john Hudson's List: Effect drugs has on human brain and behavior

• Does drug abuse cause mental disorders, or vice versa?

   

  Drug abuse and mental disorders often co-exist. In some cases, mental diseases may precede addiction; in other cases, drug abuse may trigger or exacerbate mental disorders, particularly in individuals with specific vulnerabilities.

• What are some effects of specific abused substances?

   
    ^25,19
   
  •   Nicotine is an addictive stimulant found in cigarettes and other forms of tobacco. Tobacco smoke increases a user's risk of cancer, emphysema, bronchial disorders, and cardiovascular disease. The mortality rate associated with tobacco addiction is staggering. Tobacco use killed approximately 100 million people during the 20th century and, if current smoking trends continue, the cumulative death toll for this century has been projected to reach 1 billion.
• • Alcohol consumption can damage the brain and most body organs. Areas of the brain that are especially vulnerable to alcohol-related damage are the cerebral cortex (largely responsible for our higher brain functions, including problem solving and decisionmaking), the hippocampus (important for memory and learning), and the cerebellum (important for movement coordination).
   
  •   Marijuana is the most commonly abused illicit substance. This drug impairs short-term memory and learning, the ability to focus attention, and coordination. It also increases heart rate, can harm the lungs, and can increase the risk of psychosis in those with an underlying vulnerability.
• • Inhalants are volatile substances found in many household products, such as oven cleaners, gasoline, spray paints, and other aerosols, that induce mind-altering effects. Inhalants are extremely toxic and can damage the heart, kidneys, lungs, and brain. Even a healthy person can suffer heart failure and death within minutes of a single session of prolonged sniffing of an inhalant.
   
  •   Cocaine is a short-acting stimulant, which can lead abusers to "binge" (to take the drug many times in a single session). Cocaine abuse can lead to severe medical consequences related to the heart and the respiratory, nervous, and digestive systems.
• • Amphetamines, including methamphetamine, are powerful stimulants that can produce feelings of euphoria and alertness. Methamphetamine's effects are particularly long lasting and harmful to the brain. Amphetamines can cause high body temperature and can lead to serious heart problems and seizures.
   
  •   Ecstasy (MDMA) produces both stimulant and mind-altering effects. It can increase body temperature, heart rate, blood pressure, and heart wall stress. Ecstasy may also be toxic to nerve cells.
   
  •   LSD is one of the most potent hallucinogenic, or perception-altering, drugs. Its effects are unpredictable, and abusers may see vivid colors and images, hear sounds, and feel sensations that seem real but do not exist. Abusers also may have traumatic experiences and emotions that can last for many hours. Some short-term effects can include increased body temperature, heart rate, and blood pressure; sweating; loss of appetite; sleeplessness; dry mouth; and tremors.
   
  •   Heroin is a powerful opiate drug that produces euphoria and feelings of relaxation. It slows respiration and its use is linked to an increased risk of serious infectious diseases, especially when taken intravenously. Other opioid drugs include morphine, OxyContin, Vicodin, and Percodan, which have legitimate medical uses; however, their nonmedical use or abuse can result in the same harmful consequences as abusing heroin.
   
  •   Prescription medications are increasingly being abused or used for nonmedical purposes. This practice cannot only be addictive, but in some cases also lethal. Commonly abused classes of prescription drugs include painkillers, sedatives, and stimulants. Among the most disturbing aspects of this emerging trend is its prevalence among teenagers and young adults, and the common misperception that because these medications are prescribed by physicians, they are safe even when used illicitly.
   
  •   Steroids, which can also be prescribed for certain medical conditions, are abused to increase muscle mass and to improve athletic performance or physical appearance. Serious consequences of abuse can include severe acne, heart disease, liver problems, stroke, infectious diseases, depression, and suicide.
   
