of the brain COMT comes in two forms., The team found that in people with two copies of the "normal" version of COMT, smoking cannabis had little effect on their mental health. In people with one normal and one "bad" form of the gene, smoking cannabis slightly increased their risk of psychosis. But for people with two copies of the bad gene, smoking cannabis as a teenager increased their likelihood of developing psychosis by a factor of 10. According to Professor Murray, 25% of the UK population carry two 'bad' copies of the COMT gene Featured Research Professor Robin Murray Research published in the British Journal of Psychiatry (2004) 181, p110 - 117 Professor Murray is Head of Psychiatry at the Institute of Psychiatry. His research examines the evidence that cannabis causes psychosis using established criteria of causality. His team identified five studies that included a well-defined sample drawn from population-based registers or cohorts and used prospective measures of cannabis use and adult psychosis His team's findings were: * On an individual level, cannabis use confers an overall twofold increase in the relative risk factor for later schizophrenia. * At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. * Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis. His team concluded that cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths but also felt that further research is needed to understand the mechanisms by which cannabis causes psychosis Professor Yasmin Hurd Her research investigates the close relationship between psychiatric disorders and drug abuse. As drug abuse is 4-7 times more common in persons with depression or schizophrenic syndromes and 35-80% of drug abusers will suffer from psychiatric disorders during their lifetime. The strong association between drug abuse and psychiatric disorders suggests similar underlying neurobiological impairments. Her research team is focused on the systematic study of human brains from subjects with drug abuse (stimulants and opiates) and psychiatric disorders. Their goal is to identify and map specific genes in which regulate emotional functions, and are thereby relevant to the disorders of interest. Additional studies carried out by this group are designed to assess how drugs affect the development of the human brain during the foetal stage, which may later lead to psychiatric problems. As complement to studies of the human brain, animal models are used in this research group to simultaneously study changes in neurotransmitter levels (e.g., dopamine) during drug self-administration behaviour. Possible neural targets for the development of future treatments against depression and drug dependence have been identified and published by the research group. (Professor Hurd's results are unpublished and have not been replicated at this time). Further Reading Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyl transferase gene: longitudinal evidence of a gene X environment interaction. Caspi et al., Biological Psychiatry. 2005 May 15; 57(10) p1117-27 Arseneault L, Cannon M, Poulton R, et al, 2002, Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study, BMJ 2002; 325:1212 -1213 Arseneault L, Cannon M, Witton J, Murray R M, 2004, Causal association between cannabis and psychosis: examination of the evidence, Br. J. Psychiatry, 2004; 184: 110 - 117 Hall W, Solowij N, 1998, Adverse effects of cannabis, Lancet 1998; 352:1611-16 van Os J, Bak M, Hanssen M, Bijl R V, de Graaf R, Verdoux H, 2002, Cannabis Use and Psychosis: A Longitudinal Population-based Study, Am. J. Epidemiol. 2002; 156: 319 - 327 David Ferguson and John Horwood "Cannabis Use and Dependence in a New Zealand Birth Cohort" New Zealand Medical Journal 12/5/2000: 113 (1109): 1506-1508 Macleod J, Oakes R, Copello A, Crome I, Egger M, Hickman M, Oppenkowski T, Stokes-Lampard H, Davey Smith G. "Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies". Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G (2002) Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ 325: 1199 Andreasson S, Allebeck P, Engstrom A, Rydberg U (1987) Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet 2:1483-1486 http://news.bbc.co.uk/2/hi/programmes/panorama/4109360.stm Psychosis, Hype And Baloney By Bruce Mirken and Mitch Earleywine, AlterNet. Posted March 7, 2005. Although the mainstream media is eating it up, a new study claiming a link between marijuana use and psychosis should be approached with great caution. As the month began, the worldwide press jumped all over a study in the March issue of the journal Addiction purporting to show a causal link between marijuana use and psychosis. "Drug Doubles Mental Health Risk," the BBC reported. "Marijuana Increases Risk of Psychosis," the Washington Times chimed in. Such purported links have lately become the darling of prohibitionists, but a close look at the new study reveals gaping holes unmentioned in those definitive-sounding headlines. Before we look at the study itself, let's consider some basics: If X causes Y, it's reasonable to expect a huge increase in X to cause at least a modest increase in Y, but this has not been the case with marijuana and psychosis. Private and government surveys have documented a massive increase in marijuana use, particularly by young people, during the 1960s and '70s, but no corresponding increase in psychosis was ever reported. This strongly suggests that if marijuana use plays any role in triggering psychosis, that effect is weak, rare, or both. For this reason, researchers should approach "proof" that marijuana causes serious mental illness with great caution. The researchers in this case, a New Zealand team led by David M. Fergusson of the Christchurch School of Medicine and Health Sciences, seem to have done just the reverse. Fergusson's team looked at a group of 1,265 New Zealand kids who were followed from birth to age 25 and assessed at various points along the way for a variety of physical, mental and social problems and issues. At ages 18, 21 and 25 they were assessed for both marijuana use and supposed psychotic symptoms. Having found a correlation with daily users reporting the highest frequency of psychotic symptoms, they then applied a series of mathematical models. These models are designed to adjust for possible variables that might confound the results and to assess whether the marijuana use caused the symptoms or vice versa. Whatever model was applied, the correlation held up. But the reported "growing evidence" that "regular use of cannabis may increase risks of psychosis" depends completely on the validity of the underlying data, and those data raise some screamingly obvious questions. Psychotic symptoms were measured using 10 items from something called Symptom Checklist 90. Participants were asked if they had certain ideas, feelings or beliefs that commonly accompany psychotic states. The researchers did not look at actual diagnoses, and the symptom checklist is not identical to the formal diagnostic criteria listed in the DSM-IV manual. Perhaps most important, they only used 10 "representative" items from a much larger questionnaire. These 10 items focus heavily on paranoid thoughts or feelings, such as "feeling other people cannot be trusted," "feeling you are being watched or talked about by others," "having ideas or beliefs that others do not share." This presents a big methodological problem, because it is well known that paranoid feelings are a fairly common effect of being high on marijuana. But the article gives no indication that respondents were asked to distinguish between feelings experienced while high and feelings experienced at other times. Thus, we are left with no indication at all as to whether these supposed psychotic symptoms are long-term effects or simply the normal, passing effects of marijuana intoxication. While it's possible the researchers had these data and didn't see a need to report them, the failure to do so is downright bizarre. It's like reporting that people who go to bars are more erratic drivers than people who don't, without bothering to look at whether they'd been drinking at the time their driving skills were assessed. Even if these were long-term effects, the researchers seem not to have considered that what might be an indication of psychosis in other circumstances could be an entirely normal reaction for people who use marijuana. Consider: Someone using a substance that is both illegal and socially frowned-upon almost by definition has "ideas or beliefs that others do not share." This is not a sign of mental illness. It's a sign of a rational person realistically assessing his or her situation. The same goes for "feeling other people cannot be trusted." Just ask Robin Prosser, the Montana medical marijuana patient arrested last summer on possession charges by the cops who came to save her life after she'd attempted suicide because she was in unbearable pain after running out of medicine. Fergusson reports very little raw data, so we don't know which symptoms came up most often, or whether the differences in average levels of symptoms between users and non-users came from a few people having a lot of symptoms or a lot of people having a couple symptoms. The heavy-user group, with the highest levels of supposed psychosis, reported an average of less than two symptoms each. So it is entirely possible that the entire case for marijuana "causing" psychosis is based on marijuana smokers having the completely reasonable feelings that they have beliefs different from mainstream society and thus should be a tad suspicious of others. "Proof" that marijuana makes you psychotic? No. Not even close. But don't expect the mainstream media to figure this out. Bruce Mirken is communications director for the Marijuana Policy Project. Mitch Earleywine, Ph.D., is associate professor of psychology at the University of Southern California and author of Understanding Marijuana (Oxford University Press, 2002). http://www.alternet.org/drugreporter/21436/

