The National Institute of Mental Health (NIMH) is part of the National Institutes of Health (NIH), a component of the U.S. Department of Health and Human Services.

Marijuana

Marijuana is the most commonly abused illicit drug in the United States. A dry, shredded green/brown mix of flowers, stems, seeds, and leaves of the hemp plant Cannabis sativa, it usually is smoked as a cigarette (joint, nail), or in a pipe (bong). It also is smoked in blunts, which are cigars that have been emptied of tobacco and refilled with marijuana, often in combination with another drug. It might also be mixed in food or brewed as a tea. As a more concentrated, resinous form it is called hashish and, as a sticky black liquid, hash oil. Marijuana smoke has a pungent and distinctive, usually sweet-andsour odor. There are countless street terms for marijuana including pot, herb, weed, grass, widow, ganja, and hash, as well as terms derived from trademarked varieties of cannabis, such as Bubble Gum, Northern Lights, Fruity Juice, Afghani #1, and a number of Skunk varieties.

The main active chemical in marijuana is THC (delta-9-tetrahydrocannabinol). The membranes of certain nerve cells in the brain contain protein receptors that bind to THC. Once securely in place, THC kicks off a series of cellular reactions that ultimately lead to the high that users experience when they smoke marijuana.

Extent of Use —

In 2004, 14.6 million Americans age 12 and older used marijuana at least once in the month prior to being surveyed. About 6,000 people a day in 2004 used marijuana for the first time—

2.1 million Americans. Of these, 63.8 percent were under age 18(1). In the last half of 2003, marijuana was the third most commonly abused drug mentioned in drug-related hospital emergency department (ED) visits in the continental United States, at 12.6 percent, following cocaine (20 percent) and alcohol (48.7 percent)(2). Percentage of 8th-Graders Who Have Used Marijuana Monitoring the Future Survey, 2005 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 Lifetime 23.1% 22.6% 22.2% 22.0% 20.3% 20.4% 19.2% 17.5% 16.3% 16.5% Annual 18.3 17.7 16.9 16.5 15.6 15.4 14.6 12.8 11.8 12.2 30-day 11.3 10.2 9.7 9.7 9.1 9.2 8.3 7.5 6.4 6.6 Daily 1.5 1.1 1.1 1.4 1.3 1.3 1.2 1.0 0.8 1.0

Percentage of 10th-Graders Who Have Used Marijuana Monitoring the Future Survey, 2005 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 Lifetime 39.8% 42.3% 39.6% 40.9% 40.3% 40.1% 38.7% 36.4% 35.1% 34.1% Annual 33.6 34.8 31.1 32.1 32.2 32.7 30.3 28.2 27.5 26.6 30-day 20.4 20.5 18.7 19.4 19.7 19.8 17.8 17.0 15.9 15.2 Daily 3.5 3.7 3.6 3.8 3.8 4.5 3.9 3.6 3.2 3.1

Percentage of 12th-Graders Who Have Used Marijuana Monitoring the Future Survey, 2005 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 Lifetime 44.9% 49.6% 49.1% 49.7% 48.8% 49.0% 47.8% 46.1% 45.7% 44.8% Annual 35.8 38.5 37.5 37.8 36.5 37.0 36.2 34.9 34.3 33.6 30-day 21.9 23.7 22.8 23.1 21.6 22.4 21.5 21.2 19.9 19.8 Daily 4.9 5.8 5.6 6.0 6.0 5.8 6.0 6.0 5.6 5.0

*“Lifetime” refers to use at least once during a respondent’s lifetime. “Annual” refers to use at least once during the year preceding an individual’s response to the survey. “30-day” refers to use at least once during the 30 days preceding an individual’s response to the survey.

Prevalence of lifetime,* annual, and use within the last 30 days for marijuana remained stable among 10th- and 12thgraders surveyed between 2003 and 2004. However, 8th-graders reported a significant decline in 30-day use and a significant increase in perceived harmfulness of smoking marijuana once or twice and regularly(3). Trends in disapproval of using marijuana once or twice and occasionally rose among 8th-graders as well, and 10th-graders reported an increase in disapproval of occasional and regular use for the same period(3).

Effects on the Brain

Scientists have learned a great deal about how THC acts in the brain to produce its many effects. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to organs throughout the body, including the brain.

In the brain, THC connects to specific sites called cannabinoid receptors on nerve cells and influences the activity of those cells. Some brain areas have many cannabinoid receptors; others have few or none. Many cannabinoid receptors are found in the parts of the brain that influence pleasure, memory, thought, concentration, sensory and time perception, and coordinated movement(4).

