fanatic4488

I think you are mistaken. There is still plenty of marijuana research going on in the U.S. by non-government afilliated research groups, mostly colleges and universities. In fact, the vast majority of THC research that I have been doing is post-2000, and every month I see new research coming out in the professional journals. Would you like me to provide you with information on these studies? There is no shortage of marijuana research in the U.S. (in fact, my university is doing plenty of marijuana research). However, there is a shortage of recent research on the effects of THC on REM and SWS. There is also a confound in research. It is my belief that laboratory marijuana research actually underestimates the effects of long-term THC use. The reason for this is that when you examine the methods of these studies, you see that they are pretty much all based on acute marijuana use. Subjects only ingest THC for short periods of time. There is a dramatic shortage of good, well-controlled research on long-term marijuana use. It would be impossible, for example, to get an ethics board to approve a study in which you will have adults smoke THC for a decade. If, for example, someone developed lung cancer, then the school would be liable. The best we can do is correlational research with long-term humans. I have seen plenty of studies in which long-term cannabis users are found to have a higher incidence of a wide variety of health problems. However, these studies are incredibly flawed because they are correlational instead of causational. They prove nothing because they are not controlled for confounds. It is difficult to get unriversity ethics boards to allow long-term research on humans (no...it's not a case of the government censoring us, it's us censoring us). You simply cannot do research in a university without the approval of the Ethics Review Board, which is your own college's staff, not the government. Also, the databases I use do include professional journals from places like the U.K., Australia, Sweden, etc. It is very common for me to site foreign research. However, I do not think they include reports that are not available in English.

Mamabudz

To do research into an illicit drug, Colleges and Universities must not only affiliate with the Government, they must receive their approval, samples and report to the Governemnt.

"Plenty" of research is an insignificant term. There are a number of universities doing research at this time, including U of California, U of F. University of Mass has had difficulty getting approval for its studies as the Governemnt continues to deny them access to growing the grade of cannabis currently marketed to the regular consumer -- in fact Senator Kerry wrote letters supporting UMass recommending that they be allowed to grow their own, but this request has been denied, yearly, for alomost 7 years now.

Of course the research you are doing is post 2000 -- it is allowed now, it wasn't prior to this time. But what you are doing is simply that RESEARCH. Findings of fact, proof of hypothesis, creation of new theories and hypothesis and proof are dcdes away. And publication in "so called" professional journals is merely a stepping stone fore individuals who wish to have bullets for their resume. Professional publication of a hypothesis or a theory is nothing new.

Plenty of research -- Many hours of the same thing is not plenty -- it is possibly thorough -- different adjective needed in your expository prose. Your university is studying one aspect. They have noticed a correlation. The conclusion you have leapt to is that Any effect is a BAD effect.

"Leaping to conclusions" is not a healthy exercise for a scientist.

Yes, it does. It is the reason why Anectdotal information is so important in this particular field of research.

Whether the subject is human or other form of mammal

Actually -- there isn't -- I suggest reviewing the research done by the World Health Organization on the Rasta cultures of Jamaica -- specifically in regards to peri-natal and birth outcomes. In addition studies have been carried out over decades throughout the world that simply require a bit more "digging" to find. marijuana is not a newly created amphetamine -- its history dates back to biblical use and ergo pre-biblical use. Archeological proofs date it's pharmacological use back to the last ice age with some evidence of use over 20,000 years ago.

Your ethics board would have little trouble finding individuals who have smoked nothing but marijuana for 10 years or so. The problem arises in getting Governemnt approval. You will have to do a bit of researchon that issue but it is truly a sticking point. As for causing lung cancer, I suggest reviewing the published data on that rather than the hearsay evidence you have been provided. There are not, as of this time, any proven cases of lung cancer caused directly by the use of smoked cannabis. While the inhalation of any burning matter and particulate smoke causes irritation ot the nose, throat and lungs, irritation itself is not a sole cause of cancerous development.

Interesting that my indications are that long term cannabis users have a higher quality of life, with less health problems as they enter middle age. Must be the "confounds" such as their awareness to eat better, take life at a slower pace, not be overwhelmed by stress and exercise regualrly. Those with chronic illnesses find that cannabis use decreases their need for other toxic medications which is beneficial in the long run. And they maintain better support systems for dealing with life traumas.

It seems to me that the indiciduals coming to your University probably have other issues to deal with than marijuana use. A very skewed population to use as a "standard".

Ethics Review Boards are comprised of your staff. Professors and Administrators. Folks who rely on the University to get their funds. FUnds for a university come from a variety of places. A small amount comes from the students in the form of privately paid tuition. The vast amount of Tuition is paid for by Federally Funded Student Loans, Federal Student Grants, Grants from Donors to the college (this usually is earmarked for building and sports however), and Federal grants for Research. Ina State University, add in State Grants, State Student Loans, and State Student Grants.

ANywhere you see Federal or State you are dealing with the Governemnt. I beleive you are still naive when it comes to the way things work in business and schools and universities are a business.

Try looking for the actual research PAPERS that are published...not the watered down version of documents that are published in so-called professional journals.

For a start try Hebrew University in Jerusalmen and the University of Bologna in Italy.

Good luck...and have another cookie

Mama Budz

Higher Logic

The statement that there are no Marijuana-related deaths is extremely misleading. I have seen for myself medical reports in which chronic Marijuana use was considered the cause of death.

It is not misleading though. Cannabis has zero toxicity. More people die per year from eating green potatoes than from cannabis intoxication. The only possible way you could die from cannabis is if a bale of it fell on your head. You would literally have to consume 1,500 pounds in 15 minutes to die from smoking. An impossible task.

“At present it is estimated that Marijuana’s LD-50 is around 1:20,000 or 1:40,000. In layman terms, this means that in order to induce death a Marijuana smoker would have to consume 20,000 to 40,000 times as much Marijuana as is contained in one Marijuana cigarette. NIDA-supplied Marijuana cigarettes weigh approximately .9 grams. A smoker would theoretically have to consume nearly 1,500 pounds of Marijuana within about fifteen minutes to induce a lethal response.”

“100% of the studies done at dozens of American universities and research facilities show [cannabis] toxicity does not exist. Medical history does not record anyone dying from an overdose of Marijuana [UCLA, Harvard, and Temple].”

In practical terms, cannabis cannot induce a lethal response as a result of drug-related toxicity.

Known drug-related deaths (in the United Kingdom, 1990):

Tobacco: .................110,000
Alcohol: ..................30,000
Volatile Substances: .........112
Morphine: .....................91
Methadone: ....................84
Heroin: .......................62
Barbiturate Type: ..............7
Anti-Depressants: ..............4
Cocaine: .......................4
Pethidine: .....................3
MDMA (ecstasy): ................3
Amphetamine Type: ..............2
Hallucinogens: .................0
LSD: ...........................0
Psilocybin: ....................0
Cannabis: ......................0

I have seen, for example, lung cancer deaths in which there is not evidence of nicotine use, but there is long-term cannabis use, and other common causes of lung cancer were eliminated.

Moreover, I have seen examples where people who have never smoked anything or had a drink in their lives die of lung cancer. What’s your point? Your point, though invalid, still has no relevance because there are other methods of consuming cannabis, such as vaporization, topical creams, ingestion, and nasal sprays.
This study compares smokers, non-smokers, and drinkers (in differing combinations) and their risk of cancer:

http://www.ccguide.org.uk/cancdata.html

If a person who is stoned crazy gets behind a wheel, wrecks, and dies, wouldn't you consider it possible that the delayed reaction and impaired judgment that certainly all of us agree are factors while you are stoned could be a contributor?

Here is an interesting quote, “[Cannabis] users also have the same or lower incidence of murders and highway deaths and accidents than the general [non-cannabis] using population as a whole.”

