Consciousness Day 1 Hook (Notes): 5 minutes Consciousness: our awareness of ourselves & our environment. o Brings varied information to the surface, enabling us to reflect & plan. o Especially important in letting us concentrate to learn a complex concept or behavior. o Voluntary control o Automatic behaviors happen ahead of us being conscious of them. Procedure 1 (Round Robin; voluntary behaviors & multi-tasking): 5 minutes o Go round robin around the room having each student give an example of a conscious action or behavior. o Have students who have volunteered their answers give examples of how they mutli-task. Pick an example from one of the students & tease out what behaviors are automatic & which ones are conscious; show them how you quickly switch your attention between these conscious ones to make that makes it feel like you are consciously thinking about multiple things. Procedure 2 (Experiments): 5 minutes o Take dominant hand & foot & move your foot in a clock wise direction while drawing a 3 with your hand. o Opposite direction big circles with your hands. o Tap 3 evenly with one hand & 4 evenly with the other in the same length of time, at the same time. Procedures 3 (Notes): 35 minutes Biological rhythms: our bodies & minds fluctuate over time with our internal “biological clocks.” o Annual cycles: Humans experience seasonal variations in appetite, sleep length, & moods. Seasonal affective disorder: Talk about tanning beds, sun lamps, extra light around the house Metabolism o Twenty-eight day cycles: the female menstrual cycle averages 28 days. Talk about female & male (nature vs. learned) o Twenty-four hour cycles: Cycles of varying alertness, body temperature, & growth hormone secretion. Circadian rhythm: Our bodies roughly synchronize with the 24 hour cycles of the day; our biological clock (for example, of temperature & wakefulness). Night owls vs. early birds Transitional time periods for this. Starts to transition in the 20s, transitions earlier for women than for men because they start puberty earlier & are therefore farther along in their development. Name things that can throw off your circadian rhythm. Think up strategies to put your circadian rhythm back on track. Bright lights, caffeine, melatonin. o Ninety-minute cycles: Various stages of 90 minutes cycles. Sleep: A state that we do not know we are in until we leave it. Stages of sleep: o Awake, relaxed Alpha waves: These are read by an EEG when you are awake but in a relaxed state. o Stage 1: May experience hallucinations. Hallucinations: Sensory experiences that occur without sensory stimuli. Sensations such as falling or floating weightlessly; sudden jerk of the body (hypnagogic) o Stage 2: 20 minutes; sleeptalking & brain spindles, bursts of rapid, rhythmic brain wave activity. o Stage 3: a few minutes; Brain starts to emit large delta waves. Delta waves: The large, slow brain waves associated with deep sleep o Stage 4: Two 30 minute stages; sleepwalking, or bed wetting. It is hard to waken a person in this stage. o Back through 3 & 2, to REM o REM sleep (rapid eye movement): This is the stage where dreaming occurs, therefore, it is accompanied by energetic brain activity. Muscles are relaxed while other body systems are active. Visual & auditory areas of the brain are still active. Heart rate rises & breathing increases. Dreams. Day 2 Procedures: Procedure 1 (Notes): 20 minutes Sleeptalking: usually garbled or nonsensical (any sleep stage). Even when you sleep, your brain still processes certain stimuli, like you manage to not fall off of your bed, if you sleep with a baby, you will not roll over & smoother them, the cry from a baby’s nursery quickly wakes a person from deep sleep, the sound of your name. o We process most information in life outside of our conscious awareness. o Story about me as a 6 week old baby with a double inner ear infection. Why do we sleep: o The amount we need to sleep is both related to our age & very individual. o Sleep debt o Just add an extra hour of sleep to feel better, both mentally & physically. Procedure 2 (Sleep Survey): 5 minutes o Have the students complete the sleep survey on page 282 Are You Sleep Deprived? Cornell University psychologist James Maas reports that most college students suffer the consequences of sleeping less than they should. To see if you are in that group, answer the following true-false questions. 1. I need an alarm clock in order to wake up at the appropriate time. 2. It’s a struggle for me to get out of bed in the morning. 3. Weekday mornings I hit the snooze bar several times to get more sleep. 4. I feel tired, irritable, & stressed out during the week. 5. I have trouble concentrating & remembering. 6. I feel slow with critical thinking, problem solving, & being creative. 7. I often fall asleep watching TV. 8. I often fall asleep in boring meeting or lectures or in warm rooms. 9. I often fall asleep after heavy meals or after a low dose of alcohol. 10. I often fall asleep while relaxing after dinner. 11. I often fall asleep within five minutes of getting into bed. 12. I often feel drowsy while driving. 13. I often sleep extra hours on weekend mornings. 14. I often need a nap to get through the day. 15. I have dark circles around my eyes. If you answered “true” to three or more items, you are probably not getting enough sleep, To determine your sleep needs, Maas recommends that you “go to bed 15 minutes earlier than usual every night for the next week—continue this practice by adding 15 more minutes each week—until you wake without an alarm clock & feel alert all day.” (Quiz reprinted with permission from James B. Maas, Power sleep: The revolutionary program that prepares your mind & body for peak performance [New York: HaperCollins, 1999].) Procedure 3 (Compare Answers & Problem Solve): 10 minutes o Have the students compare their answers & come up with solutions to help combat the effects of not having enough sleep & ways to get more sleep in the future. Procedure 4 (Notes): 15 minutes o Sleep debt: Your body keeps track of sleep deprivation for 2-3 weeks. Suppresses our immune system, difficulty studying, diminished productivity, tendency to make mistakes, irritability, fatigue, alters metabolic & hormonal functioning in ways that mimic aging & are conducive to obesity, hypertension, & memory impairment. o Sleep Theories: Offers protection (hunters & gatherers) Helps us recuperate Restore & repair brain tissue Remembering; helps restore & rebuild our fading memories Pituitary gland releases growth hormone during sleep. o Sleep disorders: Insomnia: persistent problem in falling or staying asleep. True insomnia isn’t the occasional inability to sleep that we experience when we’re anxious or excited. o For any stressed being, being vigilant is natural & adaptive. From middle age on, sleep is rarely uninterrupted. Some people unnecessarily fret over how long it takes them to get to sleep (overestimate) & they underestimate how long that they sleep. The most common quick fixes for true insomnia, alcohol & medication, tend to make the problem worse. o These can reduce REM sleep. o Tolerance o Worsens when treatment is stopped. o Ask the students for suggests to increase the likelihood of sleep. These are suggestions from scientists: Relax before bedtime, using dimmer light. Avoid caffeine (this includes chocolate) after late afternoon, & avoid rich foods before bedtime. A glass of milk may help (milk provides raw materials for the manufacture of serotonin, a neurotransmitter that facilitates sleep). Sleep on a regular schedule (rise at the same time even after a restless night) & avoid naps. A regular sleep schedule boosts daytime alertness, too, as shown in an experiment in which University of Arizona students averaged 7.5 hours of sleep a night on either a varying or consistent schedule (Manber & others, 1996). Exercise regularly but not late in the evening (late afternoon is best). Reassure yourself that a temporary loss of sleep causes no great harm, certainly noting worth losing sleep over. Hide the clock face so you aren’t tempted to check it repeatedly. If nothing else works, aims for less sleep; go to bed later or get up earlier. Narcolepsy: Story about my grandpa. People with this condition experience periodic overwhelming sleepiness. Usually lasts less than 5 minutes, but it can happen at the most inconvenient times. In severe cases, the person may collapse directly into REM sleep, without the accompanying loss of muscular tension. 1 in 2,000 people. Sleep apnea: They intermittently stopping breathing while sleeping. After an airless minute or so, decreased blood oxygen arouses, the sleeper to awaken & snort in air for a few seconds. Can happen more than 400 times a night; they can be deprived of slow-wave sleep. Apart from sleepiness & irritability during the day, most people do not remember these episodes. 1 in 20; mostly overweight men Anyone who snores at night, feels tired during the day, & who possibly has high blood pressure should be checked for apnea. For severe cases, doctors give the sleeper a masklike device with an air pump that keeps the airway open & breathing regular. Night terrors: These occur mostly in children, who may sit up or walk around, talk incoherently, experience a doubling of heart & breathing rates, & appear terrified. Seldom wake up fully during an episode & they recall little or nothing the next morning. o At the most it is usually a fleeting, frightening image. o Usually occur during the first few hours of stage 4. o Dreams: hallucinations of the sleeping mind that vivid, emotional, & bizarre. So vivid that we may confuse them with reality Occur during REM sleep. Lucid dreams: When a person is sufficiently awake during a dream to wonder whether or not they are dreaming. In some such cases, people are able to test their state of consciousness. If they can perform an absurd act, they know that they are dreaming. People who are blind from birth experience dreams with the other senses: hearing, touching, smelling, & tasting. Sometimes though, even these people experience visual images in dreams. 8 in 10 dreams are negative Failing in an attempt to do something. Being attacked, pursued, or rejected. Experiencing misfortune. The story line of dreams is called the manifest content. Previous days’ experiences & preoccupations. o After a trauma, people commonly experience nightmares. Sometimes the sensory stimuli of our sleeping environment intrudes. Anything that happens during the 5 minutes just before we fall asleep is typically lost to memory. o Reasons for dreaming: To satisfy our own wishes/Freud’s wish-fulfillment: A psychic safety valve that gets rid of otherwise unacceptable feelings. Latent content: unconscious drives & wishes that would be threatening if expressed directly (Freud). To file away memories/information-processing: Dreams sift, sort, & fix the day’s experiences in our memory. REM sleep helps convert memories into long-term learning. To develop & preserve neural pathways/physiological function: Physiological needs: REM sleep provides periodic stimulation, which may develop & preserve neural pathways. To make sense of neural static/activation-synthesis: Activation-synthesis theory: the neural activity is random, & dreams are the brain’s attempt to make sense of it. The parts of the brain that process visual images are activated, but not the visual cortex area. To reflect cognitive development/cognitive theory: Brain maturation & cognitive development. Dream content reflects dreamers’ cognitive development— their knowledge & understanding. Day 3 o Hook (Dream Interpretations): 50 minutes o Lay out the rules. The dreams don’t leave the room. No inappropriate topics. No leading questions. No Yes/No questions No This or That questions. Use open-ended questions. o Tell the students to take 2 column notes (left side dream notes, right side dream interpretation) o Have students volunteer their dreams. Day 4 o Hook (Dream Interpretations): 50 minutes o Lay out the rules. The dreams don’t leave the room. No inappropriate topics. No leading questions. No Yes/No questions No This or That questions. Use open-ended questions. o Tell the students to take 2 column notes (left side dream notes, right side dream interpretation) o Have students volunteer their dreams. Day 5 Procedures: Hook (Stories of Sleep): __ minutes o Story of the brain during different stages of sleep. Books from King? Articles online? Day 6 Procedures (Notes): 50 minutes Hypnosis: a social interaction in which one person (the hypnotist) suggests to another (the subject) that certain perceptions, feelings, thought, or behaviors will spontaneously occur. o Virtually anyone will experience some degree of hypnotic responsiveness if led to expect it. Posthypnotic suggestions: These have helped alleviate headaches, asthma, & stress-related skin disorders. Dissociation: A split between different levels of consciousness. Like dissociative disorder. Psychoactive drugs: Are chemicals that change perceptions & moods. Tolerance: The user experiences neuroadaptation (the brain adapts its chemistry to offset the drug effect). o This happens due to the continued use of alcohol & other psychoactive drugs. o The user ends up requiring increasingly larger doses to experience the drug’s effect. Withdrawal: The body’s response to the drug’s absence; including physical pain & intense cravings, indicating, physical dependence. Psychological dependence: This happens particularly with stress-relieving drugs. Addiction: A craving for a substance despite adverse consequences & often with physical symptoms such as aches, nausea, & distress following sudden withdrawal. o Abrupt changes in work or school attendance, quality of work, work output, grades and discipline o Unusual flare-ups or outbreaks of temper o Withdrawal from responsibility, family and social groups o General changes in overall attitude o Deterioration of physical appearance and grooming o Wearing of sunglasses at inappropriate times o Continual wearing of long-sleeved garments particularly in hot weather or reluctance to wear short-sleeved attire when appropriate o Association with known substance abusers o Unusual borrowing of money from friends, co-workers or parents o Stealing small items from employer, home or school o Secretive behavior regarding actions and possessions o Poorly concealed attempts to avoid attention and suspicion such as frequent trips to storage rooms, restrooms, basement, etc. o Size of pupils - blown out pupils are indicative of stimulant use, such as crack, methamphetamine or cocaine; Pinpoint pupils can be indicative of depressant use, such as heroin or opiates. Depressants: are drugs such as alcohol, barbiturates (tranquilizers), & opiates that clam neural activity & slow body functions. o Alcohol: slows down the brain activity that controls judgment & inhibitions. o Barbiturates: Also known as tranquilizers, they depress the activity of the central nervous system, reducing anxiety but impairing memory & judgement. o Opiates: Opium & its derivatives, morphine & heroin, also depress neural functioning. The pupils constrict, the breathing slows, & the user becomes lethargic. Temporarily lessens pain & anxiety. Stimulants: Temporarily excite neural activity & arouse body functions. These people stay awake, lose weight, or boost mood or athletic performance. Caffeine, nicotine, etc. o Amphetamines: Cocaine, Ecstasy. Drugs that stimulate neural activity, causing speeded-up body functions & associated energy & mood changes. o Methamphetamine: “Speed;” a powerfully addictive drug that stimulates the central nervous system, with speeded-up body functions & associated energy & mood changes; over time, appears to reduce baseline dopamine levels. o Cocaine: Sniffed, injected, or smoked. In enters the bloodstream quickly & causes a “rush” of euphoria that lasts 15 to 30 minutes. It depletes the brain’s supply of the neurotransmitters dopamine, serotonin, & norepinephrine. o Ecstasy: MDMA is both a stimulant & a mild hallucinogen. An amphetamine derivative, it triggers the release of the neurotransmitter dopamine. But its major effect is to release stored serotonin & to block its reabsorption. Hallucinogens: These distort perceptions & evoke sensory images in the absence of sensory input. o LSD: a powerful hallucinogenic drug, also known as acid. o Marijuana/THC: The leaves & flowers of the hemp plant, which for 5000 years has been cultivated for its fiber. Smoked or eaten; smoking produces a greater effect than eating. It relaxes, disinhibits, & may produce a euphoric high. Near-death experience: Those who have come close to death through cardiac arrest or other physical traumas. An altered state of consciousness reported after a close brush with death (such as through cardiac arrest); often similar to drug-induced hallucinations. Dualists: The presumption that mind & body are two distinct entities that interact. Monists: The presumption that mind & body are different aspects of the same thing. Day 7 Procedures: Hook (Sleep Stage Facts Research): 30 minutes o Have the students look in materials besides their textbooks to discover more information on the different stages of sleep & what happens in those stages. Groups: Stage 1 Stage 2 Stage 3 Stage 4 REM sleep Procedure 1 (Share): 10 minutes o Have the groups share the information that they learned. Procedure 2 (Reflect): 10 minutes o Have the students describe the processing of falling to sleep & then going through the sleep stages as the brain & body experiences it. Sleep Stages Research Name: Date: Period: 1. What do the brain waves of this stage of sleep look like? Also, please draw them. 2. What is happening to the body during this stage of sleep? 3. What is happening in the brain during this stage of sleep? 4. Approximately how long does this stage of sleep last? 5. What is the purpose of this stage of sleep? 6. Find 3 additional facts about this stage of sleep. Day 8 Procedures: Hook (Article): 10 minutes o Read the article together as a class. Procedure 1 (Questions): 10 minutes o Have the students work on the questions together in groups. Procedure 2 (Promoting a side): 15 minutes o Have the students get into 2 big groups & work on a way to convince people of either the existence or nonexistence of global warming. Procedure 3 (Presentation & Debate: 15 minutes o Have the groups each present their sides & then present arguments to weaken the position of the opposing side. The Science of Why We Don't Believe Science How our brains fool us on climate, creationism, and the vaccine-autism link. By Chris Mooney | Mon Apr. 18, 2011 3:00 AM PDT "A MAN WITH A CONVICTION is a hard man to change. Tell him you disagree and he turns away. Show him facts or figures and he questions your sources. Appeal to logic and he fails to see your point." So wrote the celebrated Stanford University psychologist Leon Festinger [1] (PDF), in a passage that might have been referring to climate change denial—the persistent rejection, on the part of so many Americans today, of what we know about global warming and its human causes. But it was too early for that—this was the 1950s—and Festinger was actually describing a famous case study [2] in psychology. Festinger and several of his colleagues had infiltrated the Seekers, a small Chicago-area cult whose members thought they were communicating with aliens—including one, "Sananda," who they believed was the astral incarnation of Jesus Christ. The group was led by Dorothy Martin, a Dianetics devotee who transcribed the interstellar messages through automatic writing. Through her, the aliens had given the precise date of an Earth-rending cataclysm: December 21, 1954. Some of Martin's followers quit their jobs and sold their property, expecting to be rescued by a flying saucer when the continent split asunder and a new sea swallowed much of the United States. The disciples even went so far as to remove brassieres and rip zippers out of their trousers—the metal, they believed, would pose a danger on the spacecraft. Festinger and his team were with the cult when the prophecy failed. First, the "boys upstairs" (as the aliens were sometimes called) did not show up and rescue the Seekers. Then December 21 arrived without incident. It was the moment Festinger had been waiting for: How would people so emotionally invested in a belief system react, now that it had been soundly refuted? [3]Read also: the truth about Climategate [4].At first, the group struggled for an explanation. But then rationalization set in. A new message arrived, announcing that they'd all been spared at the last minute. Festinger summarized the extraterrestrials' new pronouncement: "The little group, sitting all night long, had spread so much light that God had saved the world from destruction." Their willingness to believe in the prophecy had saved Earth from the prophecy! From that day forward, the Seekers, previously shy of the press and indifferent toward evangelizing, began to proselytize. "Their sense of urgency was enormous," wrote Festinger. The devastation of all they had believed had made them even more certain of their beliefs. In the annals of denial, it doesn't get much more extreme than the Seekers. They lost their jobs, the press mocked them, and there were efforts to keep them away from impressionable young minds. But while Martin's space cult might lie at on the far end of the spectrum of human selfdelusion, there's plenty to go around. And since Festinger's day, an