From ???@??? Sat Oct 19 04:46:48 1996 Received: from gulik.dymaxion.edu(root@line222.nwm.mindlink.net [204.191.202.222]) by gold.interlog.com(8.7.6/8.6.10) with ESMTP id RAA28142 for <iorfida@interlog.com>;Thu, 17 Oct 1996 17:38:43 -0400 (EDT) From: ccletters@hempbc.com Received:from hempbc.com (root@localhost [127.0.0.1]) by gulik.dymaxion.edu (8.7.5/8.6.9)with SMTP id OAA00515 for ccletters; Thu, 17 Oct 1996 14:35:48 -0700 Date:Thu, 17 Oct 1996 14:35:48 -0700 Message-Id: <199610172135.OAA00515@gulik.dymaxion.edu>Reply-To: ai256@chebucto.ns.ca Subject: CC#03 First LTE Campaign VancouverHarm Reduction Rally X-UIDL: 38089601294c29a9136b83bdc25ddbf3
The Vancouver Harm Reduction protest event will be the subject of ourfirst letter campaign. It is detailed in the following announcement, whichyou all should have received from CClist last weekend. Please refer tothe next post to CCletters, titled "First LTE Campaign Info:...",before writing, as in that post I have outlined the nature of this letterwriting effort. I've given us all lots of time for this - almost a week- so relax and take your time. Chris ---------------------------------------------------------------------------
The following is excerpted from a full page ad that will soon appearin Vancouver weekly newspaper "Terminal City". The full ad isat least eight times as long and goes into the history of the drug warand the current situation with the Controlled Drugs and Substances Act.For more info email growpotkin@hempbc.com, or call (604) 253-6357
* Harm Reduction Club Free Market Tam-Tam
Free speech. Free music. Cheap pot.
SATURDAY, OCTOBER 19, 3PM (sharp) Grandview Park (William & CommercialDrive) For more info call 253-6357
Pot will be openly sold, but on and after the 19th, and only to clubmembers.
- In 1993, the hemp movement began to remove the shame from "possession"by holding rallies where many people could commit that crime, shamelessly.The government's reaction was to back off.
Well, it's now time to do the same thing with "trafficking".The Harm Reduction Club is an experiment. Right now it's just a personwho knows he has little to lose by risking five years less a day for trafficking,rather than letting the shame remain unchallenged, thereby risking a lifetimein a Singapore-style police state - or perhaps even an environmental nightmare.
Let's get together and remove the last remaining bits of shame associatedwith marijuana, using the profits from the sale of good organic herb to:
1) provide free legal services 2) fund education projects to teach peoplesmarter smoking strategies 3) provide medicinal and nutritional hemp information4) promote soft, natural drugs over hard, synthetic ones 5) teach druglessmethods of getting high 6) create an atmosphere of safety and toleranceto enjoy marijuana in 7) educate the public about the dangers of prohibition.
These are the seven goals of the Club.
Any money collected above a living wage will be put towards the sevengoals of the club. In addition, in exchange for cooperation from the government,we will donate 10% of all earnings to cash strapped charities - the needleexchange and the medical marijuana buyers club, for example.
But if the government continues to arrest us for something that theythemselves have indicated is a health issue, well then that 10% will goto legal defense - possession, trafficking, causing a disturbance, resistingarrest, toplessness, whatever - you're covered.
That's right, you heard correctly, free legal advice and defense, asafer-smarter-smoking guide and a gram sized joint for just 20 bucks. When'sthe next time you're gonna hear an offer like that?
Join the club.
The club will kick off it's illegal-yet-noble activities at the "FreeMarket Tam Tam" on Saturday, October 19th, at 3pm sharp, in GrandviewPark on William Street and Commercial Drive.
There will be an open microphone, and the club invites anyone who disagreeswith legalization to come out and give reasons why, and see if it can withstandcriticism (and see if the criticism can withstand criticism.... it shouldn'ttake too long to exhaust all the arguments to prohibition and get to thebottom of this mess).
If it turns out that someone possesses a compelling reason why we shouldn'tsell pot to anyone over the age of thirteen who a) signs a pledge not tooperate heavy machinery while impaired on our marijuana, and b) agreesto read our "safer-smarter-smoking" kit - hey, we'll bow to reason.We'll take our buds and split. The shame of being a pot "pusher"will remain. Big Brother will have won the day.
About the rally: Interstellar Rootcellar, SKAB, Wes and a number ofother musicians will perform some acoustic sets, and the club will smoke-upany other musicians or drummers who perform that day. We will also passthe joint to any videographers who hang out all day, ready to preserveand distribute the magic moment if and when the cops decide to bust us.
Bring Cameras, food, pot etc. to sell (this is, after all, a free market)but leave your aggression, hard drugs (especially alcohol) and shame athome. Be prepared to hug anyone who is getting arrested without reason- we may be stoned, but we're not going down so easy.
"Washing one's hands of the conflict between the powerful and thepowerless means to side with the powerful, not to be neutral." -PauloFriere
A new world is growing inside the old one.
The club could end up becoming the path to freedom for many people,economically and politically. The medical marijuana buyers club in SanFrancisco had 90 employees - four people got hired full time just to weighout buds. The Vancouver Harm Reduction Club itself is non-profit and collectivelyrun.
The government is really to blame for this enterprise. They denied usany legal mode of evolution nor justification for a lack of evolution.If they use force, it will be because they lack reason. If the police getcaught on film using force without reason, prohibition is done for. Ifthey leave us alone, we'll out-grow the synthetics. The only way they canwin is to intimidate people away from joining up.
The Harm Reduction Club non-transaction info line is 253-6357. Pot willopenly be sold, but only on/after the 19th and only to club members.
Almost everybody knows the drugwar is a joke. The real crime is thatgood, potent, organic bud isn't easily available from a reliable, responsiblesource. How many times in your life will you again be given the opportunityto party, dance, sing, smoke pot and hug people in order to fight the powers-that-beand save the economy and ecology?
See you on the 19th.
*
-- Dana Larsen (muggles@hempbc.com) Editor, Cannabis Canada, "Canada'sNational Magazine of Marijuana & Hemp" Visit Cannabis Canada onlineat http://www.hempbc.com
Subscribe to Cannabis Canada Magazine! Suite 405, 21 Water St., Vancouver,BC, CANADA, V6B 1A1 Call Toll Free for more information: 1-800-330-HEMP
Join the Cannabis Canada News and Information Email List! Send an emailto cclist@hempbc.com with a subject of "subscribe"
From ???@??? Sat Oct 19 04:46:51 1996 Received: from gulik.dymaxion.edu(root@line222.nwm.mindlink.net [204.191.202.222]) by gold.interlog.com(8.7.6/8.6.10) with ESMTP id RAA04792 for <iorfida@interlog.com>;Thu, 17 Oct 1996 17:52:42 -0400 (EDT) From: ccletters@hempbc.com Received:from hempbc.com (root@localhost [127.0.0.1]) by gulik.dymaxion.edu (8.7.5/8.6.9)with SMTP id OAA00669 for ccletters; Thu, 17 Oct 1996 14:50:11 -0700 Date:Thu, 17 Oct 1996 14:50:11 -0700 Message-Id: <199610172150.OAA00669@gulik.dymaxion.edu>Reply-To: ai256@chebucto.ns.ca Subject: CC#04 First LTE campaign info:Vancouver Harm Reduction Rally (fwd) X-UIDL: d6c4a6d16b8a1fd82e85b45ac89c90dd
Welcome to Cannabis Canada's CCletters! For our first letter (LTE) campaign,this event is perfect. It will allow all of us to write about the War onDrugs in general, instead of limiting our focus to a single misrepresentationin a single article, with a single editor receiving the brunt of our displeasure.It will allow us to prepare before hand, in stages, and let first timewriters refine their prose over a couple of days, instead of a couple ofhours. It will also, hopefully, result in everyone having a generic letterof their distilled disgust about the WoD, complete with damning evidence,to store for future use when time does not allow them to fully take partin a LTE campaign they wish to have an impact upon. For this campaign,read over the post on the Vancouver Harm Reduction Rally scheduled forSaturday, Oct. 19 (I've titled it "First LTE campaign subject:...").The letter format that I suggest for new writers is a brief paragraph specificto the rally as an intro to your letter, and then around 200ish words ofwhy YOU think the prohibition of some substances is insane, immoral, evil,wasteful, destructive, nonsense, etc etc etc. Start the letter with a variationof "RE: your coverage of the Harm Reduction Rally last saturday etc."Please read my post entitled "Brief LTE Writers Guide" beforeyou start. If you don't want to clip that post, a version of it can befound on Mark Greer's MAP homepage, or Matt Elrod's homepage sometime nextweek. If you wish, you can wait until Friday to write, when I will posta fact/quote/cite page of relevant information that Matt Elrod and I willput together. However, for first time writers I suggest you get all youhave to say on the subject out of your system, and then edit it down toaround 200 to 250 words. Once you have distilled the essence of your ownviews on the subject, use the facts sheet to replace portions of your ownprose with cites and quotes to the same effect (making sure not to thensay the same thing in their own words), or just to add a damning quoteor two near the start of your letter. Don't be afraid to write too much,as often the best prose comes out of a long session where a sense of flowdevelops. The trick is to go back later and cut all the best prose out,and paste it onto a new page which then becomes your letter. This processwill hopefully leave most writers between 200-300 words, which they cansend to me over the weekend for feedback (I'll post my new email addresson Friday). I say 300 words knowing that it is a little long, but for thisLTE campaign some leeway on length seems appropriate. Remember though,the closer to 200 words your letter is, the more competitive it is forgetting published. Sunday and Monday, as press reports from Dana and Mattstart arriving, we can collect all the email addresses, and have each writereither send their letter off, or respond to the good, bad or ugly coverageof the event by modifying their letter. Hopefully some writers will takethe time to debunk any cliched pot myths that get repeated in a specificpaper's/TV station's coverage, or even just tailor the intro of their letterto the specific coverage they are responding to (ie. I applaud or am dismayedby your coverage). If you are looking for ideas for your first LTE anddon't want to wait until Friday, visit Matt's homepage at "www.islandnet.com/~creator/mattalk.htm"and look at some of the links. The Lindesmith center link should have thedefinitive debunking of Marijuana Myths, and that's always a good read.
If this seems a little complicated, don't worry. Future weekly LTE campaignswill consist of the article to be responded to, a post of relevant factualinfo, and that will be all. For this campaign I wanted to ease anyone unsureof their abilities into the process. Whether or not you use my addressor "letters@drcnet.org" for editing, please cc me a single copyof all letters written and sent in response to CCletters, so that Danaand I have a measure of the impact of the list. And please, this is CANNABISCanada's letters list. Though the prohibition of any substance is, in purelyphilosophical terms, difficult to defend, let's keep our focus on cannabisfor now. However, though I've seen this subject debated ad nauseum on DRCtalk,I will suggest that if you disagree with me, Matt is looking for a gooddebate on his MATTALK maillist, and you can discuss it there. For thoseof you not familiar with Mattalk, you should be subscribed to that listif you can handle 20-30 posts a day of mostly Canadian news on prohibition.Surf to Matt's homepage if you want to know more. Good luck on your letters,and don't worry if it's hard going at first. I've consciously given youalmost a week's notice, and I think you'll find that if you work at theletter a couple of days in a row and read my style guide, you'll have noproblems getting published. If nothing else, look at the letters publishedin any daily newspaper to see what style of writing DOES get published,and pattern your work after that.
Chris
-------------------------------------------------------------------------> Visit Cannabis Canada online at http://www.hempbc.com > > Subscribeto Cannabis Canada Magazine! > Suite 405, 21 Water St., Vancouver, BC,CANADA, V6B 1A1 > Call Toll Free for more information: 1-800-330-HEMP> > Join the Cannabis Canada News and Information Email List! >Send an email to cclist@hempbc.com with a subject of "subscribe">
From ???@??? Sat Oct 19 04:46:53 1996 Received: from gulik.dymaxion.edu(root@line222.nwm.mindlink.net [204.191.202.222]) by gold.interlog.com(8.7.6/8.6.10) with ESMTP id SAA09324 for <iorfida@interlog.com>;Thu, 17 Oct 1996 18:04:37 -0400 (EDT) From: ccletters@hempbc.com Received:from hempbc.com (root@localhost [127.0.0.1]) by gulik.dymaxion.edu (8.7.5/8.6.9)with SMTP id PAA00784 for ccletters; Thu, 17 Oct 1996 15:01:38 -0700 Date:Thu, 17 Oct 1996 15:01:38 -0700 Message-Id: <199610172201.PAA00784@gulik.dymaxion.edu>Reply-To: ai256@chebucto.ns.ca Subject: CC#05 A Brief Style Guide for LTEWriting X-UIDL: 45fed50b73c5aaa588ad51dfb774ccf2
All sentences should have simple structures and be brief. If a sentencecan be easily written as two sentences, it should be.
ALWAYS use the spell checker, and do a visual check for the to/too andfrom/form typos the spell checker will miss.
Letters should be no more than 1 to 1 1/2 pages long, and the shorterthe better. This length restriction can be stretched for magazines or papersthat you know agree with your POV, but with our efforts the latter willbe rare.
Paragraphs are usually only one or two sentences long, with maybe onethree sentence paragraph per full page. Look at any front page news story,and you'll see exactly what I mean.
The lead sentence should not be more than 70 words long, should containthe name of the article or letter you are responding to, and a positionon that article. If you come up with a witty one liner, you can use itas your lead, as that is where it will have a chance to catch an editor'seye. Remember that editors are themselves writers who appreciate a cleveruse of words. If you do this, then include the name of the article (orsubject) you are responding to either as a title (re. blah blah) or inthe second sentence/paragraph.