Here is an interesting article published on 31 October 2001:

“Studies had found it impossible to prove cannabis adversely affected driving, an Adelaide University researcher said yesterday. Professor Jack MacLean, director of the Road Accident Research Unit, said, while there was no doubt alcohol affected driving adversely, [which] was not the case with Marijuana. ‘It has been impossible to prove Marijuana affects driving adversely,’ he told the Australian Driver Fatigue Conference in Sydney. ‘There is no doubt Marijuana affects performance but it may be it affects it in a [favorable] way by reducing risk-taking.’ Professor MacLean said a study of blood samples taken by SA hospitals from people injured in road accidents found Marijuana was the second most common drug, after alcohol, in the bloodstream. Those with Marijuana in their blood, however, were at fault in less than half of the accidents.”

Another study actually demonstrated that under certain doses of cannabis [0.15 mg of cannabis, or about half a joint], “drivers demonstrated superior reaction times to those who had not.” They concluded, “The results of our tests clearly indicate that a small or moderate amount of cannabis is actually quite beneficial to someone's driving performance.”

I’m sure most of us would agree that driving while under the influence of anything, even a cold medicine or fatigue, is a bad idea, but this is where you inability to understand exactly what it’s like to be “high” comes into play. You have no idea what “delayed reaction times” are or any of the other factors associated with being high are like.

In addition, your theory implies that every person who drives is driving under heavy doses. I would wager that a great majority of people that do smoke do not immediately get up and then start driving. We would much rather enjoy ourselves.

There are lots of studies done about cannabis and driving, and here are some more quotes from other articles:

“Although the cannabis affected reaction time in regular users, its effects appear to be substantially less dangerous than fatigue or drinking. Research by the Australian Drugs Foundation found that cannabis was the only drug tested that decreased the relative risk of having an accident.”

“Tiredness is now blamed for causing 10% of all fatal accidents, compared with 6% for alcohol and 3% for drugs.”

“"Simulated driving scores for subjects experiencing a normal social 'high' and the same subjects under control conditions are not significantly different. However, there are significantly more errors for alcohol intoxicated than for control subjects [Crancer Study, Washington Department of Motor Vehicles]”

Professor Olaf Drummer, a forensic scientist the Royal College of Surgeons in Melbourne in 1996 "Compared to alcohol, which makes people take more risks on the road, Marijuana made drivers slow down and drive more carefully. Cannabis is good for driving skills, as people tend to overcompensate for a perceived impairment."

“This program of research has shown that Marijuana, when taken alone, produces a moderate degree of driving impairment which is related to the consumed THC dose. The impairment manifests itself mainly in the ability to maintain a steady lateral position on the road, but its magnitude is not exceptional in comparison with changes produced by many medicinal drugs and alcohol. Drivers under the influence of Marijuana retain insight in their performance and will compensate, where they can, for example, by slowing down or increasing effort. As a consequence, THC's adverse effects on driving performance appear relatively small.”

It is possible that 30 days is nothing to you. It is possible that you are not addicted to cannabis. It is also possible that you are in the early stages of addiction. I certainly don't know enough about you. I know that there are many people who smoke weed that aren't addicted to it. But I challenge long-term cannabis users to take the 30-day challenge (seriously). You may learn a lot about yourself in the process.

You just told me that cannabis is highly addictive! If that were the case, then I would already be addicted. I already demonstrated that cannabis has essentially zero addiction properties. People are more addicted to soft drinks and sugar than they are cannabis. You certainly do not know enough about me, and you keep bringing up this “long-term” or heavy user point. Explain exactly what you define as “long-term user?” I am a long-term cannabis user, and I have no problem taking a break, and you will find that all of the users on here that are long-term also have no problem doing so. You keep contradicting yourself, you say cannabis is highly addictive, and then say there are many people who are not.

Did you know that less than 1% of cannabis users are daily users? That means the rest of us out there aren’t smoking every day, or even every week.

You have to understand what addiction is.

That’s laughable. I think you need to understand what addiction is, and that there are varying degrees of it. There are certain people out there who are naturally predisposed to be “addicted” to something. I smoke cigarettes, and I know that those are highly addictive. I also smoke cannabis as well, and can say without a doubt that cannabis is not addictive in terms of the “slant” you are applying to the word. Eating chocolate is also addictive, but is that a “bad” thing in your book?

“Abuse is no argument against proper use.”

The following two quotes were approved by judges, doctors, and scientists regarding cannabis and addiction:

“One must make clear from the outset that, by definition, 'subjective preference' or a 'liking' for something, even when the liking is strong, is not 'dependence', nor is it 'addiction'. Dependence and addiction are words, which define and describe the morbid [sick] states inevitably induced in humans by their use of particular substances. A person's repeated indulgence in chemically non-addictive substances, such as cornflakes and milk, can be called a habit, but categorically, for Prohibition purposes, this is not a condition definable as addiction or dependence of any type. The word 'dependence' indicates reliance, only if one cannot lead a life without some substance, does one depend upon it.”

“It is empirically established and repeatedly confirmed by clinical studies that even frequent use of cannabis over prolonged or lifetime periods produces no mental, physical, or social dysfunction. It is a fact that were cannabis to be the object of fixation of a psychologically disturbed person's fixation of dependence, the cannabis itself would do no harm to that individual.”

There is a scale given to substances that determines the relative addictiveness of them. Nicotine is rated at the top, with 100. Caffeine is rated at 68. Cannabis is at the bottom, with 21. The only thing lower are hallucinogens such as LSD, “magic mushrooms” or psilocybin, and mescaline. The reason for this is because hallucinogen drugs do not relieve anxiety, and this has been proven by many people that drugs that do no relieve anxiety have the smallest scale of “addiction” simply because of that. Cannabis is a well-known anti-anxiety substance, which can be linked to CBD, a cannabinoid.

"Addiction is continued use despite negative consequences (i.e. problems). There is a DSM-IV diagnosis of substance dependence that gets much more detailed, and physical dependence and addiction, although related, are NOT synonymous.”

Moreover, what, may I ask, are the negative consequences of cannabis consumption? Your very definition implies that cannabis is not addictive, for I have yet to see where the negatives outweigh the positives. Stress is the number one killer in this world, and cannabis is a great stress reliever. It has a variety of medicinal qualities, many of which are unknown. Substance dependence is having to carry a pack of cigarettes with you no matter where you go. Substance dependence is asking a random stranger if you can “bum a cigarette” from them. Check out what the Dutch have to say about cannabis use. For a place where cannabis is legal, you would think that, since cannabis is so addictive, many people would be using it compared to say a place like the States where it is not legal.

I’m going to end this with some links I think you should check out.

Ireland
http://www.cannabisireland.com/

Israel
http://ale-yarok.org.il/

Canada
http://www.iamm.com/pcparty/links/links.htm

United States
http://www.americancannabissociety.com/

Germany
http://www.acmed.org/

Drug Library
http://www.druglibrary.org/

Australia
http://www.hemp.on.net.au/

Spain
http://kalamudia.kender.es/

New Zealand
http://www.alcp.org.nz/

Drug Text
http://www.drugtext.org/

Japan
http://www.taima.org/en/sitemap.htm

Judge Francis Young
http://www.ukcia.org/pollaw/lawlibrary/young.htm

Erowid
http://www.erowid.org/

2002 Canadian Study
http://www.parl.gc.ca/37/1/parlbus/c.../summary-e.pdf

Holland Study
http://www.ccguide.org.uk/holland.html

2001 Jamaican Study
http://www.stcl.edu/faculty_pages/fa...a/jamacrpt.doc

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fanatic4488

As always, I'm on a pretty restrictive schedule, but I'll reply to a few comments (I have opened quite the can of worms). I'll start with Mama Budz. First off, I am confused. First, you stated my research on THC and REM was outdated (I agree that most, thought not all, of it is, and have been very consistent in pointin that out). I replied by stating that my research is outdated because their doesn't seem to be much research since the 80's on THC and REM. I then got a response that the reason for this lack of research was that the government had banned cannbis research (I assumed you meant from the 80's on). I then replied by saying that I have plenty of post-80's research on cannabis (just not on THC and REM). You then stated that this is because the ban was lifted. When was this supposed ban? The only option left is pre-70's, which was before most drug research in this country. I have tons of research from every decade since the 70's, and I fail to say any gap where this mysterious ban would have occurred.