array of new discoveries in psychology and neuroscience has further demonstrated how our preexisting beliefs, far more than any new facts, can skew our thoughts and even color what we consider our most dispassionate and logical conclusions. This tendency toward so-called "motivated reasoning [5]" helps explain why we find groups so polarized over matters where the evidence is so unequivocal: climate change, vaccines, "death panels," the birthplace and religion of the president [6] (PDF), and much else. It would seem that expecting people to be convinced by the facts flies in the face of, you know, the facts. The theory of motivated reasoning builds on a key insight of modern neuroscience [7] (PDF): Reasoning is actually suffused with emotion (or what researchers often call "affect"). Not only are the two inseparable, but our positive or negative feelings about people, things, and ideas arise much more rapidly than our conscious thoughts, in a matter of milliseconds—fast enough to detect with an EEG device, but long before we're aware of it. That shouldn't be surprising: Evolution required us to react very quickly to stimuli in our environment. It's a "basic human survival skill," explains political scientist Arthur Lupia [8] of the University of Michigan. We push threatening information away; we pull friendly information close. We apply fight-or-flight reflexes not only to predators, but to data itself. We apply fight-or-flight reflexes not only to predators, but to data itself. We're not driven only by emotions, of course—we also reason, deliberate. But reasoning comes later, works slower—and even then, it doesn't take place in an emotional vacuum. Rather, our quick-fire emotions can set us on a course of thinking that's highly biased, especially on topics we care a great deal about. Consider a person who has heard about a scientific discovery that deeply challenges her belief in divine creation—a new hominid, say, that confirms our evolutionary origins. What happens next, explains political scientist Charles Taber [9] of Stony Brook University, is a subconscious negative response to the new information—and that response, in turn, guides the type of memories and associations formed in the conscious mind. "They retrieve thoughts that are consistent with their previous beliefs," says Taber, "and that will lead them to build an argument and challenge what they're hearing." In other words, when we think we're reasoning, we may instead be rationalizing. Or to use an analogy offered by University of Virginia psychologist Jonathan Haidt [10]: We may think we're being scientists, but we're actually being lawyers [11] (PDF). Our "reasoning" is a means to a predetermined end—winning our "case"—and is shot through with biases. They include "confirmation bias," in which we give greater heed to evidence and arguments that bolster our beliefs, and "disconfirmation bias," in which we expend disproportionate energy trying to debunk or refute views and arguments that we find uncongenial. That's a lot of jargon, but we all understand these mechanisms when it comes to interpersonal relationships. If I don't want to believe that my spouse is being unfaithful, or that my child is a bully, I can go to great lengths to explain away behavior that seems obvious to everybody else—everybody who isn't too emotionally invested to accept it, anyway. That's not to suggest that we aren't also motivated to perceive the world accurately—we are. Or that we never change our minds—we do. It's just that we have other important goals besides accuracy— including identity affirmation and protecting one's sense of self—and often those make us highly resistant to changing our beliefs when the facts say we should. Modern science originated from an attempt to weed out such subjective lapses—what that great 17th century theorist of the scientific method, Francis Bacon, dubbed the "idols of the mind." Even if individual researchers are prone to falling in love with their own theories, the broader processes of peer review and institutionalized skepticism are designed to ensure that, eventually, the best ideas prevail. Scientific evidence is highly susceptible to misinterpretation. Giving ideologues scientific data that's relevant to their beliefs is like unleashing them in the motivated-reasoning equivalent of a candy store. Our individual responses to the conclusions that science reaches, however, are quite another matter. Ironically, in part because researchers employ so much nuance and strive to disclose all remaining sources of uncertainty, scientific evidence is highly susceptible to selective reading and misinterpretation. Giving ideologues or partisans scientific data that's relevant to their beliefs is like unleashing them in the motivated-reasoning equivalent of a candy store. Sure enough, a large number of psychological studies have shown that people respond to scientific or technical evidence in ways that justify their preexisting beliefs. In a classic 1979 experiment [12] (PDF), pro- and anti-death penalty advocates were exposed to descriptions of two fake scientific studies: one supporting and one undermining the notion that capital punishment deters violent crime and, in particular, murder. They were also shown detailed methodological critiques of the fake studies—and in a scientific sense, neither study was stronger than the other. Yet in each case, advocates more heavily criticized the study whose conclusions disagreed with their own, while describing the study that was more ideologically congenial as more "convincing." Since then, similar results have been found for how people respond to "evidence" about affirmative action, gun control, the accuracy of gay stereotypes [13], and much else. Even when study subjects are explicitly instructed to be unbiased and even-handed about the evidence, they often fail. And it's not just that people twist or selectively read scientific evidence to support their preexisting views. According to research by Yale Law School professor Dan Kahan [14] and his colleagues, people's deep-seated views about morality, and about the way society should be ordered, strongly predict whom they consider to be a legitimate scientific expert in the first place—and thus where they consider "scientific consensus" to lie on contested issues. In Kahan's research [15] (PDF), individuals are classified, based on their cultural values, as either "individualists" or "communitarians," and as either "hierarchical" or "egalitarian" in outlook. (Somewhat oversimplifying, you can think of hierarchical individualists as akin to conservative Republicans, and egalitarian communitarians as liberal Democrats.) In one study, subjects in the different groups were asked to help a close friend determine the risks associated with climate change, sequestering nuclear waste, or concealed carry laws: "The friend tells you that he or she is planning to read a book about the issue but would like to get your opinion on whether the author seems like a knowledgeable and trustworthy expert." A subject was then presented with the résumé of a fake expert "depicted as a member of the National Academy of Sciences who had earned a Ph.D. in a pertinent field from one elite university and who was now on the faculty of another." The subject was then shown a book excerpt by that "expert," in which the risk of the issue at hand was portrayed as high or low, well-founded or speculative. The results were stark: When the scientist's position stated that global warming is real and human- caused, for instance, only 23 percent of hierarchical individualists agreed the person was a "trustworthy and knowledgeable expert." Yet 88 percent of egalitarian communitarians accepted the same scientist's expertise. Similar divides were observed on whether nuclear waste can be safely stored underground and whether letting people carry guns deters crime. (The alliances did not always hold. In another study [16] (PDF), hierarchs and communitarians were in favor of laws that would compel the mentally ill to accept treatment, whereas individualists and egalitarians were opposed.) Head-on attempts to persuade can sometimes trigger a backfire effect, where people not only fail to change their minds when confronted with the facts—they may hold their wrong views more tenaciously than ever. In other words, people rejected the validity of a scientific source because its conclusion contradicted their deeply held views—and thus the relative risks inherent in each scenario. A hierarchal individualist finds it difficult to believe that the things he prizes (commerce, industry, a man's freedom to possess a gun to defend his family [16]) (PDF) could lead to outcomes deleterious to society. Whereas egalitarian communitarians tend to think that the free market causes harm, that patriarchal families mess up kids, and that people can't handle their guns. The study subjects weren't "anti-science"—not in their own minds, anyway. It's just that "science" was whatever they wanted it to be. "We've come to a misadventure, a bad situation where diverse citizens, who rely on diverse systems of cultural certification, are in conflict," says Kahan [17]. And that undercuts the standard notion that the way to persuade people is via evidence and argument. In fact, head-on attempts to persuade can sometimes trigger a backfire effect, where people not only fail to change their minds when confronted with the facts—they may hold their wrong views more tenaciously than ever. Take, for instance, the question of whether Saddam Hussein possessed hidden weapons of mass destruction just before the US invasion of Iraq in 2003. When political scientists Brendan Nyhan and Jason Reifler showed subjects fake newspaper articles [18] (PDF) in which this was first suggested (in a 2004 quote from President Bush) and then refuted (with the findings of the Bush-commissioned Iraq Survey Group report, which found no evidence of active WMD programs in pre-invasion Iraq), they found that conservatives were more likely than before to believe the claim. (The researchers also tested how liberals responded when shown that Bush did not actually "ban" embryonic stem-cell research. Liberals weren't particularly amenable to persuasion, either, but no backfire effect was observed.) Another study gives some inkling of what may be going through people's minds when they resist persuasion. Northwestern University sociologist Monica Prasad [19] and her colleagues wanted to test whether they could dislodge the notion that Saddam Hussein and Al Qaeda were secretly collaborating among those most likely to believe it—Republican partisans from highly GOPfriendly counties. So the researchers set up a study [20] (PDF) in which they discussed the topic with some of these Republicans in person. They would cite the findings of the 9/11 Commission, as well as a statement in which George W. Bush himself denied his administration had "said the 9/11 attacks were orchestrated between Saddam and Al Qaeda." One study showed that not even Bush's own words could change the minds of Bush voters who believed there was an Iraq-Al Qaeda link. As it turned out, not even Bush's own words could change the minds of these Bush voters—just 1 of the 49 partisans who originally believed the Iraq-Al Qaeda claim changed his or her mind. Far more common was resisting the correction in a variety of ways, either by coming up with counterarguments or by simply being unmovable: Interviewer: [T]he September 11 Commission found no link between Saddam and 9/11, and this is what President Bush said. Do you have any comments on either of those? Respondent: Well, I bet they say that the Commission didn't have any proof of it but I guess we still can have our opinions and feel that way even though they say that. The same types of responses are already being documented on divisive topics facing the current administration. Take the "Ground Zero mosque." Using information from the political myth-busting site FactCheck.org [21], a team at Ohio Statepresented subjects [22] (PDF) with a detailed rebuttal to the claim that "Feisal Abdul Rauf, the Imam backing the proposed Islamic cultural center and mosque, is a terrorist-sympathizer." Yet among those who were aware of the rumor and believed it, fewer than a third changed their minds. A key question—and one that's difficult to answer—is how "irrational" all this is. On the one hand, it doesn't make sense to discard an entire belief system, built up over a lifetime, because of some new snippet of information. "It is quite possible to say, 'I reached this pro-capitalpunishment decision based on real information that I arrived at over my life,'" explains Stanford social psychologist Jon Krosnick [23]. Indeed, there's a sense in which science denial could be considered keenly "rational." In certain conservative communities, explains Yale's Kahan, "People who say, 'I think there's something to climate change,' that's going to mark them out as a certain kind of person, and their life is going to go less well." This may help explain a curious pattern Nyhan and his colleagues found when they tried to test the fallacy [6] (PDF) that President Obama is a Muslim. When a nonwhite researcher was administering their study, research subjects were amenable to changing their minds about the president's religion and updating incorrect views. But when only white researchers were present, GOP survey subjects in particular were more likely to believe the Obama Muslim myth than before. The subjects were using "social desirabililty" to tailor their beliefs (or stated beliefs, anyway) to whoever was listening. Which leads us to the media. When people grow polarized over a body of evidence, or a resolvable matter of fact, the cause may be some form of biased reasoning, but they could also be receiving skewed information to begin with—or a complicated combination of both. In the Ground Zero mosque case, for instance, a follow-up study [24] (PDF) showed that survey respondents who watched Fox News were more likely to believe the Rauf rumor and three related ones—and they believed them more strongly than non-Fox watchers. Okay, so people gravitate toward information that confirms what they believe, and they select sources that deliver it. Same as it ever was, right? Maybe, but the problem is arguably growing more acute, given the way we now consume information—through the Facebook links of friends, or tweets that lack nuance or context, or "narrowcast [25]" and often highly ideological media that have relatively small, like-minded audiences. Those basic human survival skills of ours, says Michigan's Arthur Lupia, are "not well-adapted to our information age." A predictor of whether you accept the science of global warming? Whether you're a Republican or a Democrat. If you wanted to show how and why fact is ditched in favor of motivated reasoning, you could find no better test case than climate change. After all, it's an issue where you have highly technical information on one hand and very strong beliefs on the other. And sure enough, one key predictor of whether you accept the science of global warming is whether you're a Republican or a Democrat. The two groups have been growing more divided in their views about the topic, even as the science becomes more unequivocal. So perhaps it should come as no surprise that more education doesn't budge Republican views. On the contrary: In a 2008 Pew survey [26], for instance, only 19 percent of college-educated Republicans agreed that the planet is warming due to human actions, versus 31 percent of noncollege educated Republicans. In other words, a higher education correlated with an increased likelihood of denying the science on the issue. Meanwhile, among Democrats and independents, more education correlated with greater acceptance of the science. Other studies have shown a similar effect: Republicans who think they understand the global warming issue best are least concerned about it; and among Republicans and those with higher levels of distrust of science in general, learning more about the issue doesn't increase one's concern about it. What's going on here? Well, according to Charles Taber and Milton Lodge of Stony Brook, one insidious aspect of motivated reasoning is that political sophisticates are prone to be more biased than those who know less about the issues. "People who have a dislike of some policy—for example, abortion—if they're unsophisticated they can just reject it out of hand," says Lodge. "But if they're sophisticated, they can go one step further and start coming up with counterarguments." These individuals are just as emotionally driven and biased as the rest of us, but they're able to generate more and better reasons to explain why they're right—and so their minds become harder to change. That may be why the selectively quoted emails of Climategate were so quickly and easily seized upon by partisans as evidence of scandal. Cherry-picking is precisely the sort of behavior you would expect motivated reasoners to engage in to bolster their views—and whatever you may think about Climategate, the emails were a rich trove of new information upon which to impose one's ideology. Climategate had a substantial impact on public opinion, according to Anthony Leiserowitz [27], director of the Yale Project on Climate Change Communication [28]. It contributed to an overall drop in public concern about climate change and a significant loss of trust in scientists. But—as we should expect by now—these declines were concentrated among particular groups of Americans: Republicans, conservatives, and those with "individualistic" values. Liberals and those with "egalitarian" values didn't lose much trust in climate science or scientists at all. "In some ways, Climategate was like a Rorschach test," Leiserowitz says, "with different groups interpreting ambiguous facts in very different ways." Is there a case study of science denial that largely occupies the political left? Yes: the claim that childhood vaccines are causing an epidemic of autism. So is there a case study of science denial that largely occupies the political left? Yes: the claim that childhood vaccines are causing an epidemic of autism. Its most famous proponents are an environmentalist (Robert F. Kennedy Jr. [29]) and numerous Hollywood celebrities (most notably Jenny McCarthy [30] and Jim Carrey). The Huffington Post gives a very large megaphone to denialists. And Seth Mnookin [31], author of the new book The Panic Virus [32], notes that if you want to find vaccine deniers, all you need to do is go hang out at Whole Foods. Vaccine denial has all the hallmarks of a belief system that's not amenable to refutation. Over the past decade, the assertion that childhood vaccines are driving autism rates has been undermined [33] by multiple epidemiological studies—as well as the simple fact that autism rates continue to rise, even though the alleged offending agent in vaccines (a mercury-based preservative called thimerosal) has long since been removed. Yet the true believers persist—critiquing each new study that challenges their views, and even rallying to the defense of vaccine-autism researcher Andrew Wakefield, after his 1998 Lancet paper [34]—which originated the current vaccine scare—was retracted and he subsequently lost his license [35] (PDF) to practice medicine. But then, why should we be surprised? Vaccine deniers created their own partisan media, such as the website Age of Autism, that instantly blast out critiques and counterarguments whenever any new development casts further doubt on anti-vaccine views. It all raises the question: Do left and right differ in any meaningful way when it comes to biases in processing information, or are we all equally susceptible? There are some clear differences. Science denial today is considerably more prominent on the political right—once you survey climate and related environmental issues, anti-evolutionism, attacks on reproductive health science by the Christian right, and stem-cell and biomedical matters. More tellingly, anti-vaccine positions are virtually nonexistent among Democratic officeholders today—whereas anti-climate-science views are becoming monolithic among Republican elected officials. Some researchers have suggested that there are psychological differences between the left and the right that might impact responses to new information—that conservatives are more rigid and authoritarian, and liberals more tolerant of ambiguity. Psychologist John Jost of New York University has further argued that conservatives are "system justifiers": They engage in motivated reasoning to defend the status quo. This is a contested area, however, because as soon as one tries to psychoanalyze inherent political differences, a battery of counterarguments emerges: What about dogmatic and militant communists? What about how the parties have differed through history? After all, the most canonical case of ideologically driven science denial is probably the rejection of genetics in the Soviet Union, where researchers disagreeing with the anti-Mendelian scientist (and Stalin stooge) Trofim Lysenko were executed, and genetics itself was denounced as a "bourgeois" science and officially banned. The upshot: All we can currently bank on is the fact that we all have blinders in some situations. The question then becomes: What can be done to counteract human nature itself? We all have blinders in some situations. The question then becomes: What can be done to counteract human nature? Given the power of our prior beliefs to skew how we respond to new information, one thing is becoming clear: If you want someone to accept new evidence, make sure to present it to them in a context that doesn't trigger a defensive, emotional reaction. This theory is gaining traction in part because of Kahan's work at Yale. In one study [36], he and his colleagues packaged the basic science of climate change into fake newspaper articles bearing two very different headlines—"Scientific Panel Recommends Anti-Pollution Solution to Global Warming" and "Scientific Panel Recommends Nuclear Solution to Global Warming"— and then tested how citizens with different values responded. Sure enough, the latter framing made hierarchical individualists much more open to accepting the fact that humans are causing global warming. Kahan infers that the effect occurred because the science had been written into an alternative narrative that appealed to their pro-industry worldview. You can follow the logic to its conclusion: Conservatives are more likely to embrace climate science if it comes to them via a business or religious leader, who can set the issue in the context of different values than those from which environmentalists or scientists often argue. Doing so is, effectively, to signal a détente in what Kahan has called a "culture war of fact." In other words, paradoxically, you don't lead with the facts in order to convince. You lead with the values—so as to give the facts a fighting chance. Source URL: http://motherjones.com/politics/2011/03/denial-science-chris-mooney Consciously Deciding Not to Believe Facts Name: Date: Period: 1. What do humans tend to do in the face of information that disagrees with their previously held beliefs? Instead of reasoning, they _____. 