NORML’s Russ Belville vs. former ONDCP’s Dr. Kevin Sabet on Marijuana Legalization at James A. Baker Institute (VIDEO)

DFW NORML’s “Truth Enforcement Vehicle” was parked out front of the Baker Institute flashing the green lights to lead people to the event.

My undying thanks go out to The James A. Baker Institute for Public Policy for the invitation to participate in this illustrious event. I learned so much from the incredible presentations of Rev. Edwin Sanders, Sen. Larry Campbell, Prof. Alex Stevens, Dr. Ethan Nadelmann, Prof. Michelle Alexander, and everyone who participated.

I also thank the crews from DFW NORML, Houston NORML, and NORML of Waco Inc. for showing up with the Truth Enforcement Vehicle, putting on a great fundraiser, and showing me a NORML (if a little traffic-laden) good time in H-town.  (Once again, like last year, wherever I go, Portland-like rain follows me, leading Professor Bluntston to exclaim, “Russ ‘Break It Down’ Belville done brought the rain!”)

Debating Kevin Sabet was fun.  Before we went up, he thanked me for devoting half of my show to him (it was only a quarter, but whatever) and suggested that maybe it isn’t a good idea for me to give up my whole debate strategy before the debate.  I told him that when you have truth, facts, logic, and reason on your side, you don’t have to have much of a strategy.

Please take the time to watch the other videos from presenters at the Baker Institute.  I’m flattered by all the hits my video is getting, but you’ll learn a whole lot more from the learned people on the other videos.

160 thoughts

  1. 2.7 million dollars for alcohol related crimes (something that is considered legal)
    847,000 for marijuana related crimes (something that is completely illegal)

    Wouldn’t we SAVE the 847,000 from legalising?

    (I know that DUIs still might occur so 847,000 might be a little overstated, however the point remains.)

  2. RUSS BELVILLE needs to be the main spokesman for NORML. He’s very good at speaking and using the facts when they’re needed. “Ol Sweaty” had a rough time trying to defend stupidity.

    [Russ responds: Hold on thar, pardner! That’s like saying “Sniper rifles need to be the main weapon of the military!” We’ve got lots of big guns here at NORML and we try to use all of them in the right battles. From our National offices with world-class expertise on cannabis science, DC politics, drug reform history, modern marijuana law, and now, newer younger, more diverse board members and staff, to our network of 177 international chapters from college campuses to Statehouses, staffed by volunteers of every age, gender, ability, race, culture, party, and religion, NORML has always been the Pot Smoker’s Lobby! I’m just honored to have been lucky enough to catch the breaks I needed to get to do this job.

    And give “ol Sweaty” a break… it was kind of warm and humid in there.]

  3. I would have to say my favorite point raised during the entirety of the discussion was addressing what constitutes abuse. I cannot recall the number of times I have heard people bring this up. I have friends that do not smoke, toke only on weekends, and whenever they’re within reaching distant of their piece. Some of them I would not consider particularly level-headed and/or intelligent, but notice how I don’t say of which group they belong. I’ve heard in the past, from quite a few friends, this phrase: “Yeah, but you’re not smoking all of the time like them. They’re so burnt out.” To which I reply, “I’ve already smoked X times today.” Usually that X is anywhere from three to nine times. Hearing me tell them that always seems to put something in perspective. The thing being, of course, that it really is predisposition to abuse which can be tackled in a much more cost efficient, less intrusive, and logical policy towards marijuana. So hearing the audience respond in a positive manner to that sort of statement brought a smile to my face. I hope to see more discussions like this in the future. Maybe Obama will eventually stay true to his word.

    [Russ responds: This is a trick I learned from NORML Advisory Board Member Rick Steves, who once said (paraphrased), “Be the kind of pot smoker that other people can’t help but like.” So I’m not afraid to say “But Kevin, I’m that guy, I’m that 9% that goes on to ‘dependence’, whatever that is. I’m smoking pot five to seven times a day, every day!” I wanted that audience to think, “Well, he’s kinda animated, but he doesn’t seem scary, and it looks like he can clean up nice and work hard and gosh, how does he remember all those statistics off the top of his head if he smokes so much pot?”

    That’s how YOU can be an ACTivist. By just being a positive example of a pot smoker. By showing people they have nothing to fear about us, and locking us up is just costing them money and not stopping us.]

  4. Russ, you fucked up when you said your dad was addicted to marijuana. There is no addiction to marijuana.

    [Russ responds: I disagree. That is what my father believes. Use of alcohol, speed, and marijuana were detrimental to him. He went into treatment to stop doing those substances. He hasn’t used them since 1980.

    There can be “addiction” to anything, but I hate throwing that word around, so, in a sense, I kind of agree with you, in that my dad’s addiction to marijuana was in no way as detrimental or difficult to recover from than his addiction to speed and alcohol… or for that matter, tobacco, which he didn’t kick until 1996. But marijuana use was not positive for him. It’s not positive for everyone. We do our cause a disservice to just throw out a blanket statement like “There is no addiction to marijuana” because it will face the reality some listeners have experienced personally or seen personally, i.e., the “burn-out stoner”.

    The question is, and I used my dad example for this, is “does even the worst marijuana ‘addict’ deserve a cage or forced rehab?” I didn’t get to tell how my dad went to rehab, which was not because a cop or court forced him to (and that never would have worked anyway), but because he stood on the edge of the Snake River Bridge in Payette, Idaho, one night and was about to jump, when Jesus told him to go get treatment so he could care for his family. Yes, Jesus. My father to this day believes it was only Divine Intervention that kept him from suiciding that night.

    We have gambling ‘addicts’, shopping ‘addicts’, hoarders, sex ‘addicts’, overeaters, bulimics, religious zealots, and yes, even some dysfunctional potheads in the world. But we only lock up that last category, and then even when they are not dysfunctional. That’s the point I was trying to make.]

    What was waiting for was a comment like this to start your discussion:

    Marijuana prohibition was founded on a bold faced lie . That lie has morphed into a masterpiece in the art of brainwashing.

    Any law based on a lie is no law at all.

  5. i love you russ and norml. i think you guys have taken a path in performing a miracle for the betterment of humanity. in my eyes that is the best path one can take in this life. you are the real life val kilmer in the movie the saint, you are the modern day rosa parks who refuses evil regardless of what form it may present itself and when your goal is acheived you will see this country doing well again and being the great place we love it for..

  6. Russ, you are a rock star! Awesome defense to this guy’s government polished attack. Anybody who wants to see Obama’s answer about pot needs to see this video. But there whole argument is based on the promise that marijuana consumers are all drug addicts and need interdiction. Notice how this guy referred to marijuana users as “zombies.” His whole case was built upon the fact that marijuana is so dangerous that the cost to enforce it are justified.

    The only way to defend against this sort of an attack is to counter it by legitimizing the marijuana consumer and marijuana effects.

    First of all, marijuana effects people differently. I get there are some people that smoke pot and then get silly and stupid, munch on some junk food and fall asleep on the couch. But then there are people who get stoned and “build a bridge!” Experienced users can easily do chores or home projects, like tending a garden, or landscaping or painting the bathroom. There are people who get stoned and write and sing songs. There are people who get stoned and have great sex. There are people who get stoned and create great works of art. There are people who get stoned and invent great things for mankind. There are people who get stoned and walk their pets in the sunshine. There are people who get stoned and write important books. There are people who get stoned and then play video games better. Etc., etc., etc. People don’t get stoned and then become whacked-out zombies!

    In other words marijuana consumers are not sick addicts, but rather NORML productive people. And I am sick and tired of marijuana consumers being equated to societal trash. The marijuana high does not make you a zombie, it allows you to go inside and pull out more creative insight. Marijuana amplifies reality, and allows a person to taste, touch, hear, feel or think things without preconditioned responses based on upbringing or the collective consciousness of society, for examples. In other words, marijuana frees the mind. The marijuana consumer needs to be discussed and legitimized by using examples from history like Carl Sagan… AND Steve Jobs, John Lennon, Wiz Kalifa, Barack Obama, Jack Nicholson, Montel Williams, Bruce Lee, Andrew Weil, Sigmund Freud, etc., etc.,

    1. Thanks, Jeedi. There is so much more in my notes I didn’t get to say. I did get a Carl Sagan reference in there. I wanted to say, “Look, any herb that Carl Sagan, Michael Phelps, Willie Nelson, and 60% of the NBA can use while achieving at the top of their professions doesn’t scare me much.” When he went the “drive and build a bridge while smoking tobacco” I wanted to launch into “I work from 8am to 10pm every day, writing thousands of words, producing hours of internet video, interviewing PhDs and cops, analyzing statistics, creating graphic designs, and managing 177 NORML chapters worldwide… and I am smoking pot as I accomplish all that. I am literally doing four jobs simultaneously – board op, video op, engineer, and host – live two hours a day every day. Before that, I was a corporate trainer, getting up at 6am, not smoking at all, wearing a suit and teaching complex software, getting stellar reviews, and then I’d come home at 6pm and smoke pot. I haven’t had so much as a traffic ticket in the 21st Century. What are you so afraid of, Kevin?”

      Only in re-watching the video did I catch more of what his argument is really based on. Did you catch where he is trying to downplay the emotional side of the argument, admitting he’s only 33, but he talked with the older folks and that much of their emotion was tied to their friends getting busted for protesting Vietnam? Um, no, much of our emotion is tied to seeing videos like this: http://www.huffingtonpost.com/russ-belville/columbia-missouri-swat-ki_b_567172.html

      I kept trying to “keep it personal”. “So we need to lock me up because some kid might smoke a joint?” “So we need to lock me up because some stoner might get behind the wheel?” It is incumbent upon us, as Dr. Sabet alluded to the “Drink Responsibly” ads, to model how to “Toke Responsibly”. We have to be the examples to the American people that yes, people you know smoke pot and they cause you no harm and they are productive vital members of society.

  7. I think Russ did a fine job as an advocate for legalization, and I somewhat agree with Owen in that Cannabis is not addicting. The reason I say somewhat is because like Russ, I have had many friends and family members who have struggled with substance abuse, and I have observed that people with substance abuse problems, have a general tendency to be unable to control their overindulgence in almost any substance, be it sugar, drugs, sex or whatever, that is why members of AA/NA have to attend meetings forever, they need that constant reminder. Having said that, responsible adults who use Cannabis need to be allowed to do so without consequences. I will not stand for anyone telling me what to do with my mind body and soul, now or ever….unless Im in a cage.

  8. Mr. PhD’s ideas and education didn’t just go to his head, but to his waistline as well –he is obese. Would this hypocrite mind having the government shut down McDonalds and Coca-Cola . . . how many die from that . . . how much does one’s choice in foods affect our medical care in our nation –how much money do we lose via healthcare . . . how many sick days do obese and diabetic workers take due to their dieting habits biting them. I’m assuming Dr. Sabet drives an automobile to and fro. How much money has dependence on vehicles cost our society in lives and healthcare and property damage? Hypocrite. Does he not care about how many die from car crashes or injured from car crashes? But he wants to keep marijuana outlawed . . . how many people get injured from contact sports –how much money do parents waste because their child got hurt playing soccer or football? He’s 33 yrs old and he wasted his time getting a PhD, while so many of his peers went to war fighting drug money in Afghanistan and Iraq –getting revenge against drug money financed 9/11. He looks at the social costs of a society using tobacco and alcohol stats to keep his ‘just say no’ mind set –but he refuses to look at the fact that the War on Drugs cost America nearly $3 trillion dollars just from 9/11 and her two Middle East drug wars . . . not once did he talk about the how the war on drugs helped create our current unemployment rate and spike in gas prices . . . what’s more harmful –a bit of pot or raising four kids with one employed family member –or a spouse in a war zone fighting drug money?

    [Russ responds: To be fair, I am more obese than Dr. Sabet, by far. Six foot, 260 lbs. Like I meant to say in one of the one-liners I had in my notes, I’m more addicted to fats and sugar than I am marijuana.]

  9. I have one question for our government if they are really so concerned about the harm legalizing marijuana will cause the people of this country…..

    Why is alcohol and tobacco legal if it directly kills millions of it’s users (the U.S. population) every year?

    [Russ responds: Dr. Sabet’s answer to that had to do with culture. Seriously, he referred to the “cultural decision” to make alcohol and tobacco legal, and then he said “some would call it a ‘cultural mistake'”. If you needed any more evidence that this is really about a culture war, here it is. He even referred to us having “thousands of years” of norms built around alcohol. I’ll cede that point – marijuana smoking as an American cultural phenomenon is really only a century old and only 50 years in mainstream usage. So if that’s the case, then we can argue at what point have enough people in an underground sub-culture developed norms and achieved enough critical mass to be deemed worthy of not punishing?

    I even had a one-liner ready for that one, “Yes, it was such a mistake to make the two most addictive and toxic recreational drugs legal, so let’s not repeat that mistake by giving people access to the least addictive non-toxic drug? You want to hurt the alcohol companies? I’m the guy who from age 16-22 was the binge drinker you said alcohol companies make their profits on, and since smoking pot at age 22, I drink about two drinks a month.” Alas, in the “heat of battle” I left many of my best arrows in the quiver.]

  10. I kept waiting for Kevin Sabet to have an opinion.

    Has he ever spoken in concrete terms about what his public policy would entail?

  11. Excellent debate! Keeping it personal was the right tactic, especially when he concedes that russ the daily toker doesn’t deserve to be put in jail. That’s when I thought he lost the debate. He’s almost like an apologetic prohibitionist but that’s the only way he can hold his ground. “I’m not going to say you should be locked up but think about the children,
    but before you respond to that I already know it’s readily available to them so don’t use that rebuttal.”

  12. I was surprised Dr. Sabet thought the price of marijuana would drop by 80% if it were legalized. Is this probable? I lived in the Netherlands for a few months and the prices for quality marijuana were only slightly cheaper than in the U.S.(once I converted the euro price to USD). I understand that it is not fully legal in the Netherlands, just tolerated, but I still believe this 80% figure is very high.

  13. If it’s a hog eat hog at the trough within the govt.than you can see why things are like they are out here.

  14. Russ, you should comment on how stoned driving is way different from driving intoxicated.
    Intoxicated drivers tend to think they are fine and can drive and attempt to do so. This causes them to swerve and do really stupid stuff.
    Stoned drivers tend to realize they are stoned and compensate for the impairment causing them to drive slow and paranoidly. They stop longer at stop signs and drive considerably slower.

    [Russ responds: True enough, but the “driving and toking” area is one where, had I taken it there, Sabet would have had a ton of stats to refute me. Folks, there is an impairment with smoking pot. It’s not as bad as alcohol and you are better aware of it and do tend to compensate, but in a “oh shit!” driving situation, awareness and compensation won’t help. So I didn’t go there… why throw him a life preserver?]

  15. Well done. I agree with the previous posts though that marijuana is not addictive. If marijuana is in fact addictive, then everyone who uses it will become addicts. And that isn’t the case. No one has died from overdosing on marijuana. People have died from using marinol though. People have even died from drinking too much water.

    I rarely here anyone mention Irv Rosenfeld’s name in debates or in any arguments in favor of marijuana. The fact that he sued the feds and won, and has been receiving marijuana for decades from them is extremely important.

    Sabet acknowledges, brushes aside, and then tries to mislead about important points such as stating that marijuana was “used 5,000 years ago,” as opposed to marijuana has been used for over 5,000 years. Or “I understand that kids can get marijuana now despite the law,” making the point that prohibition does not, and will not work.

  16. There are so many things Dr. Kevin Sabet doesn’t want to talk about, but you Russ can say it all in 20 minutes. That is amazing.

    I would theorize that if a person really wants to feel high and euphoric on marijuana, they would need to stop for a few days and then light one up.
    I understand for medical purposes that a person who smokes five times or more everyday doesn’t get as high no matter how strong the marijuana is.
    That is how I see the difference between recreational and medical uses on marijuana.
    (A joint after work would mellow out a person nicely.)

    [Russ responds: It would be nice to get into that discussion of the “high”. I don’t get “high” when I smoke pot anymore, I get “adjusted”. I don’t have a better word than that. Without pot, I feel like a car with slightly-off timing. I can still run just fine, but there’s the occasional sputter. Pot is like adjusting that timing belt for me. I run far more efficiently and smoothly with it.]

  17. I watched the whole video. You did a very good job, Russ. Very good indeed! Keep up the good work!

    But I wasn’t even sure what points Sabet was trying to make some of the time, since he talked more about alcohol and tobacco than he did about marijuana. Or the points that he did make usually had at least one logical hole in them.

    Anyway, I was glad you brought up the issue of Marinol being 100% THC while the government whines about the THC potency of weed increasing. After all, it simply doesn’t make sense to recommend something that contains 100% THC while saying that recent weed is “harmful” because it contains something like 15-25% THC. I’ve been waiting for this contradiction to be addressed ever since I started paying attention to marijuana news. It’s too bad that it was brought up at the end of the allotted time. It would have loved to see Russ nail Sabet over that one. 😀

  18. Why doesn’t this Sabet want to clean up the cultural mistake of alcohol and tobacco? Imagine if tobacco and alcohol were reformed to model after medical marijuana laws and distribution where you needed to go see a doctor first to get a license before you could walk into a liquor or nicotine dispensary. Doctors could at least recognize substance abuse symptoms and offer eduction. This is far better than allowing convenience store clerks to be in charge. Alcohol advertising should be banned! No more beer commercials! All alcohol or tobacco menus should be dispensed by a highly regulated, tracking system and under the supervision of a qualified pharmacist.

    Instead Sabet would rather just play lip service to legal drug failures and not reform anything at all. Business as usual. But with a kinder and gentler twist to the same old drug war on marijuana.

  19. To begin with Cannabis Can be come additive Not As in your Body will need to have so much to stop the with draws. But psychological additive yes very much so. I my self was like that at one time. I seen alot of persons that can not control it. As in wanting to smoke all day long. Ples save be I dont know what I am saying. Hell 55 years old.

  20. Russ,

    Thanks for your reply. I think by the same token we should NOT be saying “some people get addicted to marijuana” because addiction conjures up images of a heroin addict speawled out in some ally with a needle hangng out of his arm.

    When I was ambushed by NJ state trooper Burgess in 2008, had a gun put to my head because he said he smelled weed in my car, sent my white ass through “the system” for the first time in my 53 years – I had to quit smoking for 45 days after smoking weed every day since 1975. The only signs of “withdrawal” were irritability which was exascerbated by the stress of going through the system.

    As to my other point, left unaddressed, you need to begin all of your public speaking events with the origins of marijuana prohibition – that it was founded on a lie, and explain to people how that lie morphed into a masterpiece in the art of brainwashing.

    Thanks for your ears and your efforts. Looking forward to your reply.

    [Russ responds: Thanks. Good tips.]

  21. Very good debate! I know it could go on for ever but one point missed was when it was stated that the Netherlands has even more trouble with marijuana now; well that’s because it is still illegal. We need to compleatley legalize then it wouldn’t be a big thing if someone was arrested for selling to a minor. As Russ stated we don’t want to go to jail for something that someone might do. Also the same thing with Cali is it’s not really legal so people from other states are going there to get it and bring it Home. We need LEGALIZATION!!!

  22. Below is my original comment with a response from Russ. To clarify the point I was trying to make, I am a Marine veteran with deployments to Iraq in the past. I became addicted to alcohol, drinking every night just to sleep. Lately I have been introduced to medical marijuana. I have smoke since I was 16, but I have never had the kind of scientifically engineered cannabis that is coming out lately. Within a week I stopped drinking and doing drugs and now I just use my medical marijuana. I guess going past all the cultural “norms” and what our society has done for the past 100 years, I want to know why war veterans are being oppressed and not allowed to use this beneficial medicine.

    I have one question for our government if they are really so concerned about the harm legalizing marijuana will cause the people of this country…..

    Why is alcohol and tobacco legal if it directly kills millions of it’s users (the U.S. population) every year?

    [Russ responds: Dr. Sabet’s answer to that had to do with culture. Seriously, he referred to the “cultural decision” to make alcohol and tobacco legal, and then he said “some would call it a ‘cultural mistake'”. If you needed any more evidence that this is really about a culture war, here it is. He even referred to us having “thousands of years” of norms built around alcohol. I’ll cede that point – marijuana smoking as an American cultural phenomenon is really only a century old and only 50 years in mainstream usage. So if that’s the case, then we can argue at what point have enough people in an underground sub-culture developed norms and achieved enough critical mass to be deemed worthy of not punishing?

    I even had a one-liner ready for that one, “Yes, it was such a mistake to make the two most addictive and toxic recreational drugs legal, so let’s not repeat that mistake by giving people access to the least addictive non-toxic drug? You want to hurt the alcohol companies? I’m the guy who from age 16-22 was the binge drinker you said alcohol companies make their profits on, and since smoking pot at age 22, I drink about two drinks a month.” Alas, in the “heat of battle” I left many of my best arrows in the quiver.]