The short-term effects of marijuana can include problems with memory and learning; distorted perception; difficulty in thinking and problem solving; loss of coordination; and increased heart rate. Research findings for long-term marijuana abuse indicate some changes in the brain similar to those seen after long- term abuse of other major drugs. For example, cannabinoid (THC or synthetic forms of THC) withdrawal in chronically exposed animals leads to an increase in the activation of the stress-response system(5) and changes in the activity of nerve cells containing dopamine(6). Dopamine neurons are involved in the regulation of motivation and reward, and are directly or indirectly affected by all drugs of abuse.

Effects on the Heart

One study has indicated that an abuser’s risk of heart attack more than quadruples in the first hour after smoking marijuana(7). The researchers suggest that such an effect might occur from marijuana’s effects on blood pressure and heart rate and reduced oxygen-carrying capacity of blood.

Effects on the Lungs

A study of 450 individuals found that people who smoke marijuana frequently but do not smoke tobacco have more health problems and miss more days of work than nonsmokers(8). Many of the extra sick days among the marijuana smokers in the study were for respiratory illnesses.

Even infrequent abuse can cause burning and stinging of the mouth and throat, often accompanied by a heavy cough. Someone who smokes marijuana regularly may have many of the same respiratory problems that tobacco smokers do, such as daily cough and phlegm production, more frequent acute chest illness, a heightened risk of lung infections, and a greater tendency to obstructed airways(9). Smoking marijuana possibly increases the likelihood of developing cancer of the head or neck. A study comparing 173 cancer patients and 176 healthy individuals produced evidence that marijuana smoking doubled or tripled the risk of these cancers(10).

Marijuana abuse also has the potential to promote cancer of the lungs and other parts of the respiratory tract because it contains irritants and carcinogens(9, 11). In fact, marijuana smoke contains 50 to 70 percent more carcinogenic hydrocarbons than does tobacco smoke(12). It also induces high levels of an enzyme that converts certain hydrocarbons into their carcinogenic form—levels that may accelerate the changes that ultimately produce malignant cells(13). Marijuana users usually inhale more deeply and hold their breath longer than tobacco smokers do, which increases the lungs’ exposure to carcinogenic smoke. These facts suggest that, puff for puff, smoking marijuana may be more harmful to the lungs than smoking tobacco.

Other Health Effects

Some of marijuana’s adverse health effects may occur because THC impairs the immune system’s ability to fight disease. In laboratory experiments that exposed animal and human cells to THC or other marijuana ingredients, the normal disease-preventing reactions of many of the key types of immune cells were inhibited(14). In other studies, mice exposed to THC or related substances were more likely than unexposed mice to develop bacterial infections and tumors(15, 16).

Effects of Heavy Marijuana Use on Learning and Social Behavior

Research clearly demonstrates that marijuana has the potential to cause problems in daily life or make a person’s existing problems worse. Depression(17), anxiety(17), and personality disturbances(18) have been associated with chronic marijuana use. Because marijuana compromises the ability to learn and remember information, the more a person uses marijuana the more he or she is likely to fall behind in accumulating intellectual, job, or social skills. Moreover, research has shown that marijuana’s adverse impact on memory and learning can last for days or weeks after the acute effects of the drug wear off(19, 20, 25).

Students who smoke marijuana get lower grades and are less likely to graduate from high school, compared with their nonsmoking peers(21, 22, 23, 24). A study of 129 college students found that, among those who smoked the drug at least 27 of the 30 days prior to being surveyed, critical skills related to attention, memory, and learning were significantly impaired, even after the students had not taken the drug for at least 24 hours(20). These “heavy” marijuana abusers had more trouble sustaining and shifting their attention and in registering, organizing, and using information than did the study participants who had abused marijuana no more than 3 of the previous 30 days. As a result, someone who smokes marijuana every day may be functioning at a reduced intellectual level all of the time.

More recently, the same researchers showed that the ability of a group of long-term heavy marijuana abusers to recall words from a list remained impaired for a week after quitting, but returned to normal within 4 weeks(25). Thus, some cognitive abilities may be restored in individuals who quit smoking marijuana, even after long-term heavy use.

Workers who smoke marijuana are more likely than their coworkers to have problems on the job. Several studies associate workers’ marijuana smoking with increased absences, tardiness, accidents, workers’ compensation claims, and job turnover. A study among postal workers found that employees who tested positive for marijuana on a preemployment urine drug test had 55 percent more industrial accidents, 85 percent more injuries, and a 75-percent increase in absenteeism compared with those who tested negative for marijuana use(26). In another study, heavy marijuana abusers reported that the drug impaired several important measures of life achievement including cognitive abilities, career status, social life, and physical and mental health(27).

Effects of Exposure During Pregnancy

Research has shown that some babies born to women who abused marijuana during their pregnancies display altered responses to visual stimuli(28), increased tremulousness, and a high-pitched cry, which may indicate neurological problems in development(29). During the preschool years, marijuana-exposed children have been observed to perform tasks involving sustained attention and memory more poorly than nonexposed children do(30, 31). In the school years, these children are more likely to exhibit deficits in problem-solving skills, memory, and the ability to remain attentive(30).