2. What is it that prevents people from believing this new information that does not agree with their previously held beliefs? 3. What can be a problem when confronting someone with facts & a persuasive argument? 4. How rational is this “defense mechanism?” 5. What place do basic human survival skills have in the information age? 6. How can we present new information so that it doesn’t trigger an emotional defensive reaction? Day 9 Procedures: Hook (Drugs Research Project): 30 minutes o Have the students look at their books & the provided articles to answer the questions about their group’s drug or drug related vocabulary word. Depressants Alcohol Barbiturates Opiates o Morphine o Heroin Stimulants Amphetamines o Cocaine o Ecstasy Methamphetamine: “Speed” Hallucinogens LSD Marijuana/THC Procedure 1 (Present): 10 minutes o Have the groups present their drug or their drug-related vocabulary word. Procedure 2 (Drug Challenge): 10 minutes o Have different account of either a person with a drug problem, a person in rehab, and/or a person who has completed rehab at different stations around the room & the students figure out what drug the person is on & what the symptoms that they are experiencing mean. These should be the student group stories. Have the groups go around and together try to figure out what drug or drug related symptom is happening in the story. Drug Research Project Name: Date: Period: 1. What is the name of the drug/symptom? If applicable, what type of drug is it? 2. What are the different forms of this drug? What ways is this drug ingested? 3. What are the symptoms of having used this drug/what does the drug symptom look like? 4. How addictive is this drug? 5. What long-term effects can this drug have on the body? 6. What are some ways to deal with an addiction to this drug? 7. On a separate sheet of paper, as a group, write a half page story about a person who is using/abusing this type of drug. Or, if applicable, a story about this drug related symptom. The story must not contain the drug’s name or the drug’s symptom name. Alcohol Alcohol affects brain chemistry. In 1997, Americans drank an average of 2 gallons (7.57 liters) of alcohol per person. This translates roughly into one six-pack of beer, two glasses of wine and three or four mixed drinks per week (see MMWR: Apparent Per Capita Ethanol Consumption for details). About 35 percent of adults don't consume alcohol, so the numbers are actually higher for those who do -- alcohol is an amazingly popular social phenomenon. If you have ever seen a person who has had too much to drink, you know that alcohol is a drug that has widespread effects on the body, and the effects vary from person to person. People who drink might be the "life of the party" or they might become sad and droopy. Their speech may slur and they may have trouble walking. It all depends on the amount of alcohol consumed, a person's history with alcohol and a person's personality. Even though you have seen the physical and behavioral changes, you might wonder exactly how alcohol works on the body to produce those effects. What is alcohol? How does the body process it? How does the chemistry of alcohol work on the chemistry of the brain? In this article, we will examine all of the ways in which alcohol affects the human body. What is Alcohol? In order to understand alcohol's effects on the body, it is helpful to understand the nature of alcohol as a chemical, so let's take a look... Here are several facts: Alcohol is a clear liquid at room temperature. Alcohol is less dense and evaporates at a lower temperature than water (this property allows it to be distilled -- by heating a water and alcohol mixture, the alcohol evaporates first). Alcohol dissolves easily in water. Alcohol is flammable (so flammable that it can be used as a fuel). Alcohol can be made by three different methods: Fermentation of fruit or grain mixtures (See How Beer Works for details). This is often followed by distillation of fermented fruit or grain mixtures (Spirits such as whiskey, rum, vodka and gin are distilled.) Chemical modification of fossil fuels such as oil, natural gas or coal (industrial alcohol) Chemical combination of hydrogen with carbon monoxide (methanol or wood alcohol) Ethyl Alcohol The alcohol found in alcoholic beverages is ethyl alcohol (ethanol). The molecular structure of ethanol looks like this: H H3 C - C - O - H H In this structure, C is carbon, H is hydrogen, O is oxygen and the hyphens are the chemical bonds between the atoms. For purposes of clarity, the bonds between the three hydrogen atoms and the left carbon atom are not shown. The OH (O-H) group on the molecule is what gives it the specific chemical properties of an alcohol. For the remainder of this article, when we say "alcohol," we mean ethanol. You will not find pure alcohol in most drinks; drinking pure alcohol can be deadly because it only takes a few ounces of pure alcohol to quickly raise the blood alcohol level into the danger zone. For various types of beverages, the ethanol concentration (by volume) is as follows: Beer = 4 to 6 percent (average of about 4.5 percent) Wine = 7 to 15 percent (average of about 11 percent) Champagne = 8 to 14 percent (average of about 12 percent) Distilled spirits (e.g. rum, gin, vodka, whiskey) = 40 to 95 percent Most of the typical spirits purchased in liquor stores are 40 percent alcohol. Some highly concentrated forms of rum and whisky (75 to 90 percent) can be purchased in liquor stores. Some highly concentrated forms of whiskey (i.e. moonshine) can be made and/or purchased illegally. In most U.S. states, you must be 21 years or older to buy alcoholic beverages, and there are penalties for serving or selling alcoholic beverages to minors. How Alcohol Enters the Body Alcohol Effects: Men vs. Women When you compare men and women of the same height, weight and build, men tend to have moremuscle and less fat than women. Because muscle tissue has more water than fat tissue, a given dose or amount of alcohol will be diluted more in a man than in a woman. Therefore, the blood alcohol concentration resulting from that dose will be higher in a woman than in a man, and the woman will feel the effects of that dose of alcohol sooner than the man will. When a person drinks an alcoholic beverage, about 20 percent of the alcohol is absorbed in the stomach and about 80 percent is absorbed in the small intestine. How fast the alcohol is absorbed depends upon several things: The concentration of alcohol in the beverage - The greater the concentration, the faster the absorption. The type of drink - Carbonated beverages tend to speed up the absorption of alcohol. Whether the stomach is full or empty - Food slows down alcohol absorption. After absorption, the alcohol enters the bloodstream and dissolves in the water of the blood. The blood carries the alcohol throughout the body. The alcohol from the blood then enters and dissolves in the water inside each tissue of the body (except fat tissue, as alcohol cannot dissolve in fat). Once inside the tissues, alcohol exerts its effects on the body. The observed effects depend directly on the blood alcohol concentration (BAC), which is related to the amount of alcohol consumed. The BAC can rise significantly within 20 minutes after having a drink. How Alcohol Leaves the Body Once absorbed by the bloodstream, the alcohol leaves the body in three ways: The kidney eliminates 5 percent of alcohol in the urine. The lungs exhale 5 percent of alcohol, which can be detected by breathalyzer devices. The liver chemically breaks down the remaining alcohol into acetic acid. As a rule of thumb, an average person can eliminate 0.5 oz (15 ml) of alcohol per hour. So, it would take approximately one hour to eliminate the alcohol from a 12 oz (355 ml) can of beer. The BAC increases when the body absorbs alcohol faster than it can eliminate it. So, because the body can only eliminate about one dose of alcohol per hour, drinking several drinks in an hour will increase your BAC much more than having one drink over a period of an hour or more. The Effects of Alcohol If you have seen someone who has had too much to drink, you've probably noticed definite changes in that person's performance and behavior. The body responds to alcohol in stages, which correspond to an increase in BAC: 1. Euphoria (BAC = 0.03 to 0.12 percent) They become more self-confident or daring. Their attention span shortens. They may look flushed. Their judgement is not as good -- they may say the first thought that comes to mind, rather than an appropriate comment for the given situation. They have trouble with fine movements, such as writing or signing their name. 2. Excitement (BAC = 0.09 to 0.25 percent) They become sleepy. They have trouble understanding or remembering things (even recent events). They do not react to situations as quickly (if they spill a drink they may just stare at it). Their body movements are uncoordinated. They begin to lose their balance easily. Their vision becomes blurry. They may have trouble sensing things (hearing, tasting, feeling, etc.). 3. Confusion (BAC = 0.18 to 0.30 percent) They are confused -- might not know where they are or what they are doing. They are dizzy and may stagger. They may be highly emotional -- aggressive, withdrawn or overly affectionate. They cannot see clearly. They are sleepy. They have slurred speech. They have uncoordinated movements (trouble catching an object thrown to them). They may not feel pain as readily as a sober person. 4. Stupor (BAC = 0.25 to 0.4 percent) They can barely move at all. They cannot respond to stimuli. They cannot stand or walk. They may vomit. They may lapse in and out of consciousness. 5. Coma (BAC = 0.35 to 0.50 percent) They are unconscious. Their reflexes are depressed (i.e. their pupils do not respond appropriately to changes in light). They feel cool (lower-than-normal body temperature). Their breathing is slower and more shallow. Their heart rate may slow. They may die. 6. Death (BAC more than 0.50 percent) - The person usually stops breathing and dies. How the Body Responds to Alcohol Alcohol acts primarily on the nerve cells within the brain. Alcohol interferes with communication between nerve cells and all other cells, suppressing the activities of excitatory nerve pathways and increasing the activities of inhibitory nerve pathways. For example, University of Chicago Medical Center: Alcohol and Anesthetic Actions talks about the ability of alcohol (and inhaled anesthetics) to enhance the effects of the neurotransmitter GABA, which is an inhibitory neurotransmitter. Enhancing an inhibitor would have the effect of making things sluggish, which matches the behavior you see in a drunk person. Glutamine is an excitatory neurotransmitter that alcohol weakens. By making this excitatory neurotransmitter less effective, you also get sluggishness. Alcohol does this by interacting with the receptors on the receiving cells in these pathways. Alcohol affects various centers in the brain, both higher and lower order. The centers are not equally affected by the same BAC -- the higher-order centers are more sensitive than the lower-order centers. As the BAC increases, more and more centers of the brain are affected. The order in which alcohol affects the various brain centers is as follows: 1. 2. 3. 4. 5. Cerebral cortex Limbic system Cerebellum Hypothalamus and pituitary gland Medulla (brain stem) Summary of alcohol's effects on the brain. Move your cursor over the colored bar in the lower left-hand corner to see which areas of the brain are affected by increasing BAC. High Times Cerebral Cortex The cerebral cortex is the highest portion of the brain. The cortex processes information from your senses, does your "thought" processing and consciousness (in combination with a structure called the basal ganglia), initiates most voluntary muscle movements and influences lower-order brain centers. In the cortex, alcohol does the following: Depresses the behavioral inhibitory centers - The person becomes more talkative, more self-confident and less socially inhibited. Slows down the processing of information from the senses - The person has trouble seeing, hearing, smelling, touching and tasting; also, the threshold for pain is raised. Inhibits thought processes - The person does not use good judgment or think clearly. These effects get more pronounced as the BAC increases. Limbic System The limbic system consists of areas of the brain called the hippocampus and septal area. The limbic system controls emotions and memory. As alcohol affects this system, the person is subject to exaggerated states of emotion (anger, aggressiveness, withdrawal) and memory loss. Balancing Act Cerebellum The cerebellum coordinates the movement of muscles. The brain impulses that begin muscle movement originate in the motor centers of the cerebral cortex and travel through the medulla and spinal cord to the muscles. As the nerve signals pass through the medulla, they are influenced by nerve impulses from the cerebellum. The cerebellum controls fine movements. For example, you can normally touch your finger to your nose in one smooth motion with your eyes closed; if your cerebellum were not functioning, the motion would be extremely shaky or jerky. As alcohol affects the cerebellum, muscle movements become uncoordinated. In addition to coordinating voluntary muscle movements, the cerebellum also coordinates the fine muscle movements involved in maintaining your balance. So, as alcohol affects the cerebellum, a person loses his or her balance frequently. At this stage, this person might be described as "falling down drunk." The Porter Knows Hypothalamus and Pituitary Gland The hypothalamus is an area of the brain that controls and influences many automatic functions of the brain through actions on the medulla, and coordinates many chemical or endocrine functions (secretions of sex, thyroid and growth hormones) through chemical and nerve impulse actions on the pituitary gland. Alcohol has two noticeable effects on the hypothalamus and pituitary gland, which influence sexual behavior and urinary excretion. Alcohol depresses the nerve centers in the hypothalamus that control sexual arousal and performance. As BAC increases, sexual behavior increases, but sexual performance declines. This observation has been known for a long time, and is referred to by William Shakespeare in "Macbeth" (Act 2 scene 3): Macduff: What three things does drink especially promote? Porter: Marry sir, nose-painting, sleep, and urine. Lechery, sir it provokes, and unprovokes; it provokes the desire, but it takes away the performance... The porter in the above excerpt also notes the effect of alcohol on urine excretion. Alcohol inhibits the pituitary secretion of anti-diuretic hormone (ADH), which acts on thekidney to reabsorb water. Alcohol acts on the hypothalamus/pituitary to reduce the circulating levels of ADH. When ADH levels drop, the kidneys do not reabsorb as much water; consequently, the kidneys produce more urine. Warning ... Danger Ahead Medulla The medulla, or brain stem, controls or influences all of the bodily functions that you do not have to think about, like breathing, heart rate, temperature and consciousness. As alcohol starts to influence upper centers in the medulla, such as the reticular formation, a person will start to feel sleepy and may eventually become unconscious as BAC increases. If the BAC gets high enough to influence the breathing, heart rate and temperature centers, a person will breathe slowly or stop breathing altogether, and both bloodpressure and body temperature will fall. These conditions can be fatal. For more information on the parts of the brain and their functions, see How Your Brain Works. Alcohol's Effects on Other Body Systems In addition to the brain, alcohol can affect other body tissues. It has the following effects on other systems in the body: Irritates the linings of the stomach and intestine - This can lead to vomiting. Increases blood flow to the stomach and intestines - This increases secretions by these organs, most notably stomach acid secretion. Increases blood flow to the skin - This causes a person to sweat and look flushed. The sweating causes body heat to be lost, and the person's body temperature may actually fall below normal. Reduces blood flow to muscles - This can lead to muscle aches, most notably when a person recovers from the alcohol (the "hangover"). All of alcohol's effects continue until the ingested alcohol is eliminated by the body. Alcohol Abuse In the United States, approximately 8 percent of people aged 18 and older suffer from alcohol abuse and/or dependence. This abuse or dependence costs upwards of $1.7 billion in medical treatment, lost earnings, casualty damages and criminal/legal costs. Alcohol abuse has been a rising problem over the past three decades. With the continued exposure to alcohol, how does the human body respond or adapt? The body's increased tolerance to alcohol involves the following changes: Increase in level of liver's enzymes that are used to break down alcohol Increase in activity of brain and nervous-system neurons These bodily adaptations change a person's behavior. The levels of alcohol dehydrogenase and aldehyde dehydrogenase in the liver increase in response to long-term alcohol exposure. This means that the body becomes more efficient at eliminating the high levels of alcohol in the blood. However, it also means that the person must drink more alcohol to experience the same effects as before, which leads to more drinking and contributes to addiction. The normal chemical and electrical functions of nerve cells increase to compensate for the inhibitory effects of alcohol exposure. This increased nerve activity helps people to function normally with higher BAC; however, it also makes them irritable when they are not drinking. Furthermore, the increased nerve activity may make them crave alcohol. Most certainly, the increased nerve activity contributes to hallucinations and convulsions (e.g. delirium tremens) when alcohol is withdrawn, and makes it difficult to overcome alcohol abuse and dependence. Long-term Effects In addition to the adaptations mentioned on the previous page, there are many adverse physical effects that result from long-term exposure to alcohol: The increased activity in the liver causes cell death and hardening of the tissue (cirrhosis of the liver). The brain cells in various centers die, thereby reducing the total brain mass. Stomach and intestinal ulcers can form because the constant alcohol use irritates and degrades the linings of these organs. Blood pressure increases as the heart compensates for the initially reduced blood pressure caused by alcohol. Male sex-cell (sperm) production decreases because of decreased sex-hormone secretion from the hypothalamus/pituitary and, possibly, direct effects of alcohol on the testes. Poor nutrition decreases levels of iron and vitamin B, leading to anemia. Because alcoholics lose balance and fall more often, they suffer more often from bruises and broken bones; this is especially true as they get older. Finally, alcohol abuse and dependence cause emotional and social problems. Because alcohol affects emotional centers in the limbic system, alcoholics can become anxious, depressed and even suicidal. The emotional and physical effects of alcohol can contribute to marital and family problems, including domestic violence, as well as work-related problems, such as excessive absences and poor performance. While alcoholism has devastating effects on a person's health and social environment, there are medical and psychological ways to treat the problem. See the