  23. Emotional warnings don’t match the reality. Treating myself for pain and institutional discrimination should not allow law enforcement to steal everything I’ve worked hard to earn without due process. Fear of drugs has been my childhood experience and the reality that came with adulthood showed a natural plant that grows everywhere to have less side effects than the perscribed medication and work wonders. I just want to have my perspective define my reality instead of letting an ignorant subserviant adminstrator tell my how to live my life.

  24. One small point in comparing tobacco/alcohol tax revenues with marijuana: Marijuana use currently exists and will likely not go away with the current policies. Therefore, the costs associated with its use are currently not being offset by any taxation.

    [Russ responds: That’s part of the argument I make when I use slides and can turn it into a math problem. If we presume marijuana costs will go up under legalization to such an extent they would offset any tax revenues, then it stands to reason there is some cost occurring NOW with 26 million people smoking pot every year and 2.6 million smoking pot every day. We take in $0 in taxes NOW and we spend around $7B in enforcement NOW, plus untold costs associated with underemployment of the drug-tested and the drug convicted.

    Dr. Sabet also made a false analogy in the tobacco smuggling exhibited in New York. I’ve reported on this. What that is a case of is the over-taxation of as highly-addictive product that one cannot grow themselves. In a legal cannabis market, over-taxation will just lead consumers to grow their own or buy it from someone who is. Dr. Sabet even concedes this as part of his argument that “legalization won’t make the black market go away” (and it won’t, just as there is a miniscule market in moonshine), without realizing he’s merely making the argument against legalization and OVER-taxation.]

  25. Russ, Thank you for being such a courages warrior for Marijuana. You are truly 1 of my hero’s in this insane war on Drugs!

  26. Thanks to RICE UNIVERSITY’S BAKER INSTITUTE’s board members for having an open mind and willingness to have such dialog on their campus.All of the speakers FOR THE MOVEMENT was FANTASTIC.And the few speaker that opposes THE MOVEMENT was clearly on DOPE and DOG FOOD.But the sad thing about those speaking rhetoric and propaganda about CANNABIS has never tried it in any of it’s many forms.Russ Break It Down Belleville was the HIGH LIGHT OF THE DEBATE,Ethan and Senator Campbell ran a close second.But ALL OF THEM GET MVP. AWARDS. PEACE

  27. The only thing the feds understand is hot lead. And what we get is don’t talk about violence. The feds started this war and no one is telling them no violence? would you not protect yourselves too? the fbi started this mess along time ago. Hothead and hot lead do not mix.

  28. Great job Russ! Your last point was powerful–you really are the picture of a marijuana addict: smart, reasonable and self-controlled.

    When drug warriors like Dr. Sabet quote data on current drug use patterns, they fail to realize that they have created an uneve playing field. Prohibition creates perverse incentives for many to use drugs irresponsibly. Let’s legalize marijuana, incorporate it as a cultural norm, and then let’s look at use patterns.

  29. I think it was completely unacceptable how Mr Sabet cherry-picked his data, particularly how he completely failed to mention ANY sources on his claims on the Netherland or Portugal drug policy. I think it’s sickening how he can claim to present a balanced approach and then launch the old tirade with arguments taken directly from the DEA’s page. I think it’s demeaning and offensive when someone presents data claiming a scientific outlook on the issue and then twists that data to suit his line of reasoning or ignores any data that goes against that. The Lancet (a prestigious British medical journal) has published several reviews that show a drastically different story from what Mr Sabet claims about the harm and dependancy coming from drugs.
    I heartily recommend Professor Nutt’s blog (who was adviser for the British government, but was sacked after saying that science unequivocally says that the drug policy is insanely misguided), his last post from December links to his paper on the comparison of harm from alcohol and cannabis and why, surprisingly, cannabis is safer BOTH for the individual AND society.

    A suggestion to Russ: get some fancy science graphs yourself! And I don’t mean that you should regurgitate Mr Sabet’s strategy, but the science is firmly on your side. Use it, and use it well. Check out Professor Nutt’s blog I mentioned, check out the Lancets publications, because there’s stacks of scientific ammunition to fight the legalization battle.

    [Russ responds: I have a whole book chock full of fancy science graphs. I’m still searching for a publisher. You can see some examples here http://stash.norml.org/bigbook. For this first time at bat, I wanted to set myself up as the personal story of marijuana users, partially because I knew so many more academicians were going to presenting many of those facts that day already. But for my next gig like this, I will blow them away with pretty pictures and compelling data.]

  30. I cannot smoke many times a day. Amotivational syndrome is the only detriment to weed that I have personally experienced. For example, I read it’s supposed to cause sexual dysfunction. That is NOT my experience.

    I realize that’s just me. It’s like if your stool floats your eating too much fat. If you have amotivational syndrome, you’re overdoing it.

    [Russ responds: Then I guess, for me, 5-7 times daily isn’t overdoing it. I produce fourteen live hours of radio per week, maintain a 24/7 radio network, write 5,000-10,000 words per day, coordinate 178 NORML Chapters worldwide, and travel nationwide once or twice a month to lecture on marijuana. I could actually use a little amotivation now and then… NORML has to force me to take vacation time!]

  31. You only have to watch a few episodes of ‘Cops’ on TV to see that alcohol is almost always the source of that belligerent, bellicose behavior that must really try an officer’s patience.

    People on crack and amphetamines even are busted all the time, but I’ve never seen the violence on ‘Cops’ that is supposed to be associated with them.

    I did see a guy on PCP put his fist through a privacy fence like he was the incredible Hulk. I don’t think I’ll be doing any PCP any time soon.

  32. I find it funny how Sabet now thinks there should be conversasion, i am sure he would change his mind if he was doing this and still working there.

    I’ll grant Sabet some credit on his formulation on deterring the debate to something opposite of what it should be. But what Sabet fails in comparison is that he follows NIDAA etc when in reality it is illegal to do studies on marijuana to places that are illegal, so it is inconsistent.

    Russ Belville you need to use graphs in a future debate and question hard on the issue of if these former drug czars or supporters of these czars if they support making marijuana illegal vs regulation.

    If they still believe it is beneficial to make marijuana illegal then ask why “losing 3.4billion dollars a year in the black market and not funding the U.S a good thing, when if we regulated marijuana, then dispensary’s would make a profit, workers could get paid 6$ more in minimum wage, and we would have more than enough to auctully pay off the 4trillion dollar deficit in half in 7 years if it is sold everywhere”.

    I still think you are great Russ, just keep fighting, i think you got it down pat on making yourself look more human out there but there needs to be some slides to help you on the statistics end. Surely science in other places etc can atleast do some good in future debates.

    [Russ responds: Thanks, and next time, it will be Graphapalooza!]

  33. I got to the video with Russ and that one kept freezing up, maybe being viewed a lot…but I watched all of the videos leading to that one and noticed a consistent tactic by the prohibitionists: they start talking about crime and the typical harms associated with the harder drugs…heroine this and crack that…it’s like they don’t even have an anti-cannabis argument.

    And that female Judge…she targeted a female age group and used references to gain a bond and just talked nonsense and scare tactics…

    …and the inner city officer and the reference to robbery murders and “stoned” people…cause he found the righteous path and those people are scum, is what I took away from his comments.

    I tried to stay open minded, thinking at first that they must believe what they say…but the comments and lack of concern for social harm has convinced me their “convictions” have more to do with their jobs.

  34. I would have to agree with Russ’ usage of term addiction. It is a subjective thing, and if a person thinks they’re addicted to something, they usually are right. They love it and hate it, the thing they’re addicted to.

    Say for instance, it were not subjective. If it were clear-cut maybe there would be some actual meaning to the term “drug treatment.” That is that, anyway? The cure/solution to a problem? What does it look like? Is it a pill or is it a hospital stay?

    What other treatment is there for drug use than to simply stop? That is a personal choice, one that no one makes for another person, it is a personal decision. Interventions force people into drug “treatment” but what is this “treatment” that people pretend is some kind of medical service rendered or some way to influence people to make their own decision to quit–because that’s the only way it’s gonna happen.

    Court ordered “treatment” or “sobriety” or “education” is a crock. of steaming BS. People usually become more resistant when they are forced to do something they don’t want to do, based on unjust policy.

    Drug treatment is a vague and nebulous term because there is no standard treatment. Twelve-steps? Extended abstinence in a tranquil environment? There’s a lot of money to be made from court ordered “treatment”

    Treatment can only be one’s own decision to stop or change their own behavior. Victor Frankl noted that no matter what people do to put you down, you always have a choice. “Between stimulus and response is a pause”-Victor Frankl. In that pause is a choice.

    Forcing people through hoops doesn’t make choices for them. Making things “illegal” doesn’t make those things wrong nor does it change people’s behavior when they know when to call a spade a spade and prohibition as BS

    [Russ responds: Damn right. As the old joke goes, “How many psychiatrists does it take to change a light bulb? Only one, but the light bulb has to want to change.”

    Studies of 12 Steps and rehabs and every method we use to try to treat addiction find this to be true. Coerced treatment rarely works – for every “jail was the best thing for me, it forced me into recovery” story out there I can find many more where that jail term began the nightmare they live today. An addict has to hit their own personal rock-bottom and want to recover before any method will have any chance of working.

    For some people, marijuana is detrimental to their lives. Some use it and become dysfunctionally dependent. But that number is a far lower proportion of all marijuana users than a comparative stat for other drug users, including alcohol. And recovery from marijuana dependence doesn’t require the physical detoxification that other drugs do (I remember well my father in 30-day detox, tubes poking in him to clean his system of alcohol and speed. I was 12.)

    There simply is no possible justification for the threat of force to compel someone to stop using marijuana. That is what I hoped to illustrate in the debate. We can throw up all the charts on the wall we like, but they all obfuscate the basic issue.]

  35. Russ, good job! The issues Sabet raises with blacks be incarcerated, but it won’t change EVERYTHING (as he says, “but is it the answer to ending race?”), no, it is not the end to racism, however, it is the end to racism inside the world of drugs (specially marijuana, white people do drugs to). He is trying to make you look bad by trying to make you do more, or make it seem like legalization would not fix more. If you keep this inside the realm of cannabis and not fixing racism or other abuse of other drugs, Sabet is dead in the water. I like how you kept it to the facts that he presented. I would have liked it if you stated smoking is not the only way of THC intake, such as foods (digestion), or vaporization, which is totally 100% safe and healthy. Keep it up.

  36. Russ – wear the mic – walk about. Looks calmer. I love your passionate energy. [Russ responds: D’oh! I didn’t know there was a lav mic!]

    I like the Canadian study you referenced on spending – public health costs verses enforcement costs. I think you should utilize it more. Applying this to the US and using the approx 7bil a year enforcement figure, (still think this is way too low when considering ancillary industries – drug testing alone is 5.9 bil industry ) We would end up with public health costs at $364,583,334 for all US cannabis users. Divide that by the 26 mil trying pot this year = $14.02 per one time toker on health care costs! Hardly a trip to the emergency room – more like a night at the Waffle House. OK, discount the one time tokers – same figure – $364,583,334 divided by 2.6mil daily tokers = $140.22 per year. Got you scared yet? You shouldn’t be – cause at $.70 per bag – it would cost you $255 to buy a bag a day of Funyuns for each daily toker!

    Keep in mind legalization of cannabis would immediately eliminate that 7bil – even if directly offset by increased hcc health care costs (grant them their funyons) would be a savings of $6,635,416,666 (6.6bil) annually.

    Ending enforcement – save 6.6 bil
    Ending incarceration – save 1 bil
    Ending pee testing – save 5.9 bil

    these 3 things would save 13.5 bil a year – or would it?

    Our economy, our system built around prohibition would crumble and fall – perhaps with the potential loss of ancillary industrial profits our whole country could sink into insolvency and poverty. How many jobs would be lost from just these 3 alone? Thousands – maybe a million? This then becomes an issue as big as oil. As big as invading another country just to keep oil flowing – jobs coming. As big as starting a war to keep our way of life safe.

    But then that’s what we have here – war. Warriors perpetuating that war against pot – now countryless, with the face of a mex cartel leader as it’s head. War to preserve and perpetuate their profiteering way of life – profit for the rich and powerful old white guys. Who teach their sons and daughters the ways of profiting off peoples misery. Many must live in poverty – or die – so that the few may live rich.

  37. Okay, I may be thinking outside the proverbial box here, but, what if we spent the savings on programs run by the DEA involving education programs for our children and overseeing drug treatment programs that focus on healing addicts rather than jailing them?

  38. lol, lol, LMAO.. Russ Belville,, SHAME on you.

    Did you have to make him into a complete babbling fool with every sentence you spoke? The poor guy has issues now for sure….

    I felt so bad for the guy, when he was so brave to even ‘sit’ at the table with a conveyer of truth like Russ Belville.

    I felt so bad for the guy that I wrote him an email congratulating him for staying on stage and being the fool for the whole truth. He stayed in his chair, he kept his tie on tight and straight all the time.

    I asked him why he would ever consider defending his criminality from Russ Belville in front of all Americans and the World.

    I reminded him that the video has been viewed in every country around the world and the olde reefer madness was fun to laugh at.

    If this guy was so smart, he would have known better to debate a real pro

    An interview with Russ Belville is not one of those you just walk away from as a Drug-Lord-Warrior with your head up.

    Nice cook-out Russ !!

  39. Russ, thanks for all you do. I have to point out that when there was a one-on-one debate you were the only one to get applause. I think it was something to the effect of Dr. Sabet saying that only 20% of the mexican drug lord’s funding comes from marijuana being illegal and you said ‘why even give that to them?’. Beautiful. My opininion is as follows McDonald’s, alcohol, tobacco are all more dangerous than marijuana, but at least there isn’t a death toll in the 10’s of thousands in the wake of the black market supplying these goods. Also, I think you mentioned this on your pod cast recently, that stoners get a bad name because we are most often portrayed by those with nothing to lose. As a person who lives deep in the heart of Texas, works for the government, and comes from a devout Christian family it is hard for me to ‘come out of the closet’ about marijuana. So I thank you for putting my thoughts in to words so I have ample ammunition for debates over my lifestyle.

    [Russ responds: I know a lot of pot smokers.

    I only know a few “stoners”.

    Christians who denigrate cannabis consumers haven’t read Genesis closely enough. It’s covered in the first chapter, people!]

  40. Finally got to the video with Russ…saw Russ apparently in thought over Dr Sabet’s talking points…saw Russ writing stuff down…kept thinking how Russ was going to shoot down several points 🙂 … then the rebuttal started and barely into it Dr Sabet politely asked if he could interject, Russ said sure, Sabet proceeded to less politely interrupt every single time Russ made valid points. It was like watching football: run out the clock.

    One thing I learned from watching this was the impact on myself in regards to the notion of locking someone in a cage. I have said the same in discussion, but hearing it made me think that the reality of that isn’t stated enough. Nothing about the consequences of current drug policy (I like that, not crime/victim but government policy) is acceptable if it means the treatment is a cage. Even Sabet said, if that’s your thing go do it…which I don’t see him saying to a sex offender… Sometimes cages are needed, and we are not flip about it when that is the case.

    [Russ responds: Ah, yes, the Drug War Filibuster tactic. I also liked how he’d say something, then mention a fact I was about to mention, and then tells me “don’t go there.” Well, gosh, if you’re going to tell me which of my best rebuttals not to use, that sure makes the debate easier, huh?]

  41. I like the Kevin Sabat’s claim that “This isn’t about rounding up everyone… If you want to smoke pot… I’m not concerned about that…” It’s a baldfaced lie. Nothing like a big lie right in people’s faces.

    He’s arguing against legalization. In effect he IS advocating that people should be rounded up who smoke pot. He’s a liar and fake.

  42. When he said if we legalize marijuana drug dealers will undercut the price he is admitting its about the money. They don’t care about what the people want. He also said most people don’t go to jail. Maybe they don’t but what about the people who lose there job because they smoke weed on Saturday or on there vacation then return to work and failed a drug test. What about those people now. O job means no income for something they never did at work.

  43. This was like a circus show. At times it reached the depth of a tenth grade culture class video… Most of it was like, a total fake. These people aren’t debating real issues. This is all false. This is all a stage show. It has nothing to do with reality.

    Reminds me of UFO rallies.

    Well, at least cannabis has roots…

  44. “but at least there isn’t a death toll in the 10?s of thousands in the wake of the black market supplying these goods.”

    Black markets are created…as a direct result of public policy that should be reviewed quickly by designers of the product, esp. in relation to the law.

    Used by the every-day workers who have to deal with strange, inaccurate tests at the lowest cost (walmart equate) Black markets are ad hoc systems where suppliers provide demand by presenting a thing but not stating why. Here there are many walmarts and 7-11’s and circle K’s.

    Take a power nap! even 10 minutes will help. I will assist you in your wake up time

    Go

    Demanders have been told by their legislators that 1) they have a right to ban Cannabis for all people, in order to belch out a song at Super Bowl Half-time show 2) somehow, your love of country and intelligence and drive will take you farther than you ever thought was useful.

  45. I need to get the word out. In Arizona I was given medical license to use medical marijuana as an amputee
    with terrible pain and sleeplessness. Despite my license, a local form of a DEA invaded my home pointing
    guns at me. They destroyed my home, broke things, confiscated things, accused me of selling and using
    other drugs, laughed at me, belittled me, tackled anyone that came to my house during this, arrested me,
    and threw me in jail. I spent three days there, being accused at one point of detoxing, stripped naked
    and thrown into a solitary confinement cell for 24 hours. I was not given shoes for my special amputee
    condition, and yelled at for not having shoes. I had to put up my house and car for bail, have to pay off
    a car title loan at 150% interest, am facing 20 years and a million dollars in fines, all this after having
    been given license to use by the very state that is trying to prosecute me and extort as much money
    from me as possible. Please help me. And help me get the word out. This is beyond abuse and
    it needs to be known, and fought. Sincerely, Brenda Whittaker 928.634.6677

  46. the antidote for “marijuana overdose is water” the lethal threshold is very high.

    Ethanol poisoning is caused by drinking too much alcohol,” and can be found with respect to “Alcohol beverages, including: beer, gin, vodka, wine, whiskey.”

    “Symptoms inlcude:
    * Abdominal pain
    * Coma
    * Intestinal bleeding
    * Moving from side to side
    * Slowed breathing
    * Slurred speech
    * Stupor
    * Unable to walk normally
    * Vomiting

    Cannabis
    1.(safety of cannabis) “Tetrahydrocannabinol is a very safe drug. Laboratory animals (rats, mice, dogs, monkeys) can tolerate doses of up to 1,000 mg/kg (milligrams per kilogram). This would be equivalent to a 70 kg person swallowing 70 grams of the drug—about 5,000 times more than is required to produce a high. Despite the widespread illicit use of cannabis there are very few if any instances of people dying from an overdose. In Britain, official government statistics listed five deaths from cannabis in the period 1993-1995 but on closer examination these proved to have been deaths due to inhalation of vomit that could not be directly attributed to cannabis (House of Lords Report, 1998). By comparison with other commonly used recreational drugs these statistics are impressive.”

    Source: Iversen, Leslie L., PhD, FRS, “The Science of Marijuana” (London, England: Oxford University Press, 2000), p. 178, citing House of Lords, Select Committee on Science and Technology, “Cannabis — The Scientific and Medical Evidence” (London, England: The Stationery Office, Parliament, 1998).

    2.(no deaths induced by marijuana) An exhaustive search of the literature finds no deaths induced by marijuana. The US Drug Abuse Warning Network (DAWN) records instances of drug mentions in medical examiners’ reports, and though marijuana is mentioned, it is usually in combination with alcohol or other drugs. Marijuana alone has not been shown to cause an overdose death.

    Source: Source: Drug Abuse Warning Network (DAWN), available on the web at http://www.samhsa.gov/ ; also see Janet E. Joy, Stanley J. Watson, Jr., and John A. Benson, Jr., “Marijuana and Medicine: Assessing the Science Base,” Division of Neuroscience and Behavioral Research, Institute of Medicine (Washington, DC: National Academy Press, 1999), available on the web at http://www.nap.edu/html/marimed/; and US Department of Justice, Drug Enforcement Administration, “In the Matter of Marijuana Rescheduling Petition” (Docket #86-22), September 6, 1988, p. 57.