  •   Drug combinations. A particularly dangerous and not uncommon practice is the combining of two or more drugs. The practice ranges from the co-administration of legal drugs, like alcohol and nicotine, to the dangerous random mixing of prescription drugs, to the deadly combination of heroin or cocaine with fentanyl (an opioid pain medication). Whatever the context, it is critical to realize that because of drug-drug interactions, such practices often pose significantly higher risks than the already harmful individual drugs.
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• To send a message a brain cell releases a chemical (neurotransmitter) into the space separating two cells called the synapse. The neurotransmitter crosses the synapse and attaches to proteins (receptors) on the receiving brain cell. This causes changes in the receiving brain cell and the message is delivered.

• How do drugs work in the brain?

   

  Drugs are chemicals. They work in the brain by tapping into the brain's communication system and interfering with the way nerve cells normally send, receive, and process information. Some drugs, such as marijuana and heroin, can activate neurons because their chemical structure mimics that of a natural neurotransmitter. This similarity in structure "fools" receptors and allows the drugs to lock onto and activate the nerve cells. Although these drugs mimic brain chemicals, they don't activate nerve cells in the same way as a natural neurotransmitter, and they lead to abnormal messages being transmitted through the network.

   

  Other drugs, such as amphetamine or cocaine, can cause the nerve cells to release abnormally large amounts of natural neurotransmitters or prevent the normal recycling of these brain chemicals. This disruption produces a greatly amplified message, ultimately disrupting communication channels. The difference in effect can be described as the difference between someone whispering into your ear and someone shouting into a microphone

• How do drugs work in the brain to produce pleasure?

   

  Most drugs of abuse directly or indirectly target the brain's reward system by flooding the circuit with dopamine. Dopamine is a neurotransmitter present in regions of the brain that regulate movement, emotion, cognition, motivation, and feelings of pleasure. The overstimulation of this system, which rewards our natural behaviors, produces the euphoric effects sought by people who abuse drugs and teaches them to repeat the behavior.

• How does stimulation of the brain's pleasure circuit teach us to keep taking drugs?

   

  Our brains are wired to ensure that we will repeat life-sustaining activities by associating those activities with pleasure or reward. Whenever this reward circuit is activated, the brain notes that something important is happening that needs to be remembered, and teaches us to do it again and again, without thinking about it. Because drugs of abuse stimulate the same circuit, we learn to abuse drugs in the same way

• Why are drugs more addictive than natural rewards?

   

  When some drugs of abuse are taken, they can release 2 to 10 times the amount of dopamine that natural rewards do.¹⁵ In some cases, this occurs almost immediately (as when drugs are smoked or injected), and the effects can last much longer than those produced by natural rewards. The resulting effects on the brain's pleasure circuit dwarfs those produced by naturally rewarding behaviors such as eating and sex.^16,17 The effect of such a powerful reward strongly motivates people to take drugs again and again. This is why scientists sometimes say that drug abuse is something we learn to do very, very well.

• What happens to your brain if you keep taking drugs?

   

  Just as we turn down the volume on a radio that is too loud, the brain adjusts to the overwhelming surges in dopamine (and other neurotransmitters) by producing less dopamine or by reducing the number of receptors that can receive signals. As a result, dopamine's impact on the reward circuit of a drug abuser's brain can become abnormally low, and the ability to experience any pleasure is reduced. This is why the abuser eventually feels flat, lifeless, and depressed, and is unable to enjoy things that previously brought them pleasure. Now, they need to take drugs just to try and bring their dopamine function back up to normal. And, they must take larger amounts of the drug than they first did to create the dopamine high - an effect known as tolerance.
• Decreased Dopamine Transporters in a Methamphetamine Abuser Methamphetamine abusers have significant reductions in dopamine transporters.

• How does long-term drug taking affect brain circuits?