next page to learn more. For more information on alcohol, treating alcoholism, and related topics, check out the links on the next page. Lots More Information Barbiturate Definition Barbiturates are a type of depressant drug that causes relaxation and sleepiness. In relatively low doses, barbiturates and alcohol have very similar clinical syndromes of intoxication. However, excessive and prolonged dosages of barbiturate drugs, such as phenobarbital, may produce the following chronic symptoms: memory loss, irritability, changes in alertness, and decreased interpersonal functioning. Barbiturates may also cause an acute overdose syndrome, which is lifethreatening. Alternative Names Intoxication - barbiturates Causes, incidence, and risk factors Barbiturate abuse is still a major addiction problem in the population, although it has been partly replaced by addiction to other depressant drugs more commonly prescribed, such as benzodiazepines. Though most people who take these medications for seizure disorders or pain syndromes do not abuse them, many abusers start by abusing medication prescribed for them or for other family members. Symptoms Symptoms of acute barbiturate intoxication include: Sluggishness Incoordination Difficulty in thinking Slowness of speech Faulty judgment Drowsiness or coma Shallow breathing Staggering Signs and tests Physical exam and clinical history are usually sufficient to make the diagnosis. Drug screens, both urine and serum, can detect barbiturates for up to 5 days after ingestion. Additional blood tests may show the severity of breathing difficulty. Treatment Most overdoses of depressant medications are mixtures of drugs, commonly alcohol and barbiturates or benzodiazepines, or barbiturates and opiates (heroin or Oxycontin). Some users use a combination of all 4 drugs. Those who take such combinations tend to be either new users who don't know that such combinations are a recipe for coma or death, or experienced users who want to entirely blot out consciousness. This second group is among the most difficult to treat. Because mixtures are the most common cause of death, an opiate-blocking drug called naloxone (Narcan) is often used to treat overdose when an opiate was part of the mix. If opiates are involved, naloxone will often rapidly restore consciousness and breathing. There is no direct antidote to barbiturates or alcohol overdose. In such overdoses, respiration must be maintained by artificial means until the drugs are removed from the body. Some drugs may help speed the removal of barbiturate. Expectations (prognosis) For barbiturate overdose or mixture overdose, the death rate is about 10%, and can be higher if proper treatment is not readily given. With current life support measures, including decontamination, supportive care, and helping the body eliminate the drugs, mortality may be less than 2 percent. Complications Barbiturates may cause prolonged coma and may damage fetuses of pregnant women. Calling your health care provider Call 911 immediately if someone has taken barbiturates and seems lethargic or has slowed breathing, or if someone has taken barbiturates with alcohol, opiates, or benzodiazepine drugs. These drugs together cause greater effects than each alone. More than half of all overdose deaths result from drug mixtures. Prevention Do not take barbiturates, except as prescribed. Do not exceed the prescribed dose. Never mix barbiturates with heroin (or other opiates), valium, benzodiazepines, or alcohol of any kind. Barbiturates Barbiturates were first introduced for medical use in the early 1900s. More than 2,500 barbiturates have been synthesized, and at the height of their popularity, about 50 were marketed for human use. Today, about a dozen are in medical use. Barbiturates produce a wide spectrum of central nervous system depression, from mild sedation to coma, and have been used as sedatives, hypnotics, anesthetics, and anticonvulsants. The primary differences among many of these products are how fast they produce an effect and how long those effects last. Barbiturates are classified as ultrashort, short, intermediate, and long-acting. The ultrashort-acting barbiturates produce anesthesia within about one minute after intravenous administration. Those in current medical use are the Schedule IV drug methohexital (Brevital®), and the Schedule III drugs thiamyl (Surital®) and thiopental (Pentothal®). Barbiturate abusers prefer the Schedule II short-acting and intermediate-acting barbiturates that include amobarbital (Amyta®), pentobarbital (Nembutal®), secobarbital (Seconal®), and Tuinal (an amobarbital/secobarbital combination product). Other short and intermediate-acting barbiturates are in Schedule III and include butalbital (Fiorina®), butabarbital (Butisol®), talbutal (Lotusate®), and aprobarbital (Alurate®). After oral administration, the onset of action is from 15 to 40 minutes, and the effects last up to six hours. These drugs are primarily used for insomnia and preoperative sedation. Veterinarians use pentobarbital for anesthesia and euthanasia. Long-acting barbiturates include phenobarbital (Luminal®) and mephobarbital (Mebaral®), both of which are in Schedule IV. Effects of these drugs are realized in about one hour and last for about 12 hours, and are used primarily for daytime sedation and the treatment of seizure disorders. History Barbituric acid was first synthesized December 6, 1864, by German researcher Adolf von Baeyer. This was done by condensing urea (an animal waste product) with diethyl malonate (an ester derived from the acid of apples). There are several stories about how the substance got its name. The most likely story is that Von Baeyer and his colleagues went to celebrate their discovery in a tavern where the town's artillery garrison were also celebrating the feast of Saint Barbara — the patron saint of artillerists. An artillery officer is said to have christened the new substance by amalgamatingBarbara with urea.[1] No substance of medical value was discovered, however, until 1903 when two German scientists working at Bayer, Emil Fischer and Joseph von Mering, discovered that barbital was very effective in putting dogs to sleep. Barbital was then marketed by Bayer under the trade name Veronal. It is said that Von Mering proposed this name because the most peaceful place he knew was the Italian city of Verona.[1] It was not until the 1950s that the behavioural disturbances and physical dependence potential of barbiturates became recognized.[2] While barbituric acid itself does not have any direct effect on the central nervous system, chemists have derived over 2,500 compounds from it that possess pharmacologically active qualities. The broad class of barbiturates is further broken down and classified according to speed of onset and duration of action. Ultrashort-acting barbiturates are commonly used for anesthesia because their extremely short duration of action allows for greater control. These properties allow doctors to rapidly put a patient "under" in emergency surgery situations. Doctors can also bring a patient out of anesthesia just as quickly, should complications arise during surgery. The middle two classes of barbiturates are often combined under the title "short/intermediate-acting." These barbiturates are also employed for anesthetic purposes, and are also sometimes prescribed for anxiety or insomnia. This is not a common practice anymore, however, owing to the dangers of long-term use of barbiturates; they have been replaced by the benzodiazepines for these purposes. The final class of barbiturates are known as long-acting barbiturates (the most notable one being phenobarbital, which has a half-life of roughly 92 hours). This class of barbiturates is used almost exclusively as anticonvulsants, although on rare occasions they are prescribed for daytime sedation. Barbiturates in this class are not used for insomnia, because, owing to their extremely long halflife, patients would awake with a residual "hang-over" effect and feel groggy. Barbiturates can in most cases be used either as the free acid or as salts of sodium, calcium, potassium, magnesium, lithium, etc. Codeine- and Dionine-based salts of barbituric acid have been developed. In 1912, Bayer introduced another barbituric acid derivative, phenobarbital, under the trade name Luminal, as a sedative-hypnotic.[3] [edit]Therapeutic uses Barbiturates like pentobarbital and phenobarbital were long used as anxiolytics and hypnotics. Today, benzodiazepines have largely supplanted them for these purposes, because benzodiazepines have less potential for lethal overdoses.[4][5][6] Barbiturates are classified as ultrashort-, short-, intermediate-, and long-acting, depending on how quickly they act and how long their effects last.[7] Barbiturates are still widely used in surgical anesthesia, especially to induce anesthesia, though their use during induction of anesthesia has largely been supplanted. Ultrashort barbiturates such as thiopental (Pentothal) produce unconsciousness within about a minute of intravenous (IV) injection. These drugs may be used to induce general anesthesia. Volatile anesthetics are then used to maintain general anesthesia until the end of the operation. Because thiopental and other ultrashort-acting barbiturates are typically used in hospital settings, they are not very likely to be abused, noted the DEA.[8] Phenobarbital is used as an anticonvulsant for people suffering from seizure disorders such as febrile seizures, tonic-clonic seizures, status epilepticus, and eclampsia.[9] Long-acting barbiturates such as phenobarbital (Luminal) and mephobarbital (Mebaral) are prescribed for few reasons. When taken at bedtime, they help treat insomnia, and when taken during the day they have sedative effects that can aid in the treatment of tension and anxiety. However, prescription for the treatment of these conditions is now rare due to the risks of physical dependence and fatal overdose. These drugs are more often prescribed in the treatment of convulsive conditions like epilepsy. Phenobarbital has also been used in the treatment of delirium tremens duringalcohol detoxification, although benzodiazepines have a more favorable safety profile and are more often used.[10] Long-acting barbiturates take effect within one to two hours and last 12 hours or longer.[8] [edit]Other uses related to their physiological properties Barbiturates in high doses are used for physician-assisted suicide (PAS), and in combination with a muscle relaxant for euthanasia and for capital punishment by lethal injection.[11][12] Thiopental, an ultra-short acting barbiturate that is marketed under the name Sodium Pentothal, is sometimes used as a "truth serum". When dissolved in water, it can be swallowed or administered by intravenous injection. The drug does not itself force people to tell the truth, but is thought to decrease inhibitions, making subjects more likely to be caught off guard when questioned.[13] [edit]Mechanism of action The principal mechanism of action of barbiturates is believed to be their affinity for the GABAA receptor (Acts on GABA : BDZ receptor Cl- channel complex). GABA is the principal inhibitory neurotransmitter in the mammalian central nervous system (CNS). Barbiturates bind to the GABAAreceptor at the alpha subunit, which are binding sites distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. In addition to this GABAergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Taken together, the findings that barbiturates potentiate inhibitory GABAA receptors and inhibit excitatory AMPA receptors can explain the CNS-depressant effects of these agents. At higher concentration, they inhibit the Ca2+-dependent release of neurotransmitters.[9] Barbiturates produce their pharmacological effects by increasing the duration of chloride ion channel opening at the GABAA receptor (pharmacodynamics: This increases the efficacy of GABA), whereas benzodiazepines increase the frequency of the chloride ion channel opening at the GABAA receptor (pharmacodynamics: This increases the potency of GABA). The direct gating or opening of the chloride ion channel is the reason for the increased toxicity of barbiturates compared tobenzodiazepines in overdose.[14][15] Further, barbiturates are relatively non-selective compounds that bind to an entire superfamily of ligandgated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. However, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.[16] Such findings implicate (non-GABAergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.[17] [edit]Tolerance, dependence, overdose, and adverse reaction Older adults and pregnant women should consider the risks associated with barbiturate use. When a person ages, the body becomes less able to rid itself of barbiturates. As a result, people over the age of sixty-five are at higher risk of experiencing the harmful effects of barbiturates, including drug dependence and accidental overdose.[18] When barbiturates are taken during pregnancy, the drug passes through the mother's bloodstream to her fetus. After the baby is born, it may experience withdrawal symptoms and have trouble breathing. In addition, nursing mothers who take barbiturates may transmit the drug to their babies through breast milk.[19] [edit]Tolerance and dependence Main article: Barbiturate dependence With regular use, tolerance to the effects of barbiturates develops. [edit]Overdose Main article: Barbiturate overdose [edit]Adverse Reaction A rare adverse reaction to barbiturates is Stevens–Johnson syndrome, which primarily affects the mucous membranes. [edit]Recreational use Like ethanol, barbiturates are intoxicating and produce similar effects during intoxication. The symptoms of barbiturate intoxication include respiratory depression, lowered blood pressure, fatigue, fever, unusual excitement, irritability, dizziness, poor concentration, sedation, confusion, impaired coordination, impaired judgment, addiction, and respiratory arrest, which may lead to death.[20] Recreational users report that a barbiturate high gives them feelings of relaxed contentment and euphoria. The main risk of acute barbiturate abuse is respiratory depression. Physical and psychological dependence may also develop with repeated use.[21] Other effects of barbiturate intoxicationinclude drowsiness, lateral and vertical nystagmus, slurred speech and ataxia, decreased anxiety, a loss of inhibitions. Barbiturates are also used to alleviate the adverse or withdrawal effects of illicit drug misuse.[22][23] Drug users tend to prefer short-acting and intermediate-acting barbiturates.[24] The most commonly abused are amobarbital (Amytal), pentobarbital (Nembutal), and secobarbital (Seconal). A combination of amobarbital and secobarbital (called Tuinal) is also highly abused. Short-acting and intermediate-acting barbiturates are usually prescribed as sedatives and sleeping pills. These pills begin acting fifteen to forty minutes after they are swallowed, and their effects last from five to six hours. Veterinarians use pentobarbital to anesthetise animals before surgery; in large doses, it can be used to euthanise animals.[8] Slang terms for barbiturates include barbs, bluebirds, blues, dolls, downers, goofballs, and tooties .[25] [edit]Legal status In the 1940s, military personnel were given "Goofballs" during WWII in the South Pacific region to allow soldiers to tolerate the heat and humidity of daily working conditions. Goofballs were distributed to lower the respiratory system and blood pressure to combat the extreme conditions. Many soldiers returned with addictions that caused several months of rehabilitation before being discharged. This led to addiction problems through the 1950s and 1960s. In the 1950s and 1960s, increasing reports began to be published about barbiturate overdoses and dependence problems, which eventually led to the scheduling of barbiturates as controlled drugs. In 1970, several barbiturates were designated in the United States as controlled substances with the passage of the American Controlled Substances Act of 1970. Pentobarbital, secobarbital and amobarbital were designated schedule II drugs, butabarbital schedule III, and barbital and phenobarbital schedule IV. In 1971, the Convention on Psychotropic Substances was signed in Vienna. Designed to regulate amphetamines, barbiturates, and other synthetics, the treaty today regulates secobarbital, amobarbital, butalbital, cyclobarbital, and pentobarbital as schedule III, and allobarbital,methylphenobarbital, phenobarbital, and vinylbital as schedule IV scheduled substances. [edit]Other uses in chemistry In 1988, the synthesis and binding studies of an artificial receptor binding barbiturates by 6 complementary hydrogen bonds was published.[26] Since this first article, different kind of receptors were designed, as well as different barbiturates and cyanurates, not for their efficiencies as drugs but for applications in supramolecular chemistry, in the conception of materials and molecular devices. [edit] Opiates Definition Opiate withdrawal is caused by stopping, or dramatically reducing, opiate use after heavy and prolonged use (several weeks or more). Opiates include heroin, morphine, codeine, Oxycontin, Dilaudid, methadone, and others. Alternative Names Withdrawal from opioids; Dopesickness Causes, incidence, and risk factors About 9% of the population is believed to misuse opiates over the course of their lifetime, including illegal drugs like heroin and prescribed pain medications such as Oxycontin. These drugs can cause physical dependence. This means that a person relies on the drug to prevent symptoms of withdrawal. Over time, greater amounts of the drug become necessary to produce the same effect. The time it takes to become physically dependent varies with each individual. When the drugs are stopped, the body needs time to recover, and withdrawal symptoms result. Withdrawal from opiates can occur whenever any chronic use is discontinued or reduced. Some people even withdraw from opiates after hospitalization for painful conditions without realizing what is happening to them. They think they have the flu, and because they don't know that opiates would fix the problem, they don't crave the drugs. Symptoms Symptoms of withdrawal include: Dilated pupils Diarrhea Runny nose Goose bumps Abdominal pain. Sweating Agitation Nausea Vomiting Signs and tests A physical exam and clinical history are often sufficient to diagnose opiate withdrawal. A urine or serum drug screen can verify the existence of opiates and any other drugs of abuse. Treatment Treatment of withdrawal includes supportive care and medications. The most commonly used medication, clonidine, primarily reduces physical symptoms. Another detox method is to use a slowly tapered (reduced overtime) dose of methadone to reduce the intensity of withdrawal symptoms. Methadone maintenance involves ongoing use of methadone. A new medication called buprenorphine has been shown to be more effective than other medications for treating withdrawal from opiates, and can shorten the length of detox. It may also be used for long-term maintenance like methadone. Some drug treatment programs have widely advertised treatments for opiate withdrawal called detox under anesthesia or rapid opiate detox. This involves anesthetizing the patient and injecting large doses of opiate-blocking drugs, with hopes that this will speed up the transition to normal opioid system function. There is no evidence that these programs actually reduce the time spent suffering withdrawal. In some cases, they may reduce the intensity of symptoms. However, there have been several deaths associated with the procedure, particularly when it is performed outside a hospital. Because opiate withdrawal produces vomiting, and vomiting during anesthesia significantly increases death risk, many specialists think the risks of this procedure significantly outweigh the potential (and unproven) benefits. Support Groups Support groups, such as Narcotics Anonymous and SMART Recovery can be enormously helpful to people suffering opiate addiction. Expectations (prognosis) Withdrawal from opiates is painful, but not life-threatening. Complications The biggest complication is return to drug use. Most opiate overdose deaths occur in people who have just withdrawn or detoxed. Because withdrawal reduces a previously-developed tolerance, recently withdrawn addicts can overdose on a much smaller dose than they used to take daily. Addicts should be warned about this possibility. Longer term treatment is recommended for most addicts following withdrawal. This can include self-help groups, like Narcotics Anonymous or SMART Recovery, outpatient counseling, intensive outpatient treatment (day hospitalization), or in-patient treatment. Addicts withdrawing from opiates should be assessed for depression and other mental illnesses. Appropriate treatment of such disorders can reduce the risk of relapse. Antidepressant medications should NOT be withheld under the assumption that the depression is only related to withdrawal, and not a pre-existing condition. Treatment goals should be discussed with the patient and recommendations for care made accordingly. If an opiate addict has withdrawn repeatedly only to relapse repeatedly, methadone maintenance is strongly recommended. Heroin What are the street names/slang terms? Big H, Blacktar, Brown sugar, Dope, Horse, Junk, Muc, Skag, Smac What is Heroin? Heroin is a highly