Addictive Potential

Long-term marijuana abuse can lead to addiction for some people; that is, they abuse the drug compulsively even though it interferes with family, school, work, and recreational activities. Drug craving and withdrawal symptoms can make it hard for long-term marijuana smokers to stop abusing the drug. People trying to quit report irritability, sleeplessness, and anxiety(32). They also display increased aggression on psychological tests, peaking approximately one week after the last use of the drug(33).

Genetic Vulnerability

Scientists have found that whether an individual has positive or negative sensations after smoking marijuana can be influenced by heredity. A 1997 study demonstrated that identical male twins were more likely than nonidentical male twins to report similar responses to marijuana abuse, indicating a genetic basis for their response to the drug(34). (Identical twins share all of their genes.)

It also was discovered that the twins’ shared or family environment before age 18 had no detectable influence on their response to marijuana. Certain environmental factors, however, such as the availability of marijuana, expectations about how the drug would affect them, the influence of friends and social contacts, and other factors that differentiate experiences of identical twins were found to have an important effect.(34)

Treating Marijuana Problems

The latest treatment data indicate that, in 2002, marijuana was the primary drug of abuse in about 15 percent (289,532) of all admissions to treatment facilities in the United States. Marijuana admissions were primarily male (75 percent), White (55 percent), and young (40 percent were in the 15–19 age range). Those in treatment for primary marijuana abuse had begun use at an early age; 56 percent had abused it by age 14 and 92 percent had abused it by 18(35).

One study of adult marijuana abusers found comparable benefits from a 14session cognitive-behavioral group treatment and a 2-session individual treatment that included motivational interviewing and advice on ways to reduce marijuana use. Participants were mostly men in their early thirties who had smoked marijuana daily for more than 10 years. By increasing patients’ awareness of what triggers their marijuana abuse, both treatments sought to help patients devise avoidance strategies. Abuse, dependence symptoms, and psychosocial problems decreased for at least 1 year following both treatments; about 30 percent of the patients were abstinent during the last 3-month followup period(36).

Another study suggests that giving patients vouchers that they can redeem for goods—such as movie passes, sporting equipment, or vocational training— may further improve outcomes(37).

Although no medications are currently available for treating marijuana abuse, recent discoveries about the workings of the THC receptors have raised the possibility of eventually developing a medication that will block the intoxicating effects of THC. Such a medication might be used to prevent relapse to marijuana abuse by lessening or eliminating its appeal.

References

1 Results from the 2004 National Survey on Drug Use and Health: National Findings (Office of Applied Studies, NSDUH Series H–27, DHHS Publication No. SMA 05–4061). Rockville, MD, 2004. NSDUH is an annual survey conducted by the Substance Abuse and Mental Health Services Administration. Copies of the latest survey are available from the National Clearinghouse for Alcohol and Drug Information at 800-729-6686.

2 These data are from the annual Drug Abuse Warning Network, funded by the Substance Abuse and Mental Health Services Administration, DHHS. The survey provides information about emergency department visits that are induced by or related to the use of an illicit drug or the nonmedical use of a legal drug. The latest data are available at 800729-6686 or online at www.samhsa.gov.

3 These data are from the 2005 Monitoring the Future Survey, funded by the National Institute on Drug Abuse, National Institutes of Health, DHHS, and conducted annually by the University of Michigan’s Institute for Social Research. The survey has tracked 12th-graders’ illicit drug use and related attitudes since 1975; in 1991, 8th- and 10th-graders were added to the study. The latest data are online at www.drugabuse.gov.

4 Herkenham M, Lynn A, Little MD, Johnson MR, et al. Cannabinoid receptor localization in the brain. Proc Natl Acad Sci, USA 87(5):1932–1936, 1990.

5 Rodriguez de Fonseca F, et al. Activation of cortocotropin-releasing factor in the limbic system during cannabinoid withdrawal. Science 276(5321):2050–2054, 1997.

6 Diana M, Melis M, Muntoni AL, et al. Mesolimbic dopaminergic decline after cannabinoid withdrawal. Proc Natl Acad Sci 95(17):10269–10273, 1998.

7 Mittleman MA, Lewis RA, Maclure M, et al. Triggering myocardial infarction by marijuana. Circulation 103(23):2805–2809, 2001.

8 Polen MR, Sidney S, Tekawa IS, et al. Health care use by frequent marijuana smokers who do not smoke tobacco. West J Med 158(6):596–601, 1993.

9 Tashkin DP. Pulmonary complications of smoked substance abuse. West J Med 152(5):525–530, 1990.

10 Zhang ZF, Morgenstern H, Spitz MR, et al. Marijuana use and increased risk of squamous cell carcinoma of the head and neck. Cancer Epidemiology, Biomarkers & Prevention 8(12):1071–1078, 1999.