   

  We know that the same sort of mechanisms involved in the development of tolerance can eventually lead to profound changes in neurons and brain circuits, with the potential to severely compromise the long-term health of the brain. For example, glutamate is another neurotransmitter that influences the reward circuit and the ability to learn. When the optimal concentration of glutamate is altered by drug abuse, the brain attempts to compensate for this change, which can cause impairment in cognitive function. Similarly, long-term drug abuse can trigger adaptations in habit or nonconscious memory systems. Conditioning is one example of this type of learning, whereby environmental cues become associated with the drug experience and can trigger uncontrollable cravings if the individual is later exposed to these cues, even without the drug itself being available. This learned "reflex" is extremely robust and can emerge even after many years of abstinence

• What other brain changes occur with abuse?

   

  Chronic exposure to drugs of abuse disrupts the way critical brain structures interact to control and inhibit behaviors related to drug abuse. Just as continued abuse may lead to tolerance or the need for higher drug dosages to produce an effect, it may also lead to addiction, which can drive an abuser to seek out and take drugs compulsively. Drug addiction erodes a person's self-control and ability to make sound decisions, while sending intense impulses to take drugs.
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• Abstract

  Rationale and background

  High relapse rates during

  abstinence are a pervasive problem in drug addiction

  treatment. Relapse is often associated with stress exposure,

  which can provoke a subjective state of drug craving that

  can also be demonstrated unde

  r controlled laboratory

  conditions. Stress-induced relapse and craving in humans

  can be modeled in mice, rats, and monkeys using a

  reinstatement model in which drug-taking behaviors are

  extinguished and then reinstated by acute exposure to

  certain stressors
• The high rate of relapse to drug use following periods of

  forced or self-imposed abstinence is a major clinical

  problem in addiction treatment (Hunt et al.

  1971

  ;O

  ’

  Brien

  and Gardner

  2005

  ). Clinical studies suggest that stress is

  among the key factors contributing to these high relapse

  rates (Brownell et al.

  1986

  ; Sinha

  2001

  ). Prospective

  human studies have shown that stress exposure (either

  acute stressors like an argument with coworkers or more

  chronic adverse life events like divorce or job loss) is

  associated with subsequent drug relapse (Baker et al.

  2004

  ;

  Brown et al.

  1990

  ; Brown et al.

  1995

  ; Epstein et al.

  2009a

  ;

  Hyman et al.

  2007

  ; Preston and Epstein

  2011

  ; Shiffman

  2005

  ; Sinha

  2001

  ).
• induced reinstatement in mice and rats and stress-

  induced craving and potentially stress-induced relapse in

  humans. We also discuss brain sites and circuits involved in

  stress-induced reinstatement of drug seeking in rats and

  those activated during stress-induced craving in humans

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• are vulnerable, and once an individual begins smoking, those with certain

  genetic variants are at higher risk to drink or smoke heavily and have extreme

  difficulty quitting
• InNovember2010,theDirectoroftheNationalInstitutesofHealth(NIH),

  Francis Collins, announced the creation of a taskforce to help move all sub-

  stance use, abuse, and addiction research programs within the NIH into a

  single, new institute (Collins, 2010). This transition would force a merger of

  the National Institute on Drug Abuse (NIDA), the National Institute on Alco-

  hol Abuse and Alcoholism (NIAAA), and the drug-related research portfolios

  from other institutes such as the National Cancer Institute (NCI) (Seffrin

  et al., 2010). Supporters justify the new institute’s creation by highlighting

  an emerging body of scientific findings: recent research in neuroscience sug-

  gests that a single mechanism underlies compulsive behavior and addiction,

  regardless of the particular substance or drug of abuse. Similar brain reward

  pathways are thought to be involved in the development and maintenance

  of addiction, raising the possibility of common risk factors and the hope for

  novel prevention and treatment strategies across substances. In addition, sup-

  porters argue that many would be better served by a single institute combining

  all substance use, including patients with comorbid drug use, as well as the

  general population, which would benefit from comprehensive early preven-

  tion efforts (Scientific Management Review Board, 2010). Collins stated that

  this new institute “makes scientific sense and would enhance NIH’s efforts to

  address the substance abuse and addiction problems that take such a terrible

  toll on our society” (Collins, 2010)
• Recent studies indicate that genes in the chromosomal region