addictive drug derived from morphine, which is obtained from the opium poppy. It is a “downer” or depressant that affects the brain’s pleasure systems and interferes with the brain’s ability to perceive pain. What does it look like? White to dark brown powder or tar-like substance. How is it used? Heroin can be used in a variety of ways, depending on user preference and the purity of the drug. Heroin can be injected into a vein (“mainlining”), injected into a muscle, smoked in a water pipe or standard pipe, mixed in a marijuana joint or regular cigarette, inhaled as smoke through a straw, known as “chasing the dragon,” snorted as powder via the nose. What are its short-term effects? The short-term effects of heroin abuse appear soon after a single dose and disappear in a few hours. After an injection of eroin, the user reports feeling a surge of euphoria (“rush”) accompanied by a warm flushing of the skin, a dry mouth, and heavy extremities. Following this initial euphoria, the user goes “on the nod,” an alternately wakeful and drowsy state. Mental functioning becomes clouded due to the depression of the central nervous system. Other effects included slowed and slurred speech, slow gait, constricted pupils, droopy eyelids, impaired night vision, vomiting, constipation. What are its long-term effects? Long-term effects of heroin appear after repeated use for some period of time. Chronic users may develop collapsed veins, infection of the heart lining and valves, abscesses, cellulites, and liver disease. Pulmonary complications, including various types of pneumonia, may result from the poor health condition of the abuser, as well as from heroin’s depressing effects on respiration. In addition to the effects of the drug itself, street heroin may have additives that do not really dissolve and result in clogging the blood vessels that lead to the lungs, liver, kidneys, or brain. This can cause infection or even death of small patches of cells in vital organs. With regular heroin use, tolerance develops. This means the abuser must use more heroin to achieve the same intensity or effect. As higher doses are used over time, physical dependence and addiction develop. With physical dependence, the body has adapted to the presence of the drug and withdrawal symptoms may occur if use is reduced or stopped. Withdrawal, which in regular abusers may occur as early as a few hours after the last administration, produces drug craving, restlessness, muscle and bone pain, insomnia, diarrhea and vomiting, cold flashes with goose bumps (“cold turkey”), kicking movements (“kicking the habit”), and other symptoms. Major withdrawal symptoms peak between 48 and 72 hours after the last does and subside after about a week. Sudden withdrawal by heavily dependent users who are in poor health can be fatal. Morphine What are the street names/slang terms? Duramorph, M, Miss Emma, Monkey, Roxanol, White Stuff What is Morphine? Morphine is an opiate, derived from the poppy plant. It is classified as a narcotic and is commonly prescribed to manage pain. What does it look like? Morphine is commonly available in the form of a tablet, syrup, injection or as a suppository. Depending on its form, morphine may be injected, swallowed, or even smoked. How is it used? Morphine is often used before or after surgery to alleviate severe pain. Morphine and other opioids act by attaching to specific proteins called opioid receptors, which are found in the brain, spinal cord, and gastrointestinal tract. When these compounds attach to certain opioid receptors in the brain and spinal cord, they can effectively change the way a person experiences pain. What are its short-term effects? Morphine affects regions of the brain that mediate what we perceive as pleasure, resulting in initial feelings of euphoria. Morphine can also produce drowsiness, cause constipation, and, depending upon the amount taken, depress breathing. Taking a large single dose could cause severe respiratory depression, coma or death. What are its long-term effects? Long-term use of morphine also can lead to physical dependence. This can also include tolerance and addiction. Individuals taking prescribed opioid medications should be given these medications under appropriate medical supervision and should be supervised when discontinuing use to mitigate withdrawal symptoms. OxyContin What is OxyContin? OxyContin is the brand name for oxycodone hydrochloride, an opioid (narcotic) analgesic (pain reliever).OxyContin is a controlled-release oral formulation of oxycodone hydrochloride. It is available by prescription only and is used to treat moderate to severe pain when around-the-clock pain relief is needed for an extended period of time. It works by changing the way the brain and nervous system respond to pain. What does it look like? OxyContin is available in tablet form in 8 doses: 10 mg 15 mg 20 mg 30 mg 40 mg 60 mg* 80 mg* 160 mg*. How is it used? As pain medication, OxyContin is taken every 12 hours because the tablets contain a controlled, timerelease formulation of the medication. Most pain medications must be taken every three to six hours. OxyContin abusers remove the sustained-release coating to get a rapid release of the medication, causing a rush of euphoria similar to heroin. What are its short-term effects? The most serious risk associated with opioids, including OxyContin, is respiratory depression — slowed breathing. Common opioid side effects are constipation, nausea, sedation, dizziness, vomiting, headache, dry mouth, sweating, mood changes, flushing, loss of appetite, and weakness. Taking a large single dose of an opioid could cause severe respiratory depression — slowed or difficulty breathing that can lead to death. What are its long-term effects? Chronic use of opioids can result in tolerance for the drugs, which means that users must take higher doses to achieve the same initial effects. Long-term use also can lead to physical dependence and addiction — the body adapts to the presence of the drug, and withdrawal symptoms occur if use is reduced or stopped. Taken exactly as prescribed, opioids can be used to manage pain effectively. Cocaine Introduction to How Crack Cocaine Works In the 1980s, a new drug emerged. Because of its cheap cost and quick and intense high, crack cocaine quickly gained popularity among users, especially in poor urban areas. Within two decades, the crack had exacted a heavy toll, leaving serious physical and emotional side effects not only on its users, but on entire communities and on the United States as a whole. In this article, we'll explain how crack is made, what effects it has on the body and how law enforcement and health officials are working to stem its spread. What is Cocaine? Crack is made from cocaine -- a powdered drug that is derived from Photo courtesy U.S. DEA the leaves of the coca plant, which grows primarily in South Coca plant America. Although cocaine didn't gain notoriety in the United States until the 1980s, it has been in use for centuries. Many generations of South American Indians have chewed its leaves to give them strength and energy. Cocaine was first isolated from coca leaves in the mid-1800s. Back then, it was used for medicinal purposes in drinks -- and yes, the legend is true: Coca-Cola did once contain cocaine. By the late 1800s, cocaine was also being used as an anesthetic and to prevent excess bleeding during surgery. By the following century, people began to realize that cocaine was an addictive narcotic, and non-medical use of the drug was made illegal with the passage of the Harrison Narcotics Tax Act in 1914. The chemical formula of cocaine is C17H21NO4. See IPCS: Cocaine for a look at its chemical structure. Cocaine as a drug is taken in one of three ways: It is snorted, injected or smoked. The snorted form, cocaine powder, is made by dissolving coca paste from the coca leaves in a mixture of hydrochloric acid and water. Potassium salt is added to the mixture to separate out undesired substances to be removed. Ammonia is then added to the remaining solution, and the solid powder cocaine separates out. To inject cocaine, the user mixes the powder with a small amount of water and uses a hypodermic needle to force the solution directly into a vein. Cocaine powder forms the base of freebase cocaine. Freebase cocaine has a low melting point, so it can be smoked. It is made by dissolving powder cocaine in water and a strong alkaloid solution such as ammonia. Then, a highly flammable solvent like ether is added, and a solid cocaine base separates out from the solution. Crack cocaine is an easier-to-manufacture form of freebase cocaine. Manufacturing Crack Cocaine Why "crack"? The word "crack" comes from the cracking sound the rock crystal makes when it is heated in a crack pipe. The sound is caused by the sodium bicarbonate Crack cocaine is also made from powder cocaine, but because its production doesn't require the use of flammable solvents, it is safer to make than freebase cocaine. To make crack, powder cocaine is dissolved in a mixture of water and either ammonia or sodium bicarbonate (baking soda). The mixture is boiled to separate out the solid, and then it's cooled. The solid is then dried and cut up into small nuggets, or "rocks." Crack rocks are white or tan in color and typically range in size from .1 to .5 grams. According to the U.S. Drug Enforcement Agency (DEA), crack rocks contain between 75 percent and 90 percent pure cocaine. Most of the cocaine that comes into the United States today originates in Colombia, Bolivia and Peru. Cocaine is usually smuggled into the United States across the Mexican border. It arrives in the country in powder form and is converted to crack by the wholesaler or retailer (gangs make up most of the retail market in the United States). Crack in the Body Most users smoke crack, although in rare cases, they may inject it. To smoke crack cocaine, the user places the drug into a small glass pipe (sometimes called a "straight shooter"). He or she then places a small piece of a steel wool at one end of the pipe tube and puts the rock on the other side of this filter. When the rock is heated from below, it produces a vapor, or smoke. The user inhales that vapor into his or her lungs. From there, the drug is taken up by the person's bloodstream. When it gets into the body, crack acts upon a part of the brain called the ventral tegmental area (VTA). It interferes with a chemical messenger in the brain called dopamine, which is involved in the body's pleasure response. Dopamine is released by cells of the nervous system during pleasurable activities such as eating or having sex. Once released, dopamine travels across a gap between nerve cells, called a synapse, and binds to a receptor on a neighboring nerve cell (also called a neuron). This sends a signal to that nerve cell, which produces a good feeling. Under normal conditions, once the dopamine sends that signal it is reabsorbed by the neuron that released it. This reabsorption happens with the help of a protein called the dopamine transporter. Crack interrupts this cycle. It attaches to the dopamine transporter, preventing the normal reabsorption process. As dopamine builds up in the synapse, it continues to stimulate the receptor, creating a lingering feeling of exhilaration or euphoria in the user. Because crack is inhaled as a smoke, it reaches the brain much faster than inhaled powder cocaine. It can get to the brain and create a high within 10 to 15 seconds, compared to the 10 to 15 minutes it takes to feel the effects of snorted cocaine. The crack cocaine high can last anywhere from five to 15 minutes. Side Effects of Crack Use While crack is creating a feeling of exhilaration in the user, it is also leaving a number of significant and potentially dangerous effects on the body. People who take it even a few times are at increased risk for heart attack, stroke, respiratory problems and severe mental disorders. As crack moves through the bloodstream, it first leaves the user feeling energized, more alert and more sensitive to sight, sound and touch. Heart rate increases, pupils dilate and blood pressure and temperature rise. The user may then start to feel restless, anxious and/or irritable. In large amounts, crack can make a person extremely aggressive, paranoid and/or delusional. Because of its effects on the heart rate and breathing, crack can cause a heart attack, respiratory failure, strokes or seizures. It can also affect the digestive tract, causing nausea, abdominal pain and loss of appetite. Alcohol and crack taken together can be deadly. If crack is taken with alcohol, the two substances can combine in the liver to produce a chemical called cocaethylene. This is a toxic and potentially fatal substance that produces a more intense high than crack alone but also raises heart rate and blood pressure more than crack alone, leading to its potentially deadly results. In the mid-1980s, when crack was a burgeoning public health issue, a related problem emerged: the phenomenon of the so-called "crack baby." In 1985, Dr. Ira Chasnoff wrote an article in the New England Journal of Medicine claiming that babies who were exposed to crack in the womb wound up with permanent cognitive impairment. Soon, images of "crack babies" were everywhere in the media. They became symbolic of the war against drugs. Since then, many researchers have challenged the idea of the crack baby. A 2004 study by the Society for Research in Child Developmentfound that prenatal cocaine exposure did not affect a child's development by age two, and it suggested that the harmful effects previously found in cocaine-exposed babies may actually have had more to do with post-natal care than with exposure to the drug in the womb. But despite the recent findings, doctors agree that crack is absolutely unsafe to take during pregnancy. Babies who are exposed to crack in the uterus are often born prematurely and tend to be smaller than other babies. Crack exposure can also contribute to developmental and cognitive delays. How Do People Get Addicted to Crack? Cocaine is a highly addictive substance. People who take it can become physically and psychologically dependant upon it to the point where they can't control their cravings. Researchers have found that cocaine-addicted monkeys will press a bar more than 12,000 times to get a single dose of it. As soon as they get it, they will start pressing the bar for more. Crack and other addictive drugs chemically alter a part of the brain called the reward system. As mentioned previously, when people smoke crack, the drug traps the chemical dopamine in the spaces between nerve cells. Dopaminecreates the feelings of pleasure we get from enjoyable activities such as eating and having sex. But in crack users, dopamine keeps stimulating those cells, creating a "high" -- a euphoric feeling that lasts anywhere from five to 15 minutes. But then the drug begins to wear off, leaving the person feeling let-down and depressed, resulting in a desire to smoke more crack in order to feel good again. The brain responds to the dopamine overload of the crack high by either destroying some of it, making less of it or shutting down its receptors. The result is that, after taking the drug for a while, crack users become less sensitive to it and find that they must take more and more of it to achieve the desired effect. Eventually, they cannot stop taking the drug because their brains have been "rewired" -- they actually need it in order to function. How long does it take to become addicted? That varies from person to person, and an exact number is difficult to pin down, especially when physical addiction is paired with psychological addition. Of course, not everyone reacts the same way to extended use. Some users actually become more sensitive to crack as they take it. Some people die after taking a very small amount because of this increased sensitization. When an addicted person stops taking crack, there is a "crash." He or she experiences the symptoms of withdrawal, including: Depression Anxiety Intense cravings for the drug Irritability Agitation Exhaustion Anger In the next section, we'll discuss just how widespread this particular addiction is. A Culture of Addicts? Street Terms for Crack Basa, french fries, real tops, base, glo, rock(s), black rock, hard rock, roxanne, CDs, hotcakes, twinkie, candy sugar, jelly beans, yam, electric kool-aid, nuggets In the mid-1980s, crack use exploded in the United States, primarily because of its quick high and relatively low cost: Crack cocaine costs significantly less than its powdered counterpart. The low cost of crack helps explain its rampant spread through poor, urban areas. The highest numbers of crack users are African-American men between the ages of 18 and 30 who come from low socioeconomic backgrounds. Crack has touched almost 4 percent of the American population. Nearly 8 million Americans ages 12 and older say they have taken crack at some point in their lives, according to the 2003 National Survey on Drug Use and Health(NSDUH). According to the same survey, the number of users currently taking crack in 2002 was about 567,000. Crack is not just a problem among adults. A 2003 Monitoring the Future Study by the University of Michigan found that nearly 4 percent of high school seniors and 2.5 percent of junior high school students said they had tried crack at least once. Crack addiction is taking a toll on America's health. In 2002, emergency rooms reported more than 42,000 crack-related cases to the Drug Abuse Warning Network. That number was down from nearly 49,000 in 2001, but up from the approximately 34,000 cases reported in 1995. America is not the only country dealing with crack addiction. Cocaine use has been on the rise in Europe over the last several years, although the biggest problem in most countries (with the exception of the United Kingdom and the Netherlands) is the powder form of the drug. The United Kingdom reports the highest crack use in Europe. Crack is associated with more prostitution, violent crimes and gang-related crimes than any other drug. In the next sections, we'll find out how the government is working to address the problem. Addressing the Problem: Imprisonment Crack, like most other recreational drugs besides alcohol, is illegal. The Harrison Narcotics Tax Act of 1914 banned the non-medical use of cocaine and prohibited its importation into the United States. With the Controlled Substances Act of 1970, the U.S. Congress classified cocaine as a Schedule II substance, meaning that it is considered a highly addictive drug. The classification stipulated that cocaine could only be used legally as an anesthetic for certain surgeries, and it is still used in this manner today. Penalties for using and dealing cocaine are stringent. In 2002, the Drug Enforcement Administration (DEA) arrested 4,400 people for crimes related to crack cocaine. Crack accounted for 15 percent of the DEA's arrests that year. Nearly 83 percent of those arrested were AfricanAmerican; 9 percent were Hispanic; and 7 percent were Caucasian. Penalties and prison terms for crack users and sellers are harsher than for most other drugs. Crackrelated prison terms are an average of nine-and-a-half years longer than other drug sentences. A dealer who sells 5 grams of crack can land in jail for up to 20 years. Selling 50 or more grams can result in a life sentence. While local law enforcement officials try to round up crack users and sellers, the government is working to stop cocaine from getting into the country. In 2002, U.S. Customs officials seized more than 171,000 pounds (about 77,560 kg) of cocaine as smugglers attempted to move it across the border. Addressing the Problem: Treatment Crack is a highly addictive drug, but there are treatments for people who use it regularly. There are two main types of treatments: medication and cognitive or behavioral therapy. As of November 2004, no medication exists to treat crack addicts, but the National Institute on Drug Abuse (NIDA) is researching several promising options. The drug Selegiline, used to treat Parkinson's disease, is under investigation for its ability to reduce dopamine metabolism. Disulfiram, which has been used to treat alcoholism, is another candidate. The drug creates a negative physical reaction (nausea, vomiting, etc.) whenever the addicted person ingests alcohol. Researchers are hoping that it might help people who are addicted to both cocaine and alcohol. Antidepressants are sometimes prescribed to treat the mood swings associated with the withdrawal process. Behavioral therapies are currently the most common way to treat crack addiction. Patients may be treated at either inpatient or outpatient centers. In 2002, 176,000 people were admitted to treatment centers for addiction to smoked cocaine, according to the Treatment Episode Data Set produced by the Substance Abuse and Mental Health Services Administration (SAMHSA). Crack admissions represented just under 10 percent of all admissions into drug- and alcohol-related treatment centers in 2002. One of the most popular behavioral therapies is contingency management, which rewards addicts for staying drug-free by giving them vouchers for everything from movies to gym memberships. Another approach is cognitive-behavioral therapy, which teaches people how to avoid and/or deal with situations in which they might be tempted to use crack. People with severe addictions, mental illness or a criminal record