  47. Medical useMain article: Medical cannabis
    Cannabis used medically has several well-documented beneficial effects. Among these are: the amelioration of nausea and vomiting, stimulation of hunger in chemotherapy and AIDS patients, lowered intraocular eye pressure (shown to be effective for treating glaucoma), as well as general analgesic effects (pain reliever).b[›]

    Less confirmed individual studies also have been conducted indicating cannabis to be beneficial to a gamut of conditions running from multiple sclerosis to depression. Synthesized cannabinoids are also sold as prescription drugs, including Marinol (dronabinol in the United States and Germany) and Cesamet (nabilone in Canada, Mexico, the United States and the United Kingdom).b[›] In 2011, an oromucosal spray for Multiple Sclerosis patients became licensed for use as a medicine from the European regulatory body, allowing it to be routinely prescribed by doctors.[18]

    Currently, the U.S. Food and Drug Administration (FDA) has not approved smoked cannabis for any condition or disease in the United States, largely because good quality scientific evidence for its use from U.S. studies is lacking. Regardless, fourteen states have legalized cannabis for medical use.[19][20] The United States Supreme Court has ruled in United States v. Oakland Cannabis Buyers’ Coop and Gonzales v. Raich that it is the federal government that has the right to regulate and criminalize cannabis, even for medical purposes. Canada, Spain, The Netherlands and Austria have legalized some form of cannabis for medicinal use.[21]

    Long-term effectsMain article: Long-term effects of cannabis
    Main article: Cannabis smoking#Smoking lung cancer risk

    Cannabis is ranked one of the least harmful drugs by a study published in the UK medical journal, The Lancet.[22]Given the limitations of the research, scientists still debate the possibility of cannabis dependence; the potential of cannabis as a “gateway drug”; its effects on intelligence and memory; its effect on the lungs; and the relationship, if any, of cannabis use to mental disorders[23] such as schizophrenia,[24] psychosis,[25] Depersonalization disorder[26] and depression.[27]

  48. Cannabis was used as a truth serum by the Office of Strategic Services (OSS), a US government intelligence agency formed during World War II. In the early 1940s, it was the most effective truth drug developed at the OSS labs at St. Elizabeths Hospital; it caused a subject “to be loquacious and free in his impartation of information.”[119]

    In May 1943, Major George Hunter White, head of OSS counter-intelligence operations in the US, arranged a meeting with Augusto Del Gracio, an enforcer for gangster Lucky Luciano. Del Gracio was given cigarettes spiked with THC concentrate from cannabis, and subsequently talked openly about Luciano’s heroin operation. On a second occasion the dosage was increased such that Del Gracio passed out for two hours.[119]

  49. In the United States, cannabis is overall the #4 value crop, and is #1 or #2 in many states including California, New York and Florida, averaging $3,000/lb.[113][114] It is believed to generate an estimated $36 billion market

  50. Main article: Cannabis cultivation
    It is often claimed by growers and breeders of herbal cannabis that advances in breeding and cultivation techniques have increased the potency of cannabis since the late 1960s and early ’70s, when THC was first discovered and understood. However, potent seedless cannabis such as “Thai sticks” were already available at that time. Sinsemilla (Spanish for “without seed”) is the dried, seedless inflorescences of female cannabis plants. Because THC production drops off once pollination occurs, the male plants (which produce little THC themselves) are eliminated before they shed pollen to prevent pollination. Advanced cultivation techniques such as hydroponics, cloning, high-intensity artificial lighting, and the sea of green method are frequently employed as a response (in part) to prohibition enforcement efforts that make outdoor cultivation more risky. It is often cited that the average levels of THC in cannabis sold in United States rose dramatically between the 1970s and 2000, but such statements are likely skewed because of undue weight given to much more expensive and potent, but less prevalent samples.[120] The average THC level in coffee shops in the Netherlands is currently about 18–19%, but new regulations adopted by the Dutch government in 2011 will force the THC content of cannabis sold in coffee shops to be limited to 15%, stating that cannabis in excess of 15% THC will be reclassified as a hard drug.

  51. AdulterantsChalk (in the Netherlands) and glass particles (in the UK) have been used to make cannabis appear to be higher quality.[50][51][52] Increasing the weight of hashish products in Germany with lead caused lead intoxication in at least 29 users.[53] In the Netherlands two chemical analogs of Sildenafil (Viagra) were found in adulterated marijuana.[54]

    According to both the “Talk to FRANK” website and the UKCIA website, Soap Bar, “perhaps the most common type of hash in the UK”, was found “at worst” to contain turpentine, tranquilizers, boot polish, henna and animal feces—amongst several other things.[55][56] One small study of five “soap-bar” samples seized by UK Customs in 2001 found huge adulteration by many toxic substances, including soil, glue, engine oil and animal feces.[57

  52. Detection of useTHC and its major (inactive) metabolite, THC-COOH, can be measured in blood, urine, hair, oral fluid or sweat using chromatographic techniques as part of a drug use testing program or a forensic investigation of a traffic or other criminal offense. The concentrations obtained from such analyses can often be helpful in distinguishing active use from passive exposure, prescription use from illicit use, elapsed time since use, and extent or duration of use. These tests cannot, however, distinguish authorized cannabis smoking for medical purposes from unauthorized recreational smoking.[58] Commercial cannabinoid immunoassays, often employed as the initial screening method when testing physiological specimens for marijuana presence, have different degrees of cross-reactivity with THC and its metabolites. Urine contains predominantly THC-COOH, while hair, oral fluid and sweat contain primarily THC. Blood may contain both substances, with the relative amounts dependent on the recency and extent of usage.[58][59][60][61]

    The Duquenois-Levine test is commonly used as a screening test in the field, but it cannot definitively confirm the presence of cannabis, as a large range of substances have been shown to give false positives. Despite this, it is common in the United States for prosecutors to seek plea bargains on the basis of positive D-L tests, claiming them definitive, or even to seek conviction without the use of gas chromatography confirmation, which can only be done in the lab.[62]

  53. Hash oil
    BHOMain article: Hash oil
    Hash oil, or “butane honey oil” (BHO), is a mix of essential oils and resins extracted from mature cannabis foliage through the use of various solvents. It has a high proportion of cannabinoids (ranging from 40 to 90%).[33] and is used in a variety of cannabis foods.

    Residue (resin)Because of THC’s adhesive properties, a sticky residue, most commonly known as “resin”, builds up inside utensils used to smoke cannabis. It has tar-like properties but still contains THC as well as other cannabinoids. This buildup retains some of the psychoactive properties of cannabis but is more difficult to smoke without discomfort caused to the throat and lungs. This tar may also contain CBN, which is a breakdown product of THC. Cannabis users typically only smoke residue when cannabis is unavailable. Glass pipes may be water-steamed at a low temperature prior to scraping in order to make the residue easier to remove

  54. For the plant genus, see Cannabis.

    Dried flowers of the Cannabis sativa plant with visible trichomes.Cannabis, also known as marijuana[1] (from the Mexican Spanish marihuana) and by other names,a[›] refers to preparations of the Cannabis plant intended for use as a psychoactive drug and as medicine.[2][3][4] Chemically, the major psychoactive compound in cannabis is delta-9-tetrahydrocannabinol (?9-THC); it is one of 400 compounds in the plant, including other cannabinoids, such as cannabidiol (CBD), cannabinol (CBN), and tetrahydrocannabivarin (THCV), which can produce sensory effects unlike the psychoactive effects of THC.[5]

    Contemporary uses of cannabis are as recreational drug, as religious rite, as spiritual rite, and as medicine; the earliest recorded uses date from the 3rd millennium BC.[6] In 2004, the United Nations estimated that global consumption of cannabis indicated that approximately 4.0 percent of the adult world population (162 million people) used cannabis annually, and that approximately 0.6 percent (22.5 million) of people used cannabis daily.[7] Since the early 20th century cannabis has been subject to legal restrictions with the possession, use, and sale of cannabis preparations containing psychoactive cannabinoids currently illegal in most countries of the world; the United Nations has said that cannabis is the most used illicit drug in the world.[8][9]

  55. EffectsMain article: Effects of cannabis

    Main short-term physical effects of cannabisCannabis has psychoactive and physiological effects when consumed. The minimum amount of THC required to have a perceptible psychoactive effect is about 10 micrograms per kilogram of body weight.[10] Aside from a subjective change in perception and, most notably, mood, the most common short-term physical and neurological effects include increased heart rate, lowered blood pressure, impairment of short-term and working memory,[11] psychomotor coordination, and concentration. Long-term effects are less clear.[12][13]

    Deaths associated to cannabis overdose are exceptionally rare. Fatalities resulting from cannabis overdose are said to most often occur after intravenous injection of hashish oil.[14]

  56. ClassificationMain article: Psychoactive effects
    While many psychoactive drugs clearly fall into the category of either stimulant, depressant, or hallucinogen, cannabis exhibits a mix of all properties, perhaps leaning the most towards hallucinogenic or psychedelic properties, though with other effects quite pronounced as well. Though THC is typically considered the primary active component of the cannabis plant, various scientific studies have suggested that certain other cannabinoids like CBD may also play a significant role in its psychoactive effects.[15][16][17]

  57. Currently, the U.S. Food and Drug Administration (FDA) has not approved smoked cannabis for any condition or disease in the United States, largely because good quality scientific evidence for its use from U.S. studies is lacking. Regardless, fourteen states have legalized cannabis for medical use.[19][20] The United States Supreme Court has ruled in United States v. Oakland Cannabis Buyers’ Coop and Gonzales v. Raich that it is the federal government that has the right to regulate and criminalize cannabis, even for medical purposes. Canada, Spain, The Netherlands and Austria have legalized some form of cannabis for medicinal use.[21]

  58. Residue (resin)Because of THC’s adhesive properties, a sticky residue, most commonly known as “resin”, builds up inside utensils used to smoke cannabis. It has tar-like properties but still contains THC as well as other cannabinoids. This buildup retains some of the psychoactive properties of cannabis but is more difficult to smoke without discomfort caused to the throat and lungs. This tar may also contain CBN, which is a breakdown product of THC. Cannabis users typically only smoke residue when cannabis is unavailable. Glass pipes may be water-steamed at a low temperature prior to scraping in order to make the residue easier to remove.[34]

  59. ProcessedKiefMain article: Kief
    Kief is a powder, rich in trichomes, which can be sifted from the leaves and flowers of cannabis plants and either consumed in powder form or compressed to produce cakes of hashish.[31]

  60. Unprocessed
    Dried Cannabis flowers in natural herbal formThe terms cannabis or marijuana generally refer to the dried flowers and subtending leaves and stems of the female cannabis plant.[citation needed] This is the most widely consumed form, containing 3% to 22% THC.[28][29] In contrast, cannabis varieties used to produce industrial hemp contain less than 1% THC and are thus not valued for recreational use.[30]

  61. In 1937 in the United States, the Marihuana Tax Act was passed, and prohibited the production of hemp in addition to cannabis. The reasons that hemp was also included in this law are disputed. Several scholars have claimed that the Act was passed in order to destroy the hemp industry,[94][95][96] largely as an effort of businessmen Andrew Mellon, Randolph Hearst, and the Du Pont family.[94][96] With the invention of the decorticator, hemp became a very cheap substitute for the paper pulp that was used in the newspaper industry.[94][97] Hearst felt that this was a threat to his extensive timber holdings. Mellon, Secretary of the Treasury and the wealthiest man in America, had invested heavily in the DuPont’s new synthetic fiber, nylon, and considered its success to depend on its replacement of the traditional resource, hemp.[94][98][99][100][101][102][103][104] The claims that hemp could have been a successful substitute for wood pulp have been based on an incorrect government report of 1916 which concluded that hemp hurds, broken parts of the inner core of the hemp stem, were a suitable source for paper production. This has not been confirmed by later research, as hemp hurds are not reported to be a good enough substitute. Many advocates for hemp have greatly overestimated the proportion of useful cellulose in hemp hurds. In 2003, 95?% of the hemp hurds in EU were used for animal bedding, almost 5?% were used as building material.[105][106][107][108] See also Hemp.

  62. in 1937, there was a war on. International Law Demands that marijuana be classified as a narcotic. At least thats how it went then. Before the 1920’s there were no laws regulating the sale of cocaine. you could buy it at any corner store. Penalizing people with jail time for possession is winning the war on freedom. If any penalty shall isssue for marijuana use, why not a 150$ fine?

  63. Lysergic acid diethylamide, abbreviated LSD or LSD-25, also known as lysergide and colloquially as acid, is a semisynthetic psychedelic drug of the ergoline family, well known for its psychological effects which can include altered thinking processes, closed and open eye visuals, synaesthesia, an altered sense of time and spiritual experiences, as well as for its key role in 1960s counterculture. It is used mainly as an entheogen, recreational drug, and as an agent in psychedelic therapy. LSD is non-addictive, is not known to cause brain damage, and has extremely low toxicity relative to dose, although in rare cases adverse psychiatric reactions such as anxiety or delusions are possible.[3]

    LSD was first synthesized by Albert Hofmann in 1938 from ergotamine, a chemical derived by Arthur Stoll from ergot, a grain fungus that typically grows on rye. The short form “LSD” comes from its early code name LSD-25, which is an abbreviation for the German “Lysergsäure-diethylamid” followed by a sequential number.[4][5] LSD is sensitive to oxygen, ultraviolet light, and chlorine, especially in solution, though its potency may last for years if it is stored away from light and moisture at low temperature. In pure form it is a colorless, odorless, and mildly bitter solid.[6] LSD is typically delivered orally, usually on a substrate such as absorbent blotter paper, a sugar cube, or gelatin. In its liquid form, it can also be administered by intramuscular or intravenous injection. LSD is very potent, with 20–30 µg (micrograms) being the threshold dose.[7]

    Introduced by Sandoz Laboratories, with trade-name Delysid, as a drug with various psychiatric uses in 1947, LSD quickly became a therapeutic agent that appeared to show great promise.[8] In the 1950s, officials at the U.S. Central Intelligence Agency (CIA) thought the drug might be applicable to mind control and chemical warfare; the agency’s MKULTRA research program propagated the drug among young servicemen and students. The subsequent recreational use of the drug by youth culture in the Western world during the 1960s led to a political firestorm that resulted in its prohibition.[9] Currently, a number of organizations—including the Beckley Foundation, MAPS, Heffter Research Institute and the Albert Hofmann Foundation—exist to fund, encourage and coordinate research into the medicinal and spiritual uses of LSD and related psychedelics.[10]

  64. Effects[edit] PhysicalLSD can cause pupil dilation, reduced appetite (for some, it increases), and wakefulness. Other physical reactions to LSD are highly variable and nonspecific, and some of these reactions may be secondary to the psychological effects of LSD. The following symptoms have been reported: numbness, weakness, nausea, hypothermia or hyperthermia (decreased or increased body temperature), elevated blood sugar, goose bumps, increase in heart rate, jaw clenching, perspiration, saliva production, mucus production, sleeplessness, hyperreflexia, and tremors. Some users, including Albert Hofmann, report a strong metallic taste for the duration of the effects.[11]

    LSD is not considered addictive by the medical community.[12] Rapid tolerance build-up prevents regular use, and there is cross-tolerance shown between LSD, mescaline[13] and psilocybin.[14] This tolerance diminishes after a few days without use and is probably caused by downregulation of 5-HT2A receptors in the brain.[citation needed]

    [edit] PsychologicalLSD’s psychological effects (colloquially called a “trip”) vary greatly from person to person, depending on factors such as previous experiences, state of mind and environment, as well as dose strength. They also vary from one trip to another, and even as time passes during a single trip. An LSD trip can have long-term psychoemotional effects; some users cite the LSD experience as causing significant changes in their personality and life perspective. Widely different effects emerge based on what Timothy Leary called set and setting; the “set” being the general mindset of the user, and the “setting” being the physical and social environment in which the drug’s effects are experienced.

    Some psychological effects may include an experience of radiant colors, objects and surfaces appearing to ripple or “breathe”, colored patterns behind the closed eyelids (eidetic imagery), an altered sense of time (time seems to be stretching, repeating itself, changing speed or stopping), crawling geometric patterns overlaying walls and other objects, morphing objects, a sense that one’s thoughts are spiraling into themselves, loss of a sense of identity or the ego (known as “ego death”), and other powerful psycho-physical reactions.[15] Many users experience a dissolution between themselves and the “outside world”.[16] This unitive quality may play a role in the spiritual and religious aspects of LSD. The drug sometimes leads to disintegration or restructuring of the user’s historical personality and creates a mental state that some users report allows them to have more choice regarding the nature of their own personality.[citation needed]

    If the user is in a hostile or otherwise unsettling environment, or is not mentally prepared for the powerful distortions in perception and thought that the drug causes, effects are more likely to be unpleasant than if he or she is in a comfortable environment and has a relaxed, balanced and open mindset.[17]

    [edit] SensoryLSD causes expansion and an altered experience of senses, emotions, memories, time, and awareness for 6 to 14 hours, depending on dosage and tolerance. Generally beginning within thirty to ninety minutes after ingestion, the user may experience anything from subtle changes in perception to overwhelming cognitive shifts. Changes in auditory and visual perception are typical.[16][18] Visual effects include the illusion of movement of static surfaces (“walls breathing”), after image-like trails of moving objects (“tracers”), the appearance of moving colored geometric patterns (especially with closed eyes), an intensification of colors and brightness (“sparkling”), new textures on objects, blurred vision, and shape suggestibility. Users commonly report that the inanimate world appears to animate in an unexplainable way; for instance, objects that are static in three dimensions can seem to be moving relative to one or more additional spatial dimensions.[19] Many of the basic visual effects resemble the phosphenes seen after applying pressure to the eye and have also been studied under the name “form constants”. The auditory effects of LSD may include echo-like distortions of sounds, changes in ability to discern concurrent auditory stimuli, and a general intensification of the experience of music. Higher doses often cause intense and fundamental distortions of sensory perception such as synaesthesia, the experience of additional spatial or temporal dimensions, and temporary dissociation.

    [edit] Potential uses
    Bottle of LSD from a Swiss clinical trial of LSD for anxiety in cancer patients, c. 2007.LSD has been used in psychiatry for its perceived therapeutic value, in the treatment of alcoholism, pain and cluster headache relief, for spiritual purposes, and to enhance creativity. However, government organizations like the United States Drug Enforcement Administration maintain that LSD “produces no aphrodisiac effects, does not increase creativity, has no lasting positive effect in treating alcoholics or criminals, does not produce a ‘model psychosis’, and does not generate immediate

  65. PsychotherapyIn the 1950s and 1960s LSD was used in psychiatry to enhance psychotherapy. Some psychiatrists believed LSD was especially useful at helping patients to “unblock” repressed subconscious material through other psychotherapeutic methods,[21] and also for treating alcoholism.[22][23] One study concluded, “The root of the therapeutic value of the LSD experience is its potential for producing self-acceptance and self-surrender,”[24] presumably by forcing the user to face issues and problems in that individual’s psyche.

    In December 1968, a survey was made of all 74 UK doctors who had used LSD in humans; 73 replied, 1 had moved overseas and was unavailable. Of the 73 replies, the majority of UK doctors with clinical experience with LSD felt that LSD was effective and had acceptable safety: 41 (56%) continued with clinical use of LSD, 11 (15%) had stopped because of retirement or other extraneous reasons, 9 (12%) had stopped because they found LSD ineffective, and 5 (7%) had stopped because they felt LSD was too dangerous.[25]

    [edit] End-of-life anxietyFrom 2008-2011 there has been ongoing research in Switzerland into using LSD to alleviate anxiety for terminally ill cancer patients coping with their impending deaths. Preliminary results from the study are promising, and no negative effects have been reported.[26][27][28]

    [edit] AlcoholismSome studies in the 1950s that used LSD to treat alcoholism professed a 50% success rate,[29][30] five times higher than estimates near 10% for Alcoholics Anonymous.[31] A 1998 review was inconclusive.[32] However, a 2012 meta-analysis of 6 randomized controlled trials found evidence that a single dose of LSD was associated with a decrease in alcohol abuse, lasting for several months.[33]

    [edit] PainLSD was studied in the 1960s by Eric Kast as an analgesic for serious and chronic pain caused by cancer or other major trauma.[34] Even at low (sub-psychedelic) dosages, it was found to be at least as effective as traditional opiates, while being much longer lasting in pain reduction (lasting as long as a week after peak effects had subsided). Kast attributed this effect to a decrease in anxiety; that is to say they were not experiencing less pain, but rather being less distressed by pain. This reported effect is being tested (though not using LSD) in an ongoing (as of 2006) study of the effects of the psychedelic tryptamine psilocybin on anxiety in terminal cancer patients.