11 Sridhar KS, Raub WA, Weatherby, NL Jr., et al. Possible role of marijuana smoking as a carcinogen in the development of lung cancer at a young age. Journal of Psychoactive Drugs 26(3):285–288, 1994.

12 Hoffman D, Brunnemann KD, Gori GB, et al. On the carcinogenicity of marijuana smoke. In: VC Runeckles, ed, Recent Advances in Phytochemistry. New York. Plenum, 1975.

13 Cohen S. Adverse effects of marijuana: Selected issues. Annals of the New York Academy of Sciences 362:119–124, 1981.

14 Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91(11):1585–1614, 1996.

15 Friedman H, Newton C, Klein TW. Microbial infections, immunomodulation, and drugs of abuse. Clin Microbiol Rev 16(2):209–219, 2003.

16 Zhu LX, Sharma M, Stolina S, et al. Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor- mediated, cytokine-dependent pathway. J Immunology 165(1):373–380, 2000.

17 Brook JS, Rosen Z, Brook DW. The effect of early marijuana use on later anxiety and depressive symptoms. NYS Psychologist 35–39, January 2001.

18 Brook JS, Cohen P, Brook DW. Longitudinal study of co-occurring psychiatric disorders and substance use. J Acad Child and Adolescent Psych 37(3):322–330, 1998.

19 Pope HG, Yurgelun-Todd D. The residual cognitive effects of heavy marijuana use in college students. JAMA 275(7):521–527, 1996.

20 Block RI, Ghoneim MM. Effects of chronic marijuana use on human cognition. Psychopharmacology 100(1–2):219–228, 1993.

21 Lynskey M, Hall W. The effects of adolescent cannabis use on educational attainment: A review. Addiction 95(11):1621–1630, 2000.

22 Kandel DB, Davies M. High school students who use crack and other drugs. Arch Gen Psychiatry 53(1):71–80, 1996.

23 Rob M, Reynolds I, Finlayson PF. Adolescent marijuana use: Risk factors and implications. Aust NZ J Psychiatry 24(1):45–56, 1990.

24 Brook JS, Balka EB, Whiteman M. The risks for late adolescence of early adolescent marijuana use. Am J Public Health 89(10):1549–1554, 1999.

25 Pope HG, Gruber AJ, Hudson JI, et al. Neuropsychological performance in long-term cannabis users. Arch Gen Psychiatry 58(10):909–915, 2001.

26 Zwerling C, Ryan J, Orav EJ. The efficacy of pre-employment drug screening for marijuana and cocaine in predicting employment outcome.

27 Gruber AJ, Pope HG, Hudson JI, et al. Attributes of long-term heavy cannabis users: A case control study. Psychological Medicine 33(8):1415–1422, 2003.

28 Fried PA, Makin JE. Neonatal behavioural correlates of prenatal exposure to marihuana, cigarettes and alcohol in a low risk population. Neurotoxicology and Teratology 9(1):1–7, 1987.

29 Lester BM, Dreher M. Effects of marijuana use during pregnancy on newborn crying. Child Development 60(23/24):764–771, 1989.

30 Fried PA. The Ottawa prenatal prospective study (OPPS): Methodological issues and findings. It’s easy to throw the baby out with the bath water. Life Sciences 56(23–24):2159–2168, 1995.

31 Fried PA, Smith AM. A literature review of the consequences of prenatal marihuana exposure: An emerging theme of a deficiency in aspects of executive function. Neurotoxicology and Teratology 23(1):1–11, 2001.

32 Kouri EM, Pope HG, Lukas SE. Changes in aggressive behavior during withdrawal from long-term marijuana use. Psychopharmacology 143(3):302–308, 1999.

33 Haney M, Ward AS, Comer SD, et al. Abstinence symptoms following smoked marijuana in humans. Psychopharmacology 141(4):395–404, 1999.

34 Lyons MJ, Toomey R, Meyer JM, et al. How do genes influence marijuana use? The role of subjective effects. Addiction 92(4):409–417, 1997.

35 These data from the Treatment Episode Data Set (TEDS) 2003: Substance Abuse Treatment Admissions by Primary Substance of Abuse, According to Sex, Age Group, Race, and Ethnicity, funded by the Substance Abuse and Mental Health Services Administration, DHHS. The latest data are available at 800-729-6686 or online at www.samhsa.gov.

36 Stephens RS, Roffman RA, Curtin L. Comparison of extended versus brief treatments for marijuana use. J Consult Clin Psychol 68(5):898–908, 2000.

37 Budney AJ, Higgins ST, Radonovich KJ, et al. Adding voucher-based incentives to coping skills and motivational enhancement improves outcomes during treatment for marijuana dependence. J Consult Clin Psychol 68(6):1051–1061, 2000.