may need to stay at a therapeutic community for a six- to 12-month period while they undergo rehabilitation and learn how to reenter society drug-free. To learn more about crack cocaine, other drugs, treatment methods and related topics, check out the links on the next page. Meth Around the world, 26 million people know this as their pick-me-up friend, meth. Humans have enjoyed stimulants probably since the beginning of human awareness of stimulants. From the distant past to the immediate present, cultures all over the world have sought out a pick-me-up. The ancient Chinese got their kick from má huáng, a tea brewed from an ephedra-producing shrub. South Americans have long ingested yerba mate from small gourds to keep themselves alert throughout the day. Somalis chew khat. Around the world, people every day are getting a boost by smoking cigarettes for the nicotine, drinking coffee for the caffeine and eating chocolate for the sugar. Legal amphetamines in the form of Adderall or Ritalin are heavily prescribed in the United States and other developed nations to treat ADHD in school-age children. Of course, these are just the stimulants that are consumed in mixed company. Those same amphetamines doled out to children to help them focus on school days are obtained by adults and crushed up and snorted to help them party on weekends. Some athletes discreetly take speed before sporting events to help them focus or give them a competitive edge over their rivals. Long-haul truck drivers have been known to seek out something on the down-low to keep their eyes open as they crisscross the continent in their rigs. The world is seemingly flooded with cocaine, which has been coming in and out of vogue for more than 150 years. As far as stimulating the human central nervous system, methamphetamine -- known also as crystal meth or just meth -- can hold its shaky, toothless head high. Users of this processed drug get a rush that leaves them wide-eyed and racing for anywhere from six to 24 hours at a time, and they often binge for days until they reach a twitchy, paranoid state known as "tweaking." In this article, we'll discuss methamphetamine -- what it is, how it's made, where it came from and what it does to the 26 million people around the planet who use it [source: PBS]. Crystal Meth 101 Crystal methamphetamine is a central nervous system stimulant. It is crystalline and white or nearly clear in color. It's usually snorted, but it's also commonly smoked and less commonly injected or consumed orally. Meth is extremely addictive and more powerful than any other speed, making it very seductive to anyone already fond of other forms of stimulants. Methamphetamine creates a rush by flooding thebrain with dopamine, a neurotransmitter that plays a role in bodily movement, emotions and the feeling of pleasure and pain. The increase in dopamine caused by methamphetamine isn't naturally duplicable. In order to feel that sensation again, a user has to use meth again. Over time, as with any addictive substance, the effects of the drug lessen as the user's tolerance grows, requiring more and more of the drug to reach similar highs. Long-term use affects the brain's very ability to produce or use dopamine naturally. Meth addicts (as well as those addicted to most drugs) generally have lower levels of dopamine receptors than nonaddicts. Because of this deficiency, the ability to feel pleasure is diminished for a newly sober addict breaking free from crystal meth. The onset of depression and hopelessness caused by low levels of dopamine lead many addicts right back to the drug, as it provides -- in the short term -- the best opportunity to feel anything close to normal again. In time, the brain's natural dopamine capabilities return to pre-addiction levels, but the length of time it takes varies. Taking meth makes the user more alert. The heart races, breathing quickens and sweat glands kick into overdrive. Users may become extremely talkative or withdraw into a private sphere of self-interest. They often feel superhuman, empowered, more intelligent and more perceptive. Users can also maintain their interest in mundane activities for great lengths of time. As a result, performance of repetitive tasks continues at a high level for hours and hours, when normally it might wane due to boredom. Assembly-line workers and others who perform the same physical motion over and over suddenly find their work to be invigorating and even fascinating when on crystal meth. Where life once seemed dreary and methodical, meth users may find that the drug keeps them "tuned in" to their work, speeding up their thoughts as well as their perception of the passing of time. Appetite is nearly nonexistent for someone on meth. This may make the drug seem tempting to a person trying to lose weight, but weight won't be the only thing that person loses. Over time, teeth decay, crack and fall out of the skull, a condition known as "meth mouth." Lesions can form on the skin from excessive scratching. Extended use of this stimulant can make people feel as if they've lost their minds. After days of staying awake, strange images dart in and out of the corners of the visual field, nonexistent sounds come from near and far, and the user's laser focus zeroes in on perceived threats or injustices. In short, you wouldn't want to spend a week in a foxhole with a Nazi who's eating the stuff like it's candy. Which is exactly what Nazis did in World War II, something we'll discuss in the next section. The History of Meth: From Hitler to Kerouac Jack Kerouac wrote the first draft of "On The Road" by taping sheets of paper into one long continuous scroll and then going on a three-week Benzedrine bender. The draft topped out at nearly 120 feet (37 meters) in length. The history of methamphetamine starts with a group of shrubs known as ephedra. These plants, found in many parts of the world, have been used for thousands of years in China, Pakistan, India and the Americas to make teas that help open airways and treat asthma, as well as congestion and cough. In 1887, ephedrine (an amphetamine) was first isolated from the plant. Six years later, methamphetamine was developed from ephedrine, and in 1919 crystallized methamphetamine was first produced from ephedrine using iodine and red phosphorus. Both amphetamine and methamphetamine initially existed without any particular purpose. These concentrated stimulants were applied to a variety of maladies and disorders in search of their function. Eventually, they were used as general pick-meups, antidepressants and diet pills. They were also used in World War II to conquer and defend much of the globe. Nazi leaders distributed millions of doses of methamphetamine in tablets called Pervitin to their infantry, sailors and airmen in World War II. It wasn't just the military that was amping up on the stuff -Pervitin was sold to the German public beginning in 1938, and over-the-counter meth became quite popular. When supplies ran low on the war front, soldiers would write to their families requesting shipments of speed. In one four-month period in 1940, the German military was fed more than 35 million speed tablets [source: Ulrich]. Though the pills were known to cause adverse health effects in some soldiers, it was also immediately realized that stimulants went a long way toward the Nazi dream of creating supersoldiers. As the war neared its conclusion, a request was sent from high command for a drug that would boost morale and fighting ability, and Germany's scientists responded with a pill called DIX that contained equal parts cocaine and painkiller (5 mg of each), as well as Pervitin (3 mg). The pill was put into a testing stage, but the war ended before it reached the general military population. Serving Your Country -- on Speed On average, every American serviceman in the Vietnam War consumed 30 to 40 amphetamine tablets each year of the conflict [source:Rasmussen]. The Nazis weren't the only ones jacking up their soldiers on pharmaceutical speed -- the Americans and the British were also consuming large amounts of amphetamines, namely Dexedrine. The Japanese had developed its own military-grade amphetamine, and when the war ended a large stockpile of the drug flooded the streets of Japan. After World War II, amphetamine was manufactured, sold and prescribed in the United States and much of the world. By the late 1950s and early '60s, it was becoming harder for the medical community to ignore the growing number of professionals-turned-speed-freaks who had become hopelessly hooked on Benzedrine and Dexedrine. Also, it had been discovered that Benzedrine inhalers (intended for use as bronchial dilators) could be cracked open, exposing a piece of paper soaked in Benzedrine that could then be swallowed for a powerful high. This led to increased American government control over amphetamines -- and therefore to Americans making their own amphetamines. In the next section, we'll learn that, no matter what controls you put on chemicals, you just can't keep an industrious speed freak down. How to Make Meth The production of methamphetamine -- and the desire to consume it -- is seemingly unstoppable. When precursor chemicals are brought under tight control in one country, like the United States, production simply moves to another country, such as Mexico. When Mexican authorities clamp down, it moves farther south, or into Europe or Asia. Then, the finished product is shipped right back into the very countries that have waged such a battle to get it out. Most meth in the United States is made in large labs --"superlabs"-- in Mexico. There are many small meth labs in operation in the United States, but these mostly serve to feed the habits of the amateur cooks themselves. The production of methamphetamine has been made more difficult by federal regulations aimed at controlling the flow of precursor chemicals such as ephedrine and pseudoephedrine, as well as other necessary components. Through theft, subterfuge, forgeries, personal connections and sheer willpower, determined cooks are able to collect enough materials to make some home-grown meth. Being determined and being safe are two different things -- almost 6 pounds (2.7 kilograms) of toxic material is produced for each pound of meth cooked [source: Snell]. This fact, however, doesn't stop crystal meth addicts from brewing sloppy batches of fuming, stinking, toxic speed in poorly ventilated environments. Houses used as meth labs are often uninhabitable afterward, and cities and states involved in meth lab busts often don't bother with seizing the property, since nobody in their right mind would purchase it at an auction, even at a steep discount. Small meth labs can be found in suburban houses, motel rooms, car trunks, in campsites or in the woods. Outdoor operations often result in water contamination and a dying-off of nearby vegetation. Large-scale labs are often located inside abandoned barns or warehouses set up specifically for the purpose of factory-line production of methamphetamine. Although superlabs only make up 4 percent of total labs, they produce about 80 percent of the meth that winds up on the street [source: Suo]. Much as a destination can be reached by taking one of several different routes, so too can crystal methamphetamine be produced by a number of different methods. All of them, though, involve ephedrine or pseudoephedrine. The entire process can involve as many as 32 different chemicals [source: Snell]. Without getting into an exact recipe, we'll look at how large-scale operations (who are more likely to use a methodical and exact approach to their production) make crystal meth. If the ephedrine or pseudoephedrine isn't already in pure powder form, then it must be separated from the tablets of cold medicine that contain it. To do this, the cold medicine tablets are mixed with a solvent and the solution is then filtered and exposed to low temperatures to separate and remove the inert material of the tablet. The pure pseudoephedrine is then mixed with red phosphorus and hydriodic acid. The red phosphorus is then filtered out (and later reused), and the remaining acid is neutralized by adding a lye solution. A substance is added that will bind to the meth, and the liquid meth is then drained out. Hydrogen chloride gas is bubbled through the liquid meth, making it a crystalline hydrochloride salt. This is poured through a filter cloth, and the meth that is left on the filter is then dried. Once dry, the meth is "stepped on" (mixed down with inert filler in order to maximize profits), weighed and packaged for shipment or sale. This process generally takes about two days' time and can result in hundreds of thousands of methamphetamine doses. Meth Production: The Need for Changing Speed In the 1970s, the hippie scene turned ugly as more and more members of the counterculture started popping uppers and shooting up speed. Motorcycle gangs such as the Hell's Angels were notorious for producing amphetamines using a chemical normally used to clean swimming pools: phenyl-2propanone, or P2P. In 1980, P2P was placed under federal control. The reasoning was that the elimination on the street of this precursor chemical necessary for the production of amphetamine would bring the trade in illegal speed to its jittery knees. The problem -- or, depending on your point of view, the solution -- emerged pretty quickly, as most do in the world of high-flying speed cooks who have nothing but time and nervous energy to find new ways to cook up crank. It was discovered that speed could be made using readily available ephedrine. However, this discovery came with a surprise -- this speed wasn't amphetamine, it was methamphetamine, and it was twice as strong as its P2P-derived ancestor. Two Mexican brothers, Jesus and Luis Amezcua, decided to make a career change in the late 1980s. Instead of continuing down the path as small-time cocaine runners, they began importing pure ephedrine from the overseas laboratories that produced it. The audacity of this scheme ensured that it was overlooked as a way to obtain the needed ingredients for meth. By the mid-1990s, the Amezcuas were responsible for about 80 percent of the meth on America's streets. The abundance of the product resulted in a very pure form of meth, bringing about a surge of crime, emergency-room visits, drug-related child abuse, and court-ordered and voluntary drug rehabilitation stays. The Amezcuas covered their tracks by never shipping any of the ephedrine into or through the United States. Instead, they would ship it from a point of origin such as India into Mexico, and then divide the large shipment into smaller quantities that could be transported to various laboratories in Mexico and America. A shipment of 3.4 metric tons of ephedrine was rerouted by a European shipping agent through America on its way to Mexico City and discovered by U.S. Customs agents. After realizing the extent of this operation, American authorities reached out to the nations with laboratories producing ephedrine to persuade them to adopt tighter export controls and standards. This change made a difference, but only for a while. Since the 1980s, many legislative efforts and changes in the law have been made in an attempt to curb the climbing abuse of methamphetamine. These haven't been, in the long term, successful. Making possession of precursor drugs and production equipment illegal has simply pushed the clandestine labs further underground without curbing production. When powdered ephedrine fell under tighter control, cooks switched to still-unregulated pseudoephedrine pills. When sellers of pseudoephedrine were required to register with the Drug Enforcement Administration (DEA), many scam operations did just that - so many, in fact, that the DEA couldn't process all the applications. Instead, it granted temporary licenses, and the pseudoephedrine continued to be sold in bulk to large meth operations. Making matters worse, efforts by the U.S. government to change over-the-counter access to ephedrine and pseudoephedrine were met with great resistance by the pharmaceutical lobby. While lobbyists fought to keep individually packaged pseudoephedrine pills available on store shelves, meth cooks were buying up as many packages as they could and unsealing each individual pill. These pill packages are called "blister packs," and larger meth operations went so far as to purchase "de-blistering" machines to save the time and effort it took to do it by hand. After much effort on the part of the DEA and other law enforcement and governmental agencies, pseudoephedrine (in the form of cough medicine) in the United States is now only available behind the counter. Is it making a difference? In 2004, an estimated 1.4 million people had used meth in the U.S. [source:PBS]. In 2006, the last year for which statistics are available, that number had risen to 1.9 million [source: NIDA]. For more articles you might like, from what an LSD trip is like to how chemical addiction works, try the links on the next page. Lots More Information LSD The psychedelic drug LSD has been called acid, blotter, California sunshine, dots, Electric Kool-Aid and countless other colorful nicknames since it was first sold on the street in the early 1960s. It makes sense that LSD would be popular. It's easy to take -- it's colorless, odorless and tasteless -- and ingesting just a tiny amount (25 micrograms, or 0.000025 grams, less than the weight of two salt grains) is enough to feel the effects. It's also easy to conceal, since today's doses are usually found on tiny squares of absorbent paper. LSD can be difficult to detect, because of the small amount ingested and the fact that it's quickly metabolized by the body. Finally, LSD is cheap compared to other drugs. A single dose usually costs no more than $5, and often it can be gotten for free. The same things about LSD that would make it popular also make it scary, and we've been warned about its many dangers at one time or another. For example, you may have been told that LSD can "fry" or put holes in your brain, or make you go insane and do dangerous things. Supposedly people have leapt from buildings or overpasses while tripping or have drowned because they thought that they could walk on water. There are tales that people seeking to hook children on LSD have put the drugs on postage stamps or lick-and-stick tattoos. Not all of these things are true. In fact, many of the things we've been told about what LSD does, and what people do under its influence, are myths or exaggerations created to frighten impressionable teenagers. The truth is, although LSD has been around for more than 60 years and been taken by thousands upon thousands of people, it's still not very well understood by most of us. Although it will forever be associated with hippies and the 1960s counterculture movement, LSD was first synthesized by researches seeking to create new medicines. Let's begin with LSD's own beginnings -- in a lab in Switzerland. LSD History A Swiss chemist named Albert Hofmann was employed in a laboratory at Sandoz, a pharmaceutical company, when he first synthesized LSD. Sandoz was working on a research project involving a parasitic fungus called ergot that grows on rye, known as Claviceps purpurea. In the Middle Ages, it poisoned thousands of people who ate rye bread infected with it. Ergot had also been used by midwives, who sometimes gave it to pregnant women to bring about and speed up labor. In the 19th century, most physicians deemed the practice too dangerous because high dosages lead to strong contractions and endanger the baby, although physicians sometimes still used ergot to stop a woman's bleeding after childbirth. In the 1930s, researchers at the Rockefeller Institute in New York isolated lysergic acid from an ergot compound. This research was the basis for Hofmann's work at Sandoz. While deriving different compounds from lysergic acid, Hofmann developed several medicines, including drugs that lowered blood pressure and improved brain function in the elderly. In 1938, Hofmann derived the 25th in a series of these derivatives. It was lysergic acid diethylamide, or LSD-25. He thought that LSD-25 might stimulate breathing and circulation. But tests didn't show anything special, and Sandoz abandoned further study. Five years later, Hofmann's thoughts returned to LSD-25's potential. He felt that it hadn't been fully explored, so he took the unusual step of synthesizing another batch for further testing. During the process, however, Hofmann began to feel strange. He stopped his work and went home early, "being affected by a remarkable restlessness, combined with a slight dizziness." While at home, he was in a "dreamlike state" and "perceived an uninterrupted steam of fantastic pictures, extraordinary shapes with intense, kaleidoscopic play of colors" [source:Hofmann]. At the time, Hofmann decided that he must've gotten some of the solution on his finger. (Later it was determined that he must have touched his finger to his mouth, as LSD can't be absorbed through the skin.) The next day, Hofmann purposely dosed himself with LSD. He took 250 micrograms, 10 times more than today's typical minimum dose. Hofmann became delirious and could barely speak. Initially he panicked and asked his laboratory assistant to call a doctor. The doctor could find nothing wrong with Hofmann other than the fact that his pupils were dilated -- he had normal blood pressure, heart rate and respiration. Soon