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Transcript
Why is marijuana illegal? Ask a cop, "Because it’s a gateway drug!" WRONG. There is no chemical in marijuana that makes you want to try other drugs. The only reason that some people who smoke try other drugs is because they are in an environment of other types of drugs. In other words, if all you did was smoke marijuana, you would have no urge to try other things like cocaine or crack unless you had some kind of outside influence, such as somebody around you smoking crack or snorting cocaine. Originally marijuana was brought into the country by Mexicans, in order to get rid of the Mexicans, the government illegalized MJ. This failed; thousands of Mexicans immigrate into the country each year. Another reason was MJ has many other uses, hemp is used for many things, and some cultures use it for fabrics, ropes, and paper. Hemp has been proved to be stronger and longer lasting than regular pulp in terms of making paper, and the fabric made from this is so much stronger than that of cotton, and corporate America with their wood cutting companies couldn’t keep up. Yes MJ is not good for you, studies have proved that it destroys some short term memory capabilities in users, and has been known to cause some illnesses similar to cigarette smokers, but yet cigs are still legal? What about alcohol? MJ has been around for over 5000 years, and until recently nobody had a problem with it. Government propaganda has trained the American society to believe that this drug is so detrimental to progress in society and users should be shunned. Disregard these facts and only prove my point more that you are a product of your government’s control. "Gateway Drug" The term is often used by governments, pressure groups and the media to describe the scientifically controversed concept that illegal drug use is a continuum. According to this concept, using one "soft" non- or only slightly addictive drug will lead to the use of other "harder" drugs and the associated criminal and social consequences – the first drug used is thus described as a gateway to further abuse. There is no scientific evidence to support the idea that use of one drug will lead to use of other drugs – that physiological and neurological changes make it unavoidable. Individual social histories show that "hard" drug users do progress from one drug to another, but the drives behind this are not clear enough to generalize a gateway.[1] Furthermore, some "hard" drugs, such as alcohol, may be legal, while other "soft" drugs, such as marijuana, may be illegal. In 1998, a French scientific report, led by Dr. Pierre-Bernard Roques from the INSERMCNRS, classed different types of drugs according to their lethality and addictiveness. Heroin, cocaine and alcohol were classed in the most addictive and lethal category; benzodiazepine, hallucinogens and tobacco in the medium category; and marijuana in the last category. Health secretary Bernard Kouchner, founder of Médecins Sans Frontières, declared that: "Scientifical facts show that, for cannabis, no neurotoxicity is demonstrated, to the contrary of alcohol and cocaine." In case you didn’t catch that, there is no scientific proof, and there is not enough data to generalize one drug as a gateway drug. Propaganda. Rest my case. However, I can rest assured that there are some people who will refuse to listen and will disagree with me no matter what with no refutable evidence. Behavioral effects It is sometimes observed, and generally stereotyped, that systematic changes in a person’s lifestyle, ambitions, motivation, and personality happen when a young person starts smoking marijuana. In fact, in many situations when people are asked to describe the personality traits of a marijuana user, they will most likely portray a person of apathy or loss of effectiveness: a person with diminished capacity or willingness to carry out complex long-term plans, endure frustration, concentrate for long periods, follow routines, or even successfully master new material. [12] The term "amotivational syndrome" is often applied to young individuals who have changed from clean, assertive, upwardly mobile achievers into the sort of person just described, with marijuana as the culprit. The syndrome, like other correlational phenomena, raises a chicken-and-egg type problem; marijuana use can just as easily be seen as the