A quote or cite soon after the lead sentence is a good idea. A citedfact or quote will give your opinion a broader context, and most journalist/editorswould publish your letter for the cite alone if they are impressed by itspertinence to the subject. Buckley's always good for a quote, and any scientificstudies that are relevant could be used as well.
If you are using cites to back yourself up, put them BEFORE your ownopinion. I've seen too many letters go by that have a good intro, thena few obvious pro-drug opinions, and then a good cite. You want the editorto see the cite and then the bulk of your opinions, as they are scanningdozens of letters and are quick to stop reading anything that strikes themas from the fringe. Also, don't waste words restating what you've cited.Draw a conclusion or apply it to the subject of your letter, but don'trestate it. Redundancy of any sort will invite the editor to move on tothe next letter, or worse, edit lines out of your letter.
If you find yourself writing way too much prose, don't worry. You'llnotice that most journalists sacrifice flow in order to put the most importantpoint first, second-most second, etc. Editors won't even notice if youtake what you think is your best line/paragraph and tack it in first, takeyour second best line and tack it in next, etc, until you hit 200 words.Use the cut and paste capabilities of your word processor, and don't worryif you leave a lot of prose out of this letter. There is always the nextone. Also, if you are using more than one quote, cut and paste them inwith an opinion, paraphrase, or other prose between them. Two or more separatequotes in a row does not look good. If a quote is really long, considercutting out part of it, or quoting half and then paraphrasing the rest(He also said....).
In general: the ideal letter is three to six short paragraphs long,with a short, witty lead sentence (that is usually a stand alone paragraph),a good quote up high in the prose, and some clear, pointed opinions tofinish. Be concise, and use tight, no nonsense prose without colloquialisms.If you quote or closely paraphrase the points you are responding to inyour letter, it makes your points look a little clearer. Flip to the editorialpage of whatever newspaper you are responding to, and use the letters thatpaper's editor[s] choose to publish as a template for your own.
Try to avoid using phrases coined by WoD propaganda: People are not"drug abusers," they are "people who choose to use currentlyprohibited substances" or "users of recreational drugs otherthan caffeine, nicotine, or alcohol" or "people who party withsubstances less harmful than alcohol" or even just "cannabissmokers." I don't want every writer quoting these, so try to makeup your own. Every time you find yourself calling pot "drugs"and pot smokers "drug users," realize that you are attachingthe baggage of a lot of WoD propaganda to your prose, and try to writearound it creatively.
An Incomplete List of points worth touching on in your first letter:(More info will follow on these subjects Friday)
The Dutch success History of Alcohol prohibition, parallels to the present(Crime and Corruption) The Frankfurt resolution Medical Uses, present andhistorical Hemp as a commercial crop The impact on courts and prisons Thewaste of peoples lives by imprisonment for non-violent, consensual "crimes"The disaster of American policy The Canadian Senates pro decrim pronouncementsBuckley/National review support for decrim Lancet support for medical usesSTATISTICS that support decrim The history of marijuana prohibition (thoughdo try to soft peddle the more extreme of Jack Herer's Emperor conspiracythemes, as some doubt has been cast on some of them. Still, Racism andthe WoD still flies, as well as hypocritical historic support (not to mentionmillions in lobbying funds) for cannabis prohibition from the alcohol,tobacco, and pharmaceutical industries).
Outside of mentioning the fact that 70% of Canadians think cannabisshould be decriminalized, and the fact that there are no deaths attributableto cannabis consumption ever, I think you should just pick a few of theabove and allude to them. If you try to mention more than a couple, itwill really make your letter either too long, or too much like a grocerylist. And if you are already an experienced writer DO YOUR OWN THING. Therewill be enough writers influenced by my posts to cause some suspiciousoverlap, so it is actually a good thing to completely ignore everythingI say;) Chris
ps. I was a journalist before my disability and chronic pain syndrome,and I've actually had to edit LTE's as part of my job at one paper I workedat. MAKE THEM BRIEF. It works.
pps. If you want to do a little research on your own go to: www.islandnet.com/~creator/mattalk.htmThere are links there to Cannabis Canada, and loads of other good placesto go in order to make your writing as informed as possible.
From ???@??? Sat Oct 19 04:46:56 1996 Received: from gulik.dymaxion.edu(root@line027.nwm.mindlink.net [204.191.202.27]) by gold.interlog.com (8.7.6/8.6.10)with ESMTP id AAA28913 for <iorfida@interlog.com>; Sat, 19 Oct 199600:18:38 -0400 (EDT) From: ccletters@hempbc.com Received: from hempbc.com(root@localhost [127.0.0.1]) by gulik.dymaxion.edu (8.7.5/8.6.9) with SMTPid UAA00651 for ccletters; Fri, 18 Oct 1996 20:50:42 -0700 Date: Fri, 18Oct 1996 20:50:42 -0700 Message-Id: <199610190350.UAA00651@gulik.dymaxion.edu>Reply-To: ai256@chebucto.ns.ca Subject: CC#06 War on Drugs and crime rateX-UIDL: 1c4a5aa80a2aa990f136cc3e6d54702f
The title and cite for the following study is a few pages in. Quotethe study, not the abstract presented in the next few pages. Chris [Thankyou Matt for posting this and the Marijuana Myths for our use]
THE WAR ON DRUGS INCREASES VIOLENT CRIME, NEW STUDY REVEALS . DIVERSIONOF CRIMINAL JUSTICE RESOURCES MAKES CITIZENS LESS SAFE.
OAKLAND, CA - Despite high hopes that America's "war on drugs"would reduce the rate of serious nondrug crime - assault, homicide, rape,robbery, and the like - the drug war has diverted scarce resources awayfrom fighting such crime, putting the lives and property of citizens atgreater risk, according to a new study released today by the IndependentInstitute. In Illicit Drugs and Crime, economists Bruce Benson and DavidRasmussen compare crime trends in Kansas (whose enforcement of drug lawslagged behind national trends) with trends in other states. They concludethat Kansans - and other states' residents - were relatively safer fromnondrug violent crime before escalating drug law enforcement. "Whena decision is made to wage a 'war on drugs,' other things that criminaljustice resources might do have to be sacrificed. Getting tough on drugsinevitably translates into getting soft on nondrug crime," Bensonand Rasmussen conclude. Policymakers mistakenly believe that combatingdrug use is an effective away to reduce violence and property crime. Butbecause only a small percentage of drug users commit large numbers of crimesagainst persons or property, efforts to combat these crimes by targetingdrug use have proven ineffective, Benson and Rasmussen argue. Combatingnondrug crime through direct means would utilize criminal justice resourcesfar more effectively, they maintain. Benson and Rasmussen are professorsof economics at Florida State University and research fellows at the IndependentInstitute, a public policy research organization in Oakland, California.The 60-page report can be obtained by contacting Carl Close, the Institute'sPublic Affairs Director, at 510/632-1366, or by e-mail at independ@dnai.com.Web site: http://www.independent.org
# # #
ILLICIT DRUGS AND CRIME An Independent Policy Report By Bruce L. Benson& David Rasmussen Professors of Economics, Florida State UniversityResearch Fellows, The Independent Institute
EXECUTIVE BRIEFING
In the early 1980s, policymakers and law enforcement officials steppedup efforts to combat the trafficking and use of illicit drugs. This wasthe popular "war on drugs," hailed by conservatives and liberalsalike as a means to restore order and hope to communities and familiesplagued by anti-social or self-destructive pathologies. By reducing illicitdrug use, many claimed, the drug war would significantly reduce the rateof serious nondrug crimes - robbery, assault, rape, homicide and the like.Has the drug war succeeded in doing so?
In ILLICIT DRUGS AND CRIME, Bruce L. Benson and David W. Rasmussen (Professorsof Economics, Florida State University, and Research Fellows, the IndependentInstitute), reply with a resounding no. Not only has the drug war failedto reduce violent and property crime but, by shifting criminal justiceresources (the police, courts, prisons, probation officers, etc.) awayfrom directly fighting such crime, the drug war has put citizens' livesand property at greater risk, Benson and Rasmussen contend.
"Getting tough on drugs inevitably translates into getting softon nondrug crime," they write. "When a decision is made to wagea 'war on drugs,' other things that criminal justice resources might dohave to be sacrificed."
To support this conclusion, Benson and Rasmussen compare data on druglaw enforcement and crime trends between states, and debunk numerous misconceptionsabout drug use and criminality.
DO DRUGS CAUSE CRIME?
One of the most prevalent misconceptions, Benson and Rasmussen, contendis the notion that a large percentage of drug users commit nondrug crimes,what might be called the "drugs-cause-crime" assumption implicitin the government's drug-war strategy. If true, then an effective crackdownon drug use would reduce nondrug crime rates. However, Benson and Rasmussenshow that the "drugs-cause-crime" assumption is false. Certainlymany violent and property criminals use drugs. But only a small percentageof drug users commit violent or property crimes. Drug offenders are farmore likely to recidivate for a drug offense than for a violent offenseor property crime.
Is drug use to blame for the crimes drug users do commit? Benson andRasmussen sug-gest that the reverse is closer to the mark: Many criminalswho use drugs did not begin to do so until after they began committingnondrug crimes. A Bureau of Justice Statistics survey of prison inmatesfound that about half of the inmates who had used a major drug, and about60 percent of those who used a major drug regularly, did not do so untilafter their first arrest for a nondrug crime.
"Similarly," Benson and Rasmussen note, "more than halfof local jail inmates who reported they were regular drug users in thesurvey . . . said that their first arrest for a crime occurred an averageof two years before their drug use. Once an individual has decided to turnto crime as a source of income, he or she may discover that drugs are moreeasily obtained within the criminal subculture and perhaps that the risksposed by the criminal justice system are not as great as initially anticipated.Furthermore, criminal activity generates income with which to buy goodsthat previously were not affordable, including drugs. Thus, crime leadsto drug use, not vice versa."
THE DRUG WAR'S FAILURE TO REDUCE CRIME
Because relatively few illicit drug offenders commit violent and propertycrimes and because criminal activity more often precedes drug use thanvice versa, targeting drugs is an inefficient strategy for combating nondrugcrime. And because it requires withdrawing a large amount of scarce criminaljustice resources from directly fighting nondrug crime, it is also an ineffective,often counterproductive, strategy for fighting such crime. Indeed, thetrade-off between fighting drugs and fighting nondrug crime is so severethat in some juris-dictions it seems to have led to an increase in nondrugcrime.
Benson and Rasmussen examined Florida crime data and found that increasingpolice efforts against drugs relative to the efforts against serious nondrugcrimes resulted in a lower probability of arrest for property crime. "Primarilyas a consequence of this reduced probability of arrest, the property crimerate in Florida rose 16.3 percent, from 6,892 offenses per 100,000 populationin 1983 to 8,019 in 1989." Violent crime also increased markedly inresponse to greater drug law enforcement, as drug dealers displaced bylaw enforcement invaded the turf of established dealers, and residentsof previously untapped markets fell prey to violent criminals. Since 1989,Florida has reduced its drug enforcement efforts, and its property crimerate has fallen.
Benson and Rasmussen also discuss how prison overcrowding due to increaseddrug law enforcement has compromised the punishment of other criminals.Although statistical studies of the impact of early prison release on overallcrime rates have not been performed yet, a growing number of violent felonshave been released early, only to commit more violent crimes.
THE DRUG WAR'S FAILURE TO REDUCE DRUG USE
Crime reduction was sold as one of the drug war's important side benefits.But what about its main mission, to reduce drug use? Despite the increasein the number of drug arrests and convictions, drug consumption overallhas not demonstrably fallen. While the drug war may have played a significantrole in reducing the demand for and supply of marijuana, access to cocainehas increased. From 1984 to 1990, the proportion of high school studentswho reported that cocaine was "fairly easy" or "very easy"to obtain rose by about 20 percent.
This failure is due in large part, Benson and Rasmussen explain, todrug entrepreneurs' adoption of new production techniques, new products,and new marketing strategies in response to greater law enforcement. Their"innovations" include lengthening the drug distribution chainand using younger drug pushers and runners (to reduce the risk of arrestand punishment), increasing domestic drug production (to avoid the riskof seizure at the border), smuggling into the country less marijuana andmore cocaine (which is harder to detect), development of "crack"cocaine (a low-cost substitute for higher priced powdered cocaine and formarijuana, which the drug war made harder to obtain), and development ofdrugs with greater potency (because they are less bulky and because punishmentis based on a drug's weight, not its potency).
WHAT TO DO ABOUT ILLICIT DRUGS AND CRIME?
Given the failure of the drug war to reduce crime and drug use, whatought to be done? Benson and Rasmussen offer seven public policy recommendations.
1) Reduce Crime and Drug Abuse by Cracking Down on Juvenile Criminals.Punishing youthful offenders early might divert them from further crimeand remove them from the crime sub-culture where they are more likely tobegin drug use.
2) Emphasize Treatment Over Drug Law Enforcement. Treatment is morecost-effective because it cuts consumption directly, whereas law enforcementworks indirectly, by raising the price of drugs.
3) Abolish Civil Forfeiture Laws. Civil forfeiture laws give the illusionthat drug law enforcement is self-financing. They give law enforcementagencies incentives to pursue counter-productive policies that violatedue process.
4) Make Public Safety the Main Police Priority. Law enforcement agenciesshould be evaluated on the basis of their effectiveness in preventing crime,not merely in responding to it after the fact. Improved citizen cooperationand sense of public safety should also be high priorities.
5) Make Sentencing Guidelines Reflect the Highest Priorities. Sentencingguidelines must allow officials to consider prison capacity, so that dangerousprisoners are not released prematurely to make space for the less dangerous.
6) Decentralize the Prisons. Keeping prosecutors and judges in the samejurisdictions as the prisons to which they send convicts would reduce thelikelihood of dangerous prisoners being released prematurely.