his panic gave way to euphoria, and Hofmann once again saw beautiful shapes and colors. The next day, he told others at Sandoz about what had happened, and they experimented with similar results. No other drug had been known to have such strong effects in such small doses. After trials on animals, Sandoz gave LSD to research institutes and doctors to use in psychiatric experiments on both healthy and mentally ill subjects. The research was compelling enough to convince Sandoz to patent LSD and market it as Delysid in 1947. It was sold in 25-microgram tablets for use in analytical psychotherapy. Sandoz also suggested that psychiatrists take the drug themselves, so that they could better understand their patients. Two years later, doctors at the Boston Psychotropic Hospital were using it on their own patients. By 1960, there had been hundreds of papers published in scientific and medical journals on the various uses of LSD -- it was the talk of the psychiatric community. But by 1966, Sandoz had stopped making it altogether. Let's see how LSD is made illegally. How to Make LSD Sandoz held the patent on LSD until 1963 and stopped making it shortly afterward. The company claimed that it was concerned about a lack of regulation and the inaccurate information being perpetuated about the drug. Naturally, this didn't stop anyone from making it themselves, which was legal to do until 1965. Making LSD requires a strong working knowledge of organic chemistry, a complete laboratory setup (including the ability to sterilize equipment as well as access to a darkroom), and several chemicals that are currently either sales restricted or have their sales closely monitored by the Drug Enforcement Agency (DEA). Unlike the chemicals used in the manufacture of methamphetamine, they can't be found in fairly ordinary household items. There a couple of different ways to make LSD. Some "recipes" may start with lysergic acid. Other online recipes call for morning glory seeds, which can be especially dangerous because they're often sold with a toxic coating to discourage consumption. Morning glory seeds and the seeds of some related plants contain LSA, or lysergic acid amide. The LSA can be extracted from the seeds and produce a mild high on its own. It's considered a precursor to LSD, although the amount of LSA in different seeds varies so much that the quality of the drug made from it would also vary. Here, we'll look at a recipe that starts with ergot. A chemist making LSD must be extremely careful and knowledgeable about working with ergot because of its toxicity. Remember the people poisoned by rye bread in the Middle Ages? Once the chemist obtains the fungus, he has to carefully and precisely culture it to extract the ergot alkaloids (an alkaloid is a compound containing basic nitrogen atoms). The darkroom setup becomes necessary here, because the fungus will decompose under bright lights. In fact, LSD itself can break down quickly when exposed to light. If working with toxic ergot weren't enough, the solvents and reagents (compounds used to bring about chemical reactions) are also incredibly dangerous. The solvent anhydrous hydrazine, for example, can explode when heated. It's extremely poisonous and a known carcinogen. Another chemical often used in the process, chloroform, can also cause cancer as well as severely damage the kidneys and liver. Both of these can be easily absorbed through the skin or inhaled. The ergot alkaloid is synthesized into a lysergic acid compound called iso-lysergic acid hydrazide, through the addition of chemicals and heating processes. Then the iso-lysergic acid hydrazide is isomerized, which means that the atoms in its molecules are rearranged through a chemical process. It's cooled, mixed with an acid and a base, and evaporated. What remains is iso-lysergic diethylamide, which is isomerized again to produce active LSD. The LSD is then purified and crystallized. What next? In the past, LSD was then made into tablets (microdots), simply dissolved in water or other liquids to be dropped, or made into gelatin squares (windowpanes). It's rare to see LSD in these forms today, however. Instead, it's usually dissolved in ethanol. Sheets of blotting paper are then dipped into the LSD solution and dried. These sheets ofblotter acid are usually printed with cartoon characters or other colorful graphics. The sheets are perforated into small squares, about a quarter of an inch (6.35 millimeters) wide. Each square is one dose, and a sheet can contain 900 doses. These squares are chewed and swallowed. Although LSD has been injected, especially in therapeutic uses, it's not necessary because it's very quickly absorbed by the body when taken orally. So what does it feel like to go on a trip? Find out next. LSD Trips: Something Happened to Me Yesterday It's often stated that LSD causes hallucinations, but that's not quite true. When a person has a hallucination, he or she believes that everything that he or she sees and feels is real. LSD changes the way people perceive the world around them, as well as what they think and feel, but people on LSD don't see things that aren't there. They see what's already there in a different way, and most of the time, they're aware that their altered perceptions are caused by the drug. After taking LSD, the effects -- known as a "trip" -- usually start within an hour and can last up to 12 hours, with a peak about halfway through the experience. Exactly how LSD affects each person varies widely. Some physical changes in the body during tripping include dilated pupils, increased blood pressure and a high body temperature. People on LSD may also feel dizzy, sweat, have blurred vision and feel tingling in their hands and feet. They may feel drowsy but not sleepy. LSD's primary effects are visual. Colors seem stronger and lights seem brighter. Objects that are stable might appear to move or have a halo of light around them. Sometimes objects have trails of light coming from them or appear smaller or larger than they really are. LSD users often see patterns, shapes, colors and textures. Sometimes it seems that time is running backward, or moving very quickly or slowly. On very rare occasions (although it's sometimes portrayed as common), tripping can cause synesthesia -- a confusion of sensations between different types of stimuli. Some people have described this as seeing colors when they hear specific sounds. There is an overall sense of happiness and euphoria. Everything is beautiful, interesting and magical. People on LSD often become very emotional and dreamlike. Large doses of may make them feel especially contemplative. They feel that their mind has burst through its normal boundaries, and they often claim to have had experiences that are spiritual or religious, with a new understanding of how the world works. People tripping on LSD are generally impulsive and have very poor judgment. This is part of why it's usually preferable among LSD users to trip in groups, especially with others who have experience, and in calm places like home or in a park. Close friendships have been formed among people who have tripped together. For people not tripping but observing, LSD users can be scary. They might spend lots of time pondering something that appears incredibly unimportant. They aren't always easy to understand, but when they do talk, they speak quickly and jump from subject to subject. The above are considered to be "good trips." Most people who have used LSD know that there's always a possibility of having a "bad trip." It's not really clear what causes a bad trip, especially since each trip can be very different depending on the person. LSD users sometimes say that it's due to the "set and setting." This means that if you are already in a bad mood, or you trip in a highly structured environment that requires you to think logically (such as school), you could have a bad trip. This may include losing sight of the illusory aspect of tripping, which results in fear and paranoia. The loss of control is frightening, and it seems like the trip will never end. Sometimes when someone has a bad trip, he or she is taken to a hospital. However, there usually isn't much that doctors do other than give the person a quiet space and reassurance. They may administer an anti-anxiety medication or a mild tranquilizer to ease the patient's panic. As the trip ends, the patient may feel dizzy or nauseous, but people usually recover with no lasting side effects. For some, one bad trip is enough to swear off LSD forever. Even if LSD users don't have a bad trip, heavy use of LSD can still cause a lot of problems. Next, we'll look at how LSD works in the body and its effects on mental and physical health. LSD Effects on the Body: Melts Your Mind, Not in Your Hands Researchers aren't 100 percent sure what LSD does in the central nervous system, or exactly how it causes those hallucinogenic effects. This is in part because there have never been scientific research studies on how LSD affects the brain. It's believed that LSD works similarly to serotonin, a neurotransmitter responsible for regulating moods, appetite, muscle control, sexuality, sleep and sensory perception. LSD seems to interfere with the way the brain's serotonin's receptors work. It may inhibit neurotransmission, stimulate it, or both. It also affects the way that the retinas process information and conduct that information to the brain. As little as 0.25 micrograms of LSD per 2.2 pounds (about 1 kilogram) of body weight can produce the effects. A typical dose today is around this amount; in the 1960s, it was up to four times as much. When a person takes LSD, it's quickly metabolized in the liver and eventually excreted in the urine. A small amount is left in the body by the end of the trip and is probably gone entirely a few weeks afterward. It has been stated before that LSD remains in the body forever in minuscule amounts in the brain or spinal fluid, but there's no evidence to support this claim. People who believe in it, however, say that the brain holds and may release molecules of LSD over time, and this is what causes flashbacks. A flashback occurs when a person who has used LSD in the past has an experience, lasting anywhere from seconds to hours, similar to that of an actual trip. Some LSD users enjoy them and consider them "free trips," while others find them incredibly upsetting. The majority of LSD users report never having flashbacks, and some people claim that they don't really exist. They're a very controversial topic among LSD users and researchers. Of those who have reported experiencing flashbacks, many are also mentally ill. Some doctors suggest that what the user perceives as a flashback is really a form of psychosis or mental illness that may have emerged due to LSD use. There's a medically recognized disorder called Hallucinogen Persisting Perceptive Disorder (HPPD), in which some people who have taken LSD constantly experience visual hallucinations (as opposed to the brief flashbacks). It's not yet known exactly what makes some people more susceptible to this than others. On the next page, we'll look at worst-case scenarios. LSD Dangers and Abuse There have been very few reports of LSD overdoses that resulted in death or permanent health problems. In 1973, a case was recorded in The Western Journal of Medicine in which eight people took massive overdoses of LSD at a party. They thought that the white powder being passed around was cocaine and snorted milligrams of it. Most of them passed out. In the hospital, they suffered from fevers, vomiting and internal bleeding. However, all of the patients recovered within 12 hours with no lasting effects. Five of them were examined regularly for a year afterwards for long-term problems. There have been reports of heart attacks, strokes and other deaths associated with LSD use, but many of these users also had other recreational drugs in their systems, so the role of LSD was inconclusive. The real physical damage associated with LSD comes from what can happen when someone loses inhibitions and has poor judgment, skewed perceptions or a sense of immortality while tripping. LSD users have accidentally killed themselves by walking in front of a car, getting into a car accident while tripping, or falling from windows or buildings. These people didn't "go crazy." LSD isn't likely to make someone go insane or become psychotic. It can interact with other drugs and cause psychotic symptoms (especially other drugs that work on neurotransmitters). Some people with histories of certain mental illnesses, such as schizophrenia or psychosis, may have their symptoms exacerbated on LSD. It may also speed the onset of these illnesses if one was already going to develop. Heavy LSD users can also develop profound social problems, completely ruin their sleep cycles and lose interest in eating and personal hygiene. They become uninterested in participating in the world going on around them and feel completely disconnected from everybody else. The real problem is that because they're taking LSD so often, they think the LSD is creating the illusion that their life is a mess instead of recognizing that it really is a mess. You won't hear about someone being in rehab for LSD abuse, however, because it's not an addictive drug. Using LSD for just a few days in a row can cause a person to build up a tolerance quickly, so it's rarely used more than once a week. A person who uses LSD twice a week is considered a heavy user. In addition, repeated trips tend to lose their novelty, and what once seemed magical becomes everyday and commonplace. The effects caused by LSD aren't dependable in the way that other drugs' effects are -you never know how you'll feel or what you'll see. Addicts crave dependability. Next, let's take a look at LSD that's used for purposes other than recreation. LSD as Medicine: Opening the Doors of Perception Before it was a recreational drug, LSD was used in psychiatric therapy. In the beginning, psychiatrists hoped that LSD would prove to be a cure for some forms of mental illness. It was thought that giving a patient LSD would remove the need for years of psychotherapy and bring about permanent changes in behavior and personality. Between 1950 and 1965, approximately 40,000 patients were given Sandoz's Delysid tablets [source: Henderson]. These included schizophrenics, obsessive- compulsives, depressives and autistic people. It was also administered to people considered mentally ill with sexual perversions, such as homosexuality. There were two main types of therapy that incorporated LSD usage. In Europe, psycholitic therapywas common. Psychiatrists gave patients low doses of LSD (50 micrograms or less) over several sessions and encouraged them to focus on their childhood and subconscious. American psychiatrists were more likely to use psychedelic therapy. They gave their patients high doses of about 200 micrograms over just a few sessions. Instead of bringing out childhood memories, these doctors hoped the high doses of LSD would elicit a positive spiritual awakening and encourage patients to find meaning in their lives and want to better themselves. The spiritual awakening approach was also used on alcoholics, who were difficult to treat through other types of therapy. Some psychiatrists attempted to induce a form of delirium tremens, which might scare alcoholics into reforming themselves. LSD was also given to criminals in the hopes that they could be reformed. Although many psychiatrists reported good results, there were few large studies. The smallscale studies are often considered flawed today because they didn't employ controls. Sandoz recommended very specific doses of LSD and stated it should only be administered by a psychiatrist in a controlled medical setting. Of course, there was a black market for the drug by 1962. As recreational use grew, the federal government became increasingly concerned about LSD's effects and took steps to restrict its official use. Many researchers felt that their studies were terminated before they could reach a definite conclusion about LSD's therapeutic effects. By 1965, very few researchers in the United States were still allowed to possess LSD. There were only six projects conducted in 1969, and by 1974, the National Institutes for Mental Health (NIMH) declared that LSD had no real therapeutic value. The last therapeutic LSD study in the United States took place in the 1980s. The researchers believed that LSD could be beneficial to terminally ill patients because it helped them to stay aware of their surroundings, relieved their pain and made them feel more connected to their families. The study ended, however, before the idea could be completely explored. There are currently studies using LSD in humans in other countries, such as Switzerland and the United Kingdom. In September 2008, the Food and Food Administration (FDA) opened the door once again for end-of-life clinical research using LSD. This may signal a renewed interest in other therapeutic uses for the drug. On the next page, we'll look at the group of people most often associated with LSD: hippies. Cultural History of LSD: Turn On, Tune In, Drop Out LSD played an important part in the 1960s counterculture movement. As use spread from research projects at universities to the street, LSD was credited with expanding the minds of young people who were disillusioned with the status quo. We'll take a closer look at just a few of the people instrumental in spreading the drug's popularity. Dr. Timothy Leary was a psychology professor at Harvard when he first tried psilocybin mushrooms in 1960. He was so changed by the experience that he and his Harvard colleague Richard Alpert founded a study to test the effects of psychedelic drugs. Leary believed that they could treat a host of mental illnesses and profoundly change those who took them. Complaints from parents and others, however, led Harvard to fire Leary in 1963. In 1964, he co-authored a book about psychedelic drugs and founded the League for Spiritual Discovery the following year. This was a religion that claimed LSD as a holy sacrament that must be kept legal for religious freedom. Leary toured the country with a presentation that attempted to demonstrate the experience of tripping. He spoke the phrase that came to exemplify the LSD movement, "turn on, tune in, drop out," during a 1967 speech in San Francisco before 30,000 hippies. Leary later stated in his biography that "'turn on' meant to go within to activate your neural and genetic equipment [...] 'Tune in' meant interact harmoniously with the world around you [...] 