  that code for brain-derived neurotropic factor (BDNF) are associated with

  smokinginitiation(TobaccoandGeneticsConsortium,2010).Similarly,some

  NIDA-funded researchers argue that genetically-based personality traits like

  risk taking and impulsivity may predispose certain individuals to experiment

  with drugs, including tobacco (Kreek et al., 2005). Neurogenetic research

  claims that people may become addicted to drugs for reasons that include

  genetic predispositions, personality predilections, and risks from a variety of

  comorbid disorders and diseases such as schizophrenia (Courtwright, 2010;

  Keane and Hamill, 2010; Kushner, 2010
• Important social consequences arise from the way neuroscience and genetic

  research is subtly, and at times not so subtly, constructing a new understanding

  of addiction as a disease of the brain or as a “genetic” or biological disorder. In

  this article, we use nicotine addiction as a case study through which to under-

  stand the changing nature of our perceptions of addiction and to anticipate

  how new frameworks will be integrated into existing public health and clinical

  programs at the federal, state, and local levels. Indeed, the issues and concerns

  we raise are not limited to the study of one phenomenon, nicotine addiction,

  but are relevant to a range of complex behaviors that involve substance use for

  which researchers seek to locate genetic underpinnings. Tobacco serves as an

  illustrative case because the medicalization of smoking/tobacco addiction has

  occurred more recently than for other substances, for example, alcoholism. It

  is also an arena where both social programs (e.g., clean air laws and higher

  taxes) and pharmaceutical interventions (e.g., nicotine replacement therapies)

  have been successful
• mplications for societal and clinical responses to nicotine addiction as well as

  for the subjectivity of smokers.

  A conception of addiction as a disease of the brain also has potential legal

  implications,thoughthesearemorerelevanttoillicitdrugsandalcoholthanto

  nicotine. Legal responsibility is distinct from the public or lay understandings

  of responsibility discussed earlier, and the courts have consistently ruled that

  addicts are responsible for illegal behavior (

  Powell v. Texas

  , 1968;

  Traynor v.

  Turnage

  , 1988;

  United States v. Moore

  , 1973). However, the disease model of

  addiction has influenced sentencing—addicts are still legally responsible for

  their actions, butthe consequences of a guiltyverdictmay be mediatedby their

  addiction. For example, the rise of drug courts presents a significant deviation

  from traditional adjudication, in which nosologic categories were irrelevant

  (Nolan, 2002). Drug courts offer an alternative that provides a space for

  law and therapy to be “a fully collaborative enterprise” (Nolan, 2002:1726).

  In drug courts, addiction is understood as a disease and not the result of

  poor moral choices; this model provides the basis for the courts to “coerce”

  treatment and replace prison with heavy surveillance and treatment (Tiger,

  2011).
• Although NIDA funds prevention

  and environmental influences on drug initiation, maintenance, and cessation,

  the bulk of NIDA research funding ($519.497 million) goes to “Basic and

  Clinical Neuroscience,” which includes work to “expand the understanding

  of the neurobiological, genetic/epigenetic, and behavioral factors underlying

  drug abuse and addiction” (National Institute on Drug Abuse, 2011). Another

  $116.017 million goes to “Pharmacotherapies and Medical Consequences”

  research, which is responsible for “medications development aimed at help-

  ing people recover from drug abuse and addiction and sustain abstinence”