Next, you stated, "The conclusion you have leapt to is that Any effect is a BAD effect." If you were able to read my directed study on THC and its effects on the adult human body, you would probably withdraw that comment. See, when I report research form a good source, I don't toss anything out. I provide all the research, whether I agree wtih it or not. For each study I presented, I attempted to note its strengths and weaknesses, responding favorably to things like double blind studies, good use of controls, etc. the common benefits you see in good research, and also pointing out when studies don't do a good enough job of contolling variables or have samples sizes that are too small or use THC dosages that are far greater than what you would find in the typical joint. I am very critical of each study I read. And when I found a study that would note something beneficial about THC use, I certainly reported it appropriately. My goal is not to demonize marijuana use...it is to find the truth. After all my research, I am quite convinced that the two extremes are both wrong...marijuana is not a harmless miracle drug, nor is it a psychosis-inducing (with some exceptions), homicide-inspiring devil that is responsible for society's ills. I have been equally disgusted with some of the government-sponsored anit-drug campaigns as I am with the propoganda crap put out by the NORML.

Next, you guys keep telling me about all this wonderful research on THC and REM that I haven't come across...please stop being general and be specific. I provided you with specific studies. If you can provide me with specific studies, I will be glad to check them out. The reason I came to this site in the first place was because I had exhausted all of the good resources I could find. Whenever I start drying up on sources, I start scanning message boards of marijuan users, where, if for nothing else, I try to find sources that I can use to illustrate the wide variation of public perception on the effects of marijuana (which I usually put in my introduction section). However, I rarely get a good specific resource from these sites. Usually, I get more NORML propoganda.

Also, I think you may be a little too pessimistic about research bias on THC. For example, the social psychologist who directed my undergrad research project, for example, couldn't care less what my conclusions are. He was only concerned about the quality of my research. He had no vested interest in whether the research glorified or demonized THC...he wasn't even very interested in the topic. He was, however, very excited about scrutinizing the quality of the research. That is the kind of attitude I usually see in the universities. I usually see folks who aren't emotionally vested in one extreme or the other so much as they are interested in finding the truth.

You said that getting government approval for research is the tough part. My experience has been that the govenrment approval is easy...it's the institutional review board that is the challenge. Whe I was still in undergrad, for example, I kept wanting to do more research on things like THC and REM. Feedback I got from some profs was that I was wasting my time beating a dead horse, trying to prove what has already been proven. Instead, I shoudl do something original, they said...but I hardly think that a dozen or so studies in the 70's and 80's is enough to thoroughly investigate this fascinating area of research.

You are right, there are a lot of confounds among correlational studies of THC users. See, the typical marijuana user is of lower socioeconomic status, more likely to have an arrest history, etc., etc. This means that in order to start drawing connections between the drug and its effects, you must control for varaibles like socioeconomic status (which also means less access to good health care), criminal history (criminals are indeed more likley to use drugs and more likely be "sensation seekers," etc.), etc., etc., etc. It gets hairy. That's why it's not a good idea to use correlational research, such as a university finding people who have smoked for 10 years and then measuring how they differ from the general population (if we went by those studies, we'd actually over-estimate the harmfulness of marijuana). Instead, it is best to randomly sample a large group of people and divide them into controls, placebo, THC groups, and maybe (just for the fun of it), groups for other drugs. The measure the differences over extended periods of time. Teh best way to get good results, but usually also unethical and too time-consuming and costly.

I stand by my consideration that peer-reviewed professional journals are the best sources. Have you ever observed what that process is like? It means that you get to have dozens of professional researchers scrutinize every aspect of your research, pointing out every little flaw and possible confound. By the time you get approved, your scientific method has soooooooo incredibly improved. Anyone can do a research paper and post it on the net. That doesn't mean too much to me.

Now for Higher Logic. I'm glad you pointed out the differences in how you ingest marijuana. See, I have learned that smoking ANYTHING increases risk of respiratory disease. I don't care whether it's nicotine, crack cocaine, weed, or if you just want to scoop some grass off your front lawn, roll it up and smoke it. Long-term smoking increases respiratory disease period. You seem to agree with me on that. Yet, you seem to deny that smoking marijuana can lead to respiratory disorders???? Anyway, that is why I prefer studies that do not have subjects smoke their cannabis. I don't want any confounds from the chemical process of smoking something. I prefer to know what THC does. The bulk of the research I use will involve orally ingesting THC. Yet, that is where a lot of these, dare I say it without being accused of being biased...HARMFUL effects are being proven in laboratory settings (yes, there are harmful as well as positive effects of THC use...let's be fair and balanced).

You opened a Pandora's box by minimizing the effect of THC on driving. Farthing, 1992 does an excellent job of summarizing Klonoff's experiment in which he had 4 groups drive a course (placebo, control, alcohol, THC). The amounts of THC and alcohol were comparable (long story). Out of the 4 groups, the THC group performed the worst. Certainly, I have had many cannabis dependent clients who have fun talking about the stupid driving errors they made while they were high. I don't think it is too uncommon to see this. I do, however, think that the typical marijuana user doesn't get high and get behind the wheel, so there is an issue here of responsible versus irresponsible use. I also have some nice studies on airline pilots who performend poorly on flight simulators while high in comparison to placebo and control groups, as well as plenty of good driving studies. Time estimation is one of the key areas that THC adversely effects. For example, researches have noted the THC subjects' tendency to poorly estimate timing when approaching a red light or a (albeit) fake approaching vehicle. I also here a lot of stories from my cannabis clientele about stopping several yards before actually coming to the intersection of a red light, etc. I don't want to exagerrate these impairments, either. Stopping before the intersection is much more safe than stopping after it, right? We also have the autokinetic effect with THC. A person on THC sitting in a dark room, for example, will see a stationary light and perceive it to actually be moving. Oh, yeah, and you said, "In addition, your theory implies that every person who drives is driving under heavy doses." I dont' recall ever mentioning any such theory. And yes, tiredness and other drugs are definitely major concerns for driving, but stop changing the subject. It is still a bad idea to drive when you are stoned. If you're going to use, use responsibly.

You said, "
Professor MacLean said a study of blood samples taken by SA hospitals from people injured in road accidents found Marijuana was the second most common drug, after alcohol, in the bloodstream. Those with Marijuana in their blood, however, were at fault in less than half of the accidents.” I bet you that several times more of those folks were using alcohol than marijuana, yet marijuana users were at fault for less than half of the accidents? You may have just shot yourself in the foot. I would need to know what exact percentage of marijuana-positive drivers there were versus what exact percentage of alcohol-positive drivers there were. I have some reports showing that marijuana-related accidents are FAR less common than alcohol-related accidents. However, FAR fewer people tested postivie for cannabis than alcohol (because alcohol us is FAR more common than marijuana use). When you examined the actual percentages, you quickly realize that a larger percentage of the marijuana-positive drivers are at fault than the alcohol-positive drivers. Food for thought.

You said you have no problem taking a break. How long have you taken a break for? I'm not trying to condemn you, I'm asking you to try those 30 days out and see how it goes with you. To some of my guys, a few days is plenty enough of a break for them, but 30 days is a whole other story.

Oh, yeah, and I guess you still are convinced that I don't know what addiction is??? What was so wrong with the way I defined it?

You said, "The following two quotes were approved by judges, doctors, and scientists regarding cannabis and addiction:" Be careful with statements like that. If someone does have credentials, I will be more likely to trust them than Joe-schmo on the street, but if you start to infer that because a statement is approved by professionals it is somehow solid, then you put yourself in a careful predicament. The majroity of professionals in our field believe, for example, that marijuana is highly pscyologically addictive, but you don't right???