7) Decriminalize Drug Use. Decriminalization would free up scarce criminaljustice resources in order to focus on violent and property crime. Prohibition,especially of less dangerous drugs, is ultimately a self-defeating policy.*
The entire text of ILLICIT DRUGS AND CRIME is on the Independent Institute'sWeb Site: http://www.independent.org. A hard copy of the 60-page reportis available for $7.95 + $3.00 (S/H) from the Independent Institute, 134Ninety-Eighth Avenue, Oakland, CA 94603 (USA). Credit card orders accepted.510-632-1366 (ph), 510-568-6040 (fax), independ@dnai.com (e-mail).
From ???@??? Sat Oct 19 04:47:00 1996 Received: from gulik.dymaxion.edu(root@line027.nwm.mindlink.net [204.191.202.27]) by gold.interlog.com (8.7.6/8.6.10)with ESMTP id AAA03034 for <iorfida@interlog.com>; Sat, 19 Oct 199600:30:16 -0400 (EDT) From: ccletters@hempbc.com Received: from hempbc.com(root@localhost [127.0.0.1]) by gulik.dymaxion.edu (8.7.5/8.6.9) with SMTPid UAA00657 for ccletters; Fri, 18 Oct 1996 20:50:45 -0700 Date: Fri, 18Oct 1996 20:50:45 -0700 Message-Id: <199610190350.UAA00657@gulik.dymaxion.edu>Reply-To: ai256@chebucto.ns.ca Subject: CC#07 According to a study by theAustralian Government: X-UIDL: f6c97ee2234ffbe02b61d87e08ccacd3
[once again, thank you Matt. More info will follow tomorrow (Saturday).]
The health and psychological consequences of cannabis use chapter 8
National Drug Strategy Monograph Series No. 25
__________________________________________________________________________
8. The therapeutic effects of cannabinoids
8.1 Historical background
Cannabis has had a long history of medical and therapeutic use in Indiaand the Middle East (Grinspoon and Bakalar, 1993; Mechoulam, 1986; Nahas,1984) where it has been variously used as an analgesic, anti-convulsant,anti-spasmodic, anti-emetic, and hypnotic. Cannabis was introduced to Britishmedicine in the mid-nineteenth century by O'Shaugnessy (1842) who had gainedclinical experience with the drug while an Army surgeon in India (Mechoulam,1986; Nahas, 1984). He recommended its use for the relief of pain, musclespasms, and convulsions occurring in tetanus, rabies, rheumatism and epilepsy(Nahas, 1984). Partly as the result of his advocacy, cannabis came to bewidely used as an analgesic, anti-convulsant and anti-spasmodic throughoutthe middle part of the 19th century in Britain and the USA.
The medical use of cannabis declined around the turn of the presentcentury. Because the active constituents of cannabis were not isolateduntil the second half of the twentieth century, cannabis continued to beused in the form of natural preparations which varied in purity and, hencein effectiveness. The use of cannabis was largely supplanted by other pharmaceuticallypurer drugs, which could be given in standardised doses to produce moredependable effects. These included the opiates, aspirin, chloral hydrate,and the barbiturates (Mechoulam, 1986; Nahas, 1984). In the early partof the century, the medical use of such crude cannabis preparations wasfurther discouraged by laws which treated cannabis as a "narcotic"drug and severely restricted its availability. It finally disappeared fromthe American pharmacopoeia in the early 1940s after the passage of theMarijuana Tax Act (Grinspoon and Bakalar, 1993), although it continuedto be used in Australia into the 1960s (Casswell, 1992).
THC, the major psychoactive ingredient of cannabis, was not isolateduntil 1964 (Goani and Mechoulam, 1964), shortly before cannabis achievedwidespread popularity as a recreational drug among American youth. Itswidespread recreational use, and its symbolic association with a rejectionof traditional social values, undoubtedly hindered pharmaceutical researchinto its therapeutic uses. Consequently, the rediscovery of some of itstraditional therapeutic uses was largely serendipitous, as was the discoveryof some newer uses. For example, its value as an anti-emetic agent in thetreatment of nausea caused by cancer chemotherapy seems to have been rediscoveredby young adults who had used cannabis recreationally prior to undergoingchemotherapy for leukemia (Grinspoon, 1990).
>From the mid-1970s some clinical research on the therapeutic valueof cannabis and cannabinoids was undertaken. On the whole, however, thisresearch has been very thin and uneven, and, consequently, many of theclaims for the therapeutic efficacy of cannabinoids rely heavily, and,in the case of rare medical conditions, solely upon anecdotal evidence,that is, the testimonies of individuals who claim to have derived medicalbenefit from its use (e.g. Grinspoon and Bakalar, 1993; Randall, 1990),and small numbers of cases reported by physicians (e.g. Consroe et al,1975; Meinck et al, 1989).
Evidence will be reviewed for the best-supported therapeutic uses ofcannabinoids. The review begins with the evidence on the effectivenessof cannabinoids as anti-emetic drugs for nausea caused by cancer chemotherapy,and as agents to control intra-ocular pressure in glaucoma. Briefer reviewsare provided of the evidence in favour of other putative therapeutic usesof cannabinoids which are less well supported by clinical evidence, chiefamong which are its uses as an anti-convulsant, an anti-spasmodic, andan analgesic agent. The value and limitations of the largely anecdotalevidence of efficacy in these latter conditions will also be briefly considered.The review will include a discussion of the controversy in the United Statesabout "marijuana rescheduling" which has coloured much recentdiscussion of the issue. This controversy concerns the vexatious issueof whether smoked cannabis should be available for medical use in additionto synthetic cannabinoids such as THC.
8.2 Cannabinoids as anti-emetic agents
Profound nausea and vomiting can be such serious complications of chemotherapyand radiotherapy for cancer that patients may discontinue potentially life-savingtreatment (Institute of Medicine, 1982). Although various types of drugs(e.g. the phenothiazines) have been shown to be effective in controllingnausea and vomiting in cancer patients, substantial minorities of patientsdo not benefit from these drugs. The seriousness of the problem of chemotherapy-inducednausea, and the incomplete success of existing treatments, prompted oncologistsin the late 1970s and early 1980s to take a particular interest in theanti-emetic properties of cannabinoids (Institute of Medicine, 1982).
8.2.1 Clinical trials
One of the earliest trials of the effectiveness of THC as an anti-emeticwas prompted by patient reports that smoking marijuana relieved nauseaand vomiting (Sallan et al, 1975). In this study, 22 patients (10 malesand 12 females, average age 30 years) with a variety of neoplasms werestudied. In 20 patients, the nausea and vomiting had proven resistant toexisting anti-emetic drugs. A randomised placebo-controlled trial withcrossover was used, in which patients were randomly assigned to receiveoral THC (10mg per m2) and placebo in one of four different orders (THC-placebo-THC;THC- placebo-placebo; placebo-THC-placebo; placebo-THC-THC). Outcome wasassessed by grading patients' self-reports of nausea and vomiting afterTHC and placebo into three categories: complete response if there was vomitingafter placebo but not after THC; partial response if there was a greaterthan 50 per cent reduction in nausea and vomiting after THC compared toplacebo; and no response if there was a less than 50 per cent reductionin nausea and vomiting.
Ten patients completed all three courses of THC and placebo and vomitedon at least one trial. After excluding one trial because of a variationin the chemotherapy dose, there were 29 trails available for analysis,14 of placebo and 15 of THC. All 14 placebo trials resulted in no response,while in the 15 THC trials there were five complete responses, seven partialresponses, and three no responses. This difference was statistically significantwhen full and partial responses were combined. Most patients (13/16) reporteda "high" after receiving THC, an experience which was correlatedwith the anti-emetic effect. The most common side-effect was somnolencewhich curtailed activities for two to six hours in a third of patients.Only two patients experienced any symptoms of toxicity, (both after receiving20mg doses of THC), namely, visual distortions and hallucinations and depressionlasting several hours. Sallan et al reported "preliminary" observationsfrom several patients that smoking marijuana produced an equivalent anti-emeticeffect to oral THC.
A trial by Chang et al (1979) largely supported the findings of Sallanet al. In this study 15 patients with osteogenic sarcoma (10 males andfive females, average age 24 years) served as their own controls in thecourse of monthly high dose methotrexate therapy. They were assigned toreceive three THC and three placebo trials in randomised order during sixtreatment sessions. THC (10mg per m2 of body area) and placebo were administeredorally five times at three hourly intervals, beginning two hours beforechemotherapy. If the patients vomited, the remaining doses of either THCor placebo were administered by smoking a cigarette using a standardisedsmoking technique. The effect of THC and placebo were assessed by nursingstaff who rated various endpoints (e.g. number of vomiting and retchingepisodes, volume of emesis, degree and duration of nausea) without beingaware of which treatment patients had received. Patient response was gradedinto three categories: excellent (greater then 80 per cent reduction afterTHC by comparison with placebo in each of these endpoints); fair (greaterthan 30 per cent and less than 80 per cent reduction), and no response(less than 30 per cent reduction).
The results showed that eight patients had an excellent response, sixa fair response, and one had no response. On all endpoints THC produceda statistically significant reduction in nausea and vomiting by comparisonwith placebo. There was also a dose-response relationship between bloodlevels of THC and the incidence of nausea and patient reports of feeling"high". Generally, higher THC blood levels were achieved whenmarijuana was smoked than when THC was taken orally. There were few sideeffects reported, with sedation being the most common (12/15 patients).Four patients experienced five dysphoric reactions in the course of 281THC drug doses (2 per cent), none of which lasted more than 30 minutes,and all of which were successfully managed with simple reassurance.
In a second phase of the study, four patients who had an excellent responseto THC in the first phase were retested under double-blind conditions usingtwo placebo trials in the next 10 treatments. A small number of patientswho had a fair response were also studied using an increased dose of THC.All patients showed a reduction in the average anti-emetic benefit of THC,decreasing from excellent to fair in the case of previous excellent responders,and from fair to no response in the case of the fair responders. Changet al hypothesised that the decline in effect reflected either the developmentof tolerance to the effects of THC, or the development of conditioned nauseaand vomiting that was resistant to the anti-emetic effects of THC.
Since these early studies, a large number of controlled clinical studieshave been conducted which compared the effectiveness of THC with eithera placebo or with other anti-emetic drugs (see Carey et al, 1983; Posteret al, 1981; Levitt, 1986 for reviews). The results of this literaturehave sometimes been unfairly described as "confused" (e.g. Careyet al, 1983; Nahas, 1984). This description betrays an unreasonably highexpectation of the consistency of results from studies which have generallyused small samples of heterogenous patients who have received various formsof chemotherapy. It also ignores the fact that the cross-over studies comparingthe anti-emetic effects of THC with placebo have generally reported greateranti-emetic effects for THC than placebo (Poster et al, 1981); the singleexception to this finding was a study which had a sample size of only eightpatients.
Comparisons of the effectiveness of oral THC with that of existing anti-emeticagents have been less consistent than the results of comparisons with placebo.Nonetheless, the results have generally indicated that THC is at leastequivalent in effectiveness to the widely used anti-emetic drug prochlorperazine(Carey et al, 1983; Levitt, 1986). The inconsistencies in this case arisebecause some studies have shown THC to be superior, probably because ofthe practice in some trials of enlisting patients whose nausea had previouslyproven resistant to prochlorperazine (Carey et al, 1983).
The equivalence of THC and prochlorperazine has been supported by theresults of one of the largest and best conducted studies (Ungerleider etal, 1982). In this study 214 patients with a variety of forms of cancer(carcinomas, sarcomas, lymphomas and leukemias) were recruited if theyhad already undergone chemotherapy and experienced nausea and vomiting,or they were to receive a form of chemotherapy which had a high emeticpotential. Patients were randomly assigned to receive a paired trial ofeither oral THC followed by prochlorperazine or vice versa. The dose ofTHC was dependent on body surface area (7.5mg if less than 1.4m2, 10mgfor 1.4 to 1.8m2, and 12.5mg for greater than 1.8m2). Separate analyseswere conducted on three groups of patients: patients who received theircancer chemotherapy on a single day some weeks apart (N=98); patients whoreceived their chemotherapy on a daily basis over several successive days(N=41); and patients who discontinued the trial after a single episodeof either THC or prochlorperazine. Outcomes were patient self-ratings ofnausea and vomiting, and a variety of mood states and behaviours.
The results showed that there "were no statistically significantdifferences in the anti-nausea/anti-emetic effect of THC and prochlorperazine"(p640) in any of the three patient groups, even though there were differencesbetween patients in the single- and multiple-day chemotherapy regimensin the time course of the nausea. There were differences in mood and behaviourbetween the THC and prochlorperazine trials, with patients reporting greaterimpairment of concentration and less social interaction after receivingTHC. There were also more side effects from THC than prochlorperazine,with sedation, sleepiness and mental clouding being the most common. Therewas no difference in the frequency of panic attacks between the two drugs.Despite these differences in side effects there was a small patient preferencein favour of THC as an anti-emetic, with 41 per cent experiencing lessnausea on THC, 31 per cent experiencing less nausea on prochlorperazine,and 29 per cent reporting no difference in effectiveness. The effectivenessof THC was not related to age or prior experience with marijuana, but itwas related to the experience of side effects, with patients experiencingthem reporting less nausea.
Given the wide variety of patients who have been studied in terms ofage and type of cancer, the wide variety of chemotherapeutic agents thathave been used to treat their cancers, and the variety of different anti-emeticswith which THC has been compared, the fact that findings of these studiesare generally positive for THC is more impressive than the apparent differencesin outcome. The positive results from the controlled trials also seem tobe borne out by clinical experience with cannabinoids in managing cancerpatients. A recent survey of a large sample of American oncologists, forexample, found that 44 per cent of oncologists had recommended marijuanato at least one cancer patient, and 64 per cent of these physicians reportedthat it was successful controlling nausea in at least half of their patients.Overall, just under half of the oncologists in the sample (44 per cent)believed that cannabinoids could be safely used in the treatment of nauseacaused by chemotherapy and radiotherapy (Dobin and Kleiman, 1991). A similarproportion (48 per cent) reported that they would prescribe marijuana fortheir patients if it was legal.