    [edit] Cluster headachesLSD has been used as a treatment for cluster headaches, an uncommon but extremely painful disorder. Researcher Peter Goadsby describes the headaches as “worse than natural childbirth or even amputation without anesthetic.”[35] Although the phenomenon has not been formally investigated, case reports indicate that LSD and psilocybin can reduce cluster pain and also interrupt the cluster-headache cycle, preventing future headaches from occurring. Currently existing treatments include various ergolines, among other chemicals, so LSD’s efficacy may not be surprising. A dose-response study testing the effectiveness of both LSD and psilocybin was planned at McLean Hospital, although the current status of this project is unclear. A 2006 study by McLean researchers interviewed 53 cluster-headache sufferers who treated themselves with either LSD or psilocybin, finding that a majority of the users of either drug reported beneficial effects.[36] Unlike use of LSD or MDMA in psychotherapy, this research involves non-psychological effects and often sub-psychedelic dosages.[37][38]

    [edit] SpiritualLSD is considered an entheogen because it can catalyze intense spiritual experiences, during which users may feel they have come into contact with a greater spiritual or cosmic order. Users claim to experience lucid sensations where they have “out of body” experiences. Some users report insights into the way the mind works, and some experience permanent shifts in their life perspective. LSD also allows users to view their life from an introspected point of view. From this point of view, a user can travel back in time to a specific moment or memory and relive that moment again.[citation needed] Some users report using introspection to resolve unresolved or negative feelings towards an individual or incident that occurred in the past. Some users consider LSD a religious sacrament, or a powerful tool for access to the divine. Stanislav Grof has written that religious and mystical experiences observed during LSD sessions appear to be phenomenologically indistinguishable from similar descriptions in the sacred scriptures of the great religions of the world and the secret mystical texts of ancient civilizations.[39]

    [edit] CreativityIn the 1950s and 1960s, psychiatrists like Oscar Janiger explored the potential effect of LSD on creativity. Experimental studies attempted to measure the effect of LSD on creative activity and aesthetic appreciation.[40][41][42][43] Seventy professional artists were asked to draw two pictures of a Hopi Indian kachina doll, one before ingesting LSD and one after.[44]

    [edit] Potential adverse effects
    Chart of dependence potential and effective dose/lethal dose of some psychoactive drugs.There have been no documented human deaths from an LSD overdose.[45] It is physiologically well tolerated and there is no evidence for long-lasting physiological effects on the brain or other parts of the human organism.[46]

    LSD may temporarily impair the ability to make sensible judgments and understand common dangers, thus making the user more susceptible to accidents and personal injury. It may cause temporary confusion, difficulty with abstract thinking, or signs of impaired memory and attention span similar to brain damage.[47]

    [edit] Adverse drug interactionsThere is some indication that LSD may trigger a dissociative fugue state in individuals who are taking certain classes of antidepressants such as lithium salts and tricyclics. In such a state, the user has an impulse to wander, and may not be aware of his or her actions, which can lead to physical injury. Anonymous anecdotal reports have attributed seizures and one death to the combination of LSD with lithium.[48] SSRIs noticeably reduce LSD’s subjective effects.[49] MAOIs are also reported to reduce the effects of LSD.[48]

    [edit] Panic and anxietyLSD may trigger panic attacks or feelings of extreme anxiety, colloquially referred to as a “bad trip”.[50]

    [edit] SuggestibilityWhile publicly available documents indicate that the CIA and Department Of Defense have discontinued research into the use of LSD as a means of mind control,[51] research from the 1960s suggests there exists evidence that both mentally ill and healthy people are more suggestible while under its influence.[52][53]

    [edit] PsychosisThere are some cases of LSD inducing a psychosis in people who appeared to be healthy before taking LSD.[54] In most cases, the psychosis-like reaction is of short duration, but in other cases it may be chronic. It is difficult to determine whether LSD itself induces these reactions or if it triggers latent conditions that would have manifested themselves otherwise. The similarities of time course and outcomes between putatively LSD-precipitated and other psychoses suggest that the two types of syndromes are not different and that LSD may have been a nonspecific trigger.[citation needed]

    Estimates of the prevalence of LSD-induced prolonged psychosis lasting over 48 hours have been made by surveying researchers and therapists who had administered LSD:

    Cohen (1960) estimated 0.8 per 1,000 volunteers (the single case among approximately 1250 study volunteers was the identical twin of a schizophrenic and he recovered within 5 days) and 1.8 per 1,000 psychiatric patients (7 cases among approximately 3850 patients, of which 2 cases were “preschizophrenic” or had previous hallucinatory experience, 1 case had unknown outcome, 1 case had incomplete recovery, and 5 cases recovered within up to 6 months).[55]
    Malleson (1971) reported no cases of psychosis among experimental subjects (170 volunteers who received a total of 450 LSD sessions) and estimated 9 per 1,000 among psychiatric patients (37 cases among 4300 patients, of which 8 details are unknown, 10 appeared chronic, and 19 recovered completely within up to 3 months).[25]
    However, in neither survey study was it possible to compare the rate of lasting psychosis in these volunteers and patients receiving LSD with the rate of psychosis found in other groups of research volunteers or in other methods of psychiatric treatment (for example, those receiving placebo).

    Cohen (1960) noted:[55]

    “The hallucinogenic experience is so striking that many subsequent disturbances may be attributed to it without further justification. The highly suggestible or hysterical individual would tend to focus on his LSD experience to explain subsequent illness. Patients have complained to Abramson that their LSD exposure produced migraine headaches and attacks of influenza up to a year later. One Chinese girl became paraplegic and ascribed that catastrophe to LSD. It so happened that these people were all in the control group and had received nothing but tap water.”
    [edit] Flashbacks and HPPDSee also: Flashback (psychology)
    “Flashbacks” are a reported psychological phenomenon in which an individual experiences an episode of some of LSD’s subjective effects long after the drug has worn off, usually in the days after typical doses. In some rarer cases, flashbacks have lasted longer, but are generally short-lived and mild compared to the actual LSD “trip”. Flashbacks can incorporate both positive and negative aspects of LSD trips, and are typically elicited by triggers such as alcohol or cannabis use, stress, caffeine, or sleepiness. Flashbacks have proven difficult to study and are no longer officially recognized as a psychiatric syndrome. However, colloquial usage of the term persists and usually refers to any drug-free experience reminiscent of psychedelic drug effects, with the typical connotation that the episodes are of short duration.

    No definitive explanation is currently available for these experiences. Any attempt at explanation must reflect several observations: first, over 70 percent of LSD users claim never to have “flashed back”; second, the phenomenon does appear linked with LSD use, though a causal connection has not been established; and third, a higher proportion of psychiatric patients report flashbacks than other users.[56] Several studies have tried to determine how likely a user of LSD, not suffering from known psychiatric conditions, is to experience flashbacks. The larger studies include Blumenfeld’s in 1971[57] and Naditch and Fenwick’s in 1977,[58] which arrived at figures of 20% and 28%, respectively.

    Although flashbacks themselves are not recognized as a medical syndrome, there is a recognized syndrome called Hallucinogen Persisting Perception Disorder (HPPD) in which LSD-like visual changes are not temporary and brief, as they are in flash-backs, but instead are persistent, and cause clinically significant impairment or distress. The syndrome is a DSM-IV diagnosis. Several scientific journal articles have described the disorder.[59]

    HPPD differs from flashbacks in that it is persistent and apparently entirely visual (although mood and anxiety disorders are sometimes diagnosed in the same individuals). A recent review suggests that HPPD (as defined in the DSM-IV) is rare and affects only a distinctly vulnerable subpopulation of users.[60] However, it is possible that the prevalence of HPPD is underestimated because most of the diagnoses are applied to people who are willing to admit to their health care practitioner that they have previously used psychotropics, and presumably many people are reluctant to admit this.[61]

    There is no consensus regarding the nature and causes of HPPD (or flashbacks). A study of 44 HPPD subjects who had previously ingested LSD showed EEG abnormalities.[62] Given that some symptoms have environmental triggers, it may represent a failure to adjust visual processing to changing environmental conditions. There are no explanations for why only some individuals develop HPPD. Explanations in terms of LSD physically remaining in the body for months or years after consumption have been discounted by experimental evidence.[56] Some say HPPD is a manifestation of post-traumatic stress disorder, not related to the direct action of LSD on brain chemistry, and varies according to the susceptibility of the individual to the disorder. Many emotionally intense experiences can lead to flashbacks when a person is reminded acutely of the original experience. However, not all published case reports of HPPD appear to describe an anxious hyper-vigilant state reminiscent of post-traumatic stress disorder. Instead, some cases appear to involve only visual symptoms.[56]

    [edit] Uterine contractionsEarly pharmacological testing by Sandoz in laboratory animals showed that LSD can stimulate uterine contractions, with efficacy comparable to ergobasine, the active uterotonic component of the ergot fungus. (Hofmann’s work on ergot derivatives also produced a modified form of ergobasine which became a widely accepted medication used in obstetrics, under the trade name Methergine.) Therefore, LSD use by pregnant women could be dangerous and is contraindicated.[4] However, the relevance of these animal studies to humans is unclear, and a 2008 medical reference guide to drugs in pregnancy and lactation stated, “It appears unlikely that pure LSD administered in a controlled condition is an abortifacient.”[63]

    [edit] GeneticBeginning in 1967, studies raised concerns that LSD might produce genetic damage[64] or developmental abnormalities in fetuses. However, these initial reports were based on in vitro studies or were poorly controlled and have not been substantiated. In studies of chromosomal changes in human users and in monkeys, the balance of evidence suggests no increase in chromosomal damage. For example, white blood cells of people who had been given LSD in a clinical setting were examined for visible chromosomal abnormalities; overall, there appeared to be no lasting changes.[64] Several studies have been conducted using illicit LSD users and provide a less clear picture. Interpretation of these data is generally complicated by factors such as the unknown chemical composition of street LSD, concurrent use of other psychoactive drugs, and diseases such as hepatitis in the sampled populations. It seems possible the small number of genetic abnormalities reported in users of street LSD is either coincidental or related to factors other than a toxic effect of pure LSD.[64] A 2008 medical review concluded, “The available data suggest that pure LSD does not cause chromosomal abnormalities, spontaneous abortions, or congenital malformations.”[63]

    [edit] AntidotesAdverse effects of psychotropics are often treated with fast-acting benzodiazepines like diazepam or triazolam that have calming and antianxiety effects but do not directly affect the specific actions of psychotropics. Theoretically, specific 5-HT2A receptor antagonists, which most commonly means atypical antipsychotics (quetiapine, olanzapine, risperidone, etc.) or other 5-HT2A antagonist such as trazodone or mirtazapine, would be direct antidotes, although some anecdotal reports claim otherwise.[65] Also, some people have reported that taking an SSRI such as fluoxetine will counteract the effects of LSD.[66] Some reports indicate that although administration of chlorpromazine (Thorazine) or similar typical antipsychotic tranquilizers will not end an LSD trip, it will either lessen the intensity or immobilize and numb the patient, a side effect of the medication.[67] While it also may not end an LSD trip, the best chemical treatment for a “bad trip” is an anxiolytic agent such as diazepam (Valium) or another benzodiazepine. As the effect of the drug is psychological as well as physical, any treatment should focus on calming the patient. Limiting stimuli such as bright lights and loud noises can help in the event of an ill reaction.

    Many rumors about home remedies to counteract psychedelic effects are circulated, including vanilla essence, and anti-histamines. These may have a placebo effect, working by making the taker think they have done something to make it better.[68]

    [edit] Chemistry and structure
    The four possible stereoisomers of LSD. Only (+)-LSD is psychoactive.LSD is an ergoline derivative. It is commonly synthesised by reacting diethylamine with an activated form of lysergic acid. Activating reagents include phosphoryl chloride[69] and peptide coupling reagents.[70] Lysergic acid is made by alkaline hydrolysis of lysergamides like ergotamine, a substance derived from the ergot fungus on rye, or from ergine (lysergic acid amide, LSA), a compound that is found in morning glory (Ipomoea tricolor) and Hawaiian baby woodrose (Argyreia nervosa) seeds.

    LSD is a chiral compound with two stereocenters at the carbon atoms C-5 and C-8, so that theoretically four different optical isomers of LSD could exist. LSD, also called (+)-D-LSD, has the absolute configuration (5R,8R). The C-5 isomers of lysergamides do not exist in nature and are not formed during the synthesis from D-lysergic acid. Retrosynthetically, the C-5 stereocenter could be analysed as having the same configuration of the alpha carbon of the naturally occurring amino acid L-tryptophan, the precursor to all biosynthetic ergoline compounds.

    However, LSD and iso-LSD, the two C-8 isomers, rapidly interconvert in the presence of bases, as the alpha proton is acidic and can be deprotonated and reprotonated. Non-psychoactive iso-LSD which has formed during the synthesis can be separated by chromatography and can be isomerized to LSD.

    A totally pure salt of LSD will emit small flashes of white light when shaken in the dark.[5] LSD is strongly fluorescent and will glow bluish-white under UV light.

    [edit] Reactivity and degradation”LSD,” writes the chemist Alexander Shulgin, “is an unusually fragile molecule.”[5] It is stable for indefinite time if stored as a solid salt or dissolved in water, at low temperature and protected from air and light exposure.

    LSD has two labile protons at the tertiary stereogenic C5 and C8 positions, rendering these centres prone to epimerisation. The C8 proton is more labile due to the electron-withdrawing carboxamide attachment, but removal of the chiral proton at the C5 position (which was once also an alpha proton of the parent molecule tryptophan) is assisted by the inductively-withdrawing nitrogen and pi electron delocalisation with the indole ring.[citation needed]

    LSD also has enamine-type reactivity because of the electron-donating effects of the indole ring. Because of this, chlorine destroys LSD molecules on contact; even though chlorinated tap water contains only a slight amount of chlorine, the small quantity of compound typical to an LSD solution will likely be eliminated when dissolved in tap water.[5] The double bond between the 8-position and the aromatic ring, being conjugated with the indole ring, is susceptible to nucleophilic attacks by water or alcohol, especially in the presence of light. LSD often converts to “lumi-LSD”, which is totally inactive in human beings (to the best of current knowledge).

    A controlled study was undertaken to determine the stability of LSD in pooled urine samples.[71] The concentrations of LSD in urine samples were followed over time at various temperatures, in different types of storage containers, at various exposures to different wavelengths of light, and at varying pH values. These studies demonstrated no significant loss in LSD concentration at 25°C for up to four weeks. After four weeks of incubation, a 30% loss in LSD concentration at 37°C and up to a 40% at 45°C were observed. Urine fortified with LSD and stored in amber glass or nontransparent polyethylene containers showed no change in concentration under any light conditions. Stability of LSD in transparent containers under light was dependent on the distance between the light source and the samples, the wavelength of light, exposure time, and the intensity of light. After prolonged exposure to heat in alkaline pH conditions, 10 to 15% of the parent LSD epimerized to iso-LSD. Under acidic conditions, less than 5% of the LSD was converted to iso-LSD. It was also demonstrated that trace amounts of metal ions in buffer or urine could catalyze the decomposition of LSD and that this process can be avoided by the addition of EDTA.

    [edit] Dosage
    White on White blotters (WoW)
    Pink Elephant Blotters Containing LSD
    Bottle of Liquid LSDA single dose of LSD may be between 100 and 500 micrograms—an amount roughly equal to one-tenth the mass of a grain of sand. Threshold effects can be felt with as little as 25 micrograms of LSD.[7][72] Dosages of LSD are measured in micrograms (µg), or millionths of a gram. By comparison, dosages of most drugs, both recreational and medicinal, are measured in milligrams (mg), or thousandths of a gram. For example, an active dose of mescaline, roughly 0.2 to 0.5g, has effects comparable to 100 µg or less of LSD.[4]

    Typical doses in the 1960s ranged from 200 to 1000 µg while street samples of the 1970s contained 30 to 300 µg. By the 1980s, the amount had reduced to between 100 and 125 µg, lowering more in the 1990s to the 20–80 µg range,[73] and even more in the 2000s (decade).[74] [75]

    Estimates for the median lethal dose (LD50) of LSD range from 200 µg/kg to more than 1 mg/kg of human body mass, though most sources report that there are no known human cases of such an overdose. Other sources note one report of a suspected fatal overdose of LSD occurring in November 1975 in Kentucky in which there were indications that ~1/3 of a gram (320 mg or 320,000 µg) had been injected intravenously. (This is a very extraordinary amount, equivalent to over 3,000 times the average LSD dosage of ~100 µg).[76][77] Experiments with LSD have also been done on animals; in 1962, an elephant named Tusko died shortly after being injected with 297 mg, but whether the LSD was the cause of his death is controversial (due, in part, to a plethora of other chemical substances administered simultaneously).[78]

    [edit] PharmacokineticsLSD’s effects normally last from 6–12 hours depending on dosage, tolerance, body weight and age.[5] The Sandoz prospectus for “Delysid” warned: “intermittent disturbances of affect may occasionally persist for several days.”[4] Contrary to early reports and common belief, LSD effects do not last longer than the amount of time significant levels of the drug are present in the blood. Aghajanian and Bing (1964) found LSD had an elimination half-life of only 175 minutes.[1] However, using more accurate techniques, Papac and Foltz (1990) reported that 1 µg/kg oral LSD given to a single male volunteer had an apparent plasma half-life of 5.1 hours, with a peak plasma concentration of 5 ng/mL at 3 hours post-dose.[2]

    [edit] Detection in biological fluidsLSD may be quantified in urine as part of a drug abuse testing program, in plasma or serum to confirm a diagnosis of poisoning in hospitalized victims or in whole blood to assist in a forensic investigation of a traffic or other criminal violation or a case of sudden death. Both the parent drug and its major metabolite are unstable in biofluids when exposed to light, heat or alkaline conditions and therefore specimens are protected from light, stored at the lowest possible temperature and analyzed quickly to minimize losses.[79]

    [edit] Pharmacodynamics
    Binding affinities of LSD for various receptors. The lower the dissociation constant (Ki), the more strongly LSD binds to that receptor (i.e. with higher affinity). The horizontal line represents an approximate value for human plasma concentrations of LSD, and hence, receptor affinities that are above the line are unlikely to be involved in LSD’s effect. Data averaged from data from the Ki DatabaseLSD affects a large number of the G protein coupled receptors, including all dopamine receptor subtypes, and all adrenoreceptor subtypes, as well as many others. LSD binds to most serotonin receptor subtypes except for 5-HT3 and 5-HT4. However, most of these receptors are affected at too low affinity to be sufficiently activated by the brain concentration of approximately 10–20 nM.[80] In humans, recreational doses of LSD can affect 5-HT1A, 5-HT2A, 5-HT2C, 5-HT5A, and 5-HT6 receptors.[1][81] 5-HT5B receptors, which are not present in humans, also have a high affinity for LSD.[82] The psychedelic effects of LSD are attributed to its strong partial agonist effects at 5-HT2A receptors as specific 5-HT2A agonists are psychedelics and largely 5-HT2A specific antagonists block the psychedelic activity of LSD.[80] Exactly how this produces the drug’s effects is unknown, but it is thought that it works by increasing glutamate release in the cerebral cortex and therefore excitation in this area, specifically in layers IV and V.[83] LSD, like many other drugs, has been shown to activate DARPP-32-related pathways.[84]

    [edit] HistoryMain article: History of LSD
    LSD was first synthesized on November 16, 1938[85] by Swiss chemist Albert Hofmann at the Sandoz Laboratories in Basel, Switzerland as part of a large research program searching for medically useful ergot alkaloid derivatives. LSD’s psychedelic properties were discovered 5 years later when Hofmann himself accidentally ingested an unknown quantity of the chemical.[86] The first intentional ingestion of LSD occurred on April 19, 1943,[87] when Hofmann ingested 250 µg of LSD. He said, this would be a threshold dose based on the dosages of other ergot alkaloids. Hofmann found the effects to be much stronger than he anticipated.[88] Sandoz Laboratories introduced LSD as a psychiatric drug in 1947.[89]

    Beginning in the 1950s the US Central Intelligence Agency began a research program code named Project MKULTRA. Experiments included administering LSD to CIA employees, military personnel, doctors, other government agents, prostitutes, mentally ill patients, and members of the general public in order to study their reactions, usually without the subject’s knowledge. The project was revealed in the US congressional Rockefeller Commission report in 1975.