National Institutes of Health – U.S. Department of Health and Human Services

This material may be used or reproduced without permission from NIDA. Citation of the source is appreciated.

Prescription Medications

Brief Description:
Prescription drugs that are abused or used for nonmedical reasons can alter brain activity and lead to dependence. Commonly abused classes of prescription drugs include opioids (often prescribed to treat pain), central nervous system depressants (often prescribed to treat anxiety and sleep disorders), and stimulants (prescribed to treat narcolepsy, ADHD, and obesity).

Street Names:
Commonly used opioids include oxycodone (OxyContin), propoxyphene (Darvon), hydrocodone (Vicodin), hydromorphone (Dilaudid), meperidine (Demerol), and diphenoxylate (Lomotil). Common central nervous system depressants include barbiturates such as pentobarbital sodium (Nembutal), and benzodiazepines such as diazepam (Valium) and alprazolam (Xanax). Stimulants include dextroamphetamine (Dexedrine) and methylphenidate (Ritalin).

Effects:

  Long-term use of opioids or central nervous system depressants can lead to physical dependence and addiction. Taken in high doses, stimulants can lead to compulsive use, paranoia, dangerously high body temperatures, and irregular heartbeat.

Statistics and Trends:

  According to NIDA's 2005 Monitoring the Future study, 9.5% of high school seniors used hydrocodone (Vicodin) in the past year. Source: NIDA Infofacts: High School and Youth Trends.

Methamphetamine is a very addictive stimulant drug that activates certain systems in the brain. It is chemically related to amphetamine but, at comparable doses, the effects of methamphetamine are much more potent, longer lasting, and more harmful to the central nervous system (CNS).

Methamphetamine is a Schedule II stimulant, which means it has a high potential for abuse and is available only through a prescription that cannot be refilled. It can be made in small, illegal laboratories, where its production endangers the people in the labs, neighbors, and the environment. Street methamphetamine is referred to by many names, such as ?speed,? ?meth,? and ?chalk.? Methamphetamine hydrochloride, clear chunky crystals resembling ice, which can be inhaled by smoking, is referred to as ?ice,? ?crystal,? ?glass,? and ?tina.? 1

Methamphetamine is taken orally, intranasally (snorting the powder), by needle injection, or by smoking. Abusers may become addicted quickly, needing higher doses and more often. At this time, the most effective treatments for methamphetamine addiction are behavioral therapies such as cognitive behavioral and contingency management interventions.

Health Hazards
Methamphetamine increases the release of very high levels of the neurotransmitter dopamine, which stimulates brain cells, enhancing mood and body movement. Chronic methamphetamine abuse significantly changes how the brain functions. Animal research going back more than 30 years shows that high doses of methamphetamine damage neuron cell endings. Dopamine- and serotonin-containing neurons do not die after methamphetamine use, but their nerve endings (?terminals?) are cut back, and regrowth appears to be limited. Noninvasive human brain imaging studies have shown alterations in the activity of the dopamine system. These alterations are associated with reduced motor speed and impaired verbal learning. Recent studies in chronic methamphetamine abusers have also revealed severe structural and functional changes in areas of the brain associated with emotion and memory, which may account for many of the emotional and cognitive problems observed in chronic methamphetamine abusers.

Taking even small amounts of methamphetamine can result in increased wakefulness, increased physical activity, decreased appetite, increased respiration, rapid heart rate, irregular heartbeat, increased blood pressure, and hyperthermia. Other effects of methamphetamine abuse may include irritability, anxiety, insomnia, confusion, tremors, convulsions, and cardiovascular collapse and death. Long-term effects may include paranoia, aggressiveness, extreme anorexia, memory loss, visual and auditory hallucinations, delusions, and severe dental problems.

Also, transmission of HIV and hepatitis B and C can be a consequence of methamphetamine abuse. Among abusers who inject the drug, infection with HIV and other infectious diseases is spread mainly through the re-use of contaminated syringes, needles, and other injection equipment by more than one person. The intoxicating effects of methamphetamine, however, whether it is injected or taken other ways, can alter judgment and inhibition and lead people to engage in unsafe behaviors. Methamphetamine abuse actually may worsen the progression of HIV and its consequences; studies with methamphetamine abusers who have HIV indicate that the HIV causes greater neuronal injury and cognitive impairment compared with HIV-positive people who do not use drugs.

Extent of Use
Monitoring the Future Study (MTF)*
Past year** methamphetamine use in 2006 was reported by 1.8 percent of 8th-graders, 1.8 percent of 10th-graders (which represents a statistically significant decline from 2.9 percent in 2005), and 2.5 percent of 12th-graders. Perceived risk of harm from trying crystal methamphetamine, collected only for 12th-graders, increased from 54.6 percent in 2005 to 59.1 percent in 2006.