The general conclusion on the available literature is that THC is superiorto placebo, and equivalent in effectiveness to other widely-used anti-emeticdrugs, in its capacity to reduce the nausea and vomiting caused by somechemotherapy regimens in some cancer patients. There are a number of issuesthat remain to be resolved in deciding upon the clinical role of cannabinoidsas anti-emetic agents in cancer chemotherapy. These issues include: thetypes of nausea against which it may be most effective, and hence the typesof patients for which they are most appropriately prescribed; the degreeof patient tolerance of the psychotropic side effects of THC and othercannabinoids; the potential seriousness of possible THC induced immunosuppressionin patients who are already immunologically compromised; the most effectivedosing schedules for THC as an anti-emetic; the potential use of THC incombination with other anti-emetic drugs; and the extent to which the motivationfor the use of THC may have been reduced by the availability of newer anti-emeticdrugs that are more effective than prochlorperazine (the main anti-emeticdrug in the 1980s).
8.2.2 Which patients?
Which patients with what types of nausea are the most suitable for treatmentwith cannabinoids as anti-emetics? Patients with various forms of cancerhave been the most extensively investigated patient group, but the numbersof different types of cancer have been too small to allow convincing analysesof differences in patient response. The same point can be made about typesof chemotherapy regimens; they have varied widely in these studies, andhave often not been reported, but there has been no systematic analysisof the effectiveness of cannabinoids in controlling emesis produced bydifferent agents. It is uncertain to what extent the cannabinoids may beeffective against nausea from other causes. The mechanisms that producenausea are not well understood but there are believed to be one or moreprotective mechanisms located in the brain stem that can be triggered bya variety of emetic agents. This raises the possibility that cannabinoidsmay be therapeutically useful against nausea from a variety of causes.
8.2.3 Side effects
The psychoactive effects of cannabis which are prized by recreationalusers - euphoria, relaxation, drowsiness - are not always welcomed by olderpatients, most of whom are cannabis-naive. In some studies a substantialminority of such patients have discontinued the use of THC because of theunwelcome dysphoria and somnolence (Levitt et al, 1986). This has not beena universal experience, so further research is required to discover towhat extent this has been the result of unnecessarily large doses, or poorpatient preparation for these effects, and failure to adequately managethem by reassurance. What does seem to be the case is that the experienceof some psychological effects of THC, including the "high", isnecessary for the occurrence of a clinically significant anti-emetic effect.This fact has led to the search, so far unsuccessful, for cannabinoid derivativesof THC which possess its anti-emetic properties but not its psychoactiveones. The recent discovery of the cannabinoid ligand and receptor, andreceptor subtypes (see pp7-8) has encouraged researchers to believe thatthis may be an achievable goal (Iversen, 1993).
A potentially more serious side effect of therapeutic THC is its possibleimmunosuppressive effect. Any such effect would limit its use as an anti-emeticin the treatment of cancer, since cancer patients experience immune suppressionas a side effect of their treatment. There are several reasons why thismay be less serious an issue that it seems at first glance. First, thereare doubts about the existence of any immunosuppressive effect of cannabinoids(see Section 6.2 on the immune system, pp62-68), and the effect is smallin those studies which report one. Second, the clinical significance ofany such effects is doubtful in the use of THC in cancer chemotherapy.Such use would be intermittent, and relatively short-term, and the possiblegain in increased life expectancy from being able to complete a courseof cancer chemotherapy is such that most patients would be prepared totake the risk, in the same way that they chose to undergo the highly toxicchemotherapy in the first place.
8.2.4 Unresolved clinical issues
If THC has a place in the management of nausea from cancer treatment(Poster et al, 1981), and perhaps other causes, a number of clinical issuesremain to be resolved (Levitt, 1986). Foremost among these is the bestway in which to administer the drug. Should it be given well in advanceof treatment at low doses to ensure a stable blood level, or should itbe given in larger doses shortly before chemotherapy or radiotherapy? Thisissue has not been systematically studied (Levitt, 1986).
An additional question is whether there is any clinical benefit to bederived from combining THC with existing anti-emetic agents. There is suggestiveevidence that there might be, since the mechanisms of action, while notwell understood, appear to be different, raising the possibility that theremay be positive synergistic effects from the combination of THC and otheranti-emetics. One single-blind study of the combination of dronabinol andprochlorperazine, for example, suggested that the combination of thesedrugs may have a superior anti-nausea effect to either drug used alone(Plasse et al, 1991). Clearly, more research is warranted on this issue,especially as it may enable cannabinoids to be used as anti-emetics atlower doses with fewer unwanted psychotropic effects.
It seems surprising that the desirability of undertaking research ondosing and combined use of cannabinoids was highlighted by Poster et alin 1981 and by the Institute of Medicine in 1982. Yet very little researchhas been done, and THC has not been routinely incorporated into the managementof nausea caused by cancer chemotherapy. One of the likely reasons hasbeen the American controversy about the rescheduling of marijuana underthe Controlled Substances Act, which some argue has discouraged clinicalresearch on cannabinoids (see below). Another reason has been that themotivation for further research on the anti-emetic properties of THC hasbeen removed by the recent development of newer anti-emetic drugs whichare superior to prochlorperazine (Iversen, 1993), the "gold standard"drug when the major controlled trials were conducted on cannabis in the1970s and 1980s. In the absence of trials comparing THC with these newerdrugs, its comparative efficacy is unknown, although given its approximateequivalence to prochlorperazine it is likely to be inferior to the newerdrugs.
8.3 Cannabinoids as anti-glaucoma agents
Glaucoma is the leading cause of blindness in the United States, affectingtwo million people and producing 300,000 new cases each year (Adler andGeller, 1986). It is a condition "which is generally characterisedby an increase in intraocular pressure ... that progressively impairs visionand may lead to absolute blindness" (Adler and Geller, 1986, p54).Although its causes are not understood, it is believed to involve an obstructionto the outflow of the aqueous humour in the eye leading to a gradual increasein intraocular pressure (IOP) which, if untreated, may damage the opticnerve, resulting in blindness. Its incidence increases over the age of35, especially among individuals who are myopic (i.e. short-sighted). Althoughvarious drugs are available which reduce IOP, all possess unwanted side-effectsand patients may become tolerant to their therapeutic effects.
The effects of cannabis in reducing IOP were discovered serendipitouslyby researchers and patients in the early and middle 1970s. Hepler and hiscolleagues (1971, 1976) observed a substantial decrease in IOP while researchingthe effects of cannabis intoxication on pupil dilation. They demonstratedthat both cannabis and oral THC produced substantial reductions in IOPin both normal volunteers and patients with glaucoma (Hepler and Petrus,1976; Hepler et al, 1976). Subsequent research identified THC as the agentresponsible for producing this effect (Adler and Geller, 1986).
Around the same time, patients with glaucoma who had used cannabis recreationallyalso discovered its therapeutic effects. One such patient, Robert Randall,used cannabis daily to control his glaucoma. When arrested for possessionand cultivation of cannabis, he successfully used the defence of "medicalnecessity" arguing, with the support of his physicians, that he wouldgo blind if he stopped his cannabis use. He subsequently was given legalaccess to cannabis for medical purposes (Randall Affidavit, in Randall,1988).
Although there have been a number of case reports of the successfuluse of cannabis in the management of glaucoma (e.g. Grinspoon and Bakalar,1993; Randall, 1990), there have not been any controlled clinical studiesof its effectiveness and safety in the long-term management of glaucoma.Informed clinical opinion has been that THC is an effective anti-glaucomaagent when used acutely, but there are doubts about its effectiveness withchronic use because of the development of tolerance to its effects on IOP(Jones et al, 1981). Ophthalmologists who are opposed to the clinical useof THC point to a number of major disadvantages. First, because THC isnot water-soluble, it cannot, unlike other anti-glaucoma agents, be appliedtopically to the eye to ensure that enough is absorbed to produce a clinicallysignificant reduction in IOP. Second, as a consequence, THC must be absorbedsystemically in order to produce a therapeutic effect on IOP, which meansthat patients must experience the psychoactive effects of THC in orderto derive its therapeutic benefits against glaucoma. Third, because glaucomais a chronic condition, THC or cannabis would need to be taken in substantialdoses on a daily basis over long periods of time, if not for the remainderof adult life. There has been an understandable concern about the healthrisks of chronic daily cannabis use (e.g. Hepler, 1990; American Academyof Ophthalmology, 1990).
The position adopted by the American Academy of Ophthalmology has beento insist that cannabis has no accepted medical use in the management ofglaucoma, and cannot have such medical use until a large controlled trialhas been conducted into its safety and effectiveness in daily chronic use.There has been no evidence that the Academy has any interest in, or hasgiven any encouragement to, the conduct of such a trial. Consequently,its position is that THC and other cannabinoids should not be used be inthe management of glaucoma.
A contrary position has been taken by Randall, who has argued that patientsshould be allowed to make the choice between the uncertain health risksof chronic cannabis use and the more certain risks to sight of poorly controlledglaucoma:
"People with life- and sense-threatening diseases are routinelyconfronted by stark choices ... [between] the devastating consequencesof a debilitating, progressive disease ... [and] often highly damagingbiological and mental consequences of the toxic chemicals required to checkthe progression of disease. .. Viewed in this medical context, marihuanais more benign and far less damaging that the synthetic toxins routinelyprescribed by physicians" (cited in Grinspoon and Bakalar, 1993, p153)
8.4 Cannabinoids and neurological disorders
8.4.1 Anti-convulsant
Historically one of the commonest medical uses of cannabis preparationshas been as an anti-convulsant. O'Shaughnessy (1842), for example, recommendedthe use of cannabis to control seizures in epilepsy, tetanus and rabies(Nahas, 1984). Animal studies have provided some support for this use inshowing that THC has dual effects on convulsions, i.e. they can produceconvulsions in susceptible animals, and suppress the maximum severity ofconvulsions from a variety of causes, while cannabidiol (CBD) appears tobe a potent anti-convulsant (Chesher and Jackson, 1974; Consroe and Snider,1986; Institute of Medicine, 1982).
Despite this animal evidence, there is very limited evidence on thetherapeutic effects of cannabinoids in humans with epilepsy. There area small number of case studies of individuals with epilepsy in which therecreational use of cannabis appeared to enhance the anti-convulsant effectsof more traditional anti-convulsant medication From ???@??? Sat Oct 1904:47:00 1996 Received: from gulik.dymaxion.edu (root@line027.nwm.mindlink.net[204.191.202.27]) by gold.interlog.com (8.7.6/8.6.10) with ESMTP id AAA03034for <iorfida@interlog.com>; Sat, 19 Oct 1996 00:30:16 -0400 (EDT)From: ccletters@hempbc.com Received: from hempbc.com (root@localhost [127.0.0.1])by gulik.dymaxion.edu (8.7.5/8.6.9) with SMTP id UAA00657 for ccletters;Fri, 18 Oct 1996 20:50:45 -0700 Date: Fri, 18 Oct 1996 20:50:45 -0700 Message-Id:<199610190350.UAA00657@gulik.dymaxion.edu> Reply-To: ai256@chebucto.ns.caSubject: CC#07 According to a study by the Australian Government: X-UIDL:f6c97ee2234ffbe02b61d87e08ccacd3
(e.g. Consroe et al, 1975; Grinspoon and Bakalar, 1993). There is asingle randomised placebo controlled study of the administration of CBDin 15 patients with epilepsy that was not well controlled by conventionalanti-convulsants. Four of the eight patients who received CBD in additionto their usual anti-convulsant drugs were free of seizures throughout thestudy period, and three were improved. By contrast, only one out of sevenpatients in the placebo condition showed any clinical improvement (Cunhaet al, 1980). Despite this suggestive evidence of efficacy in epilepsy,CBD has not been widely used in clinical management. Perhaps this is notsurprising given the absence of evidence of its efficacy, the existenceof other effective anti-convulsant drugs, and concerns about the safetyof chronic use in the management of a chronic disease. It is perhaps moresurprising that there has been no further research on the anti-convulsantproperties of CBD, especially as it has no psychoactive side effects (Nahas,1984).
8.4.2 Anti-spasmodic
Cannabinoids have been used in an empirical way in the management ofsome patients with movement disorders, a variety of syndromes that havein common a deficit in non-pyramidal motor control function, which is expressedin usually one or more of the non-epileptic, abnormal involuntary movements,such as those found in Parkinson's disease, Huntington's disease, multiplesclerosis, and spasticity. Although a number of drugs may be of benefitin the management of these conditions, they are not always effective, andmay produce troublesome side-effects (Consroe and Snider, 1986).
There has been some animal evidence which indicates that THC and itsanalogues produce a broad spectrum of neurological effects, which includealterations in motor function, and changes in muscle tone and reflexes.The acute motor effects in normal humans - ataxia, tremulousness and subjectiveweakness - also suggest a potential for therapeutic effects in some movementdisorders (Consroe and Snider, 1986).
The evidence that cannabinoids have therapeutic effects in patientswith movement disorders is largely anecdotal. Grinspoon and Bakalar (1993),for example, present four case histories of individuals with multiple sclerosiswhose condition improved while they smoked marijuana, and deterioratedafter they stopped smoking. Meinck et al (1989) report a case history ofa young man with multiple sclerosis with severe limb and gait ataxia whocomplained of erectile impotence. After smoking marijuana his gait improvedsufficiently to be able to walk unaided, and he was able to achieve andsustain an erection. When cannabis was withdrawn under medical supervision,the patient's motor function deteriorated to the point where he was unableto walk without assistance.