    In 1963 the Sandoz patents expired on LSD.[73] Also in 1963, the US Food and Drug Administration classified LSD as an Investigational New Drug, which meant new restrictions on medical and scientific use.[73] Several figures, including Aldous Huxley, Timothy Leary, and Al Hubbard, began to advocate the consumption of LSD. LSD became central to the counterculture of the 1960s.[90] On October 24, 1968, possession of LSD was made illegal in the United States.[91] The last FDA approved study of LSD in patients ended in 1980, while a study in healthy volunteers was made in the late 1980s. Legally approved and regulated psychiatric use of LSD continued in Switzerland until 1993.[92] Today, medical research is resuming around the world.[93]

    [edit] Production
    Glassware seized by the DEABecause an active dose of LSD is very minute, a large number of doses can be synthesized from a comparatively small amount of raw material. Beginning with ergotamine tartrate, for example, one can manufacture roughly one kilogram of pure, crystalline LSD from five kilograms of the ergotamine salt. Five kilograms of LSD—25 kilograms of ergotamine tartrate—could provide 100 million doses, according to the DEA, more than enough to meet what is believed to be the entire annual U.S. demand. Since the masses involved are so small, concealing and transporting illicit LSD is much easier than smuggling other illegal drugs like cocaine or cannabis.[94]

    Manufacturing LSD requires laboratory equipment and experience in the field of organic chemistry. It takes two to three days to produce 30 to 100 grams of pure compound. It is believed that LSD is not usually produced in large quantities, but rather in a series of small batches. This technique minimizes the loss of precursor chemicals in case a step does not work as expected.[94]

    [edit] Forms
    LSD BlotterLSD is produced in crystalline form and then mixed with excipients or redissolved for production in ingestible forms. Liquid solution is either distributed in small vials or, more commonly, sprayed onto or soaked into a distribution medium. Historically, LSD solutions were first sold on sugar cubes, but practical considerations forced a change to tablet form. Appearing in 1968 as an orange tablet measuring about 6 mm across, “Orange Sunshine” acid was the first largely available form of LSD after its possession was made illegal. Tim Scully, a prominent chemist, made some of it, but said that most “Sunshine” in the USA came by way of Ronald Stark, who imported approximately thirty-five million doses from Europe.[95]

    Over a period of time, tablet dimensions, weight, shape and concentration of LSD evolved from large (4.5–8.1 mm diameter), heavyweight (?150 mg), round, high concentration (90–350 µg/tab) dosage units to small (2.0–3.5 mm diameter) lightweight (as low as 4.7 mg/tab), variously shaped, lower concentration (12–85 µg/tab, average range 30–40 µg/tab) dosage units. LSD tablet shapes have included cylinders, cones, stars, spacecraft and heart shapes. The smallest tablets became known as “Microdots”.[96]

    After tablets came “computer acid” or “blotter paper LSD”, typically made by dipping a preprinted sheet of blotting paper into an LSD/water/alcohol solution.[95][96] More than 200 types of LSD tablets have been encountered since 1969 and more than 350 blotter paper designs have been observed since 1975.[96] About the same time as blotter paper LSD came “Windowpane” (AKA “Clearlight”), which contained LSD inside a thin gelatin square a quarter of an inch across.[95] LSD has been sold under a wide variety of often short-lived and regionally restricted street names including Acid, Trips, Uncle Sid, Blotter, Lucy, Alice and doses, as well as names that reflect the designs on the sheets of blotter paper.[97][98] Authorities have encountered the drug in other forms—including powder or crystal, and capsule.[99]

    [edit] Modern distributionLSD manufacturers and traffickers in the United States can be categorized into two groups: A few large-scale producers, and an equally limited number of small, clandestine chemists, consisting of independent producers who, operating on a comparatively limited scale, can be found throughout the country.[100] As a group, independent producers are of less concern to the Drug Enforcement Administration than the larger groups, as their product reaches only local markets.[101]

    [edit] Mimics
    LSD blotter acid mimic actually containing DOC
    Different blotters which could possibly be mimicsSince 2005, law enforcement in the United States and elsewhere has seized several chemicals and combinations of chemicals in blotter paper which were sold as LSD mimics, including DOB,[102][103] 2C-I,[104][105] DOC,[105] a mixture of DOC and DOI,[106] and a mixture of DOC and DOB.[107] Street users of LSD are often under the impression that blotter paper which is actively hallucinogenic can only be LSD because that is the only chemical with low enough doses to fit on a small square of blotter paper. While it is true that LSD requires lower doses than most other hallucinogens, blotter paper is capable of absorbing a much larger amount of material. The DEA performed a chromatographic analysis of blotter paper containing 2C-C which showed that the paper contained a much greater concentration of the active chemical than typical LSD doses, although the exact quantity was not determined.[108] Blotter LSD mimics can have relatively small dose squares; a sample of blotter paper containing DOC seized by Concord, California police had dose markings approximately 6 mm apart.[105]

    [edit] Legal statusThe United Nations Convention on Psychotropic Substances (adopted in 1971) requires its parties to prohibit LSD. Hence, it is illegal in all parties to the convention, which includes the United States, Australia, New Zealand, and most of Europe. However, enforcement of extant laws varies from country to country. Medical and scientific research with LSD in humans is permitted under the 1971 UN Convention.

    [edit] CanadaIn Canada, LSD is a controlled substance under Schedule III of the Controlled Drugs and Substances Act.[109] Every person who seeks to obtain the substance, without disclosing authorization to obtain such substances 30 days before obtaining another prescription from a practitioner, is guilty of an indictable offense and liable to imprisonment for a term not exceeding 3 years. Possession for purpose of trafficking is an indictable offense punishable by imprisonment for 10 years.

    [edit] United KingdomIn the United Kingdom, LSD is a class ‘A’ drug. This means possession of the drug without a license is punishable with 7 years imprisonment and/or an unlimited fine, and trafficking is punishable with life imprisonment and an unlimited fine (see main article on drug punishments Misuse of Drugs Act 1971).

    In 2000, after consultation with members of the Royal College of Psychiatrists’ Faculty of Substance Misuse, the UK Police Foundation issued the Runciman Report which recommended “the transfer of LSD from Class A to Class B”.[110]

    In November 2009, the UK Transform Drug Policy Foundation released in the House of Commons a guidebooks to the legal regulation of drugs, After the War on Drugs: Blueprint for Regulation, which details options for regulated distribution and sale of LSD and other psychedelics.[111]

    [edit] United StatesLSD is Schedule I in the United States, according to the Controlled Substances Act of 1970.[112] This means LSD is illegal to manufacture, buy, possess, process, or distribute without a DEA license. By classifying LSD as a Schedule I substance, the Drug Enforcement Administration holds that LSD meets the following three criteria: it is deemed to have a high potential for abuse; it has no legitimate medical use in treatment; and there is a lack of accepted safety for its use under medical supervision. There are no documented deaths from chemical toxicity; most LSD deaths are a result of behavioral toxicity.[113]

    There can also be substantial discrepancies between the amount of chemical LSD that one possesses and the amount of possession with which one can be charged in the U.S. This is because LSD is almost always present in a medium (e.g. blotter or neutral liquid), and the amount that can be considered with respect to sentencing is the total mass of the drug and its medium. This discrepancy was the subject of 1995 United States Supreme Court case, Neal v. U.S.[114]

    Lysergic acid and lysergic acid amide, LSD precursors, are both classified in Schedule III of the Controlled Substances Act. Ergotamine tartrate, a precursor to lysergic acid, is regulated under the Chemical Diversion and Trafficking Act.

    [edit] Notable individualsSome notable individuals have commented publicly on their experiences with LSD.[115][116] Some of these comments date from the era when it was legally available in the US and Europe for non-medical uses, and others pertain to psychiatric treatment in the 1950s and 1960s. Still others describe experiences with illegal LSD, obtained for philosophic, artistic, therapeutic, spiritual, or recreational purposes.