I am well aware of the difference between liking something and being addicted to it. Not sure why you brought it up. '

Oh, yeah, and you really hurt yourself when you started talking about marijuana and anxiety. It is true that marijuana decreases anxiety when the user experiences a high (just like a cigaretter smoker experiences relief from anxiety when he/she lights up). However, for both of these drugs, studies have been pretty consistent that, in the long run, continued use will cause the person to become more anxious when NOT under the influence. Consider operant conditioning and Pavlov's dogs. If you light up every time you are highly stressed, your body experiences a relief from anxiety. However, after this process is repeated day after day, year after year, your body becomes use to the connection between hightened anxiety and the reaction of smoking to relieve it. Because of this, the body tends to rely on the foreign chemical (in this case THC) to decrease anxiety, much like for the nicotine addict or the alcohol addict. If you want some specific references, consider two expeiements by Haney et al. in 1998, Wiesbeck et al., 1996, or the decade of research that Gardners's team reported on in 1999 (just access a resource database and type those reference in and you can view abstracts...I have full reports). BTW...that anxiety factor is another sign of dependence.

What are the negative consequences that are associated with marijuan use, you ask? Well, I'll tell you some of them, but I caution you to understand that I'm not saying that EVERYONE will always EXPERIENCE these. To put things in perspective, I occasionally drink alcohol. There are tons of negative consequences that SOME people experience from alcohol that I don't. Keep that in mind when you read this list. These are possible negative effects int the research, and many are ones that some of my clients have experienced: interpersonal conflict (changes in friends, arguments with family, etc.), cardiovascular conditions, respiratory ailment (complications in asthma, chronic bronchitis, emphysema, sinusitis, and yes....even lung cancer), conjunctivital congestion, severe postural hypotension, bradycardia (vasovagal syndrome), decreased motivational syndrome (commonly branded as "amotivational syndrome"), sudden change in eating patterns (for some, resulting in overeating, you know...classic munchies), hypthermia, catalepsy, impaired motor activities (for some of my guys, resulted in accidents), difficulty reading or concentration (which has sometimes translated to problems in educational settings), short-term memory impairment, depression, anxiety, impaired spatial memory, psychotic episodes (particularly with those who already have a pre-existing condition, like schizophrenia...or for those who have ingested ungodly amounts of THC that are far greater than a typical marijuana user), decreased immune system functioning, decreased restful sleep (decreased SWS and REM sleep), mild insomnia (during withdrawal), difficulty staying awake in class/at work, decreased testosterone, lowered follicle-stimulating homrone and sperm counts (dose-dependent effects), sperma abnormalities, decreased sperm motility (that was a good study with humans), permature sperm apoptosis, impaired spermatogenesis, shorter luteal phases (in the female cycle), pregnancy complications (including effects similar to FAS), etc. In general, it is difficult for my cannabis-dependent clients to draw connections between their use and negative consequences. Their grades typically drop as their use increases, they typically lose motivation, slowly become depressed or anxious (when not using), stop performing as well in athletic settings, etc., etc., but how can they tell that the effects result from their use if it happens so slowly. I use a little story for some of them: If you take a frog and throw him in a pot of boiling, hot water, it will jump out. However, if you put him in a cold pot of water and slowly heat it, he will die. He doesn't recognize slow, gradual changes. That's part of the problem with tobacco users and cannabis users....they don't draw these connections well, and they are uncomfortable with any information that might suggest that what they are doing isn't in their best interest. I've also had guys who decided enough was enough when their habit got to be too expensive, they spent too much time being preoccupied with the drug (and neglected things like school, social relationships, family responsibilities, etc.) in the process. Not uncommon to see some social withdrawal/isolation and gradual dropping out of things previously thought of as important, etc.

BTW...just because something is highly addictive doesn't mean that EVERYONE will be addicted to it. You seem to think that I am inconsistent by calling something highly addictive and then offering that YOU may not be addicted to it. Cigarettes are highly addictive, but not everyone who smokes them is addicted, for example. Or take alcohol as another example.

It's late and I'm prolly not even making sense anymore. Until next time!

Higher Logic

I'm going to highlight just a few of the negative consequences you mentioned, which I have heard over and over before, and are nothing more than scare tactics used based on flawed studies. This is the exact type of research and information we are talking about when we say flawed studies that are government sponsored and/or funded.

1. Cannabis use produces amotivational syndrome.
The concept of an amotivational syndrome first appeared in the late 1960s, as cannabis use was increasing among American youth. In the years since, 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 no difference in grade-point averages between cannabis users and non-users. One study found lower grades among students reported to be daily users of cannabis, but the authors failed to identify a causal relationship and concluded that both phenomena were part of a complex of inter-related social and emotional problems.

In one longitudinal study of college students, after controlling for other factors, cannabis users were found to have higher grades than non-users and to be equally as likely to successfully complete their educations. Another study found that cannabis users in college scored higher than non-users on standardized "achievement values" scales.

Field studies conducted in Jamaica, Costa Rica and Greece also found no evidence of an amotivational syndrome cannabis-using populations.

In these samples of working-class males, the educational and employment records of cannabis users were, for the most part, similar to those of non-users. In fact, in Jamaica, cannabis was often smoked during working hours as an aid to productivity.

The results of laboratory studies have been nearly as consistent.

In one study lasting 94 days, cannabis had no significant impact on learning, performance or motivation.

In another 31-day study, subjects given cannabis worked more hours than controls and turned in an equal number of tokens for cash at the study's completion.

However, in a Canadian study that required subjects in the cannabis group to consume unusually high doses, some reduction in work efficiency was noted in the days following intoxication.

Undoubtedly, when cannabis is used in a way that produces near-constant intoxication, other activities are likely to be neglected.

However, the weight of scientific evidence suggests that there is nothing in the pharmacological properties of cannabis that alter people's attitudes, values, or abilities regarding work.

2. Cannabis is a major cause of highway accidents.
All of your studies that conclude that cannabis results in poor driving performance come to that conclusion on the basis that the user takes in large quantities. Moreover, you are right, in high doses, cannabis probably produces driving impairment in most people. However, there is no evidence that cannabis, in current consumption patterns, contributes substantially to the rate of vehicular accidents in America.

A number of studies have looked for evidence of drugs in the blood or urine of drivers involved in fatal crashes. All have found alcohol present in 50% or more. Cannabis has been found much less often. Furthermore, in the majority of cases where cannabis has been detected, alcohol has been detected as well.

For example, a recent study sponsored by the U.S. National Highway Traffic Safety Administration (NHTSA) involving analysis of nearly 2000 fatal accident cases, found 6.7 % of drivers positive for cannabis. In more than two-thirds of those, alcohol was present and may have been the primary contributor to the fatal outcome.

To accurately assess cannabis's contribution to fatal crashes, the positive rate among deceased drivers would have to be compared to the positive rate from a random sample of drivers not involved in fatal accidents. Since the rate of past-month cannabis use for Americans above the legal driving age is about 12 percent, on any given day a substantial proportion of all drivers would test positive, particularly since cannabis s metabolites remain 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 positive for cannabis only. To be meaningful, these test results would have to be compared to those from a matched control group of drivers.

A number of driving simulator studies has shown that cannabis does not produce the kind of psychomotor impairment evident with modest doses of alcohol. In fact, in a recent NHTSA study, the only statistically significant outcome associated with cannabis was that drivers drove more slowly.

A recent study of actual driving ability under the influence of cannabis - employing the same protocol used to test the impairment-potential of medicinal drugs - evaluated the 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 maintain steady lateral position. However, even with the highest dose of THC, impairment was relatively minor - comparable to that with blood-alcohol concentrations of between .03 and .07 % and many legal medications. Drivers under the influence of cannabis also tended to decrease their speed and approach other cars more cautiously.

While recognizing some limitations of this study, the authors conclude, "THC is not a profoundly impairing drug."