'Drop out' meant self-reliance" [source: Leary]. He was disappointed that people thought he meant "Get stoned and abandon all constructive activity." Ken Kesey was an author whose first experience with LSD came when he volunteered in 1959 to take part in a CIA study of the effects of psychedelic drugs. He and his friends, known as The Merry Pranksters, traveled across the country in a school bus called "Furthur" as a social experiment. Their adventures were documented by author Tom Wolfe in "The Electric Kool-Aid Acid Test." While Timothy Leary originally advocated a more serious, controlled use of LSD, Kesey was an "acid populist" who believed that if enough people used it, society as a whole could be transformed. In 1965, he began holding psychedelic parties advertised with signs that read "Can you pass the acid test?" Kesey believed that the acid tests expanded consciousness and started a revolution. Girl with Kaleidoscope Eyes Is the Beatles' "Lucy in the Sky with Diamonds" an LSD song? John Lennon didn't deny that the lyrics were inspired by drug experiences, but he claimed that he didn't notice that the title spelled out "LSD" until someone pointed it out. He said the title was from his son Julian, who painted a picture of his classmate Lucy surrounded by sparkling stars. When Lennon asked Julian what the painting was called, he replied, "Lucy in the sky with diamonds." Lennon showed off the painting and maintained that it was the origin of the title until his death. Owsley Stanley was a self-taught chemist who helped to make LSD popular and accessible in the influential Haight-Ashbury section of San Francisco. While a student at the University of California at Berkley, Stanley tried LSD but was frustrated with the wide differences in quality and purity. He set up his own lab to make pure, high-quality LSD, which became known as "Owsley LSD" or simply "Owsley." It became the standard by which other LSD was measured after Sandoz stopped making the drug and it became illegal. He often distributed it freely, and it has been estimated that Stanley made half a kilo of LSD, enough for 10 million 50-microgram trips, in his lifetime. He also created an LSD synthesis that was 99 percent pure called White Lightning, as well as another psychedelic drug, STP. Stanley also became friends with the band the Grateful Dead (who performed at Kesey's acid tests) and worked as their sound engineer. He not only heavily influenced the band's sound, but also designed their Lightning Bolt Skull logo and was the inspiration for the Dancing Bears logo because of his nickname, "The Bear." So what happened between the 1960s and today? LSD Drug Laws Today In the United States today, LSD is a Schedule I controlled substance under theControlled Substances Act (CSA). This means that the federal government believes LSD to have high abuse potential, a lack of accepted safe use when taken under medical supervision, and no current medical use. The last criterion is important; LSD is a Schedule I drug, but cocaine is Schedule II due to some medical use (such as local anesthesia). There are higher legal ramifications, in other words, for LSD than for cocaine. The federal penalty for the first offense of LSD possession is a maximum of one year in prison or a minimum fine of $1,000. Additional offenses can raise the prison time to as much as three years. The penalties for making or selling LSD are based not only on the number of offenses, but the amount involved. So even if it's the first offense, if the amount is up to 10 grams, the offender can spend five to 40 years in jail and face a fine of $2 million. Higher amounts can result in a life sentence. A 1991 Supreme Court ruling found that when weighing blotter acid, the weight of the paper can be included. Since the actual amount of LSD in the paper is so minute, some people have claimed that this results in unfairly harsh sentences. There are few federal arrests for LSD, however -- they number less than 2 percent of all DEA arrests. And who are these LSD users? According to the 2007 National Household Survey on Drug Use & Health, about 9 percent of people in the United States over the age of 12 have used LSD at least once in their lifetimes. This is the profile of the average LSD user: He is a white male between the ages of 18 and 22 who usually first tried the drug between the ages of 15 and 19. He's most likely to live in the Western United States, come from a fairly affluent family and have educated parents. He's only used LSD a few times but is also likely to use alcohol, marijuana and cocaine. As the age groups in the survey increased, LSD use generally declined, meaning that LSD users have a "short career." There was a slight increase in the use of LSD among high school seniors in the early 1990s, but it has generally remained between 8 and 10 percent since the survey began in 1975. For more articles on drugs, from the CIA's LSD experiments to the Salem witch trials, try the links on the next page. Lots More Information Marijuana Photo courtesy Marijuana.com Marijuana comes from the Cannabis sativa plant and is the most commonly used illicit drug in the United States. See more controlled substance pictures. Although banned by the U.S. federal government in 1937, it is estimated that 14.8 million Americans use marijuana, which is roughly the population of Calcutta, India. The United States drug market is one of the world's most commercially viable and attracts drug traffickers from every corner of the globe. On American soil, marijuana costs between $400 and $2000 per pound. A pound of higher quality marijuana, known as sinsemilla, costs between $900 and $6,000. Marijuana is the buds and leaves of the Cannabis sativa plant. This plant contains more than 400 chemicals, including delta-9-tetrahydrocannabinol (THC), the plant's main psychoactive chemical. THC is known to affect our brain's short-term memory. Additionally, marijuana affects motor coordination, increases your heart rate and raises levels of anxiety. Studies also show that marijuana containscancercausing chemicals typically associated with cigarettes. In this article, you will learn about marijuana, why this drug is so popular and what effects it has on your mind and body. The history of marijuana use reaches back farther than many would guess. Cultivation of the Cannabis sativa plant dates back thousands of years. The first written account of cannabis cultivation (ostensibly used as medical marijuana) is found in Chinese records dating from 28 B.C. That means Chinese cultures were growing marijuana more than 2,000 years ago. However, the plant may have been cultivated long before then -- there have been reports of a nearly 3,000-year-old Egyptian mummycontaining traces of THC, the main psychoactive chemical in marijuana. Cannabis sativa is perhaps the most recognizable plant in the world. Pictures of the ubiquitous green cannabis leaf show up in the news media, textbooks and drug-prevention literature, and the leaf's shape is made into jewelry, put on bumper stickers and clothing and spray-painted on walls. The leaves are arranged palmately, radiating from a common center like the fingers of a hand spreading apart. Although most people know what the cannabis plant looks like, they may know very little about its horticulture. Hemp Products The marijuana plant has many uses. Its stiff, fibrous stalk can be used to make lots of products, from food to ship sails. The stalk is comprised of two parts -- the hurd and thebast. The bast provides fibers that can be woven into many fabrics. These fibers (also called hemp) are woven to create canvas, which has been used to make ship sails for centuries. The hurd provides pulp to make paper, oil to make paints and varnishes, and seed for food. Marijuana plants produce a high-protein, high-carbohydrate seed that is used in granola and cereals. Hemp oil and seed contain only trace amounts of psychoactive chemicals. Owning hemp products, such as hemp rope or a hemp shirt, is legal. However, it is illegal to grow or possess marijuana in plant or drug form in the United States. Possession of the cannabis plant or marijuana seeds is punishable by fines and possible jail sentences. Cannabis sativa is believed to be a native plant of India, where it possibly originated in a region just north of the Himalayan mountains. It's a herbaceous annual that can grow to a height of between 13 and 18 feet (4 to 5.4 meters). The plant has flowers that bloom from late summer to mid-fall. Cannabis plants usually have one of two types of flowers, male or female, and some plants have both. Male flowers grow in elongated clusters along the leaves and turn yellow and die after blossoming. Female flowers grow in spikelike clusters and remain dark green for a month after blossoming, until the seed ripens. Hashish, which is more powerful than marijuana, is made from the resin of the cannabis flowers. Marijuana plants contain more than 400 chemicals, 60 of which fit into a category called cannabinoids. THC is just one of these cannabinoids, but it's the chemical most often associated with the effects that marijuana has on the brain. Cannabis plants also contain choline, eugenol, guaicacol and piperidine. The concentration of THC and other cannabinoids varies depending on growing conditions, plant genetics and processing after harvest. You'll learn more about the potency of THC and the toxicity of marijuana next. Marijuana in the Body Every time a user smokes a marijuana cigarette or ingests marijuana in some other form, THC and other chemicals enter the user's body. The chemicals make their way through the bloodstream to the brain and then to the rest of the body. The most powerful chemical in marijuana is THC (delta-9tetrahydrocannabinol), which is primarily responsible for the "high" associated with the drug. The most common way of using marijuana is smoking. Smoking is also the most expedient way to get the THC and other chemicals into the bloodstream. When the smoke from marijuana is inhaled, the THC goes directly to the lungs. Your lungs are lined with millions of alveoli, the tiny air sacs where gas exchange occurs. These alveoli have an enormous surface area -- 90 times greater than that of your skin -- so they make it easy for THC and other compounds to enter the body. The smoke is absorbed by the lungs just seconds after inhaling. You can also eat marijuana. In this case, the marijuana enters the stomach and the blood absorbs it there. The blood then carries it to the liver and the rest of the body. The stomach absorbs THC more slowly than the lungs. When marijuana is eaten, the levels of THC in the body are lower, but the effects last longer. Marijuana and the Brain THC is a very potent chemical compared to other psychoactive drugs. An intravenous (IV) dose of only 1 milligram can produce serious mental and psychological effects. Once in your bloodstream, THC typically reaches the brain within seconds after it is inhaled and begins to go to work. Marijuana users often describe the experience of smoking marijuana as initially relaxing and mellow, creating a feeling of haziness and light-headedness. The user's eyes may dilate, causing colors to appear more intense, and other senses may be enhanced. Later, feelings of a paranoia and panic may be felt by the user. The interaction of the THC with the brain is what causes these feelings. To understand how marijuana affects the brain, you need to know about the parts of the brain that are affected by THC. Here are the basics: Neurons are the cells that process information in the brain. Chemicals called neurotransmitters allow neurons to communicate with each other. Neurotransmitters fill the gap, or synapse, between two neurons and bind to protein receptors, which enable various functions and allow the brain and body to be turned on and off. Some neurons have thousands of receptors that are specific to particular neurotransmitters. Foreign chemicals, like THC, can mimic or block actions of neurotransmitters and interfere with normal functions. In your brain, there are groups of cannabinoid receptors concentrated in several different places. These cannabinoid receptors have an effect on several mental and physical activities, including: Short-term memory Coordination Learning Problem solving Cannabinoid receptors are activated by a neurotransmitter called anandamide. Anandamide belongs to a group of chemicals called cannabinoids. THC is also a cannabinoid chemical. THC mimics the actions of anandamide, meaning that THC binds with cannabinoid receptors and activates neurons, which causes adverse effects on the mind and body. High concentrations of cannabinoid receptors exist in the hippocampus, cerebellum and basal ganglia. The hippocampus is located within the temporal lobe and is important for short-term memory. When the THC binds with the cannabinoid receptors inside the hippocampus, it interferes with the recollection of recent events. THC also affects coordination, which is controlled by the cerebellum. The basal ganglia controls unconscious muscle movements, which is another reason why motor coordination is impaired when under the influence of marijuana. Other Physiological Effects of Marijuana In addition to the brain, the side effects of marijuana reach many other parts of the body. Marijuana is filled with hundreds of chemicals, and when it is burned, hundreds of additional compounds are produced. When marijuana is inhaled or ingested in some other form, several short-term effects occur. Some of marijuana's side effects are: Problems with memory and learning Distorted perception Difficulty with thinking and problem solving Loss of coordination Increased heart rate Anxiety, paranoia and panic attacks The initial effects created by the THC in marijuana wear off after an hour or two, but the chemicals stay in your body for much longer. The terminal half-life of THC is from about 20 hours to 10 days, depending on the amount and potency of the marijuana used. This means that if you take one milligram of THC that has a half-life of 20 hours, you will still have 0.031 mg of THC in your body more than four days later. The longer the half-life, the longer the THC lingers in your body. The Munchies One peculiar phenomenon associated with marijuana use is the increased hunger that users feel, often called the "munchies." Research shows that marijuana increases foodenjoyment and the number of times a person eats each day. Until recently, the munchies were a relative mystery. However, a recent study by Italian scientists may explain what happens to increase appetite in marijuana users. Molecules called endocannabinoids bind with receptors in the brain and activate hunger. This research indicates that endocannabinoids in the hypothalamus of the brain activate cannabinoid receptors that are responsible for maintaining food intake. The debate over the addictive capacity of marijuana continues. Ongoing studies now show a number of possible symptoms associated with the cessation of marijuana use. These symptoms most commonly include irritability, nervousness, depression, anxiety and even anger. Other symptoms are restlessness, severe changes in appetite, violent outbursts, interrupted sleep or insomnia. In addition to these possible physical effects, psychological dependence usually develops because a person's mind craves the high that it gets when using the drug. Beyond these effects that marijuana has, marijuana smokers are susceptible to the same health problems as tobacco smokers, such as bronchitis, emphysema and bronchial asthma. Other effects include dry mouth, red eyes, impaired motor skills and impaired concentration. Long-term use of the drug can increase the risk of damaging the lungs andreproductive system, according to the U.S. Drug Enforcement Agency (DEA). It has also been linked to heart attacks. Although marijuana is known to have negative effects on the human body, there is a raging debate over the use of medicinal marijuana. Some say that marijuana should be legalized for medical use because it has been known to suppress nausea, relieve eye pressure, decrease muscle spasms, stimulate appetite, stop convulsions and eliminatemenstrual pain. Because of its therapeutic nature, marijuana has been used in the treatment of several conditions including: cancer and AIDS (to supress nausea and stimulate appetite), glaucoma (to alleviate eye pressure), epilepsy(to stop convulsions) and multiple sclerosis (to decrease muscle spasms). Others believe the negative effects of marijuana usage outweigh the positive. There are currently nine U.S. states that have legalized marijuana for medical purposes: Alaska, Arizona, California, Colorado, Hawaii, Maine, Nevada, Oregon and Washington. Marijuana Potency Whether marijuana is more potent today than it was 30 or 40 years ago is at the center of much debate. The U.S. federal government has released information saying that the levels of potency have risen anywhere from 10 to 25 times since the 1960s. Is this a myth or reality? Testing for Marijuana An estimated 20 million workers are drug-tested annually in the United States at a cost of more than $1 billion. The body metabolizes THC into about five metabolites before passing it into the body's urine, so drug tests are designed to detect the metabolites instead of THC. Detectable amounts of these metabolites remain in the system for several days to several weeks following marijuana use, depending on the level of use. The most common test for detecting marijuana or any drug is the immuno-assay. In this test, the urine is mixed with a solution containing an antibody specific to certain metabolites. The antibody is usually tagged with a fluorescent dye or radioactive substance. The amount of fluorescent light or radioactivity is measured to determine the concentration of metabolites in the sample. Gas chromatography/mass spectrometrymay also be used to test for THC metabolites. "There's no question that marijuana, today, is more potent than the marijuana in the 1960s. However, if you were to look at the average marijuana potency which is about 3.5 percent, it's been relatively stable for the last 20 years. Having said that, it's very important that what we have now is a wider range of potencies available than we had in the 1970s, in particular," Director of the National Institute on Drug Abuse Alan Leshner said in 1999 while testifying in front of the U.S. House Subcommittee on Crime. Those who support the legalization of marijuana say that the data is skewed because testing was only performed on marijuana of specific geographic origins in the 1960s and 1970s, and therefore isn't representative of marijuana potency overall. Officials obtained the samples from a type of Mexican marijuana that is known to contain low levels of THC -- 0.4 to 1 percent. When these levels are compared to other types of marijuana, it looks as if potency levels have risen in the last 30 years. Typical THC levels, which determines marijuana potency, range from 0.3 to 4 percent. However, some specially grown plants can contain THC levels as high as 15 percent. Several factors are involved in determining the potency of a marijuana plant, including: Growing climate and conditions Plant genetics Harvesting and processing The time at which the plant is harvested affects the level of THC. Additionally, female varieties have higher levels of THC than male varieties. As a cannabis plant matures, its chemical composition changes. During early development,cannabidiolic acid is the most prevalent chemical. Later, cannabidiolic acid is converted to cannabidiol, which is later converted to THC when the plant reaches its floral maturation. To determine the average potency levels of marijuana, researchers need to examine a cross section of cannabis plants, which wasn't done in the 1960s and 1970s. This makes it difficult to make accurate comparisons between the THC levels of that time period and the THC levels of today. Marijuana Usage Marijuana is readily available in almost every corner of the United States. It's found growing in homes, on farms, in the suburbs and in the city. Cannabis is frequently found growing on public land, often in remote locations to prevent observation and identification of the growers. In 2003, drug law enforcement authorities seized 2.7 million pounds (1.2 million kilograms) of marijuana from illegal operations. Marijuana is also smuggled into the United States from Mexico, Cambodia and Thailand, among other countries. There is a growing trend toward indoor cultivation of marijuana in the United States because of the DEA's efforts to curtail outdoor cultivation. Indoor marijuana growers cultivate cannabis in closets, fish tanks and elaborate greenhouses. Some marijuana growers have even built structures that look like real homes but lack interior walls, all to hide their marijuana-growing operations. More than 71 million Americans over the age of 12 had tried marijuana as of 1998, which is more than 25 percent of the national population. Frequent usage is lower than it was in 1979, when 13.2 percent of the U.S. population over the age of 12 was using marijuana on a monthly basis. In 1999, it had declined to 5.1 percent. There are several ways in which people use marijuana, and the way in which it is used determines the amount of chemicals transferred into the body. Here are the most common methods of use: Street Slang There are hundreds of slang words that mean "marijuana" (some refer to specific types). Here are just a few: Airplane Astro turf Aunt Mary Black Bart Boom Bud Charge Chiba chiba Chunky Dagga Dank Dinkie dow Endo Ganja Haircut Hay Herb Mary Jane Matchbox Maui wauie Sezz Yellow submarine Weed Zambi Source: U.S. Drug Enforcement Agency (DEA) Cigarette - Also called a joint, dried marijuana buds are rolled into a cigarette. Approximately 10 percent to 20 percent of the THC is transferred into the body when smoking a joint. Cigar - Some users slice open a cigar, remove the tobacco and refill it with marijuana. The marijuana-filled cigar is often called a blunt. Pipe - You've probably seen people smoke pipes of tobacco, but these pipes are also used to smoke marijuana. About 40 percent to 50 percent of the THC is transferred into the body when using a pipe. Bong - These are water pipes that typically have a long tube rising out of a bowlshaped base. Water pipes trap the smoke until it's inhaled, raising the amount of THC taken in. Food - Marijuana is sometimes baked into foods, such as brownies, or brewed as tea. With millions of users, marijuana use isn't limited to one demographic group. It cuts across all racial and economic boundaries. However, marijuana use is highest among younger people. The prevalence of marijuana use in teenagers doubled from 1992 to 1999: One out of every 13 kids aged 12 to 17 were current users of marijuana in 1999. The 1998 National Center on Addiction and Substance Abuse indicates that marijuana is very easy to obtain. Half of all 13-year-olds said that they can find and purchase marijuana, according to the study. Of teens surveyed, 49 percent said that they had first tried marijuana at age 13 or younger. Buying, selling, using or growing marijuana is illegal in every part of the United States. Penalties vary from place to place, but usually consist of jail time, a fine or both. In some states, you can be arrested for just being in a place where you know drug activity is taking place. The severity of the penalty varies on several factors: Quantity - Penalties vary based on the amount of marijuana found in the person's possession. Selling - Penalties are more severe for those intending to sell marijuana. Growing - Penalties are also more severe for those cultivating cannabis. Location - A person arrested for selling marijuana near a school will often face harsher penalties. (There's a state-by-state guide to facts about marijuana penalties at NORML.) Jail sentences and fines have done little to suppress the use of marijuana in the United States. Despite the health and legal risks that come with using marijuana (or any illicit drug), it continues to be the illegal drug of choice for many Americans, as it has for decades. For more articles you might be interested in, from how LSD trips work to the science behind addiction, try the next page. 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