    Steve Jobs, co-founder and CEO of Apple Inc. said, “Taking LSD was a profound experience, one of the most important things in my life.”[117]
    In a 2004 interview, Paul McCartney said that The Beatles songs “Day Tripper” and “Lucy in the Sky with Diamonds” are about LSD. John Lennon, George Harrison, and Ringo Starr also experimented with the drug, although McCartney cautioned that “it’s easy to overestimate the influence of drugs on the Beatles’ music.”[118]
    Kary Mullis is reported to credit LSD with helping him develop DNA amplification technology.[119]
    Aldous Huxley, author of Brave New World became a user of psychedelics after moving to Hollywood, CA. He was at the forefront of the counterculture’s experimentation with psychedelic drugs, which led to his 1954 work The Doors of Perception. Dying of cancer, on November 22, 1963, he asked his wife to inject him with 100 µg of LSD. He died from the cancer later that day.[120]
    [edit] See alsoALD-52, chemical analogue of LSD
    Ayahuasca
    Dimethyltryptamine
    Ergine, Lysergic acid amide (LSA), chemical analogue of LSD
    Icaro, shamanic tool to prepare Ayahuasca
    Methysergide, headache medication, chemically related to LSD
    Psychedelic drug
    Psychedelic experience
    Unethical human experimentation in the United States
    Urban legends about LSD
    [edit] References1.^ a b c Aghajanian, George K.; Bing, Oscar H. L. (1964). “Persistence of lysergic acid diethylamide in the plasma of human subjects” (PDF). Clinical Pharmacology and Therapeutics 5: 611–614. PMID 14209776. http://www.maps.org/w3pb/new/1964/1964_aghajanian_2224_1.pdf. Retrieved 2009-09-17.
    2.^ a b Papac, DI; Foltz, RL (May/June 1990). “Measurement of lysergic acid diethylamide (LSD) in human plasma by gas chromatography/negative ion chemical ionization mass spectrometry” (PDF). Journal of Analytical Toxicology 14 (3): 189–190. PMID 2374410. http://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&C=ref&ID=6265&DocPartID=6624. Retrieved 2009-09-17.
    3.^ Passie T, Halpern JH, Stichtenoth DO, Emrich HM, Hintzen A (2008). “The Pharmacology of Lysergic Acid Diethylamide: a Review”. CNS Neuroscience & Therapeutics 14 (4): 295–314. doi:10.1111/j.1755-5949.2008.00059.x. PMID 19040555. http://www.maps.org/w3pb/new/2008/2008_Passie_23067_1.pdf.
    4.^ a b c d Hofmann, Albert. LSD—My Problem Child (McGraw-Hill, 1980). ISBN 0-07-029325-2.
    5.^ a b c d e Alexander and Ann Shulgin. “LSD”, in TiHKAL (Berkeley: Transform Press, 1997). ISBN 0-9630096-9-9.
    6.^ Shulgin, Alexander; Shulgin, Ann (1991). “Burt”. PiHKAL (1st ed.). Transform Press. p. 21. ISBN 978-0-9630096-0-9.
    7.^ a b Greiner T, Burch NR, Edelberg R (1958). “Psychopathology and psychophysiology of minimal LSD-25 dosage; a preliminary dosage-response spectrum”. AMA Arch Neurol Psychiatry 79 (2): 208–10. PMID 13497365.
    8.^ Arthur Stoll and Albert Hofmann LSD Patent April 30, 1943 in Switzerland and Mar. 23, 1948 in the United States.
    9.^ “LSD: cultural revolution and medical advances”. Royal Society of Chemistry. http://www.rsc.org/chemistryworld/Issues/2006/January/LSD.asp. Retrieved 2007-09-27.
    10.^ “The Albert Hofmann Foundation”. Hofmann Foundation. http://www.hofmann.org/. Retrieved 2007-09-27.
    11.^ Albert Hofmann. “LSD: My Problem Child”. http://www.psychedelic-library.org/child5.htm. “”taste of metal on the palate””
    12.^ Lüscher C, Ungless MA (November 2006). [“http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030437” “The Mechanistic Classification of Addictive Drugs”]. PLoS Med. 3 (11): e437. doi:10.1371/journal.pmed.0030437. PMC 1635740. PMID 17105338. “http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030437”.
    13.^ Wolbach AB Jr, Isbell H, Miner EJ (1962). “Cross tolerance between mescaline and LSD-25, with a comparison of the mescaline and LSD reactions”. Psychopharmacologia 3: 1–14. doi:10.1007/BF00413101. PMID 14007904. http://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&C=ref&ID=2032&DocPartID=1893.
    14.^ Isbell H, Wolbach AB, Wikler A, Miner EJ (1961). “Cross Tolerance between LSD and Psilocybin”. Psychopharmacologia 2 (3): 147–59. doi:10.1007/BF00407974. PMID 13717955. http://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&C=ref&ID=1979&DocPartID=1843.
    15.^ The Good Drugs Guide. “LSD psychedelic effects”. http://www.thegooddrugsguide.com/lsd/psychedelic.htm. Retrieved 2008-03-03.
    16.^ a b Linton Harriet B., Langs Robert J. (1962). “Subjective Reactions to Lysergic Acid Diethylamide (LSD-25)” (PDF). Arch. Gen. Psychiat 6: 352–68. http://www.maps.org/w3pb/new/1962/1962_linton_2052_1.pdf.
    17.^ “LSD dangers”. The Good Drugs Guide. http://www.thegooddrugsguide.com/lsd/dangers.htm. Retrieved 2008-10-20.
    18.^ Katz MM, Waskow IE, Olsson J (1968). “Characterizing the psychological state produced by LSD”. J Abnorm Psychol 73 (1): 1–14. doi:10.1037/h0020114. PMID 5639999.
    19.^ See, e.g., Gerald Oster’s article “Moiré patterns and visual hallucinations”. Psychedelic Rev. No. 7 (1966): 33–40.
    20.^ DEA Public Affairs (2001-11-16). “DEA – Publications – LSD in the US – The Drug”. Web.petabox.bibalex.org. http://web.petabox.bibalex.org/web/20011116091659/www.usdoj.gov/dea/pubs/lsd/lsd-4.htm. Retrieved 2010-11-27.
    21.^ Cohen, S. (1959). The therapeutic potential of LSD-25. A Pharmacologic Approach to the Study of the Mind, p251–258.
    22.^ http://www.erowid.org/references/texts/show/1852docid1733
    23.^ “Use of d-Lysergic Acid Diethylamide in the Treatment of Alcoholism”. Hofmann.org. 2003-11-14. http://www.hofmann.org/papers/blewett_1.html. Retrieved 2012-02-22.
    24.^ Chwelos N, Blewett D.B., Smith C.M., Hoffer A. (1959). “Use of d-lysergic acid diethylamide in the treatment of alcoholism”. Quart. J. Stud. Alcohol 20: 577–90. PMID 13810249.
    25.^ a b Malleson, Nicholas (1971). “Acute Adverse Reactions to LSD in Clinical and Experimental Use in the United Kingdom” (PDF). Br J Psychiatry 118 (543): 229–30. doi:10.1192/bjp.118.543.229. PMID 4995932. http://www.maps.org/w3pb/new/1971/1971_malleson_5136_1.pdf.
    26.^ “Psychiater Gasser bricht sein Schweigen”. July 28, 2009. http://bazonline.ch/wissen/medizin-und-psychologie/Psychiater-Gasser-bricht-sein-Schweigen/story/25732295.
    27.^ “LSD-Assisted Psychotherapy for Anxiety Associated with Life-Threatening Illness”. http://www.maps.org/research/psilo-lsd/principal_investigator_peter_gasser_m.d._with_co-therapist_barbara_spe/.
    28.^ David Jay Brown (May 27, 2011). “Landmark Clinical LSD Study Nears Completion”. Patch.com. http://santacruz.patch.com/articles/landmark-clinical-lsd-study-nears-completion.
    29.^ BBC – LSD “helps alcoholics to give up drinking”
    30.^ Maclean, J.R.; Macdonald, D.C.; Ogden, F.; Wilby, E., “LSD-25 and mescaline as therapeutic adjuvants.” In: Abramson, H., Ed., The Use of LSD in Psychotherapy and Alcoholism, Bobbs-Merrill: New York, 1967, pp. 407–426; Ditman, K.S.; Bailey, J.J., “Evaluating LSD as a psychotherapeutic agent,” pp.74–80; Hoffer, A., “A program for the treatment of alcoholism: LSD, malvaria, and nicotinic acid,” pp. 353–402.
    31.^ Minogue SJ (May 1948). “Alcoholics Anonymous”. Med. J. Aust. 1 (19): 586. PMID 18868217.
    32.^ Mangini M (1998). “Treatment of alcoholism using psychedelic drugs: a review of the program of research”. J Psychoactive Drugs 30 (4): 381–418. doi:10.1080/02791072.1998.10399714. PMID 9924844.
    33.^ Krebs, Teri S and Johansen, Pal-Orjan, “Lysergic acid diethylamide (LSD) for alcoholism: meta-analysis of randomized controlled trials”, Journal of Psychopharmacology, March 8, 2012.
    34.^ Kast, Eric (1967). “Attenuation of anticipation: a therapeutic use of lysergic acid diethylamide” (PDF). Psychiat. Quart. 41 (4): 646–57. doi:10.1007/BF01575629. PMID 4169685. http://www.maps.org/w3pb/new/1967/1967_kast_3881_1.pdf.
    35.^ Goadsby is quoted in “Research into psilocybin and LSD as cluster headache treatment”, and he makes an equivalent statement in an Health Report interview on Australian Radio National (August 9, 1999). Pages accessed 2007-01-31.
    36.^ Sewell, R. A.; Halpern, J. H.; Pope, H. G. Jr. (2006-06-27). “Response of cluster headache to psilocybin and LSD”. Neurology 66 (12): 1920–2. doi:10.1212/01.wnl.0000219761.05466.43. PMID 16801660.
    37.^ Summarized from “Research into psilocybin and LSD as cluster headache treatment” and the Clusterbusters website. Pages accessed 2007-01-31.
    38.^ Berlin pilot cluster headaches treatment with LSD study. LSD Alleviates ‘Suicide Headaches’.
    39.^ Grof, Stanislav; Joan Halifax Grof (1979). Realms of the Human Unconscious (Observations from LSD Research). London: Souvenir Press (E & A) Ltd. pp. 13–14. ISBN 0285648829. http://www.csp.org/chrestomathy/realms_of3.html.
    40.^ Sessa, B. (2008). “Is it time to revisit the role of psychedelic drugs in enhancing human creativity?”. J Psychopharmacol 22 (8): 821–7. doi:10.1177/0269881108091597. PMID 18562421.
    41.^ Janiger, O.; Dobkin de Rios M. (1989). “LSD and creativity”. J Psychoactive Drugs 21 (1): 129–34. PMID 2723891. http://www.erowid.org/culture/characters/janiger_oscar/janiger_oscar.shtml.
    42.^ Stafford, Peter G.; B. H. Golightly (1967). LSD, the problem-solving psychedelic. ASIN B0006BPSA0. http://www.psychedelic-library.org/staf3.htm.
    43.^ McGlothlin, W.; Cohen S, McClothlin MS (1967). “Long lasting effects of LSD on normals”. Archives of General Psychiatry 17 (5): 521–532. PMID 6054248. http://www.maps.org/w3pb/new/1967/1967_mcglothlin_4655_1.pdf.
    44.^ Whalen, John (1998-07-09). “The Trip: Cary Grant on acid, and other stories from the LSD Studies of Dr. Oscar Janiger”. LA Weekly.
    45.^ Passie, Torsten; Halpern, John H.; Stichtenoth, Dirk O.; Emrich, Hinderk M.; Hintzen, Annelie (11 November 2008). “The Pharmacology of Lysergic Acid Diethylamide: A Review”. CNS Neuroscience & Therapeutics 14 (4): 295–314. doi:10.1111/j.1755-5949.2008.00059.x. PMID 19040555.
    46.^ http://www.maps.org/research/cluster/psilo-lsd/cns-neuroscience+therapeutics_2008-passie.pdf
    47.^ LSD AND ORGANIC BRAIN IMPAIRMENT S Cohen, AE Edwards – Drug dependence, 1969
    48.^ a b “LSD and Antidepressants” (2003) via Erowid.
    49.^ Kit Bonson, “The Interactions between Hallucinogens and Antidepressants” (2006).
    50.^ “Erowid LSD (Acid) Vaults: Health: Excerpt from Strassman’s Adverse Reactions to Psychedelic Drugs”. Erowid.org. 1993-03-25. http://www.erowid.org/chemicals/lsd/lsd_health1.shtml. Retrieved 2010-11-27.
    51.^ “Is Military Research Hazardous to Veterans Health? Lessons Spanning Half A Century, part F. HALLUCINOGENS”. December 8, 1994 John D. Rockefeller IV, West Virginia: 103rd Congress, 2nd Session-S. Prt. 103-97; Staff Report prepared for the committee on veterans’ affairs. 1994-12-08. http://www.gulfweb.org/bigdoc/rockrep.cfm#hallucinogens.
    52.^ Middlefell R (March 1967). “The effects of LSD on body sway suggestibility in a group of hospital patients” (PDF). Br J Psychiatry 113 (496): 277–80. doi:10.1192/bjp.113.496.277. PMID 6029626. http://www.lycaeum.org/research/researchpdfs/1489.pdf.
    53.^ Sjoberg BM, Hollister LE (November 1965). “The effects of psychotomimetic drugs on primary suggestibility”. Psychopharmacologia 8 (4): 251–62. doi:10.1007/BF00407857. PMID 5885648.
    54.^ [Rick Strassman (1984). “Adverse reactions to psychedelic drugs. A review of the literature”. J Nerv Ment Dis 172 (10): 577–95. doi:10.1097/00005053-198410000-00001. PMID 6384428.
    55.^ a b Cohen, Sidney (January 1960). “Lysergic Acid Diethylamide: Side Effects and Complications” (PDF). Journal of Nervous and Mental Disease 130 (1): 30–40. doi:10.1097/00005053-196001000-00005. PMID 13811003. http://www.maps.org/w3pb/new/1960/1960_cohen_1848_1.pdf.
    56.^ a b c David Abrahart (1998). “A Critical Review of Theories and Research Concerning Lysergic Acid Diethylamide (LSD) and Mental Health”. http://www.maps.org/research/abrahart.html#chp1. Retrieved 2007-02-02.
    57.^ Blumenfield M (1971). “Flashback phenomena in basic trainees who enter the US Air Force”. Military Medicine 136 (1): 39–41. PMID 5005369.
    58.^ Naditch MP, Fenwick S (1977). “LSD flashbacks and ego functioning”. Journal of Abnormal Psychology 86 (4): 352–9. doi:10.1037/0021-843X.86.4.352. PMID 757972.
    59.^ See, for example, Abraham HD, Aldridge AM (1993). “Adverse consequences of lysergic acid diethylamide”. Addiction 88 (10): 1327–34. doi:10.1111/j.1360-0443.1993.tb02018.x. PMID 8251869.
    60.^ Halpern JH, Pope HG Jr (2003). “Hallucinogen persisting perception disorder: what do we know after 50 years?”. Drug Alcohol Depend 69 (2): 109–19. doi:10.1016/S0376-8716(02)00306-X. PMID 12609692. ; Halpern JH (2003). “Hallucinogens: an update”. Curr Psychiatry Rep 5 (5): 347–54. doi:10.1007/s11920-003-0067-4. PMID 13678554. [1]
    61.^ Baggott et al. (2006). “Prevalence of chronic flashbacks in hallucinogen users: a web-based questionnaire” (PDF). http://www.cpdd.vcu.edu/Pages/Meetings/Meetings_PDFs/2006abstractbook.pdf. Retrieved 2009-09-25.
    62.^ Abraham, H. D., & Duffy, F. H. ((1996)). “Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: Evidence for disinhibition”. Psychiatry Research 67 (3): 173–187. doi:10.1016/0925-4927(96)02833-8. PMID 8912957.
    63.^ a b Gerald G. Briggs,Roger K. Freeman,Sumner J. Yaffe (2008). Drugs in pregnancy and lactation. Lippincott Williams & Wilkins. ISBN 9780781778763. http://books.google.com/?id=YOEV2w3XTxsC.
    64.^ a b c Dishotsky NI, Loughman WD, Mogar RE, Lipscomb WR (1971). “LSD and genetic damage” (PDF). Science 172 (3982): 431–40. doi:10.1126/science.172.3982.431. PMID 4994465. http://www.maps.org/w3pb/new/1971/1971_dishotsky_5148_1.pdf.
    65.^ Huxley, Aldous The Doors of Perception and Heaven & Hell, Harper & Row, 1954.
    66.^ Bonson, Kit (1994). “The Interactions between Hallucinogens and Antidepressants – Summary of Results from Online Survey and Online Interviews”. Erowid. http://www.erowid.org/chemicals/maois/maois_info4.shtml. Retrieved 2008-07-28.
    67.^ Gilberti, F. and Gregoretti, L. L. (1955). “Prime esperienze di antaonismo psicofarmacologico” (PDF). Sistema Nervoso 4: 301–309. http://www.maps.org/w3pb/new/1955/1955_giberti_3993_1.pdf.
    68.^ RaveSafe (1999). “RaveSafe Q&A – Can you actually end an acid trip?”. http://www.ravesafe.org/qna/qna-2.htm. Retrieved 2008-07-28.
    69.^ Monte AP, Marona-Lewicka D, Kanthasamy A, Sanders-Bush E, Nichols DE (March 1995). “Stereoselective LSD-like activity in a series of d-lysergic acid amides of (R)- and (S)-2-aminoalkanes”. J. Med. Chem. 38 (6): 958–66. doi:10.1021/jm00006a015. PMID 7699712.
    70.^ Nichols DE, Frescas S, Marona-Lewicka D, Kurrasch-Orbaugh DM (September 2002). “Lysergamides of isomeric 2,4-dimethylazetidines map the binding orientation of the diethylamide moiety in the potent hallucinogenic agent N,N-diethyllysergamide (LSD)”. J. Med. Chem. 45 (19): 4344–9. doi:10.1021/jm020153s. PMID 12213075.
    71.^ Li Z., McNally A. J., Wang H., Salamone S. J. (October 1998). “Stability study of LSD under various storage conditions”. J. Anal. Toxicol. 22 (6): 520–5. PMID 9788528. http://designer-drugs.com/pte/12.162.180.114/dcd/pdf/lsd.storage.stability.pdf.
    72.^ Stoll, W.A. (1947). Ein neues, in sehr kleinen Mengen wirsames Phantastikum. Schweiz. Arch. Neur. 60,483.
    73.^ a b c Henderson, Leigh A.; Glass, William J. (1994). LSD: Still with us after all these years. San Francisco: Jossey-Bass. ISBN 978-0787943790.
    74.^ Erowid & Eduardo Hidalgo, Energy Control (Spain) (2009). “LSD Samples Analysis”. Erowid. http://www.erowid.org/chemicals/lsd/lsd_article3.shtml. Retrieved 2010-02-08.
    75.^ Fire & Earth Erowid (2003). “LSD Analysis – Do we know what’s in street acid?”. Erowid. http://www.erowid.org/chemicals/lsd/lsd_article1.shtml. Retrieved 2010-02-08.
    76.^ “LSD Vault: Dosage”. 2006-07-06. http://www.erowid.org/chemicals/lsd/lsd_dose.shtml. Retrieved 2007-01-31.
    77.^ “LSD Toxicity: A Suspected Cause of Death”. Journal of the Kentucky Medical Association. http://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&ID=1389&DocPartID=1151. Retrieved 2007-11-26.
    78.^ Erowid & R. Stuart (2002). “LSD Related Death of an Elephant – Controversy surrounding the 1962 death of an elephant after an injection of LSD”. Erowid. http://www.erowid.org/chemicals/lsd/lsd_history4.shtml. Retrieved 2008-07-28.
    79.^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 871-874.
    80.^ a b Nichols, David E. (2004). “Psychotropics”. Pharmacology & Therapeutics 101 (2): 131–81. doi:10.1016/j.pharmthera.2003.11.002. PMID 14761703. http://www.erowid.org/references/refs_view.php?A=ShowDoc1&ID=6318.
    81.^ “PDSP database”. http://pdsp.cwru.edu/pdsp.php. Retrieved 2009-11-02.
    82.^ Nelson, DL (February 2004). “5-HT5 receptors”. Current drug targets. CNS and neurological disorders 3 (1): 53–8. doi:10.2174/1568007043482606. PMID 14965244.
    83.^ BilZ0r. “The Neuropharmacology of Hallucinogens: a technical overview”. Erowid, v3.1 (August 2005).
    84.^ Svenningsson P. , Nairn A. C., Greengard P. (2005). “DARPP-32 mediates the actions of multiple drugs of abuse”. AAPS Journal 7 (2): E353–E360. doi:10.1208/aapsj070235. PMC 2750972. PMID 16353915. http://www.aapsj.org/view.asp?art=aapsj070235.
    85.^ Albert Hofmann; translated from the original German (LSD Ganz Persönlich) by J. Ott. MAPS-Volume 6 Number 69 Summer 1969
    86.^ Nichols, David (2003-05-24). “Hypothesis on Albert Hofmann’s Famous 1943 “Bicycle Day””. Hofmann Foundation. http://www.erowid.org/general/conferences/conference_mindstates4_nichols.shtml. Retrieved 2007-09-27.
    87.^ Albert Hofmann. “LSD My Problem Child”. http://www.psychedelic-library.org/child1.htm. Retrieved 2010-04-19.
    88.^ Hofmann, Albert. “History Of LSD”. http://www.a1b2c3.com/drugs/lsd01.htm. Retrieved 2007-09-27.
    89.^ DEA Public Affairs (2001-11-16). “LSD: The Drug”. Web.petabox.bibalex.org. http://web.petabox.bibalex.org/web/20011116091659/www.usdoj.gov/dea/pubs/lsd/lsd-4.htm. Retrieved 2010-11-27.
    90.^ Brecher, Edward M; et al. (1972). “How LSD was popularized”. Consumer Reports/Drug Library. http://www.druglibrary.org/schaffer/Library/studies/cu/CU50.html. Retrieved 2008-07-14.
    91.^ United States Congress (1968-10-24). “Staggers-Dodd Bill, Public Law 90-639”. http://www.erowid.org/psychoactives/law/law_fed_staggers-dodd.pdf. Retrieved 2009-09-08.
    92.^ Gasser, Peter (1994). “Psycholytic Therapy with MDMA and LSD in Switzerland”. http://www.maps.org/news-letters/v05n3/05303psy.html. Retrieved 2009-09-08.
    93.^ Psychedelic Research Around the World: MDMA Studies: In Progress
    94.^ a b DEA (2007). “LSD Manufacture – Illegal LSD Production”. LSD in the United States. U.S. Department of Justice Drug Enforcement Administration. Archived from the original on 2007-08-29. http://web.archive.org/web/20070829023659/http://www.fas.org/irp/agency/doj/dea/product/lsd/lsd-5.htm.
    95.^ a b c Stafford, Peter (1992). “Chapter 1 – The LSD Family”. Psychedelics Encyclopaedia (Third Expanded ed.). Ronin Publishing Inc. p. 62. ISBN 0-914171-51-8.
    96.^ a b c Laing, Richard R.; Barry L. Beyerstein, Jay A. Siegel (2003). “Chapter 2.2 – Forms of the Drug”. Hallucinogens: A Forensic Drug Handbook. Academic Press. pp. 39–41. ISBN 0124339514. http://books.google.co.uk/books?id=l1DrqgobbcwC&printsec=frontcover&source=gbs_summary_r&cad=0#PPA39,M1.
    97.^ Honig, David. Frequently Asked Questions via Erowid
    98.^ “Street Terms: Drugs and the Drug Trade”. Office of National Drug Control Policy. 2005-04-05. http://www.whitehousedrugpolicy.gov/streetterms/ByType.asp?intTypeID=6. Retrieved 2007-01-31.
    99.^ DEA (2008). “Photo Library (page 2)”. US Drug Enforcement Administration. http://www.usdoj.gov/dea/photo_library2.html#lsd. Retrieved 2008-06-27.
    100.^ ^ Maclean, J.R.; Macdonald, D.C.; Ogden, F.; Wilby, E., “LSD-25 and mescaline as therapeutic adjuvants.” In: Abramson, H., Ed., The Use of LSD in Psychotherapy and Alcoholism, Bobbs-Merrill: New York, 1967, pp. 407–426; Ditman, K.S.; Bailey, J.J., “Evaluating LSD as a psychotherapeutic agent,” pp.74–80; Hoffer, A., “A program for the treatment of alcoholism: LSD, malvaria, and nicotinic acid,” pp. 353–402.
    101.^ ^ LSD: The Drug
    102.^ United States Drug Enforcement Administration (October 2005). Microgram Bulletin 38 (10). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1005/mg1005.html. Retrieved 2009-08-20.
    103.^ United States Drug Enforcement Administration (November 2006). Microgram Bulletin 39 (11). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1106/mg1106.html. Retrieved 2009-08-20.
    104.^ United States Drug Enforcement Administration (February 2007). Microgram Bulletin 40 (2). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0207/mg0207.html. Retrieved 2009-08-20.
    105.^ a b c United States Drug Enforcement Administration (December 2007). Microgram Bulletin 40 (12). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1207/mg1207.html. Retrieved 2009-08-20.
    106.^ United States Drug Enforcement Administration (March 2008). Microgram Bulletin 41 (3). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0308/mg0308.html. Retrieved 2009-08-20.
    107.^ United States Drug Enforcement Administration (March 2009). Microgram Bulletin 42 (3). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0309/mg0309.html. Retrieved 2009-08-20.
    108.^ United States Drug Enforcement Administration (November 2005). Microgram Bulletin 38 (11). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1105/mg1105.html. Retrieved 2009-08-20.
    109.^ Canadian government (1996). “Controlled Drugs and Substances Act”. Justice Laws. Canadian Department of Justice. http://laws.justice.gc.ca/en/showdoc/cs/C-38.8//20070705/en?command=HOME&caller=SI&fragment=lsd&search_type=all&day=5&month=7&year=2007&search_domain=cs&showall=L&statuteyear=all&lengthannual=50&length=50. Retrieved 2007-07-05.
    110.^ Drugs and the law: Report of the inquiry into the Misuse of Drugs Act 1971 London: Police Foundation, 2000, Runciman Report
    111.^ After the War on Drugs: Blueprint for Regulation Transform Drug Policy Foundation 2009
    112.^ From [2]: LSD is a Schedule I substance under the Controlled Substances Act.
    113.^ “Toxicity, Hallucinogens – LSD”. Emedicine.medscape.com. http://emedicine.medscape.com/article/1011615-overview. Retrieved 2010-11-27.
    114.^ Neal v. United States, U.S. 284 (1996). , originating from U.S. v. Neal, 46 F.3d 1405 (7th Cir. 1995)
    115.^ “Famous LSD users”. The Good Drugs Guide. http://www.thegooddrugsguide.com/articles/famous_users/lsd.htm. Retrieved 2008-10-20.
    116.^ “Publicly expressed thoughts and ideas about the effects of psychedelic drugs”. Tietoiseen.fi. 2010-05-12. http://www.tietoiseen.fi/w/index.php?title=Main_Page. Retrieved 2010-11-27.
    117.^ Bosker, Bianca (21 October 2011). “The Steve Jobs Reading List: The Books And Artists That Made The Man”. The Huffington Post. http://www.huffingtonpost.com/2011/10/21/the-steve-jobs-reading-list-the-books_n_1024021.html. Retrieved 23 October 2011.
    118.^ Matus, Victorino (June 2004). “The Truth Behind “LSD””. The Weekly Standard. http://www.weeklystandard.com/Content/Public/Articles/000/000/004/197vgrel.asp?page=1.
    119.^ Ann Harrison (2006-01-16). “LSD: The Geek’s Wonder Drug?”. Wired. Wired. http://www.wired.com/science/discoveries/news/2006/01/70015. Retrieved 2008-03-11. “Like Herbert, many scientists and engineers also report heightened states of creativity while using LSD. During a press conference on Friday, Hofmann revealed that he was told by Nobel-prize-winning chemist Kary Mullis that LSD had helped him develop the polymerase chain reaction that helps amplify specific DNA sequences.”
    120.^ Colman, Dan. “Aldous Huxley’s LSD Death Trip”. http://www.openculture.com/2011/10/aldous_huxleys_lsd_death_trip.html. Retrieved 1 November 2011.
    [edit] Further readingBBC News: Pont-Saint-Esprit poisoning: Did the CIA spread LSD?
    Bebergal, Peter, “Will Harvard drop acid again? Psychedelic research returns to Crimsonland”, The Phoenix (Boston), June 2, 2008
    Grof, Stanislav. LSD Psychotherapy. (April 10, 2001)
    Lee, Martin A. and Bruce Shlain. Acid Dreams: The Complete Social History of LSD: The CIA, the Sixties, and Beyond (1992) ISBN 978-0-8021-3062-4
    Marks, John. The Search for the Manchurian Candidate: The CIA and Mind Control (1979), ISBN 0-8129-0773-6
    Roberts, Andy. Albion Dreaming: A Popular History of LSD in Britain (2008), Marshall Cavendish,U.K, ISBN 1-905736-27-4
    Stevens, Jay. Storming Heaven: LSD And The American Dream (1998) ISBN 978-0-8021-3587-2
    Hofmann, Albert. LSD My Problem Child: Reflections on Sacred Drugs, Mysticism and Science (1983) ISBN 978-0-9660019-8-3
    Henderson, Leigh A. and William J. Glass. LSD: Still With Us After All These Years: Based on the National Institute of Drug Abuse Studies on the Resurgence of Contemporary LSD Use (1st edition 1994, 2nd edition 1998) ISBN 978-0-7879-4379-0
    de Rios, Marlene Dobkin and Oscar Janiger. LSD, spirituality, and the creative process (2003, Inner Traditions) ISBN 978-0-89281-973-7 – “An exploration of how LSD influences imagination and the creative process. Based on the results of one of the longest clinical studies of LSD that took place between 1954 and 1962, before LSD was illegal. Includes personal reports, artwork, and poetry from the original sessions as testimony of the impact of LSD on the creative process.”
    Passie T, Halpern JH, Stichtenoth DO, Emrich HM, Hintzen A (2008). “The pharmacology of lysergic acid diethylamide: a review”. CNS Neuroscience & Therapeutics 14 (4): 295–314. doi:10.1111/j.1755-5949.2008.00059.x. PMID 19040555

  66. Cancer can be treated by surgery, chemotherapy, radiation therapy, immunotherapy, monoclonal antibody therapy or other methods. The choice of therapy depends upon the location and grade of the tumor and the stage of the disease, as well as the general state of the patient (performance status). A number of experimental cancer treatments are also under development.

    Complete removal of the cancer without damage to the rest of the body is the goal of treatment. Sometimes this can be accomplished by surgery, but the propensity of cancers to invade adjacent tissue or to spread to distant sites by microscopic metastasis often limits its effectiveness. The effectiveness of chemotherapy is often limited by toxicity to other tissues in the body. Radiation can also cause damage to normal tissue.

    Because “cancer” refers to a class of diseases,[1][2] it is unlikely that there will ever be a single “cure for cancer” any more than there will be a single treatment for all infectious diseases.[3] Angiogenesis inhibitors were once thought to have potential as a “silver bullet” treatment applicable to many types of cancer, but this has not been the case in practice.[4]

  67. any with AMA wanna comment? This is an open forum you didnt get your voice heard in the 1930’s. Where is the AMA on this?

  68. SurgeryIn theory, non-hematological cancers can be cured if entirely removed by surgery, but this is not always possible. When the cancer has metastasized to other sites in the body prior to surgery, complete surgical excision is usually impossible. In the Halstedian model of cancer progression, tumors grow locally, then spread to the lymph nodes, then to the rest of the body. This has given rise to the popularity of local-only treatments such as surgery for small cancers. Even small localized tumors are increasingly recognized as possessing metastatic potential.

    Examples of surgical procedures for cancer include mastectomy for breast cancer, prostatectomy for prostate cancer, and lung cancer surgery for non-small cell lung cancer. The goal of the surgery can be either the removal of only the tumor, or the entire organ. A single cancer cell is invisible to the naked eye but can regrow into a new tumor, a process called recurrence. For this reason, the pathologist will examine the surgical specimen to determine if a margin of healthy tissue is present, thus decreasing the chance that microscopic cancer cells are left in the patient.

    In addition to removal of the primary tumor, surgery is often necessary for staging, e.g. determining the extent of the disease and whether it has metastasized to regional lymph nodes. Staging is a major determinant of prognosis and of the need for adjuvant therapy.

    Occasionally, surgery is necessary to control symptoms, such as spinal cord compression or bowel obstruction. This is referred to as palliative treatment.

    If surgery is possible and appropriate, it is commonly performed before other forms of treatment, although the order does not affect the outcome.[5] In some instances, surgery must be delayed until other treatments are able to shrink the tumor.

    [edit] Radiation therapyMain article: Radiation therapy
    Radiation therapy (also called radiotherapy, X-ray therapy, or irradiation) is the use of ionizing radiation to kill cancer cells and shrink tumors. Radiation therapy can be administered externally via external beam radiotherapy (EBRT) or internally via brachytherapy. The effects of radiation therapy are localised and confined to the region being treated. Radiation therapy injures or destroys cells in the area being treated (the “target tissue”) by damaging their genetic material, making it impossible for these cells to continue to grow and divide. Although radiation damages both cancer cells and normal cells, most normal cells can recover from the effects of radiation and function properly. The goal of radiation therapy is to damage as many cancer cells as possible, while limiting harm to nearby healthy tissue. Hence, it is given in many fractions, allowing healthy tissue to recover between fractions.

    Radiation therapy may be used to treat almost every type of solid tumor, including cancers of the brain, breast, cervix, larynx, lung, pancreas, prostate, skin, stomach, uterus, or soft tissue sarcomas. Radiation is also used to treat leukemia and lymphoma. Radiation dose to each site depends on a number of factors, including the radiosensitivity of each cancer type and whether there are tissues and organs nearby that may be damaged by radiation. Thus, as with every form of treatment, radiation therapy is not without its side effects.

    [edit] ChemotherapyMain article: Chemotherapy
    Chemotherapy is the treatment of cancer with drugs (“anticancer drugs”) that can destroy cancer cells. In current usage, the term “chemotherapy” usually refers to cytotoxic drugs which affect rapidly dividing cells in general, in contrast with targeted therapy (see below). Chemotherapy drugs interfere with cell division in various possible ways, e.g. with the duplication of DNA or the separation of newly formed chromosomes. Most forms of chemotherapy target all rapidly dividing cells and are not specific to cancer cells, although some degree of specificity may come from the inability of many cancer cells to repair DNA damage, while normal cells generally can. Hence, chemotherapy has the potential to harm healthy tissue, especially those tissues that have a high replacement rate (e.g. intestinal lining). These cells usually repair themselves after chemotherapy.