3. Cannabis impairs memory and cognition.
Cannabis produces immediate, temporary changes in thoughts, perceptions, and information processing. The cognitive process most clearly affected by cannabis is short-term memory. In laboratory studies, subjects under the influence of cannabis have no trouble remembering things they learned previously. However, they display diminished capacity to learn and recall new information. This diminishment only lasts for the duration of the intoxication. There is no convincing evidence that heavy long-term cannabis use permanently impairs memory or other cognitive functions.

4. Cannabis impairs immune system functioning.
The principal study fueling the original claim of immune impairment involved preparations created with white blood cells that had been removed from cannabis smokers and controls. After exposing the cells to known immune activators, researchers reported a lower rate of "transformation" in those taken from cannabis smokers.

However, numerous groups of scientists, using similar techniques, have failed to confirm this original study.

In fact, a 1988 study demonstrated an increase in responsiveness when white blood cells from cannabis smokers were exposed to immunological activators.

Studies involving laboratory animals have shown immune impairment following administration of THC, but only with the use of extremely high doses. For example, one study demonstrated an increase in herpes infection in rodents given doses of 100 mg/kg/day - a dose approximately 1000 times the dose necessary to produce a psychoactive effect in humans.

There have been no clinical or epidemiological studies showing an increase in bacterial, viral, or parasitic infection among human cannabis users. In three large field studies conducted in the 1970s, in Jamaica, Costa Rica, and Greece, researchers found no differences in disease susceptibility between cannabis users and matched controls.

Cannabis use does not increase the risk of HIV infection; nor does it increase the onset or intensity of symptoms among AIDS patients. In fact, the FDA decision to approve the use of Marinol (synthetic THC) for use in HIV-wasting syndrome relied upon the absence of any immunopathology due to THC.

Today, thousands of people with AIDS are smoking cannabis daily to combat nausea and increase appetite. There is no scientific basis for claims that this practice compromises their immune responses. Indeed, the recent discovery of a peripheral cannabinoid receptor associated with lymphatic tissue should encourage aggressive exploration of THC's potential use as an immune-system stimulant.

5. Cannabis harms sexual reproduction and maturation.
There is no evidence that cannabis impairs male reproductive functioning.

The Jamaican and Costa Rican field studies detected no differences in hormone levels between cannabis users and non-users.

In epidemiological surveys of cannabis users, no problems with fertility have emerged as important.

In 1974, researchers reported diminished testosterone, reduced sexual function, and abnormal sperm cells in males identified as chronic cannabis users. In a laboratory study, the same researchers reported an acute decrease in testosterone, but no chronic effect after nine weeks of smoking; they did not evaluate sperm volume or quality. In other laboratory studies, researchers have been generally unable to replicate these findings, although by administering very high THC doses - up to 20 cigarettes per day for 30 days - one study found a slight decrease in sperm concentrations. In all studies, test results remained within normal ranges and probably would not have affected actual fertility.

Severe adverse consequences have also been produced in male laboratory animals, although only with extremely high daily THC doses.

More importantly, in both the human and animal laboratory studies, all observed changes were reversed once THC administration was halted.

The claim that cannabis impairs female reproductive functioning in humans has no support in the scientific literature.

There have been no epidemiological studies indicating diminished fertility in female users of cannabis, and a recent survey found no impact of chronic cannabis use on female sex hormones.

Animal studies show hormonal changes and depressed ovulation following extremely high daily doses of THC. As occurs with males, these changes disappear once the experiment is completed. In addition, when THC was administered to female monkeys for an entire year, they developed tolerance to its hormonal effects and normal cycles were reestablished.

Almost immediately following publication of the few studies showing a cannabis impact on reproductive hormones, warnings about cannabis's potential impact on adolescent sexual development began to appear.

Other than one case report of a 16-year old cannabis smoker who had failed to progress to puberty, there has been nothing to indicate that such a potential exists. In whatever other ways one might consider cannabis to be bad for adolescents; it does not retard their sexual development.

6. Cannabis decreases the motility of sperm and lowers the sperm count.
It was already stated above why this study was flawed, but to further clarify, though sperm motility and levels do drop, they do not fall below normal or average levels.

7. Cannabis use during pregnancy harms the fetus.
A number of studies claimed reported low birth weight and physical abnormalities among babies exposed to cannabis in utero. However, when other factors known to affect pregnancy outcomes were controlled for - for example, maternal age, socioeconomic class, and alcohol and tobacco use - the association between cannabis use and adverse fetal effects disappeared.

Numerous other studies have failed to find negative impacts from cannabis exposure. However, when negative outcomes are found, they tend to be widely publicized, regardless of the quality of the study.

It is now often claimed that cannabis use during pregnancy causes childhood leukemia. The basis for this claim is one study, in which. 5% of the mothers of leukemic children admitted to using cannabis prior to or during pregnancy. A "control group" of mothers with normal children was then created and questioned by telephone about previous drug use. Their reported .5 % cannabis use-rate was used to calculate a 10-fold greater risk of leukemia for children born to cannabis users. Given national surveys showing cannabis prevalence rates of at least 10%, these "control group" mothers almost certainly under-reported their drug use to strangers on the telephone.

Also used as evidence of cannabis-induced fetal harm are two longitudinal studies, in which the children of cannabis users were examined repeatedly. However, on closer examination, the effects of cannabis appear to be minimal, if existent at all.

After finding a slight deficit in visual responsiveness among cannabis-exposed newborns, no differences were found at six months, 12 months, 18 months, or 24 months. At age 3, the only difference (after controlling for confounding variables) was that children of "moderate" smokers had superior psychomotor skills. At age 4, children of "heavy" cannabis users (averaging 18.7 joints per week) had lower scores on one subscale of one standardized test of verbal development. At age 6, these same children scored 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 cannabis-exposed and unexposed three year-olds. Researchers found no differences in the overall scores. However, by dividing the sample by race, they found - among African-American children only - lower scores on one subscale for those exposed during the first trimester and lower scores on a different subscale for those exposed during the second trimester.

Although it is sensible to advise pregnant women to abstain from using most drugs - including cannabis - the weight of scientific evidence indicates that cannabis has few adverse consequences for the developing human fetus.

Also, check out my other post regarding pregnancy, breast-feeding, etc.

http://www.cannabis.com/420/showpost...9&postcount=28

Back to the addiction claim:

Essentially all drugs are used in "an addictive fashion" by some people. However, for any drug to be identified as highly addictive there should be evidence that substantial numbers of users repeatedly fail in their attempts to discontinue use and develop use-patterns that interfere with other life activities.

National epidemiological surveys show that the large majority of people who have had experience with cannabis do not become regular users.

In 1993, among Americans age 12 and over, about 34% had used cannabis sometime 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 in high school also found a high "discontinuation rate" for cannabis. While 77% had used the drug, 74% of those had not used in the past year and 84% had not used in the past month.

Of course, even people who continue using cannabis for several years or more are not necessarily "addicted" to it. Many regular users - including many daily users - consume cannabis in a way that does not interfere with other life activities, and may in some cases enhance them.

There is only scant evidence that cannabis produces physical dependence and withdrawal in humans.

When human subjects were administered daily oral doses of 180-210 mg of THC - the equivalent of 15-20 joints per day - abrupt cessation produced adverse symptoms, including disturbed sleep, restlessness, nausea, decreased appetite, and sweating. The authors interpreted these symptoms as evidence of physical dependence. However, they noted the syndrome's relatively mild nature and remained skeptical of its occurrence when cannabis is consumed in usual doses 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 following the administration of very high doses. 6Recently, at a NIDA-sponsored conference, a researcher described unpublished observations involving rats pretreated with THC and then dosed with a cannabinoid receptor-blocker. Not surprisingly, this provoked sudden withdrawal, by stripping receptors of the drug. This finding has no relevance to human users who, upon ceasing use, experience a very gradual removal of THC from receptors.

The most avid publicizers of cannabis's addictive nature are treatment providers who, in recent years, have increasingly admitted insured cannabis users to their programs. The increasing use of drug-detection technologies in the workplace, schools, and elsewhere has also produced a group of cannabis users who identify themselves as "addicts" in order to receive treatment instead of punishment.