  (National Institute on Drug Abuse, 2011).
• Imaging studies, including positron emission tomography (PET), magnetic

  resonance imaging (MRI), and functional MRI (fMRI) (Illes, Kirschen, and

  Gabrieli, 2003; Li and Sinha, 2008; Volkow et al., 2007) have intensified un-

  derstandings of addiction as a brain disease in profound ways because of the

  power of brain images to make objective claims not only about our brains, but

  also about who we are (Dumit, 2004). As Wayne Hall has noted, “a ‘disease’

  that can be ‘seen’ in the many-hued splendour of a PET scan carries more con-

  viction than . . . self-reports of addicts who claim they are unable to control

  their drug use” (Hall, Carter, and Morley, 2003:867). Because brain images

  are fluid signifiers that are easily (if at times inaccurately) made meaningful

  by society and laypersons (McCabe and Castel, 2007), they can serve differ-

  ent meanings simultaneously (Dumit, 2004). As Campbell states, “the social

  power of this tool is lodged in its potential to change public perceptions—to

  effectively change the ‘truths’ upon which members of the public proceed on

  the path to recovery” (Campbell, 2010:100). As a consequence, independent

  of researchers’ intentions and prior to any clinical applications, neuroimag-

  ing research on addiction is creating novel relationships between brain im-

  ages, “brain types,” and individual perceptions of self and disease that hav
• Tobacco use has followed alcohol and other drugs in

  a conceptual shift from being viewed as a habit to, in many scientific and

  medical circles, a disease (cf. Kessler et al., 1997; Kmietowicz, 2000). Smok-

  ing, with roots in spiritual and medicinal ceremonies in native New World

  cultures, has long been considered a “habit,” possibly even beneficial to one’s

  health and capable of stimulating virility and vigor and staving off syphilis

  (Robicsek, 2004).
• ur interviews show that addiction is widely understood as an uncontrollable

  behavior, with individuals unable to quit on their own. These statements are

  consistent with the fact that diagnosis for substance-use disorders remains

  focused on behavior; although there is increasing use of pharmaceutical inter-

  ventions for addiction (e.g., nicotine replacement therapy and non-nicotine

  pharmaceuticals like bupropion and varenicline), treatment programs con-

  tinue to focus on behavior modification in order to facilitate smoking cessa-

  tion.

  Probes about addiction etiology yielded a stakeholder view of addiction

  that is consistent with the conception that the potential for addiction exists

  in our bodies prior to drug use, waiting to be triggered, especially for those

  with certain genetic profiles. Most stakeholders believed the environmental

  factors (e.g., peers, family, stress) to be the primary causal factor for smoking

  initiation, but the speed and severity with which one became dependent on

  tobacco was determined by biology—once you initiate smoking, it flips a

  biological “switch” that perpetuates the behavior. A typical comment wa
• or utilizing concepts including compulsive use, “needing the drug

  to feel well,” loss of control, “bad decision making,” craving, inability or

  difficulty quitting, increased tolerance, or use that interferes with a productive

  lifestyle. These results may be consistent with either environmental variables

  or biological ones; etiology is not clear. Examples include
• The NIDA paradigm does not preclude and, in fact, seems to include,

  genetic predispositions to addiction; NIDA publications cite the estimate that

  40to60percentofaperson’svulnerabilitytoaddictionisduetogeneticfactors

  (National Institute on Drug Abuse, 2007:8). Further, NIDA funds research

  that seeks to identify genetic predispositions that were initially identified

  through classic approaches such as twin studies: genome-wide association

  studies (GWAS) (Bierut et al., 2007) and recent meta-analyses of GWAS

  (Thorgeirsson et al., 2010) are part of the body of literature that utilizes the

  most recent techniques for examining possible genetic influences on smoking

  initiation, maintenance, and cessation (Amos, Spitz, and Cinciripini, 2010).

  Smoking thus parallels a common understanding of alcoholism: certain people
• An addiction is something that once you start doing it, the behavior or the

  drug or whatever it is, that you find it hard to stop, despite it having negative

  impacts on your health or how you feel. (clinician practicing on the East

  Coast)
• Individuals become addicted not just to the drug,

  but to neurotransmitters like dopamine and serotonin released in the brain

  (Keane and Hamill, 2010; Schull, 2003). Even for those without genetic or

  other risk factors, because of the power of the reward system of the brain, these

  artificial substances purportedly “flip a switch” in the brain such that, once

  activated, drug use moves from being voluntary to involuntary and “beyond

  one’s control” (Brower, 2006), especially as continued heavy use changes an

  individual’s brain structure and function
• Nicotine addiction . . . also leads to other diseases, . . . but I think in and

  to itself, it’s a disease.” (tobacco cessation specialist in a state public health

  department in the Pacific Northwest

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• Why Do Teens Use Alcohol and Other Drugs (AODs)?