    Because some drugs work better together than alone, two or more drugs are often given at the same time. This is called “combination chemotherapy”; most chemotherapy regimens are given in a combination.[6]

    The treatment of some leukaemias and lymphomas requires the use of high-dose chemotherapy, and total body irradiation (TBI). This treatment ablates the bone marrow, and hence the body’s ability to recover and repopulate the blood. For this reason, bone marrow, or peripheral blood stem cell harvesting is carried out before the ablative part of the therapy, to enable “rescue” after the treatment has been given. This is known as autologous stem cell transplantation. Alternatively, hematopoietic stem cells may be transplanted from a matched unrelated donor (MUD).

    [edit] Targeted therapiesMain article: Targeted therapy
    Targeted therapy, which first became available in the late 1990s, has had a significant impact in the treatment of some types of cancer, and is currently a very active research area. This constitutes the use of agents specific for the deregulated proteins of cancer cells. Small molecule targeted therapy drugs are generally inhibitors of enzymatic domains on mutated, overexpressed, or otherwise critical proteins within the cancer cell. Prominent examples are the tyrosine kinase inhibitors imatinib (Gleevec/Glivec) and gefitinib (Iressa).

    Monoclonal antibody therapy is another strategy in which the therapeutic agent is an antibody which specifically binds to a protein on the surface of the cancer cells. Examples include the anti-HER2/neu antibody trastuzumab (Herceptin) used in breast cancer, and the anti-CD20 antibody rituximab, used in a variety of B-cell malignancies.

    Targeted therapy can also involve small peptides as “homing devices” which can bind to cell surface receptors or affected extracellular matrix surrounding the tumor. Radionuclides which are attached to these peptides (e.g. RGDs) eventually kill the cancer cell if the nuclide decays in the vicinity of the cell. Especially oligo- or multimers of these binding motifs are of great interest, since this can lead to enhanced tumor specificity and avidity.

    Photodynamic therapy (PDT) is a ternary treatment for cancer involving a photosensitizer, tissue oxygen, and light (often using lasers). PDT can be used as treatment for basal cell carcinoma (BCC) or lung cancer; PDT can also be useful in removing traces of malignant tissue after surgical removal of large tumors.[7]

    [edit] Immunotherapy
    A renal cell carcinoma (lower left) in a kidney specimen.Main article: Cancer immunotherapy
    Cancer immunotherapy refers to a diverse set of therapeutic strategies designed to induce the patient’s own immune system to fight the tumor. Contemporary methods for generating an immune response against tumours include intravesical BCG immunotherapy for superficial bladder cancer, and use of interferons and other cytokines to induce an immune response in renal cell carcinoma and melanoma patients. Vaccines to generate specific immune responses are the subject of intensive research for a number of tumours, notably malignant melanoma and renal cell carcinoma. Sipuleucel-T is a vaccine-like strategy in late clinical trials for prostate cancer in which dendritic cells from the patient are loaded with prostatic acid phosphatase peptides to induce a specific immune response against prostate-derived cells.

    Allogeneic hematopoietic stem cell transplantation (“bone marrow transplantation” from a genetically non-identical donor) can be considered a form of immunotherapy, since the donor’s immune cells will often attack the tumor in a phenomenon known as graft-versus-tumor effect. For this reason, allogeneic HSCT leads to a higher cure rate than autologous transplantation for several cancer types, although the side effects are also more severe.

    The cell based immunotherapy in which the patients own Natural Killer cells(NK) and Cytotoxic T-Lymphocytes(CTL) are used has been in practice in Japan since 1990. NK cells and CTLs primarily kill the cancer cells when they are developed. This treatment is given together with the other modes of treatment such as Surgery, radiotherapy or Chemotherapy and called as Autologous Immune Enhancement Therapy (AIET)[8] [9]

    [edit] Hormonal therapyMain article: Hormonal therapy (oncology)
    The growth of some cancers can be inhibited by providing or blocking certain hormones. Common examples of hormone-sensitive tumors include certain types of breast and prostate cancers. Removing or blocking estrogen or testosterone is often an important additional treatment. In certain cancers, administration of hormone agonists, such as progestogens may be therapeutically beneficial.

  69. Dopamine — a simple organic chemical in the catecholamine family — plays a number of important physiological roles in the bodies of animals. Its name derives from its chemical structure, which consists of an amine group (NH2) linked to a catechol structure called dihydroxyphenylalanine (acronym DOPA). In the brain, dopamine functions as a neurotransmitter — a chemical released by nerve cells to send signals to other nerve cells. The human brain uses five known types of dopamine receptors, labeled D1, D2, D3, D4, and D5. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.

    Dopamine plays a major role in the brain system that is responsible for reward-driven learning. Every type of reward that has been studied increases the level of dopamine transmission in the brain, and a variety of highly addictive drugs, including stimulants such as cocaine and methamphetamine, act directly on the dopamine system. There is evidence that people with extraverted (reward-seeking) personality types tend to show higher levels of dopamine activity than people with introverted personalities. Several important diseases of the nervous system are associated with dysfunctions of the dopamine system. Parkinson’s disease, an age-related degenerative condition causing tremor and motor impairment, is caused by loss of dopamine-secreting neurons in the substantia nigra. Schizophrenia has been shown to involve elevated levels of dopamine activity in the mesolimbic pathway and decreased levels of dopamine in the prefrontal cortex.[1][2] Attention deficit hyperactivity disorder (ADHD) is also believed to be associated with decreased dopamine activity.[citation needed]

    Dopamine is available as an intravenous medication acting on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure. However, because dopamine cannot cross the blood–brain barrier, dopamine given as a drug does not directly affect the central nervous system. To increase the amount of dopamine in the brains of patients with diseases such as Parkinson’s disease and dopa-responsive dystonia, L-DOPA (the precursor of dopamine) is often given because it crosses the blood-brain barrier relatively easily.

  70. Limbic regulation From Wikipedia, the free encyclopediaJump to: navigation, search It has been suggested that Limbic resonance be merged into this article or section. (Discuss) Proposed since April 2011.

    Limbic regulation, mood contagion or emotional contagion is the effect of contact with other people upon the development and stability of personality and mood.

    The concept was advanced in the book A General Theory of Love (2000), and is one of three interrelated concepts central to the book’s premise: that our brain chemistry and nervous systems are measurably affected by those closest to us (limbic resonance); that our systems synchronize with one another in a way that has profound implications for personality and lifelong emotional health (limbic regulation); and that these set patterns can be modified through therapeutic practice (limbic revision).

    Contents [hide]
    1 Definition
    2 Importance and history
    3 Subsequent use and definitions of the term
    4 References

    [edit] DefinitionAs the authors poetically frame it: “Human physiology finds a hub … in the harmonizing activity of nearby limbic brains. Our neural architecture places relationships at the crux of our lives, where, blazing and warm, they have the power to stabilize [italics in original]. When people are hurting and out of balance, they turn to regulating affiliations: groups, clubs, pets, marriages, friendships, masseuses, chiropractors, the Internet. All carry at least the potential for emotional connection.”[1]:170

    [edit] Importance and historyLewis, Amini and Lannon make a compelling case for the centrality of limbic regulation to our physiological as well as emotional well-being. They begin with a story from the dawn of scientific experimentation in human development—albeit heinously misguided—when in the thirteenth century Frederick II raised a group of infants to be completely cut off from human interaction, other than the most basic care and feeding, so as to discover what language would spontaneously arise absence of any communication prompts. The result of this notorious experiment was that the infants, deprived of any human discourse or affection, all died.[1]:68,69

    The authors find the hegemony of Freudian theory in the early days of psychology and psychiatry to be almost as harmful as the ideas of Frederick the Great. They condemn the focus on cerebral insight, and the ideal of a cold, emotionless analyst, as negating the very benefit that psychotherapy can confer by virtue of the empathetic bond and neurological reconditioning that can occur in the course of sustained therapeutic sessions. “Freud’s enviable advantage is that he never seriously undertook to follow his own advice. Many promising young therapists have their responsiveness expunged, as they are taught to be dutifully neutral observers, avoiding emotional contact….But since therapy is limbic relatedness, emotional neutrality drains life out of the process…” [1]:184

    A General Theory of Love is scarcely more sympathetic to Dr. Benjamin Spock and his “monumentally influential volume” Baby and Child Care, especially given Spock’s role in promoting the movement against co-sleeping, or allowing infants to sleep in the same bed as their parents. Lewis, Amini and Lannon cite the research of sleep scientist James McKenna, which seems to suggest that the limbic regulation between sleeping parents and infants is essential to the neurological development of the latter and a major factor in preventing Sudden Infant Death Syndrome (SIDS). “The temporal unfolding of particular sleep stages and awake periods of the mother and infant become entwined….on a minute to minute basis, throughout the night, much sensory communication is occurring between them.”[1]:195

    [edit] Subsequent use and definitions of the termIn Living a connected life (2003), Dr. Kathleen Brehony looks at recent brain research which shows the importance of proximity of others in our development. “Especially in infancy, but throughout our lives, our physical bodies are influencing and being influenced by others with whom we feel a connection. Scientists call this limbic regulation.” [2]

    Brehony goes on to describe the parallels between the “protest/despair” cycles of an abandoned puppy and human development. Mammals have developed a tendency to experience distraction, anxiety and measurable levels of stress in response to separation from their care-givers and companions, precisely because such separation has historically constituted a threat to their survival. As anyone who has owned a puppy can attest, when left alone it will cry, bark, howl, and seek to rejoin its human or canine companions. If these efforts are unsuccessful and the isolation is prolonged, it will sink into a state of dejection and despair. The marginal effectiveness of placing a ticking clock in the puppy’s bed is based on a universal need in mammals to synchronize to the rhythms of their fellow creatures.

    Limbic resonance and limbic regulation are also referred to as “mood contagion” or “emotional contagion” as in the work of Sigal Barsade. Barsade and colleagues at the Yale School of Management build on research in social cognition, and find that some emotions, especially positive ones, are spread more easily than others through such “interpersonal limbic regulation”.[3]

    Author Daniel Goleman has explored similar terrain across several works: in Emotional Intelligence (1995), an international best seller, The Joy Of Living, coauthored with Yongey Mingyur Rinpoche, and the Harvard Business Review on Breakthrough Leadership. In the latter book, Goleman considers the “open loop nature of the brain’s limbic system” which depends on external sources to manage itself, and examines the implications of interpersonal limbic regulation and the science of moods on leadership.[4]

    In Mindfully Green: A Personal and Spiritual Guide to Whole Earth Thinking (2003) author Staphine Kaza defines the term as follows: “Limbic regulation is a mutual simultaneous exchange of body signals that unfolds between people who are deeply involved with each other, especially parents and children.” She goes on to correlate love with limbic engagement and asserts that children raised with love learn and remember better than those who are abused. Kaza then proposes to “take this work a step further from a systems perspective, and imagine that a child learns through some sort of limbic regulation with nature”.[5]

    [edit] References1.^ a b c d Lewis, Thomas L.; Amini, Fari; Lannon, Richard (2000). A general theory of love. New York: Random House. ISBN 0-375-50389-7.
    2.^ Brehony, Kathleen A. PhD (2003). Living a connected life: creating and maintaining relationships that last. New York: Henry Holt & Co.. p. 26. ISBN 0-8050-7023-0.
    3.^ Barsade, Sigal (December 2002). “The Ripple Effect: Emotional Contagion and Its Influence on Group Behavior”. Administrative Science Quarterly (Johnson Graduate School of Management, Cornell University.): 644–675. JSTOR 3094912.
    4.^ Goleman, Dan; Peace, William J.; Pagonis, William G.; Peters, Tom F.; Jones, Gareth Stedman; Collingwood, Harris. Harvard Business Review on Breakthrough Leadership. Harvard Business School Press. pp. 31. ISBN 1-57851-805-9.
    5.^ Kaza, Stephanie (2008). Mindfully Green: A Personal and Spiritual Guide to Whole Earth Thinking. Shambhala. pp. 45, 46. ISBN 1-59030-583-3.

  71. Psychology is the study of the mind, occurring partly via the study of behavior.[1][2] Grounded in scientific method,[1][2] psychology has the immediate goal of understanding individuals and groups by both establishing general principles and researching specific cases,[3][4] and for many it ultimately aims to benefit society.[5][6] In this field, a professional practitioner or researcher is called a psychologist, and can be classified as a social scientist, behavioral scientist, or cognitive scientist. Psychologists attempt to understand the role of mental functions in individual and social behavior, while also exploring the physiological and neurobiological processes that underlie certain cognitive functions and behaviors

  72. The high lipid-solubility of cannabinoids results in their persisting in the body for long periods of time. Even after a single administration of THC, detectable levels of THC can be found in the body for weeks or longer (depending on the amount administered and the sensitivity of the assessment method). A number of investigators have suggested that this is an important factor in marijuana’s effects, perhaps because cannabinoids may accumulate in the body, particularly in the lipid membranes of neurons.[39]

    Until recently, little was known about the specific mechanisms of action of THC at the neuronal level. However, researchers have now confirmed that THC exerts its most prominent effects via its actions on two types of cannabinoid receptors, the CB1 receptor and the CB2 receptor, both of which are G-Protein coupled receptors. The CB1 receptor is found primarily in the brain as well as in some peripheral tissues, and the CB2 receptor is found exclusively in peripheral tissues.[40] THC appears to alter mood and cognition through its agonist actions on the CB1 receptors, which inhibit a secondary messenger system (adenylate cyclase) in a dose dependent manner. These actions can be blocked by the selective CB1 receptor antagonist SR141716A (rimonabant), which has been shown in clinical trials to be an effective treatment for smoking cessation, weight loss, and as a means of controlling or reducing metabolic syndrome risk factors.[41]

  73. HistoryJohn W. Huffman, an organic chemist at Clemson University, synthesized analogues and metabolites of ?9-tetrahydrocannabinol (THC), the principal active component of cannabis. JWH-018 is one of these analogues, with studies showing an affinity for the cannabinoid (CB1) receptor five times greater than that of THC. Cannabinoid receptors are found in mammalian brain and spleen tissue; however, the structural details of the active sites are currently unknown.[7][8]

    On December 15, 2008, it was reported by the German pharmaceutical company THC Pharm that JWH-018 was found as one of the active components in at least three versions of the herbal blend Spice, which has been sold as an incense in a number of countries around the world since 2002.[9][10][11] An analysis of samples acquired four weeks after the German prohibition of JWH-018 took place found that the compound had been replaced with JWH-073.[12

  74. HistoryJohn W. Huffman, an organic chemist at Clemson University, synthesized analogues and metabolites of ?9-tetrahydrocannabinol (THC), the principal active component of cannabis. JWH-018 is one of these analogues, with studies showing an affinity for the cannabinoid (CB1) receptor five times greater than that of THC. Cannabinoid receptors are found in mammalian brain and spleen tissue; however, the structural details of the active sites are currently unknown.[7][8]

    On December 15, 2008, it was reported by the German pharmaceutical company THC Pharm that JWH-018 was found as one of the active components in at least three versions of the herbal blend Spice, which has been sold as an incense in a number of countries around the world since 2002.[9][10][11] An analysis of samples acquired four weeks after the German prohibition of JWH-018 took place found that the compound had been replaced with JWH-073.[12

  75. JWH-018 (1-pentyl-3-(1-naphthoyl)indole) or AM-678[1] is an analgesic chemical from the naphthoylindole family that acts as a full agonist at both the CB1 and CB2 cannabinoid receptors, with some selectivity for CB2. It produces effects in animals similar to those of THC, a cannabinoid naturally present in cannabis, leading to its use in synthetic cannabis products such as “legal cannabis herbal incense blends”, including Spice, Relaxinol, and Mr. Nice Guy, which are ‘legally’ sold as “incense” and labeled as “not for human consumption.

  76. A GABA agonist is a drug which acts to stimulate or increase the action at the GABA receptor, producing typically sedative effects, and may also cause other effects such as anxiolytic and muscle relaxant effects.

  77. ethanol (C2H5OH) is the type of alcohol found in alcoholic beverages, and in common speech the word alcohol refers specifically to ethanol.

  78. Applications
    Total recorded alcohol per capita consumption (15+), in litres of pure alcohol[6]Alcohols can be used as a beverage (ethanol only), as fuel and for many scientific, medical, and industrial utilities. Ethanol in the form of alcoholic beverages has been consumed by humans since pre-historic times. A 50% v/v solution of ethylene glycol in water is commonly used as an antifreeze.

    Some alcohols, mainly ethanol and methanol, can be used as an alcohol fuel. Fuel performance can be increased in forced induction internal combustion engines by injecting alcohol into the air intake after the turbocharger or supercharger has pressurized the air. This cools the pressurized air, providing a denser air charge, which allows for more fuel, and therefore more power.

    Alcohols have applications in industry and science as reagents or solvents. Because of its relatively low toxicity compared with other alcohols and ability to dissolve non-polar substances, ethanol can be used as a solvent in medical drugs, perfumes, and vegetable essences such as vanilla. In organic synthesis, alcohols serve as versatile intermediates.

    Ethanol can be used as an antiseptic to disinfect the skin before injections are given, often along with iodine. Ethanol-based soaps are becoming common in restaurants and are convenient because they do not require drying due to the volatility of the compound. Alcohol is also used as a preservative for specimens.

    Alcohol gels have become common as hand sanitizers.

  79. ProductionIn industry, alcohols are produced in several ways:

    By fermentation using glucose produced from sugar from the hydrolysis of starch, in the presence of yeast and temperature of less than 37 °C to produce ethanol, for instance, the conversion of invertase to glucose and fructose or the conversion of glucose to zymase and ethanol.
    By direct hydration using ethylene (ethylene hydration)[7] or other alkenes from cracking of fractions of distilled crude oil.

  80. Nucleophilic substitutionThe OH group is not a good leaving group in nucleophilic substitution reactions, so neutral alcohols do not react in such reactions. However, if the oxygen is first protonated to give R?OH2+, the leaving group (water) is much more stable, and the nucleophilic substitution can take place. For instance, tertiary alcohols react with hydrochloric acid to produce tertiary alkyl halides, where the hydroxyl group is replaced by a chlorine atom by unimolecular nucleophilic substitution. If primary or secondary alcohols are to be reacted with hydrochloric acid, an activator such as zinc chloride is needed. In alternative fashion, the conversion may be performed directly using thionyl chloride.[1]

    Alcohols may, likewise, be converted to alkyl bromides using hydrobromic acid or phosphorus tribromide, for example:

    3 R-OH + PBr3 ? 3 RBr + H3PO3
    In the Barton-McCombie deoxygenation an alcohol is deoxygenated to an alkane with tributyltin hydride or a trimethylborane-water complex in a radical substitution reaction.

    DehydrationAlcohols are themselves nucleophilic, so R?OH2+ can react with ROH to produce ethers and water in a dehydration reaction, although this reaction is rarely used except in the manufacture of diethyl ether.

    More useful is the E1 elimination reaction of alcohols to produce alkenes. The reaction, in general, obeys Zaitsev’s Rule, which states that the most stable (usually the most substituted) alkene is formed. Tertiary alcohols eliminate easily at just above room temperature, but primary alcohols require a higher temperature.

    This is a diagram of acid catalysed dehydration of ethanol to produce ethene:

    A more controlled elimination reaction is the Chugaev elimination with carbon disulfide and iodomethane.

    EsterificationTo form an ester from an alcohol and a carboxylic acid the reaction, known as Fischer esterification, is usually performed at reflux with a catalyst of concentrated sulfuric acid:

    R-OH + R’-COOH ? R’-COOR + H2O
    In order to drive the equilibrium to the right and produce a good yield of ester, water is usually removed, either by an excess of H2SO4 or by using a Dean-Stark apparatus. Esters may also be prepared by reaction of the alcohol with an acid chloride in the presence of a base such as pyridine.

    Other types of ester are prepared in a similar manner — for example, tosyl (tosylate) esters are made by reaction of the alcohol with p-toluenesulfonyl chloride in pyridine.

    OxidationMain article: Alcohol oxidation
    Primary alcohols (R-CH2-OH) can be oxidized either to aldehydes (R-CHO) or to carboxylic acids (R-CO2H), while the oxidation of secondary alcohols (R1R2CH-OH) normally terminates at the ketone (R1R2C=O) stage. Tertiary alcohols (R1R2R3C-OH) are resistant to oxidation.

    The direct oxidation of primary alcohols to carboxylic acids normally proceeds via the corresponding aldehyde, which is transformed via an aldehyde hydrate (R-CH(OH)2) by reaction with water before it can be further oxidized to the carboxylic acid.