Basically, what this comes down to is a lot of your research is not "literate." You may be finding credible people and whatnot, but you are not factoring in the most important part: how the study was done and if it was replicated.

I urge you to check out the Jamaican studies and LaGuardia studies down back in the 30s and 40s as well.

Mamabudz

Yes dear, we realize that. That is why you have been taking repeated time from your busy schedule to enlighten us wayward demon weed smokers of the errors of our way and lead us to salvation. It is also why we are trying very carefully to explain to you why the information you are spewing at us -- when reviewed systematically -- makes no clear sense whatsoever. It is drivel we are very familiar with and is so much Reefer madness propoganda.

Your definition was incorrect, ergo, it was wrong. To base an entire analogy then on an imprecise defintion is moot. It merely demonstrates that you don't know what you are talking about and that is why we are not "convinced" by your statements. You go off on tangents beyond the point you wish to make.

Try this on for size as a Summation:
Does smoking pot interfere with REM sleep? Yes. How? We have some ideas but nothing specific. Is it bad? It might be, on the other hand, interference with REM sleep may be helpful in some ways with some diseases. What we do know right now is there is an effect.
Research to be continued.

We are still ignorant as to what REM sleep is. We are still trying to figure ou the unconcious mind and the purpose of dreams. To say that effecting dreams is good or bad assumes that you have full knowledge of a topic you can't possibly have knowledge of at all.

No scientist or doctor has the right to make those kinds of conclusions. A college student has even less of that right.

And herein lies further proof of naivete. Your estimation of the "typical Marijuana user" is the ultimate proof of your lack of knowdege on this entire subject.

My personal experience in the Marijuana Culture, shows me a very different picture. With the number and variety of individuals with whom it has been my pleasure to share the ritual and enjoyment of smoking and or imbibing marijauna throughout my life, the "typical" Marijuana smoker is educated, computer literate, middle to upper middle class, has a family and extended family. Most have a strong moral and spiritual life and are active civically voting and sitting on juries. Often they are highly creative and have strong bonds of communication with their children. Their children perform well in school and score well on standardized testing. These results cross the board regardless of race and religion.

Actually, it is quite early -- we amotivated types are up and about our business. What you are "prolly" doing is anyone's guess; however, I suggest that when you awaken from your slumber, perhaps you should look up the references Higher Logic was kind enough to foward to you.

You are young and excited about your field -- that is excellent. Do not however, become so blinded that you fail to see that there is a world beyond your microscope.

Have a pleasant day.

Mama Budz

Higher Logic

I knew I forgot to mention something. Thanks for pointing that out about the typical user, Mama. I think a lot of your views are coming with these people that you work with, who seem to be coming to you not because they use cannabis, but have other factors surrounding them and you are equating it with cannabis use. Mama correctly defined the typical user. You're typical user isn't a poor black male living in an urban setting, and you'll find that the culture itself is so diverse that you really can't generalize anyone. I know people across the entire spectrum that use cannabis: mothers, fathers, grandparents, homosexuals, college students, CEOs of companies, professors, blacks, whites, Asians, Mexicans, Indians, Native Americans, etc. However, statistically speaking Mama did do a pretty good job, and "we" aren't as unmotivated and unstable as you'd point us out to be.

fanatic4488

Thanks for the research information.
1) First off, I want to clarify that I provided you a listing of possible negative effects of mairjuana use (and indeed, ones often cited). That doesn't mean I bleieve whholeheartedly in some of them (I thought I cautioned you guys on that). Here is an excerpt from my old directed study on immune system impairment:Immune System Impairment
Human studies, although sometimes contradictory, generally demonstrate mild immunologic impairment as a result of marijuana use, although such impairment was shown to be reversible with abstinence. Moreover, impairment only resulted in greater susceptibility to disease for patients who were already suffering from immunologic damage or impairment of some sort, so an interaction between marijuana use, pre-existing immune system impairment, and susceptibility to disease is suggested. Animal studies have been shown to be more conclusive, and generally suggest a detrimental effect of marijuana on immune system functioning (Gold, 1989). However, sources for this paper did not specify if these studies involved THC ingestion exclusively or the more broad marijuana inhalation technique. Recall that THC binds to CB2 receptors, which are largely located in the areas of the human body associated with the immune system (Lichtman et al., 2001). Thus, it is quite feasible that immune system functioning could be effected by THC molecules binding to receptor sites in these areas of the body.

I suppose that doesn't sound well-balanced and impartial to you, but it does to me, considering what I saw in those studies. Anything that implies negative effects of THC seems to be perceived by you two as biased (or am I just going nuts)?