There has been one controlled study by Clifford (1983) who examinedthe effects of THC on tremor in eight patients (four male and four female)with advanced multiple sclerosis who had ataxia and tremor. Five patientsreported subjective benefit from THC and there was objective evidence ofbenefit in two of these cases. Single-blind placebo challenge in thesecases produced evidence that their clinical condition deteriorated whengiven placebo and improved with the reinstatement of THC.
Grinspoon and Bakalar (1993) described several case histories of individualswith paraplegia and quadriplegia who reported that cannabis use helpedto reduce muscle spasm. The experiences of these individuals were supportedby similar reports obtained from a survey of 43 individuals with spinalcord injuries, 22 of whom reported that they used cannabis to control theirmuscle spasm.
The only controlled trial of a cannabinoid in a movement disorder hasbeen an evaluation of the effects of CBD on severity of chorea in patientswith advanced Huntington's disease (Consroe et al, 1991). This study wasprompted by the authors' observation that CBD had improved the conditionof an individual with Huntington's disease (Sandyck et al, 1988). In thisstudy 19 Huntington's patients were enrolled in a double-blind controlledtrial in which they received six weeks administration of CBD or placeboin a cross-over design. The outcome was the severity of chorea, as assessedby blind clinical ratings, patient self-report, and a variety of measuresof motor function. Although the study had sufficient statistical powerto detect a relatively small clinical benefit, there was no evidence ofimprovement in chorea on any of the clinical, self-report or motor measures.In the light of Consroe et al's failure to replicate the earlier favourablesingle case, further controlled trials are warranted before any of thecannabinoids can be routinely used in treating movement disorders.
8.5 Cannabinoids as anti-asthmatic agents
Smoked cannabis, and to a lesser extent oral THC, have an acute bronchodilatoryeffect in both normal persons and persons with asthma (Tashkin et al, 1975;Tashkin et al, 1976). Tashkin et al (1975), for example, compared the bronchodilatoreffect of smoked cannabis with that of a standard clinical dose of thebronchodilator isoproterenol in relieving experimentally induced asthmain asthmatic patients. They found that smoking a 2 per cent-THC cannabiscigarette produced a bronchodilator nearly equivalent to that of a clinicaldose of isoproterenol.
Despite this early suggestion of a therapeutic effect in asthma, cannabinoidshave not been used therapeutically, nor have they been extensively investigatedas anti-asthmatic agents other than by Tashkin and his colleagues (Tashkin,1993). A major obstacle to therapeutic use has been the route of administration.Oral THC produces a smaller bronchodilator effect after a substantial delay,and when used as an inhalant produces irritation and reflex bronchoconstriction.Hence, smoking marijuana has been the most dependable way of deliveringa clinically effective dose of THC. There is an understandable concernamong clinical researchers that smoking is an unsuitable mode of administeringany drug, and an especially inappropriate way to administer a drug to patientswith asthma, because it would inevitably involve the delivery of othernoxious chemicals that would nullify its therapeutic value in the shortterm, and carry an increased risk of other respiratory disease and possiblycancer in the long term (Tashkin, 1993). The unwanted psychotropic effectsfrom marijuana smoking have also been a barrier to its use as an anti-asthmaticdrug. Some investigators (e.g. Graham, 1986) have nonetheless argued thatthe suitability of THC as a spray should be further investigated becauseof the possible hazards of the chronic use of the more widely-used beta-blockerantagonists. The recent discovery of the cannabinoid receptor and ligandmay prompt a re-examination of this question.
8.6 Cannabinoids as analgesics
There is some animal evidence that THC has an analgesic effect whichoperates via a different mechanism from that of the opioid drugs (Segal,1986). There is a small amount of human experimental studies which havereported mixed evidence of an analgesic effect (Nahas, 1984). There hasbeen little clinical evidence beyond historical use for various forms ofchronic pain, including migraine, dysmenorrhoea, and neuralgia, and thesmall number of case histories of its use in chronic pain, dysmenorrhoea,labour pain, and migraine reported by Grinspoon and Bakalar (1993).
Only one double-blind controlled cross-over study has been reported.This study compared the analgesic effect of THC and codeine in patientswith cancer pain (Noyes et al, 1975). The findings suggested that 20mgof THC was of equivalent analgesic effect to 120mg of codeine. However,neither drug produced substantial analgesia in these patients, and themajority of patients found the psychotropic effects of 20mg of THC sufficientlyaversive that they discontinued its use. Clearly, much more basic pharmacologicaland animal investigation is required before cannabinoids or their derivativeshave any clinical use as analgesics. Nevertheless, such investigationsmay be worth pursuing because of the dependence potential of the more potentopioid analgesics, and the likelihood that any cannabinoid mediated analgesiceffect operates by a different mechanism to that of the opioids.
8.7 Other possible therapeutic uses
A variety of other therapeutic uses have been suggested, although fewhave been investigated in any depth. In the late 1940s, for example, therewere some investigations of the therapeutic uses of the euphoriant propertiesof cannabis, as a possible anti-depressant agent in the form of synhexil,a synthetic cannabis analogue. The results in one uncontrolled study werepositive, but these were not replicated in later studies using lower doses(Nahas, 1984; Grinspoon and Bakalar, 1993). None of these suggestions havebeen further investigated, probably because of the potential for THC toproduce dysphoric and other unwanted psychotropic side effects.
8.8 Cannabis and AIDS
One of the areas of greatest contemporary interest in the therapeuticuses of cannabinoids and cannabis has been their possible roles as an anti-nauseaagent, an appetite stimulant and an analgesic in patients with AIDS (Randall,1989). The development of this interest seems to have replicated the earlierdiscovery of the anti-emetic effects of cannabis in young cancer patientsin the 1970s. AIDS patients often experience nausea and weight loss, eitherwhile receiving cytotoxic drugs to suppress HIV, or as a direct effectof the AIDS spectrum diseases. Many patients have been recreational cannabisusers, and so have reported that the smoking of marijuana produces a diminutionin their nausea, an increased appetite, reduced pain, and general improvementsin well being. AIDS advocacy groups have accordingly argued that marijuanashould be made legally available to AIDS patients (e.g. Randall, 1991).
So far the bulk of evidence for these therapeutic claims has been providedby case reports (see Randall, 1989). There has been one small uncontrolledstudy of 10 symptomatic AIDS patients which suggested that dronabinol (syntheticTHC) may be effective in reducing nausea and stimulating appetite (Plasseet al, 1991). The evidence of its anti-emetic properties in cancer patientsseems to support its potential application in AIDS treatment, and is deservingof further investigation.
A potential concern with the use of cannabinoids in HIV positive individualsand AIDS patients is the possible immunosuppressive effects of cannabinoids.Although, as argued above, this effect is likely to be small and of limitedconcern when used intermittently in cancer patients, it is of potentiallygreater significance in AIDS patients, since cannabis would be used regularlyby patients with a major immune system disorder. Even a small impairmentin immunity may have major consequences for HIV and AIDS affected individuals.Recent epidemiological evidence does something to allay this concern. Alarge prospective cohort study of HIV/AIDS in homosexual and bisexual menrecently failed to find any relationship between cannabis use, or any otherpsychoactive drug use, and the rate at which HIV positive men developedclinical AIDS (Kaslow et al, 1989). Nonetheless, the issue of immunosuppressionneeds to be explicitly investigated in any research which is undertakeninto the therapeutic uses of cannabinoids in the treatment of AIDS.
8.9 The limitations of anecdotal evidence
Much of the case for the therapeutic uses of cannabinoids as other thananti-emetic agents depends upon anecdotal evidence from case histories.Such evidence has justifiably come to be distrusted as evidence of therapeuticeffectiveness in clinical medicine, especially in the case of chronic conditionswhich have a fluctuating course of remission and exacerbation. In suchdiseases, it is difficult to exclude alternative explanations of any apparentrelationship between the use of a drug (e.g. THC) and an improvement ina patient's condition. Among the alternative explanations that are mostdifficult to exclude in a single case or even a succession of single casesis simple coincidence: that is, there may be no relationship between theuse of the drug and improvement; the apparent relationship between thetwo may have arisen because the use of the drug preceded an improvementin the patient's condition that would have occurred in its absence. Thisis especially likely to occur in a chronic condition with a fluctuatingcourse. In addition, the well-known placebo effect which is observed inmany conditions may explain the apparent benefits of a drug or other treatment.It is for these reasons that this review has relied upon evidence fromcontrolled clinical trials in appraising the therapeutic uses of cannabinoids.
Grinspoon and Bakalar (1993) have attempted to defend anecdotal evidenceof therapeutic efficacy of cannabinoids. They argue that a double standardhas been used in the appraisal of the safety and efficacy of cannabinoids:anecdotal evidence of harm has been readily accepted while anecdotal evidenceof benefit has been discounted. Although at first glance "double standards"may seem to describe the behaviour of the regulatory authorities, it isdefensible to use different standards of proof when evaluating the benefitsand the costs of therapeutic drugs. It is reasonable to err on the sideof caution by requiring stronger evidence of benefit from putatively therapeuticdrugs in order to ensure that the possible risks incurred by their therapeuticuse do not outweigh their benefits. Moreover, this behaviour is not peculiarto the therapeutic appraisal of cannabinoids; it is standard practice inthe therapeutic appraisal of all drugs. Medical practitioners are encouragedto report cases histories of possible adverse effects of prescribed drugs.Such reports are treated as a noisy but necessary way of detecting rarebut serious side effects of drugs that have not been detected in clinicaltrials or animal studies.
8.10 The politics of therapeutic cannabinoid use
A puzzle in the field of cannabinoid therapeutics is that despite thepositive appraisal of the therapeutic potential of cannabinoids as anti-emeticsand anti-glaucoma agents, they have not been widely used. Nor has the detailedtype of clinical pharmacological research been undertaken on optimal methodsof clinical use in those areas where the cannabinoids do have therapeuticpotential (e.g. as anti-emetics). Part of the reason for this is that researchon the therapeutic use of these compounds has become a casualty of thedebate in the United States about the legal status of cannabis. This emergesfrom an inspection of the arguments recently advanced for and against anapplication to the United States Drug Enforcement Agency to change thestatus of marijuana under the Controlled Substances Act, 1970 from a scheduleI drug which has no accepted medical use to a schedule II drug which hasan accepted medical use (see Randall, 1988, 1989, 1990).
The proponents of rescheduling (National Organisation for the Reformof Marijuana Laws, Alliance for Cannabis Therapeutics, and Cannabis Corporationof America) have argued that marijuana should be available for medicaluse, as smoking is the most effective mode of delivering THC for some therapeuticpurposes. The opponents of rescheduling (Drug Enforcement Agency, InternationalChiefs of Police, The National Federation of Parents for a Drug Free Youth)have countered that marijuana has no therapeutic use, since its few usesare better met, either by other more effective drugs which do not havethe psychoactive effects of THC, or by the oral delivery of synthetic cannabinoids.They have been supported by medical researchers and practitioners who arguefor the therapeutic superiority of pharmaceutically pure drugs which canbe given in defined doses (e.g. Levitt, 1986; Mechoulam, 1988; Nahas, 1984).
Medical researchers who have supported the rescheduling of marijuana(e.g. Grinspoon and Bakalar, 1993; Merritt, 1988; Mikuriya, 1990; Morgan,1990; Weil, 1988) have argued that smoked cannabis is superior to oralsynthetic cannabinoids in effectiveness and has a lower risk of producingunwanted psychoactive side-effects. Apart from the unsuitability of oralmedication for patients who are vomiting, their main arguments in favourof smoking as a route of THC administration are similar to the reasonsrecreational users often give for preferring smoking to the oral use ofcannabis. The greater bioavailability of THC via smoking produces a moredependable therapeutic effect, which is more easily controlled becauseusers have a greater ability to titrate their dose, and hence, to maximisethe desired effects while minimising the unpleasant effects. An additionalargument sometimes used is that there may be other cannabinoids presentin the crude plant product which modulate the undesired side effects, includingthe unpleasant dysphoric effects of THC (Grinspoon and Bakalar, 1993).There is also suggestive evidence that smoked cannabis is as effectiveas oral THC, and may be preferred by patients because of the greater controlthey have over dose (Chang et al, 1979).
Opponents of marijuana rescheduling argue that the undesirable psychoactiveside effects of THC disqualify it from widespread medical use, whateverthe route of administration. Most also believe that smoking is a medicallyunacceptable route of administration of THC because it is unsuitable forvery young and very old patients, there is a risk of infection with micro-organismswhich may contaminate the plant material, and there is the danger thatchronic smoke inhalation may produce or exacerbate bronchitis, and exposethe user to carcinogens (e.g. Levitt, 1986; Mechoulam, 1988; Nahas, 1984).
The proponents of rescheduling respond that none of these are compellingreasons for rejecting smoked marijuana for therapeutic purposes until morepotent and specific therapeutic cannabinoids have been identified and synthesised.Smoking, they point out, would not be a compulsory method of administration;only an option for those patients who preferred it, as would the use ofcannabinoids if patients did not like their psychoactive effects. The contaminationof micro-organisms reported with blackmarket cannabis can be overcome,they argue, by standardising dose and using an anti-microbial treatment,as has been done by National Institute on Drug Abuse (NIDA) in preparingcannabis cigarettes for research (Randall, 1988). The risks of bronchitisand respiratory tract cancers, it is argued, are small with the intermittentand time-limited smoking of cannabis that would occur in the course ofcancer chemotherapy. In any case, proponents of rescheduling argue, itis probably a risk that many patients with a life-threatening illness maybe prepared to run, as shown by their preparedness to take highly toxicand carcinogenic anti-cancer agents.