    Mechanism of oxidation of primary alcohols to carboxylic acids via aldehydes and aldehyde hydratesReagents useful for the transformation of primary alcohols to aldehydes are normally also suitable for the oxidation of secondary alcohols to ketones. These include Collins reagent and Dess-Martin periodinane. The direct oxidation of primary alcohols to carboxylic acids can be carried out using potassium permanganate or the Jones reagent.

    ToxicityMain articles: Short-term effects of alcohol and Long-term effects of alcohol

    Most significant of the possible long-term effects of ethanol. In addition, in pregnant women, it causes fetal alcohol syndrome.Ethanol in alcoholic beverages has been consumed by humans since prehistoric times for a variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of large doses of ethanol causes drunkenness (intoxication), which may lead to a hangover as its effects wear off. Depending upon the dose and the regularity of its consumption, ethanol can cause acute respiratory failure or death. Because ethanol impairs judgment in humans, it can be a catalyst for reckless or irresponsible behavior. The LD50 of ethanol in rats is 10.3 g/kg.[8]

    Ethanol’s toxicity is largely caused by its primary metabolite; acetaldehyde[9] and secondary metabolite; acetic acid.[10][11][12][13] All primary alcohols are broken down into aldehydes then to carboxylic acids, and whose toxicities are similar to acetaldehyde and acetic acid.

    Some secondary and tertiary alcohols are less poisonous than ethanol because the liver is unable to metabolise them into these toxic by-products. This makes them more suitable for recreational[14][15] and medicinal[16] use as the chronic harms are lower. Ethchlorvynol is a good example of a tertiary alcohol which saw both medicinal and recreational use.

    Other alcohols are substantially more poisonous than ethanol, partly because they take much longer to be metabolized and partly because their metabolism produces substances that are even more toxic. Methanol (wood alcohol), for instance, is oxidized to formaldehyde and then to the poisonous formic acid in the liver by alcohol dehydrogenase and formaldehyde dehydrogenase enzymes, respectively; accumulation of formic acid can lead to blindness or death.[17] Likewise, poisoning due to other alcohols such as ethylene glycol or diethylene glycol are due to their metabolites, which are also produced by alcohol dehydrogenase.[18][19] An effective treatment to prevent toxicity after methanol or ethylene glycol ingestion is to administer ethanol. Alcohol dehydrogenase has a higher affinity for ethanol, thus preventing methanol from binding and acting as a substrate. Any remaining methanol will then have time to be excreted through the kidneys.[17][20][21]

    Methanol itself, while poisonous, has a much weaker sedative effect than ethanol. Some longer-chain alcohols such as n-propanol, isopropanol, n-butanol and t-butanol do, however, have stronger sedative effects, but also have higher toxicity than ethanol.[22][23] These longer chain alcohols are found as contaminants in some alcoholic beverages and are known as fusel alcohols,[24][25] and are reputed to cause severe hangovers although it is unclear if the fusel alcohols are actually responsible.[26] Many longer chain alcohols are used in industry as solvents and are occasionally abused by alcoholics,[27][28] leading to a range of adverse health effects.[29]

  81. ToxicityMain articles: Short-term effects of alcohol and Long-term effects of alcohol

    Most significant of the possible long-term effects of ethanol. In addition, in pregnant women, it causes fetal alcohol syndrome.Ethanol in alcoholic beverages has been consumed by humans since prehistoric times for a variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of large doses of ethanol causes drunkenness (intoxication), which may lead to a hangover as its effects wear off. Depending upon the dose and the regularity of its consumption, ethanol can cause acute respiratory failure or death. Because ethanol impairs judgment in humans, it can be a catalyst for reckless or irresponsible behavior. The LD50 of ethanol in rats is 10.3 g/kg.[8]

    Ethanol’s toxicity is largely caused by its primary metabolite; acetaldehyde[9] and secondary metabolite; acetic acid.[10][11][12][13] All primary alcohols are broken down into aldehydes then to carboxylic acids, and whose toxicities are similar to acetaldehyde and acetic acid.

    Some secondary and tertiary alcohols are less poisonous than ethanol because the liver is unable to metabolise them into these toxic by-products. This makes them more suitable for recreational[14][15] and medicinal[16] use as the chronic harms are lower. Ethchlorvynol is a good example of a tertiary alcohol which saw both medicinal and recreational use.

    Other alcohols are substantially more poisonous than ethanol, partly because they take much longer to be metabolized and partly because their metabolism produces substances that are even more toxic. Methanol (wood alcohol), for instance, is oxidized to formaldehyde and then to the poisonous formic acid in the liver by alcohol dehydrogenase and formaldehyde dehydrogenase enzymes, respectively; accumulation of formic acid can lead to blindness or death.[17] Likewise, poisoning due to other alcohols such as ethylene glycol or diethylene glycol are due to their metabolites, which are also produced by alcohol dehydrogenase.[18][19] An effective treatment to prevent toxicity after methanol or ethylene glycol ingestion is to administer ethanol. Alcohol dehydrogenase has a higher affinity for ethanol, thus preventing methanol from binding and acting as a substrate. Any remaining methanol will then have time to be excreted through the kidneys.[17][20][21]

    Methanol itself, while poisonous, has a much weaker sedative effect than ethanol. Some longer-chain alcohols such as n-propanol, isopropanol, n-butanol and t-butanol do, however, have stronger sedative effects, but also have higher toxicity than ethanol.[22][23] These longer chain alcohols are found as contaminants in some alcoholic beverages and are known as fusel alcohols,[24][25] and are reputed to cause severe hangovers although it is unclear if the fusel alcohols are actually responsible.[26] Many longer chain alcohols are used in industry as solvents and are occasionally abused by alcoholics,[27][28] leading to a range of adverse health effects.[29]

  82. Metastasis, or metastatic disease (sometimes abbreviated mets), is the spread of a disease from one organ or part to another non-adjacent organ or part.[1][2] It was previously thought that only malignant tumor cells and infections have the capacity to metastasize; however, this is being reconsidered due to new research.[3] The word metastasis means “displacement” in Greek, from ????, meta, “next”, and ??????, stasis, “placement”. The plural is metastases.

    Cancer occurs after a single cell in a tissue is progressively genetically damaged to produce a cancer stem cell possessing a malignant phenotype. These cancer stem cells are able to undergo uncontrolled abnormal mitosis, which serves to increase the total number of cancer cells at that location. When the area of cancer cells at the originating site becomes clinically detectable, it is called a primary tumor. Some cancer cells also acquire the ability to penetrate and infiltrate surrounding normal tissues in the local area, forming a new tumor. The newly formed “daughter” tumor in the adjacent site within the tissue is called a local metastasis.

    Some cancer cells acquire the ability to penetrate the walls of lymphatic and/or blood vessels, after which they are able to circulate through the bloodstream (circulating tumor cells) to other sites and tissues in the body. This process is known (respectively) as lymphatic or hematogeneous spread.

    After the tumor cells come to rest at another site, they re-penetrate through the vessel or walls, continue to multiply, and eventually another clinically detectable tumor is formed. This new tumor is known as a metastatic (or secondary) tumor. Metastasis is one of three hallmarks of malignancy (contrast benign tumors).[4] Most tumors and other neoplasms can metastasize, although in varying degrees (e.g. basal cell carcinoma) rarely metastasize.[4]

    When tumor cells metastasize, the new tumor is called a secondary or metastatic tumor, and its cells are like those in the original tumor. This means, for example, that, if breast cancer metastasizes to the lungs, the secondary tumor is made up of abnormal breast cells, not of abnormal lung cells. The tumor in the lung is then called metastatic breast cancer, not lung cancer.

  83. Treatment and survival is determined by whether or not a cancer is local or has spread to other locations. If the cancer spreads to other tissues and organs, it may decrease a patient’s likelihood of survival. However, there are some cancers (i.e., some forms of leukemia, a cancer of the blood) that can kill without spreading at all.

    When cancer has metastasized, it may be treated with radiosurgery, chemotherapy, radiation therapy, biological therapy, hormone therapy, surgery or a combination of these. The choice of treatment generally depends on the type of primary cancer, the size and location of the metastasis, the patient’s age and general health, and the types of treatments used previously. In patients diagnosed with CUP, it is still possible to treat the disease even when the primary tumor cannot be located.

    The treatment options currently available are rarely able to cure metastatic cancer, though some tumors, such as testicular cancer and thyroid cancer, are usually still curable.

  84. Apoptosis ( /?æp??to?s?s/)[1][2] is the process of programmed cell death (PCD) that may occur in multicellular organisms.[3] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation. (See also apoptotic DNA fragmentation.) Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytic cells are able to engulf and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage.[4]

    In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis, in general, confers advantages during an organism’s life cycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.[5]

    Research in and around apoptosis has increased substantially since the early 1990s. In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in an extensive variety of diseases. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer.

  85. Atrophy
    Classification and external resources

    Mice with spinal muscular atrophy
    MeSH D001284

    Atrophy is the partial or complete wasting away of a part of the body. Causes of atrophy include mutations (which can destroy the gene to build up the organ), poor nourishment, poor circulation, loss of hormonal support, loss of nerve supply to the target organ, excessive amount of apoptosis of cells, and disuse or lack of exercise or disease intrinsic to the tissue itself. Hormonal and nerve inputs that maintain an organ or body part are referred to as trophic [noun] in medical practice (‘trophic” is an adjective that can be paired with various nouns). Trophic describes the trophic condition of tissue. A diminished muscular trophic is designated as atrophy.

    Atrophy is the general physiological process of reabsorption and breakdown of tissues, involving apoptosis on a cellular level. When it occurs as a result of disease or loss of trophic support due to other disease, it is termed pathological atrophy, although it can be a part of normal body development and homeostasis as well.

  86. Homeostasis (from Greek: ??????, hómoios, “similar”[1], and ??????, stásis, “standing still”[2]) is the property of a system that regulates its internal environment and tends to maintain a stable, constant condition of properties like temperature or pH. It can be either an open or closed system.

  87. Positive feedback
    Positive feedback is a mechanism by which an output is enhanced, such as protein levels. However, in order to avoid any fluctuation in the protein level, the mechanism is inhibited stochastically (I), therefore when the concentration of the activated protein (A) is past the threshold ([I]), the loop mechanism is activated and the concentration of A increases exponentially if d[A]=k [A]Positive feedback mechanisms are designed to accelerate or enhance the output created by a stimulus that has already been activated.

    Unlike negative feedback mechanisms that initiate to maintain or regulate physiological functions within a set and narrow range, the positive feedback mechanisms are designed to push levels out of normal ranges. To achieve this purpose, a series of events initiates a cascading process that builds to increase the effect of the stimulus. This process can be beneficial but is rarely used by the body due to risks of the acceleration’s becoming uncontrollable.

    One positive feedback example event in the body is blood platelet accumulation, which, in turn, causes blood clotting in response to a break or tear in the lining of blood vessels. Another example is the release of oxytocin to intensify the contractions that take place during childbirth.[10]

    [edit] Negative feedbackNegative feedback mechanisms consist of reducing the output or activity of any organ or system back to its normal range of functioning. A good example of this is regulating blood pressure. Blood vessels can sense resistance of blood flow against the walls when blood pressure increases. The blood vessels act as the receptors and they relay this message to the brain. The brain then sends a message to the heart and blood vessels, both of which are the effectors. The heart rate would decrease as the blood vessels increase in diameter (known as vasodilation). This change would cause the blood pressure to fall back to its normal range. The opposite would happen when blood pressure decreases, and would cause vasoconstriction.

    Another important example is seen when the body is deprived of food. The body would then reset the metabolic set point to a lower than normal value. This would allow the body to continue to function, at a slower rate, even though the body is starving. Therefore, people who deprive themselves of food while trying to lose weight would find it easy to shed weight initially and much harder to lose more after. This is due to the body readjusting itself to a lower metabolic set point to allow the body to survive with its low supply of energy. Exercise can change this effect by increasing the metabolic demand.

    Another good example of negative feedback mechanism is temperature control. The hypothalamus, which monitors the body temperature, is capable of determining even the slightest variation of normal body temperature (37 degrees Celsius). Response to such variation could be stimulation of glands that produce sweat to reduce the temperature or signaling various muscles to shiver to increase body temperature.

    Both feedbacks are equally important for the healthy functioning of one’s body. Complications can arise if any of the two feedbacks are affected or altered in any way.

    [edit] Homeostatic imbalanceMany diseases are a result of disturbance of homeostasis, a condition known as homeostatic imbalance. As it ages, every organism will lose efficiency in its control systems. The inefficiencies gradually result in an unstable internal environment that increases the risk for illness. In addition, homeostatic imbalance is also responsible for the physical changes associated with aging. Even more serious than illness and other characteristics of aging is death. Heart failure has been seen where nominal negative feedback mechanisms become overwhelmed, and destructive positive feedback mechanisms then take over.[10]

    Diseases that result from a homeostatic imbalance include diabetes, dehydration, hypoglycemia, hyperglycemia, gout, and any disease caused by a toxin present in the bloodstream. All of these conditions result from the presence of an increased amount of a particular substance. In ideal circumstances, homeostatic control mechanisms should prevent this imbalance from occurring, but, in some people, the mechanisms do not work efficiently enough or the quantity of the substance exceeds the levels at which it can be managed. In these cases, medical intervention is necessary to restore the balance, or permanent damage to the organs may result.

    According to the following quote, every illness has aspects to it that are a result of lost homeostasis:

    “Just as we live in a constantly changing world, so do the cells and tissues survive in a constantly changing microenvironment. The ‘normal’ or ‘physiologic’ state then is achieved by adaptive responses to the ebb and flow of various stimuli permitting the cells and tissues to adapt and to live in harmony within their microenvironment. Thus, homeostasis is preserved. It is only when the stimuli become more severe, or the response of the organism breaks down, that disease results – a generalization as true for the whole organism as it is for the individual cell.” (Pathologic Basis of Disease, third edition, S.L. Robbins MD, R.S. Cotran MD, V.K. Kumar MD. 1984, W.P. Saunders Company)

  88. You may hear people ask, “If it’s dangerous, why do so many people have medical marijuana cards?”40 It’s true that scientists have determined that the cannabis plant has the potential for addressing a range of medical conditions. But it’s also true that when you’re young and your body is still growing, marijuana actually has the potential of inflicting a long-lasting, negative impact on your developing brain.

    Using marijuana at a young age can result in structural and functional deficits of the brain. This could cause you to develop weakened verbal and communication skills, lowered learning capabilities and a shortened attention span.40

    wonder why NIDA????

  89. LONG-TERM EFFECTS
    In addition to the possible effects on your brain, smoking marijuana may also be hazardous to your developing lungs. Marijuana smoke contains 50% to 70% more carcinogenic hydrocarbons than tobacco smoke.41

    You may have heard people argue that marijuana is a “gateway drug” to harder drug use. Some say this is a myth, others insist it is a fact. The truth is that there is a link. Research shows that the earlier you start using marijuana, the more likely you are to become dependent on it or other types of drugs later in life.42

    THE BOTTOM LINE
    Some movies and music make “stoner” culture seem cool, natural and like it’s not a big deal. But if being fit and getting good grades are some of your goals, using marijuana can become a big deal, fast. Marijuana limits your brain’s effectiveness, slows your thinking and impairs your coordination. A number of studies have also shown an association between chronic marijuana use and increased rates of anxiety, depression and schizophrenia. 41

    Is there a causal link NIDA?

  90. The menonites have a very primitive culture. They dont even believe in using the internet…is it a bad thing? exposure to anything can be pretty bad… The essence of the belief is to figure that out for yourself

  91. What did the NASA paper do? Scientists started out the project with extremophile bacteria from Mono Lake in California. This is not a pleasant place for most living creatures: it’s an alkali lake with a pH of close to 10, and it also has high concentrations of arsenic (high being about 200 µM) dissolved in it. The bacteria living there were already adapted to tolerate the presence of arsenic, and the mechanism of that would be really interesting to know…but this work didn’t address that.

    Next, what they did was culture the bacteria in the lab, and artificially jacked up the arsenic concentration, replacing all the phosphate (PO43-) with arsenate (AsO43-). The cells weren’t happy, growing at a much slower rate on arsenate than phosphate, but they still lived and they still grew. These are tough critters.

    They also look different in these conditions. Below, the bacteria in (C) were grown on arsenate with no phosphate, while those in (D) grew on phosphate with no arsenate. The arsenate bacteria are bigger, but thin sections through them reveal that they are actually bloated with large vacuoles. What are they doing building up these fluid-filled spaces inside them? We don’t know, but it may be because some arsenate-containing molecules are less stable in water than their phosphate analogs, so they’re coping by generating internal partitions that exclude water.

  92. HERE ARE THE FEDERAL PENALTIES:

    Any amount (first offense) misdemeanor 1 year $1,000
    Any amount (second offense) misdemeanor 15 days MMS* $2,500
    Any amount (subsequent offense) misdemeanor or felony 90 days MMS* – 3 years $5,000
    *Mandatory minimum sentence.

  93. Less than 50 plants/50 kg (first offense) felony not more than 5 years $250,000
    50-99 plants/50-99 kg (first offense) felony
    not more than 20 years
    $1,000,000
    100-999 plants/100-999 kg (first offense) felony 5 – 40 years $2M-$5M
    1000 plants/1000 kg or more (first offense) felony 10 years – life $4M-$10M
    To a minor felony double penalty double penalty
    Within 1,000 feet of a school, or other specified areas felony double penalty double penalty
    Gift of small amount
    see Possession

  94. we should have a national referendum on the issue of making the penalty of personal possession at the federal level a 150$ fine

  95. DETAIL:

    possession of marijuana is punishable by up to one year in jail and a minimum fine of $1,000 for a first conviction. For a second conviction, the penalties increase to a 15-day mandatory minimum sentence with a maximum of two years in prison and a fine of up to $2,500. Subsequent convictions carry a 90-day mandatory minimum sentence and a maximum of up to three years in prison and a fine of up to $5,000.

    Distribution of a small amount of marijuana, for no remuneration, is treated as possession. Manufacture or distribution of less than 50 plants or 50 kilograms of marijuana is punishable by up to five years in prison and a fine of up to $250,000. For 50-99 plants or 50-99 kilograms the penalty increases not more than 20 years in prison and a fine of up to $1 million if an individual, $5 million if other than an individual for the first offense. Manufacture or distribution of 100-999 plants or 100-999 kilograms carries a penalty of 5 – 40 years in prison and a fine of $2-$5 Million. For 1000 plants or 1000 kilograms or more, the penalty increases to 10 years – life in prison and a fine of $4-$10 Million.

    Distribution of greater than 5 grams of marijuana to a minor under the age of 21 doubles the possible penalties. Distribution within 1,000 feet of a school, playground, public housing or within 100 feet of a youth center, public pool or video arcade also doubles the possible penalties.

    The sale of paraphernalia is punishable by up to three years in prison.

    The sentence of death can be carried out on a defendant who has been found guilty of manufacturing, importing or distributing a controlled substance if the act was committed as part of a continuing criminal enterprise – but only if the defendant is (1) the principal administrator, organizer, or leader of the enterprise or is one of several such principal administrators, organizers, or leaders, and (2) the quantity of the controlled substance is 60,000 kilograms or more of a mixture or substance containing a detectable amount of marijuana, or 60,000 or more marijuana plants, or the if the enterprise received more than $20 million in gross receipts during any 12-month period of its existence.

    Applicable Statute:

  96. If the supreme court upholds 1000 dollar penalties for medical marijuana….i would like to see if pennsylvanians would uphold it

  97. golly we better… we organized the tea party that defeated the British. If tony doesnt believe marijuana is good for you… i guess you cant convince any can you?

  98. maybe i just need a little more alcohol psu… but i just dont get it… Lincoln said prohibition was an evil that should be fought… this man who freed slaves thought we shouldnt interfere with an individual’s right to put whatever they want into their body…I want to say something about addiction… any addiction stimulates dopamine… if an addict is to have anything…why not marijuana??? It seems completely reasonable to allow people to drink. No one should mix marijuana and alcohol though. there would be like a 1,000,000% chance there would be an accident. I don’t see any insurance liabilities there

  99. If i were to write the state referendum for medicinal use of marijuana, i would make the penalty a 150$ fine. Dont take up jail cells with people smoking marijuana… its that simple…if we want blood for smoking pot y dont we tar some people up good RENDELL?

  100. how about probation for medical use? you piss in a cup once in a while or give them blood once a month and if its only marijuana wouldnt that be okay? is that a gray area?

  101. i wonder if the bus would play a cypress hill song for me… i will make that request from here. Psu would love it.. its called insane in the brain

  102. When George Zimmerman murdered Trayvon Martin he became a victim of the “drug war” violence! Unending prohibitionist propaganda out of bloodthirsty Washington is claiming a vast number of lives! We need to recognize, & recalculate the true amount of casualties & deaths caused by the “drug war”! Then we must demand, KILL, NO, MORE ! ! !

Leave a Reply