2) You said there are no studie showing adverse effects of THC on the reproductive study? Please do not be offended If I chuckle to myself....
Effects on Reproductive System
THC has been found to bind to androgen receptors, and marijuana also seems to act on estrogenic receptors. For males, diminished testosterone production and inhibited reproductive functioning are believed to be the results. In a study of 20 men who used marijuana at least 4 days a week for 6 months, lowered testosterone levels were present, although still within the normal range for all but two of the subjects. Levels of follicle-stimulating hormone (FSH) and sperm counts were also lower than in non-users, and impairment was dose-dependent (Gold, 1989). However, this study consisted of marijuana use rather than THC-ingestion, so it is difficult to conclude a direct relationship between THC and reproductive impairment from this study alone.
THC effects in the reproductive system are explained in part by the discovery of the existence of cannabinoid receptors in the reproductive system. For example, a series of studies using sea urchins revealed that THC reduced sperm fertility by inhibiting the egg jelly-stimulated acrosome reaction. This THC fertility reduction phenomenon was shown to be dose-dependant. Sperm fertility was able to be restored after abstinence from THC was achieved. The effects were attributed to the ability of cannabinoids to block the membrane fusion step in exocytosis. Researchers were able to determine that functional cannabinoid receptors did in fact exist in the sperm of both sea urchins and humans (Schuel et al., 1999).
Another study investigated the effect of THC on sperm generation in mice. Mice ingesting THC showed a statistically significant elevation in abnormal sperm production in comparison to controls. While normal sperm tended to contain a smooth kidney-shaped head with a prominent hook, abnormal sperm displayed amorphous heads, folded heads, banana-shaped heads, and even heads without hooks. The researchers in this experiment, however, were unable to identify the mechanism by which these mutations occurred, but one of their speculations was that cannabinoids interfere with spermatogenesis (Zimmerman, Zimmerman, & Raj, 1999).
Fortunately, there is no shortage of studies investigating this possibility. One study duplicated earlier results, but focused solely on the process of spermatogenesis in rats. Although a dose-dependent relationship was strongly evidenced between THC ingestion and defects in spermatogenesis, the exact mechanism by which this occurred was still unknown. (In this study, heavy THC use was also associated with decreased epididymal sperm count and decreased testis and seminal vesicle size.) However, it is important to note that very small doses of THC did not appear to cause any reproductive deficits, while larger doses that are “comparable to that used in humans” did (Huang, Nahas, & Hembree, 1999).
“High-dose marihuana smoking” in 11 human males smoking marijuana for 4 weeks in a laboratory setting was shown to correlate significantly with a reduction in sperm concentration, total sperm count, amount of sperm with normal morphology, and sperm motility. The experimenters were able to determine that a direct cannabinoid effect on the germinal epithelim during spermiogenesis was the most likely explanation for their results. The same abnormally shaped sperm heads as those observed in rodent experiments were witnessed in this study. These sperm abnormalities were found to be more severe than those in chronic tobacco smokers and moderate alcohol drinkers. Once again, sperm abnormalities were shown to be temporary, as abstinence from cannabis was eventually shown to eliminate these sperm defects (Hembree et al., 1999).
Nahas et al. (2002a) summarized the last few decades of research on THC effects on spermatogenesis in males. According to these researchers, a significant decline in sperm count and concentrations, decreased sperm motility, tubular degeneration, abnormal sperm morphology, premature sperm apoptosis (cell death), and impaired spermatogenesis have been shown to be effects of THC in a variety of studies and experiments, using humans in psychiatric wards, lab settings, hospital settings, and in the field. The same effects have been observed in studies using monkeys, rats, mice, dogs, sea urchins, and toads. The specific mechanism for many of these observations is believed to be the observed attachment of THC to a receptor located on the sperm cell. However, most of these impairments were found to diminish or disappear entirely after short periods of abstinence from THC ingestion. In addition, the researchers pointed out that, fortunately, fat storage prevents THC from rapidly reaching toxic levels in spermatogenic cells (recall that THC is highly fat soluble). However, slow release of THC from fat still maintains testicular barrier concentrations of THC in the blood and bilipid layer, and these concentrations are sufficient enough to deregulate the membrane molecular signaling mechanism. In other words, THC actually has the ability to interfere with the normal spermatogenesis process for much longer than initially expected. Moreover, these researchers caution that THC and all other cannabinoids are “xenobiotics which have to be entirely eliminated form the body after being transformed into metabolites which are excreted in faeces of urine, and are in part reabsorbed in the body and tissues by enterohepatic recirculation” (Nahas et al. 2002a). The researchers summarized research indicating that THC still affects the body in one way or another long after abstinence from cannabis. These findings are perhaps significant for males who chronically smoke marijuana and wonder why they are experiencing reproductive impairment.
In females, hormonal disruption of the female reproductive cycle, shorter luteal phases resulting in shorter menstrual cycles, elevated plasma prolactin levels, depressed testosterone levels, galactorrhea, impaired fertility, suppression of ovarian function, interference with gonadotropin and estrogenic activity, and amenorrhea have been associated with marijuana use. However, little can be inferred about THC exclusively from these results, since subjects used marijuana rather than THC itself (Gold, 1989).
A series of studies using rhesus monkeys examined THC’s tendency to decrease circulating levels of folicle-stimulating hormone (FSH) and luteinizing hormone (LH). THC-ingesting monkeys were administered a hypothalamic gonadotropin releasing hormone (GnRH). Administration of GnRH was found to reverse the inhibitory effect of THC on FSH and LH circulating levels. This finding supported the hypothesis of a hypothalamic site of action for THC. The researchers interpreted this finding as evidence that progesterone levels were not mediated by direct effects on ovarian synthesis and secretion of progesterone, but rather by the indirect acute effect of THC on pituitary gonadotropins. THC ingestion was also found to have the effect of inhibition of gonadotropin secretion in the menstrual cycle of monkeys, and the disruption was shown to last as long as several months. Levels of THC ingestion were created in a way that compared accurately to moderate-to-heavy marijuana use in humans. It is also relevant to point out that rhesus monkeys are, according to the researchers, “one of the best experimental animal models for extrapolating to the human reproductive cycle” (Smith et al., 1999).
Despite significant findings of THC’s inhibitory effect on gonadal hormones in female rhesus monkeys, a study with 16 female human subjects found little disruption in the menstrual cycle of adult females. A small but statistically significant decrease in luteinizing hormone (LH) levels was observed after marijuana (THC level of marijuana cigarettes was 1.8%) use in the luteal phase of the menstrual cycle, but the results were considered by the researchers to not be biologically significant. Small but statistically significant prolactin levels were also evidenced in the women, but again the researchers did not feel the results were biologically significant, and normal ovulatory menstrual cycles were observed in heavy, moderate, or occasional marijuana smokers. However, it is important to note that unlike the previously mentioned studies involving rhesus monkeys, these women were only analyzed for 21 days of marijuana use (Mendelson & Mello, 1999). It is therefore possible that THC ingestion for a short period of time does not interfere too heavily with gonadal hormone levels in females, but long-term use does.
Animal studies using primates and rodents have found significant and severe complications in the pregnancies of animals ingesting THC, sometimes resulting even in death (e.g. Paria, Das, & Dey, 1999; Sassenrath, Chapman, & Goo, 1999). However, this paper is concerned with THC effects on the adult human rather than on developing fetuses, embryos, infants, or children. Therefore, such findings are considered beyond the scope of this paper.

BTW...I attended a lecture with Dr. Robert Lowe, a license clinical psychologist, LMHC, Certified Addiction Professional (like myself), and a recovering addict. He gave a rather interesting lecture on cananbis and its effects on reporduction. You might be interested in noting that he provides the same definition for addiction as I do. If you have tuned in to Dr. Drew Pinsky on Love Line (Certified Addiction Medicine Specialist and psychiatrist who heads a detox unit in California), you will find that he also provides the same definition of addiction that I do. And you will find that the Florida Certification Board for Addiction Professionals provides the same defniition. I am humored by your claims that my defnition shows that "I don't know what I'm talking about." It's the same definition that is widely accepted in our field!!! Are you perhaps attempting to redefine it? If you prefer, I will get a little more detailed and provide to you the APA's DSM-IVTR clinical diagnostic criteria for both substance abuse and substance dependence, though:
The DSM-IV defines the diagnostic criteria for substance abuse as a maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one or more of the following, occurring within a 12-month period:
Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions, or expulsions from school; neglect of children or household).
Recurrent substance use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by substance use).
Recurrent substance-related legal problems (e.g., arrests for substance-related disorderly conduct).
Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance (e.g., arguments with spouse about consequences of intoxication, physical fights).

Figure 2-2
DSM-IV Diagnostic Criteria for Substance Dependence

The DSM-IV defines the diagnostic criteria for substance dependence as a maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three or more of the following, occurring at any time in the same 12-month period:
Tolerance, as defined by either of the following:
The need for markedly increased amounts of the substance to achieve intoxication or desired effect.
Markedly diminished effect with continued use of the same amount of the substance.
Withdrawal, as manifested by either of the following:
The characteristic withdrawal syndrome for the substance.
The same (or closely related) substance is taken to relieve or avoid withdrawal symptoms.
Taking the substance often in larger amounts or over a longer period than was intended.
A persistent desire or unsuccessful efforts to cut down or control substance use.
Spending a great deal of time in activities necessary to obtain or use the substance or to recover from its effects.
Giving up social, occupational, or recreational activities because of substance use.
Continuing the substance use with the knowledge that it is causing or exacerbating a persistent or recurrent physical or psychological problem.

Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Copyright 1994, American Psychiatric Association.