    

  Even though it is illegal for anyone in the U.S. under age 21 to buy or be caught with alcohol or illegal drugs, many teens are still using. Alcohol use and the abuse of prescription drugs are common among teens. The most common drugs teens report using include alcohol, tobacco, caffeine, pot or weed (marijuana), and pills that were not prescribed to them. Other less used drugs include opiates, cocaine, amphetamines, hallucinogens, depressants, inhalants, club drugs, and performance enhancing drugs (Goldstein, 2011).

• Experts believe there are a number of reasons youth use AODs. First, recent research shows that the brain does not fully develop until around a person’s mid-twenties (Winters & Arria, 2011). The area of the brain that is last to develop is the pre-frontal cortex, which is in charge of judgment and decisionmaking. This is thought to be one reason why risky behaviors among teens is so common and why adults always puzzle over poor decisions teens make.

    

  Researchers have found that teens start using drugs and alcohol for four main reasons: (1) to improve their mood; (2) to receive social rewards; (3) to reduce negative feelings; and (4) to avoid social rejection (Kuntsche, Knibbe, Gmel, & Engels, 2005). Teens who reported social reasons for drinking were more likely to report moderate drinking. Those who wanted to improve their mood reported heavy alcohol use while those looking to reduce negative feelings showed problematic drinking patterns. Experts point to peer pressure and other social reasons for initial use of substances during teen years (Terry-McElrath, O’Malley, & Johnston, 2009). Teens will sometimes copy what their friends do to feel accepted, and some are curious about the effects of drugs on their mood and behavior.

• What Are the Problems with Teen Drug and Alcohol Use?

    

  Drug and alcohol use during teen and young adult years can lead to many problems for teens and their families. Teen AOD misuse can lead to skipping school, bad grades, conflict in relationships with friends and peers, rocky family relationships, and can cause poor brain function, concentration, and other areas of brain development (NIAAA, 2009). Some teens also get in trouble with the law and end up in court, involved with police and Social Services, and may spend time in juvenile detention (USDOJ, 2003). Teens that begin using AODs earlier are more likely to be heavy users and may become chemically dependent on substances later (NIAAA, 2009). These problems have a negative impact on the life of the teen and on their future work life, family relationships, friendships, and overall health

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• As the most commonly abused illicit drug in the United States (http://www.medicinenet.com/marijuana/page3.htm), marijuana has received its fair share of negative publicity. According to the National Survey on Drug Use and Health, in 2007, 14.4 million Americans aged 12 or older used marijuana at least once in the month prior to being surveyed, and about 6,000 people a day in 2007 used marijuana for the first time—2.1 million Americans, 62.2 percent of which were younger than 18 years of age
• One of these myths was that marijuana damages brain cells, and that this damage causes memory loss, cognitive impairment, and learning difficulties. They report that this claim is based on a study by Heath et. al (1980),  in which structural changes in several regions of the brain were found in two rhesus monkeys exposed to THC, the active chemical in marijuana. These changes occurred primarily in the hippocampus, the area of the brain known to play an important role in learning and memory, which suggested that exposure to THC in humans would yield similar negative results.
• However, according to Morgan and Zimmer, in order to achieve these damaging results, doses of up to 200 times the psychoactive dose in humans would have to be given. Even studies in which subjects were given 100 times the human dose failed to cause any structural impairment of the brain. Additionally, in a more recent study of rhesus monkeys by Slikker et. al (1992), in which the monkeys were exposed to the equivalent of 4-5 joints per day through face-mask inhalation for an entire year, seven months later there was no observed change in hippocampal structure, cell size, cell number, or synaptic configuration. As a result of these studies, Morgan and Zimmer concluded that the claim that marijuana causes physiological damage to brain cells is incorrect.
• A study by Block et. al (1999) yielded similar results, finding that “frequent marijuana use does not produce clinically apparent MRI abnormalities or detectable global or regional changes in brain tissue volumes of gray or white matter, or both combined”. However, the study notes that anatomical abnormalities could occur at a microscopic level that cannot be measured by an MRI, so the true results of the study remain somewhat unclear.
• Despite this, Morgan and Zimmer acknowledge that there is evidence that marijuana, especially in high doses, can interfere with users’ ability to transfer new information into long-term memory. Thus, although while under the influence of marijuana, learning is less efficient, there is no evidence that marijuana users suffer permanent structural impairment.