Methamphetamine Prevalence of Abuse
Monitoring the Future Survey, 2006

8th Grade 10th Grade 12th Grade
Lifetime 2.7% 3.2% 4.4%
Past Year 1.8 1.8 2.5
Past Month 0.6 0.7 0.9

Community Epidemiology Work Group (CEWG)***
In eight areas with data available from 2002 to 2005, sizable increases in primary methamphetamine treatment admissions as a proportion of total treatment admission, excluding alcohol, occurred in six; the increases were greatest in Arizona, Minneapolis/St. Paul, Los Angeles County, Denver, and Atlanta. Trend data show decreases in lab incidents from 2002 to 2005 in all CEWG States except Florida (up from 157 to 273), Michigan (from 225 to 341), and Pennsylvania (up from 30 to 79).

In the 2005 reporting period, primary treatment admissions for methamphetamine abuse as a proportion of all admissions, excluding alcohol, continued to be highest in Hawaii (56.3 percent) and San Diego (49.4 percent). Trend data from 2004 to 2005 show increases in methamphetamine treatment admissions as a proportion of all admissions, excluding alcohol, of between 4.1 and 4.7 percentage points in Atlanta, Los Angeles, and San Diego. The proportion of primary methamphetamine treatment admissions declined 5 percentage points in Arizona.

Demographic data available from seven CEWG areas suggest that, compared with cocaine and heroin admissions, primary methamphetamine admissions are more likely to be female, White, and younger than 25.

Unweighted DAWN Live! data for 2005 show that methamphetamine emergency department reports exceeded those for all other illicit drugs, excluding alcohol, in Phoenix and San Diego, and accounted for the second highest number of reports in San Francisco.

National Survey on Drug Use and Health (NSDUH)****
According to the 2005 NSDUH, 10.4 million Americans age 12 and older had tried methamphetamine at least once in their lifetimes. The rates for past month and past year methamphetamine use did not change between 2004 and 2005, but the lifetime rate declined from 4.9 percent to 4.3 percent. From 2002 to 2005, decreases were seen in lifetime (5.3 percent to 4.3 percent) and past year (0.7 percent to 0.5 percent) use, but not past month use.

Rates of past year methamphetamine use among persons aged 12 or older were among the highest in Nevada (2.0 percent), Montana (1.5 percent), and Wyoming (1.5 percent). Young adults aged 18 to 25 were more likely to use methamphetamine in the past year than youths aged 12 or 17 and adults aged 26 or older.

Other Information Resources
For more information on the effects of methamphetamine abuse and addiction, visit www.drugabuse.gov/drugpages/methamphetamine.html.

To find publicly-funded treatment facilities by state, visit www.findtreatment.samhsa.gov.

Stress and Substance Abuse

In the aftermath of the terrorist attacks on New York City and Washington, D.C., people across the country and abroad are struggling with the emotional impact of large-scale damage and loss of life, as well as the uncertainty of what will happen next. These are stressful times for all and may be particularly difficult times for people who are more vulnerable to substance abuse or may be recovering from an addiction. For example, we know that stress is one of the most powerful triggers for relapse in addicted individuals, even after long periods of abstinence. NIDA-supported ethnographers are already reporting increases in street sales of various drugs. Given that individuals may turn to drugs to cope with life's stressors, it is more important than ever that NIDA supports a comprehensive research portfolio that better informs how we prevent and treat drug abuse and addiction.

Stress and Drug Abuse; Stress and Relapse to Drug Abuse
Many clinicians and addiction medicine specialists suggest that stress is the number one cause of relapse to drug abuse, including smoking. Now, research is elucidating a scientific basis for these clinical observations. In both people and animals, stress leads to an increase in the brain levels of a peptide known as corticotropin releasing factor (CRF). The increased CRF levels in turn triggers a cascade of biological responses. Animal and human research has implicated this cascade in the pathophysiology of both substance use disorders and Posttraumatic Stress Disorder (PTSD) (Jacobsen, et al. Am J Psychiatry 2001). Research also has shown that administering CRF or a chemical that mimics the action of CRF in animals produces increases in stress-related behaviors (Koob, Heinrichs. Brain Research 1999; Jones, et al. Psychopharmacology 1998). And, mice that lack a receptor for CRF (CRF1) have impaired stress responses and express less anxiety-related behavior (Smith, et al. Neuron 1998; Timpl, et al. Nature Genetics 1998). Furthermore, people subjected to chronic stress or those who show symptoms of PTSD often have hormonal responses that are not properly regulated and do not return to normal when the stress is over. This may make these individuals more prone to stress-related illnesses and may prompt patients to relapse to drug use.

Selected Research Findings on Stress and Drug Abuse; Stress and Relapse to Drug Abuse.
Studies have reported that individuals exposed to stress are more likely to abuse alcohol and other drugs or undergo relapse.