Nexzt item, it's easy for you to call me naive by saying that my statement that cannabis is more common among lower soioeconomic status. I could just as easily call you naive for relying solely on your personal experience with marijuana users to draw the unproven claim that marijuana users are of higher (or at least not lower) socioeconomic status. First of all, let me clarify that when I use the term "typical marijuana user," I am referring to averages, not ranges. I fully know that cannabis use spawns all socioeconomic levels, and that some cannabis users are extermely intelligent while some are significantly below average in intelligence. They work in all kinds of occupations and have a tremendous range of educational background, etc. However, and please read very carefully: There is a higher percentage of marijuana users among the criminal population, and a higher percentage of marijuana users among lower socioeconomic income levels (in comparison to higher ones). Note that I do not imply that this coves "all," etc. I suppose you would like some sources. Again, the Florida Certification Board, my accrediting agency, publishes the Certification Exam Study Guide, which provides information that is found in the State Exam for Certified Addiction Professionsals. Theses trends in cannabis use are noted there. They are also noted at this website: http://www.whitehousedrugpolicy.gov/...marijuana.html, and I quote, "The different sources, however, are more uniform in reporting racial/ethnic distributions: Whites and Blacks tend to be the predominant marijuana users in approximately equal numbers of cities, according to all the sources. Similarly, all sources generally agree that marijuana use cuts across all socioeconomic groups, although, during this reporting period, low socioeconomic status is slightly more represented than high and middle status." Please note that this source is the U.S. Office of Drug Control Policy, and I don't trust them much more than I trust NORML. I prefer non-government sources. So, I will provide you with the abstracts of some of a few studies confirming this (there are several...this is well-established wtihin the field). I have the hard copies, but I can only provide cut-and-paste of abstracts:
Title: Marijuana Use From Adolescence to Young Adulthood: Multiple Developmental Trajectories and Their Associated Outcomes.
Author(s): Ellickson, Phyllis L., RAND, Santa Monica, CA, US, Phyllis_Ellickson@rand.org
Martino, Steven C., RAND, Santa Monica, CA, US
Collins, Rebecca L., RAND, Santa Monica, CA, US
Address: Ellickson, Phyllis L., RAND, 1700 Main Street, P.O. Box 2138, Santa Monica, CA, US, Phyllis_Ellickson@rand.org
Source: Health Psychology, Vol 23(3), May 2004. pp. 299-307.
Journal URL: http://www.apa.org/journals/hea.html
Publisher: US: American Psychological Assn
Publisher URL: http://www.apa.org
ISSN: 0278-6133 (Print)
Digital Object Identifier: 10.1037/0278-6133.23.3.299
Language: English
Keywords: marijuana use; developmental patterns; favorable outcomes; early adolescence; young adulthood; light users; early high users; stable light users; steady increase users; health outcomes
Abstract: This study used latent growth mixture modeling to identify discrete developmental patterns of marijuana use from early adolescence (age 13) to young adulthood (age 23) among a sample of 5,833 individuals. After the a priori removal of abstainers, 4 trajectory groups were identified: early high users, who decreased from a relatively high level of use at age 13 to a more moderate level: stable light users, who maintained a low level of use: steady increasers, who consistently increased use; and occasional light users, who began use at age 14 and used at low levels thereafter. Analyses of covariance comparing the trajectory groups on behavioral, socioeconomic, and health outcomes at age 29 revealed that abstainers consistently had the most favorable outcomes, whereas early high users consistently had the least favorable outcomes. (PsycINFO Database Record (c) 2004 APA, all rights reserved)(journal abstract)

Title: A longitudinal study of ethnicity and socioeconomic status in relation to family decision-making style, peer group affiliation, drug use, and educational achievement of students in their 10th and 12th grades.
Author(s): Engerman, Kimarie, Howard U., US
Source: Dissertation Abstracts International Section A: Humanities & Social Sciences, Vol 63(10-A), 2003. pp. 3470.
Publisher: US: Univ Microfilms International
Publisher URL: http://www.il.proquest.com/umi/
ISSN: 0419-4209 (Print)
Order Number: AAI3066494
Language: English
Keywords: family decision making style; peer group affiliation; SES; educational achievement; ethnicity; drug use; high school students
Abstract: This longitudinal study examined parent oriented, joint oriented, and teen oriented family decision-making style in relation to affiliation with learning oriented and delinquent oriented peer groups, low, middle, and high educational achievement quartiles, and the use of cigarettes, alcohol, marijuana, and cocaine for the same set of students in their 10th and 12th grade. This study also looked at the role of ethnicity and socioeconomic status. Data was documented from the National Education Longitudinal Study of 1988 (NELS:88). The sample for this study was 16,489 students who participated in both the first follow-up (10th grade) and second follow-up (12th grade) student questionnaire. Descriptive and inferential statistical techniques in the form of percentages, chi-square, and logistic regression were used to test the study's 17 hypotheses. Significant differences were found in 10th and 12th grade. In 10th grade, parent oriented family decision-making style adolescents were more likely to be affiliated with more learning oriented peers, be in the low educational achievement quartile, and not use cigarettes, alcohol, and marijuana. Furthermore, in 12th grade, teen oriented family decision-making style adolescents were more likely to be affiliated with more delinquent oriented peers, be in the high educational achievement quartile, and use cigarettes, alcohol, marijuana, and cocaine. An ancillary analysis was conducted with a stepwise logistic regression to determine if family decision-making style, peer group affiliation, drug use, and educational achievement in 10th grade, when controlled for ethnicity and SES, predicted peer group affiliation, drug use, and educational achievement in 12th grade. (PsycINFO Database Record (c) 2004 APA, all rights reserved)
Subjects: *Academic Achievement; *Decision Making; *Family Relations; *Peer Relations; *

Title: Socioeconomic status, depressive symptoms and adolescent substance use.
Author(s): Reading, Richard
Source: Child: Care, Health & Development, Vol 28(5), Sep 2002. pp. 434.
Journal URL: http://www.blackwell-science.com/~cg...cchd&File=cchd
Publisher: United Kingdom: Blackwell Publishing
Publisher URL: http://www.blackwellpublishing.com
Reviewed Item: E. Goodman and B. Huang (2002). Socioeconomic status, depressive symptoms and adolescent substance use; Arch. Pediatr. Adolesc. Medical, 156, 448-453
ISSN: 0305-1862 (Print)
Language: English
Keywords: socioeconomic status; depressive symptoms; adolescents; substance abuse
Abstract: Reviews the article by E. Goodman and B. Huang which hypothesized that the graded relationship between SES and substance abuse among teenagers was mediated, in part, through increased rates of depression among teenagers from poorer backgrounds. They therefore used data on 15,112 adolescents from Wave I of the National Longitudinal Study of Adolescent Health (1995) and performed linear regression analyses of cross-sectional data to determine the relationships between measures of SES, depression and the use of cigarettes, alcohol, marijuana and cocaine. The author of this review believes that the weak modifying effect of depression at best suggests that other mechanisms than depression account for the greater substance use among poorer youngsters. (PsycINFO Database Record (c) 2004 APA, all rights reserved)

It's tough to get the full skinny on the socioeconomic results simply by looking at the abstracts...wish I could give you full articles. Anyway, this correlation kind of makes sense. Criminals are more likely to use illicit drugs of all kinds than non-criminals. Why...because criminals are more likely to participate in all "antosicial" (be careful about how you interpret that word...I am using it by its psychiatric defnition) behaviors. And yes, people in lower socioeconomic classes are also more prone to criminal behaviors and drug use than the middle and upper socioeconomic status. You can probably hypothesize quite a few reasons on why (e..g desperation, lower education)

I am not attempting to stereotype people who use marijuana. I am relying instead on research. I consider it possible that you are offended by my statements and personalizing the information I present. Please don't be...I assure you that I do not want to lump all cananbis users into one neatly packaged category. As I said before, I don't want to demonize cannabis nor go out of my way to rationalize it...I want the well-balanced truth. If I didn't know better, I'd say you two WANT me to think cannabis is the devil, because you keep putting words in my mouth that imply that. In my papers, I include research that doesn't show negative consequences of cananbis use just as I include research that does.

Higher Logic

Regarding just the aspect of addiction (we've gone off on so many tangents that it's hard to stay on topic here).

This is from the Report of the FCDA Europe titled "Cannabis Addiction and Cannabis Dependency." I like their definition a little better. Also realize that just because some is certified in addiction or whatnot, doesn't mean they are informed enough to make a call on issues. Sometimes they say things for the sake of saying them.

fanatic4488

That defniition is a very long way of saying...well, I'm not sure. I really can't tell how they define addiction from that excerpt. I can tell why they don't like the phrase "psychological addiction." The only diagnosis for substance dependence that is accepted in medical and psychological fields is DSM-IVTR diagnosis.

I visited the website FCDA (I think), and checked out their page on cannabinoids (http://www.fcda.org/cannabinoids.htm). They appear to be another one-sided, biased special interest group, not a good source for research. Just as bad as using the National Partnership for a Drug Free America or, on the flip-side NORML. I prefer non-biased and objective sources. Institutions of research that are not connected to special interest groups or government afilliations. Sure, you can say that universities are loosely connected to the government if you want, but that's a stretch (I don't know many govenrment puppets in universities...they are pretty freethinking and objective). Again, I stress the importance of peer-reviewed professional journals, which pool from research pro's that are as diverse as they come. Both people who probably disagree with you, agree with you, and frankly don't care enough to take a side are involved in that gruellsome review process. Thanks again for the exchange of information.