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• The most common amphetamine in Australia is methamphetamine, which comes in three forms:  
   
  • Speed – is the most common amphetamine and usually comes in the form of a powder.  
  • Base – is an oily, sticky or waxy paste.  
  • Ice (crystal methamphetamine) – is a crystal or crystalline powder, and is a stronger form of methamphetamine. It is also known as ‘crystal meth’, ‘shabu’ or ‘glass’.

• How amphetamines work

  
   When we are stressed or under threat, the central nervous system prepares us for physical action by creating particular physiological changes. Amphetamines prompt the brain to initiate this ‘fight or flight’ response. These changes include:  
   
  • The release of adrenalin and other stress hormones 
  • Increased heart rate and blood pressure 
  • Redirected blood flow into the muscles and away from the gut.
• Risk of damage to brain cells
• • Amphetamine psychosis, which includes hallucinations, paranoia and other symptoms similar to schizophrenia. This can lead to behaviour dangerous to the person and to others. 
  • Malnutrition, because the drug suppresses appetite 
  • Reduced immunity, due to malnutrition and lack of sleep 
  • Mood swings, depression and panic attacks 
  • The need to use other drugs, such as sleeping tablets, to balance the effects of amphetamines 
  • Aggression and increased susceptibility to violent rages.

• Social effects of long-term amphetamine use

  
   People who regularly use speed can also experience problems with: 
   
  • Relationships – such as arguments and break-ups. 
  • Work or study – including trouble concentrating and reduced performance. 
  • The law – being arrested for possession and use, violence or crimes committed to support use. 
  • Finances – such as debt because of an inability to hold down a job or from spending money on amphetamines.
• Amphetamines are psychostimulant drugs that abnormally speed up the functions of the brain and body.
• Long-term amphetamine misuse can damage the brain and may lead to psychosis, malnutrition and violent behaviour

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• Doctors that favor medical marijuana state:   

  Mollie Fry, MD, told ProCon.org in an Apr. 7, 2006 interview:

  "I took an oath to do no harm.  If a doctor is willing to give you a prescription for a drug that is addictive or could kill you, then why should you not be able to choose a non-toxic drug like marijuana?

• Leslie Iversen, PhD, Professor in the Department of Pharmacology at the University of Oxford, wrote in his Oct. 2000 book The Science of Marijuana:

  "Cannabis is a safer drug than aspirin and can be used long-term without serious side effects

• Side Effects of Smoking:

  About half of all Americans who continue to smoke will die because of the habit. Each year about 438,000 people in the United States die from illnesses related to cigarette smoking. Cigarettes kill more Americans than alcohol, car accidents, suicide, AIDS, homicide, and illegal drugs combined. 

• Cancer:

  Cigarette smoking accounts for at least 30% of all cancer deaths. It is a major cause of cancers of the lung, larynx (voice box), oral cavity, pharynx (throat), esophagus (swallowing tube connected to the stomach), and bladder, and it contributes to the development of cancers of the pancreas, cervix, kidney, stomach, and also some leukemias

• Marijuana can be used instrumentally.

  THC can be used to treat pain and decrease nausea in people with Cancer.  The only thing that makes it illegal is the law.
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