Kosten TR, Rounsaville BJ, Kleber HD: A 2.5 year follow-up of depressions, life crises, and treatment effects on abstinence among opioid addicts. Arch Gen Psychiatry 1986; 43:733-739.
Dawes MA, Antelman SM, Vanyukov MM, Giancola P, Tarter RE, Susman EJ, Mezzich A, Clark DB: Developmental sources of variation in liability to adolescent substance use disorders. Drug and Alcohol Dependence 2000; 61(1): 3-14.
Sinha R, Fuse T, Aubin LR, O'Malley SS: Psychological stress, drug-related cues, and cocaine craving. Psychopharmacology 2000; 152:140-148.

In an analysis of studies regarding factors that can lead to continued drug use among opiate addicts, high stress was found to predict continued drug use.

Brewer DD, Catalano RF, Haggerty K, Gainey RR, Fleming CB: A meta-analysis of predictors of continued drug use during and after treatment for opiate addiction. Addiction 1998; 93:73-92.

Research has shown that in animals not previously exposed to illicit substances, stressors increase vulnerability for drug self-administration.

Piazza PV, Deminiere JM, Le Moal M, Simon H: Stress- and pharmacologically-induced behavioral sensitization increases vulnerability to acquisition of amphetamine self-administration. Brain Research 1990; 514:22-26.

Acute stress can improve memory, whereas chronic stress can impair memory and may impair cognitive function.

McEwan BS, Sapolsky RM: Stress and Cognitive Function. Current Opinion in Neurobiology 1995; 5:205-216.

Research has shown that there is overlap between neurocircuits that respond to drugs and those that respond to stress.

Piazza PV, Le Moal M: Pathophysiological basis of vulnerability to drug abuse: role of an interaction between stress, glucocorticoids, and dopaminergic neurons. Annu Rev Pharmacol Toxicol 1996; 36:359-378.
Kreek MJ, Koob G: Drug dependence: Stress and dysregulation of brain reward pathways. Drug Alcohol Depend 1998; 51:23-47.
Piazza PV, Le Moal M: The role of stress in drug self-administration. Trends Pharmacol Sci 1998; 19(2):67-74.

Researchers have shown that, among drug-free cocaine abusers in treatment, exposure to personal stress situations led to consistent and significant increases in cocaine craving, along with activation of emotional stress and a physiological stress response. In another study of cocaine abusers in treatment, significant increases in cocaine and alcohol craving were observed with stress and drug cues imagery but not with neutral-relaxing imagery.

Sinha R, Catapano D, O'Malley S: Stress-induced craving and stress response in cocaine dependent individuals. Psychopharmacology 1999; 142:343-351.
Sinha R, Fuse T, Aubin LR, O'Malley SS: Psychological stress, drug-related cues, and cocaine craving. Psychopharmacology 2000; 152:140-148.

A follow-up study of smokers who had completed a national smoking cessation program showed that there is a strong relationship between stress coping resources and the ability to sustain abstinence.

Matheny KB, Weatherman KE: Predictors of Smoking Cessation and Maintenance. Journal of Clinical Psychology 1998; 54(2):223-235.

Animal studies have shown that stress induces relapse to heroin, cocaine, alcohol, and nicotine self-administration.

Shaham Y, Stewart J: Stress reinstates heroin-seeking in drug-free animals: an effect mimicking heroin, not withdrawal. Psychopharmacology 1995; 119:334-341.
Erb S, Shaham Y, Stewart J: Stress reinstates cocaine-seeking behavior after prolonged extinction and a drug-free period. Psychopharmacology 1996; 128:408-412.
Stewart J: Pathways to relapse: the neurobiology of drug- and stress-induced relapse to drug-taking. Journal of Psychiatry & Neuroscience 2000; 25:125-136
Ahmed SH, Koob GF: Cocaine- but not food-seeking behavior is reinstated by stress after extinction. Psychopharmacology 1997; 132:289-295.
Lê AD, Quan B, Juzytch W, Fletcher PJ, Joharchi N, Shaham Y: Reinstatement of alcohol-seeking by priming injections of alcohol and exposure to stress in rats. Psychopharmacology 1998; 135:169-174.
Y. Buczek, Lê AD, Wang A, Stewart J, Shaham Y: Stress reinstates nicotine seeking but not sucrose solution seeking in rats. Psychopharmacology 1999; 144:183-188.
Posttraumatic Stress Disorder (PTSD) and Substance Abuse
Research shows that Posttraumatic Stress Disorder (PTSD), a psychiatric disorder, may develop in people after they experience or witness life-threatening events such as terrorist incidents, military combat, natural disasters, serious accidents, or violent personal assaults like rape. Research also shows that PTSD is a risk factor for substance abuse and addiction. Because the events that occurred on September 11, 2001, were experienced by thousands of people, as well as rescue workers in and around the vicinity of the attacks, and were televised to millions across the world, it is likely that some individuals may develop behavioral and emotional re-adjustment problems. Symptoms of PTSD can include reexperiencing the trauma; avoidance of people, places, and thoughts connected to the event; and arousal, which may include trouble sleeping, exaggerated startle response, and hypervigilance. People who develop such symptoms may be more prone to escape from the realities of the day by self-medicating with drugs (Khantzian. Am J Psychiatry 1985). In fact, clinical observations suggest that PTSD patients may use psychoactive substances without a physician?s directions to relieve traumatic memories and other symptoms associated with PTSD (Brown. Drug Alcohol Dependence 1994).