result of such a personality shift as it can be the cause of it. Regardless, studies to raise this and other questions, like the prevalence of such "syndrome" in the population, and proving a biological or psychological connection of the "syndrome" to substance use, have not happened. Instead, a political tug of war has ensued with each point of view claiming their own scientific research as evidence. Government studies often point to statistical data accumulated by methods like the National Household Survey on Drug Abuse (NHSDA), the Monitoring the Future study (MTF), and the Arrestee Drug Abuse Monitoring (ADAM) program, which claim lower school averages and higher dropout rates among users than nonusers, even though these differences are not great. However, the problem is that in many cases, like with NHSDA and MTF, these surveys are usually self-administered and may or may not be anonymous. The likeliness of over or under representing data definitely undermines the effectiveness of these instruments. [2] The MTF study is conducted anonymously, but only seeks information from a sample of people who have been arrested for drug-related offenses. Clearly, the case can easily be made that socially deviant behavior will be found more frequently in individuals of the criminal justice system compared to those in the general population. In response, independent studies of college students have shown that there was no difference in grade point average, and achievement, between marijuana users and nonusers, but the users had more difficulty deciding on career goals, and a smaller number were seeking advanced professional degrees. [13] Laboratory studies of the relationship between motivation and marijuana outside of the classroom, where volunteers worked on operant tasks for a wage representing a working world model, also fail to distinguish a noticeable different between users and non users. [14] Different and fewer risks than tobacco The process most popularly used to ingest cannabis is smoking. Tobacco smoking has well-established risks such as bronchitis, coughing, overproduction of mucus, and wheezing. Similar risks for smoking cannabis related to airway inflammation have been suggested in a study of healthy cannabis users who exhibited similar early characteristics to tobacco smoking. [23] The effects of tobacco and cannabis smoking differ, however, as they affect different parts of the respiratory tract: whereas tobacco tends to penetrate to the smaller, peripheral passageways of the lungs, cannabis tends to concentrate on the larger, central passageways. One consequence of this is that cannabis, unlike tobacco, does not appear to cause emphysema. Also unlike tobacco, regular cannabis use does not appear to cause chronic obstructive pulmonary disease, either. [24] It is important to note that in some cases, a cannabis user may encounter commercial tobacco in joints (popular in Europe), added tobacco with hash in chillum (India), or cannabis rolled in tobacco leaves (seen occasionally the U.S.), which would expose the user to the additional risks of tobacco, though nothing on the same order as regular tobacco use. No cancer link A recent study [26] on a much larger population sample (about 1200), however, not only failed to establish a cancer risk, but showed a slight negative correlation between longterm cannabis use and lung cancers, suggesting a possible theraputic effect. This followed an even larger 1997 study [27] examing the records of 64,855 Kaiser patients, and concluding no correlation between cannabis use and cancer. It has been noted, separately, that THC, a dilative agent, may help clense the lungs by dilating the bronchia, and could actively reduce the instance of tumors. [28] Yet another study failed to establish a link between cannabis use and oral cancer. [29] Although the carcinogenicity of tobacco is thought to be caused mainly by tar, it has been suggested that it could be the result of radioactive substances present in tobacco soils. This problem may not pertain to cannabis, the vast majority of which is grown in wild, organic, or hydroponic conditions. Attempts at harm reduction Often, the risk has been simply presumed, leading many to make harm reduction recommendations such as choosing bongs or vaporizers. Although vaporisers, by heating the cannabis oils to be inhaled without combustion, avoid altogether the risk [30], bong users may not fare so well, as they reduce the concentration of THC, necessitating inhalation of a greater quantity of smoke in order to receive the same amount of THC. A 2000 study conducted by NORML and MAPS found that the unfiltered joint outperformed all devices except the vaporizers, with a ratio of about 1 part cannabinoids to 13 parts tar. This ratio is still rather low; according to the report, "This poor ratio may be explained by low-potency (2.3%) of the NIDA-supplied marijuana used in the study". Short term memory loss? Sure, but only temporary. One of the primary effects of marijuana in humans is the disruption of short-term memory, which is consistent with the abundance of CB1 receptors on the hippocampus. The effects of THC at these receptor sites produce what is called a "temporary hippocampal lesion." [1] As a result of this lesion, several neurotransmitters like acetylcholine, norepinephrine, and glutamate, are released that trigger a major decrease in neuronal activity in the hippocampus and its inputs. In the end, this procedure leads to the blocking of cellular processes that are associated with memory formation. There is no scientific evidence to suggest that these effects are permanent, and normal neurological functionality is usually achieved as the drug is metabolized. Legal and political constraints on open research In many countries, experimental science suffers from legal restrictions because cannabis is illegal. Thus, cannabis as a drug is often hard to fit into the structural confines of medical research because appropriate, research-grade samples are impossible to obtain legally for research purposes, unless granted under authority of national governments. The phenomenon of legitimate scientific curiosity in conflict with governmental agenda was most recently exemplified in the United States by the clash between Multidisciplinary Association for Psychedelic Studies (MAPS), an independent research group, versus the National Institute on Drug Abuse (NIDA), a federal agency charged with the application of science to the study of drug abuse, under the general control of the Office of National Drug Control Policy (ONDCP), a White House office responsible for the direct coordination of all legal, legislative, scientific, social and political aspects of federal drug control policy. The cannabis that is available for research studies in the United States is solely controlled by the NIDA, which even has veto power over the Food and Drug Administration (FDA) to define accepted protocols. Since 1942, when cannabis was removed from the U.S. pharmacopoeia and its medical use was prohibited, there is no history of a legal (under federal law) privately funded cannabis production project. The result is that a very limited number of research opportunities take place, and these must use the product that NIDA produces, which is generally of very low potency and inferior quality. 1. ^ Emboden, W. A. 1981. The genus Cannabis and the correct use of taxonomic categories. J. Psychoactive Drugs 13: 15–21. 2. ^ Schultes, R. E., and A. Hofmann. 1980. Botany and Chemistry of Hallucinogens. C. C. Thomas, Springfield, IL., pp. 82–116. 3. ^ Small, E., and A. Cronquist. 1976. A practical and natural taxonomy for Cannabis. Taxon 25: 405–435. 4. ^ Schultes, R. E., et. al. 1974. Cannabis: an example of taxonomic neglect. Harvard University Botanical Museum Leaflets 23: 337–367. 5. ^ Anderson, L. C. 1974. A study of systematic wood anatomy in Cannabis. Harvard University Botanical Museum Leaflets 24: 29–36. 6. ^ Anderson, L. C. 1980. Leaf variation among Cannabis species from a controlled garden. Harvard University Botanical Museum Leaflets 28: 61–69. 7. ^ Hillig, K.W. 2005. Genetic evidence for speciation in Cannabis (Cannabaceae). Genetic Resources and Crop Evolution 52: 161-180. Retrieved from "http://en.wikipedia.org/wiki/Cannabis" ^ a b c d Marijuana and Medicine: Accessing The Science Base, by J.E. Joy, S. J. Watson, Jr., and J.A. Benson, Jr, Washington D.C: National Academy of Sciences Press 1999 [32] ^ a Drugs: An Introduction (5th edition), by H. Abadinsky, 2004, 62-77; 160-166 ^ Erowid Cannabis (Marijuana) Vault, accessed 08/18/05 [33] ^ Pharmacology of Cannabinoid CB1 and CB2 Receptors, by R.G. Pertwee, Pharmacology and Therapeutics, 1997, 129-180 ^ Acute and residual effects of marijuana in humans, by R.V