Weil (1988) has argued that some opponents have used double standardsin appraising the risks of marijuana smoking. According to Weil, the mostcommon psychoactive effects of marijuana (euphoria, somnolence and dysphoria)are minor, non-life-threatening and self-limiting effects that can be easilymanaged, and are of much less severity than the side effects of many otherwidely-used therapeutic drugs. Medical witnesses for the government, heclaims, "do not contrast marijuana's supposed adverse effects withthe known adverse effects of drugs routinely prescribed for the treatmentof conditions like cancer, glaucoma and multiple sclerosis. Instead, ...[they] compare marijuana to some abstract, unobtainable standard of perfection"(p437).
Merritt (1988) has made a similar point in criticising the argumentsraised against the therapeutic use of marijuana to manage glaucoma: ".. each drug family used in glaucoma therapy is capable of producing alethal response, even when properly prescribed and used .. [p470] [but]these drugs are all deemed "safe" for use in glaucoma therapy.. because their adverse consequences are considered less threatening tothe patient than blindness" (p472). Yet marijuana is excluded fromtherapeutic use because of a possible risk of cancer from long-term dailysmoking. "I cannot see", observes Merritt, "how an allegedcase of marijuana-induced lung cancer which results in death is significantlydifferent in result from an acute adverse reaction to a myotic drug whichresults in respiratory failure, except, of course, that the patient withcancer is likely to outlive the patient who is unable to draw in a breathof air" (p474).
Although the debate about the rescheduling of marijuana has been ostensiblyabout the safety and efficacy of marijuana use, it has been driven by thedebate about the legal status of recreational marijuana use. For example,some of the groups advocating the therapeutic use of cannabis have alsobeen proponents of cannabis legalisation (e.g. NORML), thereby fuellingthe fears of opponents of cannabis use that success in the campaign formarihuana rescheduling will be the thin edge of a wedge to legalise cannabis.Other proponents of legalisation (e.g. Grinspoon and Bakalar, 1993) haveturned this reasoning around, by arguing for the legalisation of cannabisas a way of making cannabis available for therapeutic purposes.
On the other side of the argument are those opponents of marijuana usewho fear that the admission that marijuana, or any of its constituents,may have a therapeutic use will send the "wrong message" to youth.This has led to the denial that cannabinoids have any therapeutic effects,and to attempts to stifle all scientific inquiry into any such effects.For example, Mr Bernstein representing the National Federation of Parentsfor a Drug Free Youth had the following to say in his summing up againstRescheduling marijuana before Judge Young (1989):
"If marijuana were to be rescheduled to Schedule II, what kindof message are we sending to a nation that is engaged in a battle for it'svery survival because of epidemic drug abuse? ... will not the messagebe that marijuana is good for cancer, good for glaucoma, good for spasticityand a host of other illnesses? Now to all of this who are the most vulnerable?The answer is, of course, our young people. Their reaction will be thatif it is good for all of these things, it can't be bad for me. We thenhave another youngster trying marijuana, the gateway drug and probablystarting down the road that leads to nowhere but destruction" (inRandall, 1989, p395).
It is unfortunate that a connection has been forged between the debatesabout the legal status of cannabis as a recreational drug and the use ofcannabinoids for therapeutic use. Any such connection is spurious, sincethere is a world of difference between the use of controlled doses of apurified drug under medical supervision and the recreational use of crudepreparations of a drug. In a rational world, clinical decisions about whetherto use pure cannabinoid drugs should not be abrogated because crude formsof the drug may be abused by those who use it recreationally. As a communitywe do not allow this type of thinking to deny us the use of opiates foranalgesia. Nor should it be used to deny access to any therapeutic usesof cannabinoids derivatives that may be revealed by pharmacological research.
8.11 Conclusions
The following provisional conclusions can be drawn on the availableevidence. First, there is good evidence for the therapeutic potential ofTHC as an anti-emetic agent. Although uncertainty exists about the mostoptimal method of dosing and the advantages and disadvantages of differentroutes of administration, there is sufficient evidence to justify it beingmade available in pure synthetic form to cancer patients. In the lightof the recent development of more effective anti-emetic agents, it remainsto be seen how widely used the cannabinoids will be. Second, there is reasonableevidence for the potential efficacy of THC in the treatment of glaucoma,especially in cases which have proved resistant to existing anti-glaucomaagents. Further research is clearly required, but this should not preventits use under medical supervision in poorly controlled cases, providedpatients make informed decisions about its use in the light of informationabout the possible health risks of long-term use. Third, there is sufficientsuggestive evidence of the potential usefulness of various cannabinoidsas analgesic, anti-asthmatic, anti-spasmodic, and anti-convulsant agentsto warrant further basic pharmacological and experimental investigation,and perhaps clinical research into their effectiveness.
Despite the basic and clinical research work which was undertaken inlate 1970s and early 1980s, the cannabinoids have not been widely usedtherapeutically, nor have further investigations been conducted along thelines suggested in the positive evaluations made by the Institute of Medicine(1982). This seems largely attributable to the fact that clinical researchon the therapeutic use of cannabinoids has been discouraged by regulationand a lack of funding in the United States, where most cannabis researchhas been conducted. The discouragement of therapeutic research, in turn,derives from the fact that THC, the most therapeutically effective cannabinoid,has the psychoactive effects sought by recreational users. In opposingthe therapeutic uses of cannabinoids, some researchers have used doublestandards in appraising efficacy and safety, setting unreasonably highstandards in assessing the evidence on the comparative therapeutic safetyand efficacy of cannabinoids and existing agents. The application of thesame demanding standards to existing agents for the candidate diseases,and more generally, to existing psychoactive drugs that are widely usedin medical practice, would denude the pharmacopoeia. The recent discoveryof the cannabinoid receptor may help to overcome some of the resistanceto research into the therapeutic uses of cannabinoids, by holding out theprospect that the psychoactive effects of the cannabinoids can be disengagedfrom their other therapeutically desirable effects.
References
Adler, M.W. and Geller, E.B. (1986) Ocular effects of cannabinoids.In R. Mechoulam (ed) Cannabinoids as Therapeutic Agents. Boca Raton, Florida:CRC Press.
American Academy of Ophthalmology. (1990) "The use of marijuanain the treatment of glaucoma", June 21, 1987, reproduced In R Randall(ed) Cancer Treatment and Marijuana Therapy. Washington, DC: Galen Press.
Carey, M.P., Burish, T.G. and Brenner, D.E. (1983) Delta-9-tetrahydrocannabinolin cancer chemotherapy: research problems and issues. Annals of InternalMedicine, 99, 106-114.
Casswell, A. (1992) Marijuana as medicine. Medical Journal of Australia,156, 497-498.
Chang, A.E., Shiling, D.J., Stillman, R.C., Goldberg, N.H., Seipp, C.A.,Barofsky, I., Simon, R.M. and Rosenberg, S.A. (1979) Delta-9-tetrahydrocannabinolas an antiemetic in cancer patients receiving high-dose methotrexate. Annalsof Internal Medicine, 91, 819-824.
Chesher, G.B. and Jackson, D.M. (1974) Anticonvulsant effects of cannabinoidsin mice: drug interactions within cannabinoids, and cannabinoid interactionswith phenytoin. Psychopharmacologia, 37, 255-264.
Clifford, D.B. (1983) Tetrahydrocannabinol for tremor in multiple sclerosis.Annals of Neurology, 13, 669-671.
Consroe, P.F., Wood, G and Buchsbaum, H. (1975) Anticonvulsant nature
From ???@??? Sat Oct 19 04:47:16 1996 Received: from gulik.dymaxion.edu(root@line027.nwm.mindlink.net [204.191.202.27]) by gold.interlog.com (8.7.6/8.6.10)with ESMTP id AAA09889 for <iorfida@interlog.com>; Sat, 19 Oct 199600:43:12 -0400 (EDT) From: ccletters@hempbc.com Received: from hempbc.com(root@localhost [127.0.0.1]) by gulik.dymaxion.edu (8.7.5/8.6.9) with SMTPid UAA00662 for ccletters; Fri, 18 Oct 1996 20:50:48 -0700 Date: Fri, 18Oct 1996 20:50:48 -0700 Message-Id: <199610190350.UAA00662@gulik.dymaxion.edu>Reply-To: ai256@chebucto.ns.ca Subject: CC#08 Lindesmith Center: ExposingMarijuan Myths(fwd) X-UIDL: ff8f5757ea5ac286f394be1b89146e75
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EXPOSING MARIJUANA MYTHS:
A REVIEW OF THE SCIENTIFIC EVIDENCE
by Lynn Zimmer, Associate Professor of Sociology Queens College
and John P. Morgan, Professor of Pharmacology, City University MedicalSchool
INTRODUCTION
Since the 1920s, supporters of marijuana prohibition have exaggeratedthe drug's dangers. In different eras, different claims have gained prominence,but few have ever been abandoned. Indeed, many of the "reefer madness"tales that were used to generate support for early anti-marijuana lawscontinue to appear in government and media reports today.
For a while in the 1970s, it seemed as if scientific inquiries werebeginning to influence the government's marijuana policies. Following thoroughreviews of the existing evidence by scholars and official commissions,criminal penalties for marijuana offenses were lessened and a number ofstates moved in the direction of decriminalization. However, in responseto lingering concerns about marijuana's potential toxicity, the governmentexpanded its funding of scientific research, mostly through the newly createdNational Instutite on Drug Abuse (NIDA).
Probably the most important studies of the 1970s were three large "fieldstudies" in Greece, Costa Rica and Jamaica. These studies, which evaluatedthe impact of marijuana on users in their natural environments, were supplementedby clinical examinations and laboratory experiments oriented toward answeringthe questions about marijuana that continued to be debated in the scientificliterature. The data from these studies, published in numerous books andscholarly journals, covered such matters as marijuana's effects on thebrain, lungs, immune and reproductive systems, its impact on personality,development, and motivational states, and its addictive potential.
Although these studies did not answer all remaining questions aboutmarijuana toxicity, they generally supported the idea that marijuana wasa relatively safe drug -- not totally free from potential harm, but unlikelyto create serious harm for most individual users or society. In the yearssince, thousands of additional studies have been conducted, many of themfunded by NIDA, and together they reaffirm marijuana's substantial marginof safety. Our review of that body of work reveals an occasional studyindicating greater toxicity than previously thought. But in nearly allsuch cases, the methodologies were seriously flawed and the findings couldnot be replicated by other researchers.
Especially since the 1980s, when the federal government's renewed waron cannabis began, both the funding of marijuana research and the disseminationof its findings have been highly politicized. Indeed, NIDA's role seemsto have become one of service to the War on Drugs. Dozens of claims oftoxicity appear in its documents, despite the existence of scores of scientificstudies refuting their validity. At the same time, studies that fail tofind serious toxicity are ignored.
In the following pages, we review the scientific evidence surroundingthe most prominent of the anti-marijuana claims.
CLAIM #1: MARIJUANA USE IS INCREASING AT AN ALARMING RATE
Reports of a recent slight increase in marijuana use, especially amongyouth, are being used to convince Americans that a renewed campaign aboutthe drug's dangers is necessary to avert an impending epidemic.
THE FACTS
According to government surveys of the general population, marijuanause began decreasing in 1980, after more than a decade of steady increase.By 1990, the downward trend showed signs of slowing, but use-rates remainedsubstantially lower than those recorded in the 1970s.
For example, among 12-17 year olds, past year marijuana use was about8 percent in 1992, compared to 24.1 percent in 1979. Among 18-25 year olds,past year use was 23 percent in 1992, compared to 46.9 percent in 1979.
A separate survey of high school students shows similar trends, withuse-rates in the 1990s well below those reported in the 1970s. However,after reaching an all-time low in 1992, they increased slightly duringthe next two years.
LIFETIME PREVALENCE OF MARIJUANA, HIGH SCHOOLS SENIORS, 1976-1994
19761978 19801982 198419861988 19901992199452.8 59.260.358.7 54.950.947.240.732.638.2
The High School Survey was originally conceived by the National Instituteon Drug Abuse (NIDA) as a measure of non-pathological drug use. This isstill what it measures. Adolescence is a time of experimentation, withdrug use as well as other activities. Most adolescent drug users do notgo on to become "drug abusers." Indeed, most adolescent drugusers, after a few years of experimentation, cease using illegal drugsaltogether.
We will probably never know why marijuana-use rates go up and down overtime. However, it is worth noting that the recent increase occurred amongthe same population of young people who had been exposed to a decade-longanti-marijuana campaign in the schools and the media. That campaign, basedon exaggerations of marijuana's harms and a "just say no" ideology,has clearly failed.
Young people, and Americans generally, need to know the scientific evidenceabout marijuana if they are to make informed decisions about both theirown drug use and the future of American drug policy.
CLAIM #2: MARIJUANA POTENCY HAS INCREASED SUBSTANTIALLY
The claim that there has been a 10-, 20- or 30-fold increase in marijuanapotency since the 1970s is used to discredit previous studies that showedminimal harm caused by the drug and convince users from earler eras thattoday's marijuana is much more dangerous.
THE FACTS
For more than 20 years the government-funded Potency Monitoring Project(PMP) at the University of Mississippi has been analyzing samples of marijuanasubmited by U.S. law enforcement officials. At no time have police seizuresreflected the marijuana generally available to users around the countryand, in the 1970s, they were over-represented by large-volume low-potencyMexican kilobricks.
During the 1970s, the PMP regularly reported potency averages of under1%, with a low of 0.4% in 1974. Quite clearly, these averages under-estimatethe THC content of marijuana smoked during this period.
Marijuana of under 0.5% potency has almost no psychoactivity. Whileit is possible that people sometimes obtained marijuana of such low potency,for the drug to have become popular in the 1960s and 1970s, most peoplemust have regularly obtained marijuana with higher THC content.
Until the late 1970s, PMP samples included none of the traditionallyhigher-potency cannabis products, such as buds and sinsemilla, even thoughthese products were available on the retail market. When changes in policepractices resulted in their seizure, PMP potency averages increased.