well you don't seem to know the core principles of it, so why should i?

well if you've been reading my posts, you would know that i always recommend moderation. i was talking about smoking for a life-time, but under a "routine of moderation."

Trained wasps could someday replace dogs for sniffing out drugs, bombs and bodies. Scientists say a species of non-stinging wasps can be trained in only five minutes and are just as sensitive to odors as man's best friend, which can require up to six months of training at a cost of about $15,000 per dog. With the use of a handheld device that contains the wasps but allows them to do their work, researchers have been able to use the insects to detect target odors such as a toxin that grows on corn and peanuts, and a chemical used in certain explosives."There's a tremendous need for a very flexible and mobile chemical detector," said U.S. Department of Agriculture entomologist Joe Lewis, who has been studying wasps since the 1960s. "Our best devices that we have currently are very cumbersome, expensive and highly fragile." The "Wasp Hound" research by Lewis and University of Georgia agricultural engineer Glen Rains is part of a larger government project to determine if insects and even reptiles or crustaceans could be recruited for defense work. That project has already resulted in scientists refining the use of bees as land-mine detectors. Through the years, Lewis and a USDA colleague, J.H. Tumlinson, discovered that a tiny, predatory wasp known as microplitis croceipes had relied on odors to locate nectar for food and hosts for its eggs caterpillars that damage crops. full article - http://abcnews.go.com/Technology/wireStory?id=1369292 what the hell? ha ha. pretty nifty...

The risk of being responsible for a fatal crash increased as the blood concentration of cannabis increased (known as a dose effect). The odds increased from 1.9 at a concentration of 0-1 ng/ml to 3.1 at or above 5 ng/ml (?). These effects were adjusted for alcohol and remained significant when also adjusted for other factors. in my view, this just means that most of the cannabis smokers who died (or what the hell ever!) had a thc concentration of above 5 ng/ml... and that's it. that's all she wrote. it doesn't say what the exact statistics are, neither does it tell us whether it's more dangerous to have 5 ng/ml of thc, or none..... i mean sure they've said it, but they haven't shown it. this study honestly makes no sense to me.

maybe you want to re-read my posts???? this study appears to prove jack shit. explain the whole 7% thing to me if you can. it looks to me that over 50% of the people that had "fatal" crashes were "sober".