Fant, S.J. Heishman, E.B. Bunker, W.B Pickworth, Pharmacology, Biochemistry, and Behavior, Aug 1998 60(4), 777-84 ^ Adverse Effects of Cannabis, by W. Hall, N. Solowij, The Lancet, Nov 1998, 1611-6 ^ Evidence that anandamide-signaling regulates human sperm functions required for fertilization, by H. Schuel et al., Molecular Reproduction and Development, Sep 2002, 63(3), 376-387 [34] ^ Analysis of facial shape in children gestationally exposed to marijuana, alcohol, and/or cocaine, by S.J. Astley, S.K. Clarren, R.E. Little, P.D. Sampson, J.R. Daling, Pediatrics, Jan 1992, 89(1), 67-77 ^ The Merck Manual of Medical Information (Home Edition), by R. Berkow MD et al, 1997, 449 ^ Five-year follow-up of rural Jamaican children whose mothers used marijuana during pregnancy, by J.S. Hayes, R. Lampart, M.C. Dreher, L. Morgan, West Indian Medical Journal, Sept 1991, 40(3). 120-3 ^ Prenatal Marijuana Exposure and Neonatal Outcomes in Jamaica: An Ethnographic Study, by M.C. Dreher, K. Nugent, R. Hudgins, Pediatrics, Feb 1994, Vol. 93 #3, 254-260 ^ Amotivational Syndrome, by W.A. McKim, Drugs and Behavior, 1993, 229-230 ^ Marihuana and Psychosocial Adjustment, by N.Q. Brill; R.L. Christie, Archives of General Psychiatry, 1974, 31, 713-719 ^ The Effects of Marihuana Use on Human Operant Behavior: Individual Data…, by H.H. Mendelson; J.C. Kuehnle, I. Greenberg; N.K. Mello, Pharmacology of Marihuana, New York: Academic Press 1976, Vol. 2, 643-653 ^ Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people, by Cécile Henquet, Lydia Krabbendam, Janneke Spauwen, Charles Kaplan, Roselind Lieb, Hans-Ulrich Wittchen and Jim van Os, British Medical Journal, December 2004, Volume 330: 11 ^ Cannabis use and mental health in young people: cohort study, by G C Patton, Carolyn Coffey, J B Carlin, Louisa Degenhardt, Micheal Lynskey and Wayne Hall, British Medical Journal, 2005, Volume 325: 1195 ^ Decreased depression in marijuana users, by: T.F. Denson; M. Earleywine, Addictive Behaviors, June 20, 2005 [35] ^ Study Finds Cannabis Triggers Transient Schizophrenia-Like Symptoms, by: J. Weaver. Yale News Release, June 14, 2004 [36] ^ Causal association between cannabis and psychosis: examination of the evidence, by: L. Arseneault et al., The British Journal of Psychiatry (2004) 184: 110117 [37] ^ Cannabis and Schizophrenia: A Longitudinal Study of Swedish Conscripts, by S. Andreasson et al, The Lancet, 1987. Vol. 2, 1483-1486 ^ Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study, by: Louise Arseneault, Mary Cannon, Richie Poulton, Robin Murray, Avshalom Caspi, Terrie E Moffitt, BMJ (British Medical Journal), 23 November, 2002, [38] ^ Moderation of the Effect of Adolescent-Onset Cannabis Use on Adult Psychosis by a Functional Polymorphism in the catechol-O-Methyltransferase Gene:Longitudinal Evidence of a Gene X Environment Interaction, by: Avshalom Caspi, Terrie E. Moffitt, Mary Cannon, Joseph McClay, Robin Murray, HonaLee Harrington, Alan Taylor, Louise Arseneault, Ben Williams, Antony Braithwaite, Richie Poulton, and Ian W. Craig, Society of Biological Psychiatry, January 18, 2005, [39] ^ Airway Inflammation in Young Marijuana and Tobacco Smokers, by: M.D. Roth et al., American Journal of Respiratory and Critical Care Medicine, Volume 157, Number 3, March 1998, 928-937 [40] ^ Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age, by: D.P. Tashkin et al., Am. J. Respir. Crit. Care Med., Vol 155, No. 1, Jan 1997, 141-148 [41] ^ Pulmonary hazards of smoking marijuana as compared with tobacco, by: T.C. Wu et al., New England Journal of Medicine, Volume 318, No. 6, Feb 11, 1988, 347351 [42] ^ Marijuana Smoking Does Not Cause Lung Cancer, Fred Gardner, Anderson Valley Advertiser, Wed, 06 Jul 2005, [43] ^ Marijuana use and cancer incidence (California, United States), by: S. Sidney, Cancer Causes and Control, Volume 8, Number 5, September 1997, 722 - 728 [44] ^ Antitumor Effects of THC, by: J. Huff & P. Chan, Environmental Health Perspectives, 108(10), Oct 2000, A442-3 [45] ^ Marijuana Use and Risk of Oral Squamous Cell Carcinoma, by: K.A. Rosenblatt et al., Cancer Research, 64, June 1, 2004, 4049-4054 [46] ^ Vaporizers for Medical Marijuana, by B. Mirken, AIDS Treatment News 327, Institute of Medicine, Sept. 17, 1999 ^ Cannabis and driving: a review of the literature and commentary (No.12), United Kingdom Department for Transport, accessed 12/27/2005, last modified 11/04/2004 [47]