Every independent analysis of potency in the 1970s found higher THCaverages than the PMP. For example, the 59 samples submitted to PharmChemLaboratories in 1973 averaged 1.62%; only 16 (27%) contained less than1% THC, more than half were over 2% and about one-fifth were over 4%. In1975, PharmChem samples ranged from 2 to 5%, with some as high as 14% --nearly 30 times the .71 average reported by the PMP.
After 1980, both the number and variety of official seizures increaseddramatically, improving the validity of the PMP's reported averages, althoughthey continue to be based on "convenience" rather than "representative"samples. As shown below, average potency has remained essentially unchangedsince the early 1980s:
MEAN PERCENTAGE THC OF SEIZED MARIJUANA, 1981-1993, MISSISSIPPI MONITORINGPROJECT
19811982 19831984 198519861987 198819891990199119921993 2.28 3.053.232.392.822.302.93 3.293.063.36 3.363.003.32
Even if potency had increased slightly since the 1970s, it would notmean that smoking marijuana had become more dangerous. In fact, since theprimary health risk of marijuana comes from smoking, higher potency productscan be less dangerous because they allow people to achieve the desiredeffect by inhaling less.
CLAIM #3: MARIJUANA IS A DRUG WITHOUT THERAPEUTIC VALUE
Proposals to make marijuana legally available as a medicine are counteredwith claims that safer, more effective drugs are available, including asynthetic version of delta-9-THC, marijuana's primary active ingredient.
THE FACTS
For thousands of years, throughout the world, people have used marijuanato treat a variety of medical conditions.
Today, in the United States, such use is prohibited. Although thirty-sixstates have passed legislation to allow marijuana's use as a medicine,federal law preempts their making marijuana legally available to patients.
A number of studies have shown that marijuana is effective in reducingnausea and vomiting, lowering intraocular pressure associated with glaucoma,and decreasing muscle spasm and spasticity. Today, many people use marijuanafor these and other medical purposes, despite its illegal status.
People undergoing cancer chemotherapy have found smoked marijuana tobe an effective anti-nauseant-often more effective than available pharmaceuticalmedications. Indeed, 44 percent of oncologists responding to a questionnairesaid they had recommended marijuana to their cancer patients; others saidthey would recommend it if it were legal.
Marijuana is also smoked by thousands of AIDS patients to treat thenausea and vomiting associated with both the disease and AZT drug therapy.Because it stimulates appetite, marijuana also counters HIV-related "wasting,"allowing AIDS patients to gain weight and prolong their lives.
In 1986, a synthetic delta-9-THC capsule (Marinol) was marketed in theUnited States and labeled for use as an anti-emetic. Despite some utility,this product has serious drawbacks, including its cost. For example, apatient taking three 5 mgm capsules a day would spend over $5,000 to useMarinol for one year. In comparison to the natural, smokeable product Marinolalso has some pharmacological shortcomings. Because THC delivered in oralcapsules enters the bloodstream slowly, it yields lower serum concentrationsper dose. Oral THC circulates in the body longer at effective concentrations,and more of it is metabolized to an active compound; thus, it more frequentlyyields unpleasant psychoactive effects. In patients suffering from nausea,the swallowing of capsules may itself provoke vomiting. In short, the smokingof crude marijuana is more efficient in delivering THC and, in some cases,it may be more effective.
The continuing illegality of medical marijuana is based more on politicalthan scientific considerations. Although during the 1970s the governmentsupported exploration into marijuana's therapeutic potential, its rolehas become one of blocking new research and opposing any change in marijuana'slegal status.
CLAIM #4: MARIJUANA CAUSES LUNG DISEASE
It is frequently claimed that marijuana smoke contains such high concentrationsof irritants that marijuana users' risk of developing lung disease is equalto or greater than that of tobacco users.
THE FACTS
Except for their psychoactive ingredients, marijuana and tobacco smokeare nearly identical. Because most marijuana smokers inhale more deeplyand hold the smoke in their lungs, more dangerous material may be consumedper cigarette. However, it is the total volume of irritant inhalation-notthe amount in each cigarette-that matters.
Most tobacco smokers consume more than 10 cigarettes per day and someconsume 40 or more. Regular marijuana smokers seldom consume more than3-5 cigarettes per day and most consume far fewer. Thus, the amount ofirritant material inhaled almost never approaches that of tobacco users.
Frequent marijuana smokers experience adverse respiratory symptoms fromsmoking, including chronic cough, chronic phlegm, and wheezing. However,the only prospective clinical study shows no increased risk of cripplingpulmonary disease (chronic bronchitis and emphysema).
Since 1982, UCLA researchers have evaluated pulmonary function and bronchialcell characteristics in marijuana-only smokers, tobacco-only smokers, smokersof both, and non-smokers. Although they have found changes in marijuana-onlysmokers, the changes are much less pronounced than those found in tobaccosmokers.
The nature of the marijuana-induced changes were also different, occuringprimarily in the lung's large airways-not the small peripheral airwaysaffected by tobacco smoke. Since it is small-airway inflamation that causeschronic bronchitis and emphysema, marijuana smokers may not develop thesediseases.
In an epidemiological survey, approximately 1200 subjects gave informationon smoking and pulmonary function at 2-year intervals. A large percentageof the subjects underwent pulmonary function testing. Although a smallgroup who reported previous marijuna smoking had significant pulmonaryabnormalities, curent marijuana smokers had no significant reduction inany pulmonary functions.
There are no epidemiological or aggregate clinical data suggesting thatmarijuana-only smokers develop lung cancer. However, since some bronchialcell changes appear to be pre-cancerous, an increased risk of cancer amongfrequent marijuana smokers is possible.
Since the pulmonary risks associated with marijuana are related to smoking,the danger is eliminated with other routes of administration. For committedsmokers, pulmonary risk might be reduced with higher-potency products,which produce desired psychoactive effects with less inhalation of irritants.Smokers could also be encouraged to abandon deep inhalation and breath-holding,which increase drug delivery only slightly.
Finally, pulmonary risk might be reduced if marijuana were smoked inwater pipes rather than cigarettes.
CLAIM #5: MARIJUANA IMPAIRS IMMUNE SYSTEM FUNCTIONING
It has been widely claimed that marijuana substantially increases users'risk of contracting various infectious diseases. First emerging in the1970s, this claim took on new significance in the 1980s, following reportsof marijuana use by people suffering from AIDS.
THE FACTS
The principal study fueling the original claim of immune impairmentinvolved preparations created with white blood cells that had been removedfrom marijuana smokers and controls. After exposing the cells to knownimmune activators, researchers reported a lower rate of "transformation"in those taken from marijuana smokers. However, numerous groups of scientists,using similar techniques, have failed to confirm this original study. Infact, a 1988 study demonstrated an increase in responsiveness when whiteblood cells from marijuana smokers were exposed to immunological activators.
Studies involving laboratory animals have shown immune impairment followingadministration of THC, but only with the use of extremely high doses. Forexample, one study demonstrated an increase in herpes infection in rodentsgiven doses of 100 mg/kg/day-a dose approximately 1000 times the dose necessaryto produce a psychoactive effect in humans.
There have been no clinical or epidemiological studies showing an increasein bacterial, viral, or parasitic infection among human marijuana users.In three large field studies conducted in the 1970s, in Jamaica, CostaRica and Greece, researchers found no differences in disease susceptibilitybetween marijuana users and matched controls.
Marijuana use does not increase the risk of HIV infection; nor doesit increase the onset or intensity of symptoms among AIDS patients. Infact, the FDA decision to approve the use of Marinol (synthetic THC) foruse in HIV-wasting syndrome relied upon the absence of any immunopathologydue to THC.
Today, thousands of people with AIDS are smoking marijuana daily tocombat nausea and increase appetite. There is no scientific basis for claimsthat this practice compromises their immune responses. Indeed, the recentdiscovery of a peripheral cannabinoid receptor asociated with lymphatictissue should encourage aggressive exploration of THC's potential use asan immune-system stimulant.
CLAIM #6: MARIJUANA HARMS SEXUAL MATURATION AND REPRODUCTION
Marijuana has been said to interfere with the production of hormonesassociated with reproduction, causing possible infertility among adultusers and delayed sexual development among adolescents.
THE FACTS
There is no evidence that marijuana impairs male reproductive functioning.The Jamaican and Costa Rican field studies detected no differences in hormonelevels between marijuana users and non-users. In epidemiological surveysof marijuana users, no problems with fertility have emerged as important.
In 1974, researchers reported diminished testosterone, reduced sexualfunction and abnormal sperm cells in males identified as chronic marijuanausers. In a laboratory study, the same researchers reported an acute decreasein testosterone, but no chronic effect after nine weeks of smoking; theydid not evaluate sperm volume or quality. In other laboratory studies,researchers have been generally unable to replicate these findings althoughby administering very high THC doses-up to 20 cigarettes per day for 30days- one study found a slight decrease in sperm concentrations. In allstudies, test results remained within normal ranges and probably wouldnot have affected actual fertility. Severe adverse consequences have alsobeen produced in male laboratory animals, although only with extremelyhigh daily THC doses. More importantly, in both the human and animal laboratorystudies, all observed changes were reversed once THC adminstration washalted.
The claim that marijuana impairs female reproductive functioning inhumans has no support in the scientific literature. There have been noepidemiological studies indicating diminished fertility in female usersof marijuana, and a recent survey found no impact of chronic marijuanause on female sex hormones.
Animal studies show hormonal changes and depressed ovulation followingextremely high daily doses of THC. As occurs with males, these changesdisappear once the experiment is completed. In addition, when THC was administeredto female monkeys for an entire year, they developed tolerance to its hormonaleffects and normal cycles were reestablished.
Almost immediately following publication of the few studies showinga marijuana impact on reproductive hormones, warnings about marijuana'spotential impact on adolescent sexual development began to appear.
Other than one case report of a 16-year old marijuana smoker who hadfailed to progress to puberty, there has been nothing to indicate thatsuch a potential exists. In whatever other ways one might consider marijuanato be bad for adolescents, it does not retard their sexual development.
CLAIM #7: MARIJUANA USE DURING PREGNANCY HARMS THE FETUS
A powerful accusation in anti-drug campaigns is that children are permanentlyharmed by their mothers' use of drugs during pregnancy. Today, it is commonlyclaimed that marijuana is a cause of birth defects and development deficits.
THE FACTS
A number of studies reported low birth weight and physical abnormalitiesamong babies exposed to marijuana in utero. However, when other factorsknown to affect pregnancy outcomes were controlled for-for example, maternalage, socio-economic class, and alcohol and tobacco use-the associationbetween marijuana use and adverse fetal effects disappeared.
Numerous other studies have failed to find negative impacts from marijuanaexposure. However, when negative outcomes are found, they tend to be widelypublicized, regardless of the quality of the study.
It is now often claimed that marijuana use during pregnancy causes childhoodleukemia. The basis for this claim is one study, in which 5% of the mothersof leukemic children admitted to using marijuana prior to or during pregnancy.A "control group" of mothers with normal children was then createdand questioned by telephone about previous drug use. Their reported .5percent marijuana use- rate was used to calculate a 10-fold greater riskof leukemia for children born to marijuana users. Given national surveysshowing marijuana prevalence rates of at least 10%, these "controlgroup" mothers almost certainly under-reported their drug use to strangerson the telephone.
Also used as evidence of marijuana-induced fetal harm are two longitudinalstudies, in which the children of marijuana users were examined repeatedly.However, on closer examination, the effects of marijuana appear to be quiteminimal, if existent at all. After finding a slight deficit in visual responsivenessamong marijuana-exposed newborns, no differences were found at 6 months,12 months, 18 months, or 24 months. At age 3, the only difference (aftercontrolling for confounding variables) was that children of "moderate"smokers had superior psycho-motor skills. At age 4, children of "heavy"marijuana users (averaging 18.7 joints/week) had lower scores on one subscaleof one standardized test of verbal development. At age 6, these same childrenscored lower on one computerized task-that measuring "vigilance."On dozens of others scales and subscales, no differences were ever found.
In another study, standardized IQ tests were administered to marijuana-exposedand unexposed 3 year-olds. Researchers found no differences in the overallscores. However, by dividing the sample by race, they found-among African-American children only-lower scores on one subscale for those exposed duringthe first trimester and lower scores on a different subscale for thoseexposed during the second trimester.
Although it is sensible to advise pregnant women to abstain from usingmost drugs-including marijuana-the weight of scientific evidence indicatesthat marijuana has few adverse consequences for the developing human fetus.
CLAIM #8: MARIJUANA CAUSES BRAIN DAMAGE
Critics state that marijuana damages brain cells and that this damage,in turn, causes memory loss, cognitive impairment, and difficulties inlearning.
THE FACTS
The original basis of this claim was a report that, upon post-mortemexamination, structural changes in several brain regions were found intwo rhesus monkeys exposed to THC. Because these changes primarily involvedthe hippocampus, a cortical brain region known to play an important rolein learning and memory, this finding suggested possible negative consequencesfor human marijuana users. Additional studies, employing rodents, reportedsimilar brain changes. However, to achieve these results, massive dosesof THC-up to 200 times the psychoactive dose in humans-had to be given.In fact, studies employing 100 times the human dose have failed to revealany damage.
In the most recently published study, rhesus monkeys, through face-maskinhalation, were exposed to the equivalent of 4-5 joints per day for anentire year. When sacraficed seven months later, there was no observedalteration of hippocampal architecture, cell size, cell number, or synapticconfiguration. The authors conclude that: "while behavioral and neuroendocrinaleffects were observed during marijuana smoke exposure in the monkey, residualneuropathological and neurochemical effects of marijuana exposure werenot observed seven months after the year-long marijuana smoke regimen."
Thus, twenty years after the first report of brain-damage in two marijuana-exposedmonkeys, the claim of physiological damage to brain cells has been effectivelydisproven.
No post-mortem examinations of the brains of human marijuana users haveever been conducted. However, numerous studies have explored marijuana'seffect on brain-related cognitive functions. Many employ an experimentaldesign-in which subjects are given marijuana in a laboratory setting, andthen compared to controls on a variety of measures involving attention,learning, and memory.
In a number of studies, no significant differences were detected. Infact, there is substantial research demonstrating that marijuana intoxicationdoes not impair the retrieval of information learned previously. However,there is evidence that marijuana, particularly in high doses, may interferewith users' ability to transfer new information into long-term memory.
While there is general agreement that, while under the influence ofmarijuana, learning is less efficient, there is no evidence that marijuanausers-even long-term users-suffer permanent impairment. Indeed, numerousstudies comparing chronic marijuana users with non-user controls have foundno significant differences in learning, memory recall, or other cognitivefunctions.
CLAIM #9: MARIJUANA IS AN ADDICTIVE DRUG
It is now frequently stated that marijuana is profoundly addicting andthat any increase in prevalence of use will lead inevitably to increasesin addiction.
THE FACTS
Essentially all drugs are used in "an addictive fashion" bysome people. However, for any drug to be identified as highly addictive,there should be evidence that substantial numbers of users repeatedly failin their attempts to discontinue use and develop use-patterns that interferewith other life activities.
National epidemiological surveys show that the large majority of peoplewho have had experience with marijuana do not become regular users.
In 1993, among Americans age 12 and over, about 34% had used marijuanasometime in their life, but only 9% had used it in the past year, 4.3%in the past month, and 2.8% in the past week.
A longitudinal study of young adults who had first been surveyed inhigh school also found a high "discontinuation rate" for marijuana.While 77% had used the drug, 74% of those had not used in the past yearand 84% had not used in the past month.
Of course, even people who continue using marijuana for several yearsor more are not necessarily "addicted" to it. Many regular users-includingmany daily users-consume marijuana in a way that does not interfere withother life activities, and may in some cases enhance them. There is onlyscant evidence that marijuana produces physical dependence and withdrawalin humans.
When human subjects were administered daily oral doses of 180-210 mgTHC-the equivalent of 15-20 joints per day-abrupt cessation produced adversesymptoms, including disturbed sleep, restlessness, nausea, decreased appetite,and sweating. The authors interpreted these symptoms as evidence of physicaldependence. However, they noted the syndrome's relatively mild nature andremained skeptical of its occurrence when marijuana is consumed in usualdoses and situations. Indeed, when humans are allowed to control consumption,even high doses are not followed by adverse withdrawal symptoms.
Signs of withdrawal have been created in laboratory animals followingthe administration of very high doses. Recently, at a NIDA-sponsored conference,a researcher described unpublished observations involving rats pre-treatedwith THC and then dosed with a cannabinoid receptor-blocker. Not surprisingly,this provoked sudden withdrawal, by stripping receptors of the drug. Thisfinding has no relevance to human users who, upon ceasing use, experiencea very gradual removal of THC from receptors.
The most avid publicizers of marijuana's addictive nature are treatmentproviders who, in recent years, have increasingly admitted insured marijuanausers to their programs. The increasing use of drug-detection technologiesin the workplace, schools and elsewhere has also produced a group of marijuanausers who identify themselves as "addicts" in order to receivetreatment instead of punishment.
CLAIM #10: MARIJUANA-RELATED MEDICAL EMERGENCIES ARE INCREASING
As evidence of its harmful effects, prohibition advocates point to dramaticincreases in emergency-room episodes related to marijuana ingestion.
THE FACTS
Data gathered by the Drug Abuse Warning Network (DAWN) show a recentincrease in "marijuana mentions" by people seeking treatmentin hospital emergency rooms. Using a one-page form, emergency-room personnelrecord "drug abuse episodes," note the presence or absence ofalcohol as a contributing factor, and list up to four other drugs recentlyconsumed by the patient.
Although DAWN began compiling data in the 1970s, recent changes in recordingprocedures, the hospital selection, and methods of statistical estimationprevent comparisons of data gathered prior to 1988 with those gatheredrecently. Thus, discussion of emergency-room trends is limited to the years1988 to 1993.
The lowest number of marijuana-mentions, recorded in 1990, was 15,706(7.1 mentions per 100,000 population). The highest was 29,166 (12.7 per100,000 population), recorded in 1993.
Using these figures, an increase of 86% has been reported. However,if 1988 is used as the "base year" instead-a year in which therewere 19,962 marijuana mentions-the increase is reduced immediately by morethan half, to 42%.
Despite marijuana being the most frequently used illicit drug, in emergencyrooms, it remains the least often mentioned illicit drug.
In 1993, marijuana accounted for 6.25% of mentions, compared to 15.3%for cocaine and 9.8% for heroin. Even over-the-counter pain medicationswere mentioned more often than marijuana-comprising 9% of the total.
For youth aged 6 to 17, there were more mentions of marijuana than ofheroin and cocaine-not because marijuana is more harmful to them but becausethese latter drugs are used so infrequently by young people. In this agegroup, mentions of over-the-counter pain medications were substantiallyhigher than those for marijuana. While marijuana accounted for 6.48% ofdrug mentions by youth, over-the-counter pain medications accounted for47%.
For the total population, not only is marijuana mentioned less frequentlythan other recreational drugs, it is seldom mentioned alone. In 1992, inmore than 80% of the drug-abuse episodes involving marijunana, at leastone other drug was mentioned; and, in more than 40%, two or more additionaldrugs were mentioned.
Of 24,000 marijuana mentions in 1992, more than 13,000 involved alcoholand nearly 10,000 involved cocaine.
Despite recent increases in marijuana mentions, hospital emergency roomsare not flooded with marijuana users seeking medical attention. In 1992,of 433,493 total drug mentions, only 4,464 -- about 1% -- involved theuse of marijuana alone.
CLAIM #11: MARIJUANA PRODUCES AN AMOTIVATIONAL SYNDROME
Marijuana is said to have a deliterious effect on society by makingusers passive, apathetic, unproductive, and unable (or unwilling) to fulfilltheir responsibilities.
THE FACTS
The concept of an amotivational syndrome first appeared in the late1960s, as marijuana use was increasing among American youth. In the yearssince, despite the absence of an agreed-upon definition of the concept,numerous researchers have attempted to verify its occurrence.
Large-scale studies of high school students have generally found nodifference in grade-point averages between marijuana users and non-users.One study found lower grades among students reported to be daily usersof marijuana, but the authors failed to identify a causal relationshipand concluded that both phenomena were part of a complex of inter-relatedsocial and emotional problems.
In one longitudinal study of college students, after controlling forother factors, marijuana users were found to have higher grades than non-usersand to be equally as likely to successfully complete their educations.Another study found that marijuana users in college scored higher thannon-users on standardized "achievement values" scales.
Field studies conducted in Jamaica, Costa Rica and Greece also foundno evidence of an amotivational syndrome among marijuana-using populations.
In these samples of working-class males, the educational and employmentrecords of marijuana users were, for the most part, similar to those ofnon-users. In fact, in Jamaica, marijuana was often smoked during workinghours as an aid to productivity. The results of laboratory studies havebeen nearly as consistent.
In one study lasting 94 days, marijuana had no significant impact onlearning, performance or motivation.
In another 31-day study, subjects given marijuana worked more hoursthan controls and turned in an equal number of tokens for cash at the study'scompletion.
However, in a Canadian study that required subjects in the marijuanagroup to consume unusually high doses, some reduction in work efficencywas noted in the days following intoxication.
Undoubtedly, when marijuana is used in a way that produces near-constantintoxication, other activities and responsibilities are likely to be neglected.
However, the weight of scientific evidence suggests that there is nothingin the pharmacological properties of cannabis to alter people's attitudes,values, or abilities regarding work.
CLAIM #12: MARIJUANA IS A MAJOR CAUSE OF HIGHWAY ACCIDENTS
The detrimental impact of alcohol on highway safety has been well documented.Marijuana's opponents claim that it, too, causes significant impairmentand that any increase in use will lead to increased highway accidents andfatalities.
THE FACTS
In high doses, marijuana probably produces driving impairment in mostpeople. However, there is no evidence that marijuana, in current consumptionpatterns, contributes substantially to the rate of vehicular accidentsin America.
A number of studies have looked for evidence of drugs in the blood orurine of drivers involved in fatal crashes. All have found alcohol presentin 50 percent or more. Marijuana has been found much less often. Furthermore,in the majority of cases where marijuana has been detected, alcohol hasbeen detected as well.
For example, a recent study sponsored by the U.S. National Highway TrafficSafety Administration (NHTSA) involving analysis of nearly 2000 fatal accidentcases, found 6.7 percent of drivers positive for marijuana. In more thantwo-thirds of those, alcohol was present and may have been the primarycontributor to the fatal outcome.
To accurately assess marijuana's contribution to fatal crashes, thepositive rate among deceased drivers would have to be compared to the positiverate from a random sample of drivers not involved in fatal accidents. Sincethe rate of past-month marijuana use for Americans above the legal drivingage is about 12 percent, on any given day a substantial proportion of alldrivers would test positive, particulary since marijuana's metabolitesremain in blood and urine long after its psychoactive effects are finished.
A recent study found that one-third of those stopped for "bad driving"between the hours of 7 p.m. and 2 a.m.-mostly young males-tested positivefor marijuana only. To be meaningful, these test results would have tobe compared to those from a matched control group of drivers.
A number of driving simulator studies have shown that marijuana doesnot produce the kind of psychomotor impairment evident with modest dosesof alcohol. In fact, in a recent NHTSA study, the only statistically significantoutcome associated with marijuana was speed reduction.
A recent study of actual driving ability under the influence of cannabis-employingthe same protocol used to test the impairment-potential of medicinal drugs-evaluatedthe impact of placebo and three active THC doses in three driving trials,including one in high-density urban traffic.
Dose-related impairment was observed in drivers' ability to maintainsteady lateral position. However, even with the highest dose of THC, impairmentwas relatively minor-similar to that observed with blood-alcohol concentrationsbetween .03 and .07 percent and many legal medications. Drivers under theinfluence of marijuana also tended to drive more slowly and approach othercars more cautiously.
While recognizing some limitations of this study, the authors concludethat "THC is not a profoundly impairing drug.
CLAIM #13: MARIJUANA IS A "GATEWAY" TO THE USE OF OTHER DRUGS
Advocates of marijuana prohibition claim that even if marijuana itselfcauses minimal harm, it is a dangerous substance because it leads to theuse of "harder drugs" such as heroin, LSD, and cocaine.
THE FACTS
Most users of heroin, LSD and cocaine have used marijuana. However,most marijuana users never use another illegal drug. Over time, there hasbeen no consistent relationship between the use patterns of various drugs.As marijuana use increased in the 1960s and 1970s, heroin use declined.And, when marijuana use declined in the 1980s, heroin use remained fairlystable.
For the past 20 years, as marijuana use-rates fluxuated, the use ofLSD hardly changed at all. Cocaine use increased in the early 1980s asmarijuana use was declining. During the late 1980s, both marijuana andcocaine declined. During the last few years, cocaine use has continuedto decline as marijuana use has increased slightly.
In 1994, less than 16 percent of high school seniors who had ever triedmarijuana had ever tried cocaine-the lowest percentage ever recorded. Infact, as shown below, the proportion of marijuana users trying cocainehas declined steadily since 1986, when a high of more than 33 percent wasrecorded.
PERCENTAGE OF MARIJUANA USERS EVER TRYING COCAINE, HIGH SCHOOL SENIORS,1975-1994
19751976 19771978 197919801981 198219831984198519861987 1988 198919901991199219931994 1919 2022 252728 27282931 333026 232222 % 181716
In short, there is no inevitable relationship between the use of marijuanaand other drugs. This fact is supported by data from other countries. InHolland, for example, although marijuana prevalence among young peopleincreased during the past decade, cocaine use decreased-and remains considerablylower than in the United States.
Whereas approximately 16 percent of youthful marijuana users in theU.S. have tried cocaine, the comparable figure for Dutch youth is 1.8 percent.Indeed, Holland's policy of allowing marijuana to be purchased openly ingovernment-regulated "coffee shops" was designed specificallyto separate young marijuana users from illegal markets where heroin andcocaine are sold.
CLAIM #14: DUTCH MARIJUANA POLICY HAS BEEN A FAILURE
While American critics of marijuana prohibition often point to Hollandas a model for an alternative policy, prohibition's supporters claim thatHolland's permissiveness has had disasterous consequences, including escalatingrates of drug use among youth.
THE FACTS
In 1976, following the recommendations of two national commissions,the Dutch government revised many aspects of its drug policy. While notlegalizing marijuana, it adopted an "expediency principle," whichdirected police and prosecutors to ignore retail sale to adults as longas the circumstances of the sale do not constitute a public nuisance.
This change in policy was based on several factors, including: * a principleof tolerance toward alternative lifestyles * a finding that, compared toother illegal drugs, marijuana poses little risk to users * a desire toprotect marijuana users from the marginalization that accompanies arrestand prosecution * a belief that separating the retail markets for "soft"and "hard" drugs decreases the likelihood that marijuana userswill experiment with cocaine or heroin
Following the policy change, marijuana sales emerged openly in coffeeshops, which were required to follow a set of regulations, including aban on advertising, sale of no more than 30 grams at a time, and a minimumpurchase age of 18. The sale of other drugs on the premises is strictlyprohibited, and constitutes grounds for immediate closure by the police.Local officials were also authorized to create additional regulations toprotect the interests of the community-for example, limiting the numberof coffee shops concentrated in any one area.
Since liberalization, marijuana use has increased in the Netherlands,although rates remain similar to those in neighboring European countries,and are generally lower than those in the United States.
MARIJUANA USE AMONG DUT