Selected Research Findings on PTSD and Substance Use Disorders
High rates of comorbidity of PTSD and substance use disorders were first reported in war-related studies, in which as many as 75% of combat veterans with lifetime PTSD also met criteria for alcohol abuse or dependence.

Kulka RA, Schlenger WE, Fairbank JA, Hough RL, Jordan BK, Marmar CR, Weiss DS: Trauma and the Vietnam War Generation: Report of Findings From the National Vietnam Veterans Readjustment Study. New York, Brunner/Mazel, 1990.

In a general population study, the overall lifetime rate of PTSD was 7.8%. Among men with a lifetime history of PTSD, 34.5% reported drug abuse or dependence at some point in their lives versus 15.1% of men without PTSD. For women, 26.9% with a lifetime history of PTSD reported drug abuse or dependence during their lives versus 7.6% of women without PTSD.

Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB: Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52:1048-1060.

Among adolescents lifetime rates of PTSD have been found ranging from 6.3%, in a community sample of older adolescents, to 29.6%, in substance-dependent adolescents aged 15 to 19 receiving treatment. And, among the substance-dependent adolescents, 19.2% currently had PTSD.

Giaconia RM, Reinherz HZ, Silverman AB, Pakiz B, Frost AK, Cohen E: Traumas and posttraumatic stress disorder in a community population of older adolescents. J Am Acad Child Adolesc Psychiatry 1995; 34:1369-1379.
Deykin EY, Buka SL: Prevalence and risk factors for posttraumatic stress disorder among chemically dependent adolescents. Am J Psychiatry 1997; 154:752-757

Persons with a lifetime history of PTSD have elevated rates of co-occurring disorders. Among men with PTSD during their lives, rates of co-occuring alcohol abuse or dependence are the highest, followed by depression, conduct disorder, and drug abuse or dependence. Among women with PTSD during their lives, rates of comorbid depression are highest, followed by some anxiety disorders, alcohol abuse or dependence, and drug abuse or dependence.

Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB: Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52:1048-1060.

Patients with PTSD commonly have substance use disorders, particularly abuse of and dependence on central nervous system depressants. This frequent co-occurrence of PTSD and substance use, suggests that the two are related.

Jacobsen LK, Southwick SM, Kosten TR: Substance Use Disorders in Patients with Posttraumatic Stress Disorder: A Review of the Literature. Am J Psychiatry 2001; 158(8):1184-1190.

The most recent thinking about the association between PTSD and substance use disorders suggests that for combat veterans (Bremner. Am J Psychiatry 1996) and civilians (Chilcoat. Arch Gen Psych 1998), the onset of PTSD typically precedes the onset of substance use disorders.

Saxon AJ, Davis TM, Sloan KL, McKnight KM, McFall ME, Kivlahan DR: Trauma, Symptoms of Posttraumatic Stress Disorder, and Associated Problems Among Incarcerated Veterans. Psychiatric Services 2001; 52(7):959-964.

In a study of 1007 young adults designed to look for a causal relationship between PTSD and substance use disorders, researchers found that when they reevaluated the participants at 3 and 5 years after an initial assessment, PTSD was associated with a more than 4-fold increased risk of drug abuse and dependence. The risk for abuse or dependence was highest for prescribed psychoactive drugs. The results suggest that drug abuse or dependence in persons with PTSD might be caused by efforts to self-medicate.

Chilcoat HD, Breslau N: Postraumatic Stress Disorder and Drug Disorders. Archives of General Psychiatry, 1998; 55:913-917.

Heroin-addicted patients who undergo so-called ultrarapid, anesthesia-assisted detoxification suffer withdrawal symptoms as severe as those endured by patients in detoxification by traditional methods, according to a NIDA-funded clinical trial. Researchers Dr. Eric Collins and colleagues at the College of Physicians and Surgeons of Columbia University concluded that there is no compelling reason to use general anesthesia in the treatment of opiate dependence, especially as it presents particular safety concerns. The new findings corroborate those of three international studies.

The ultrarapid detox technique, developed about 15 years ago by clinicians who hoped to mitigate the discomfort of withdrawal and speed the initiation of relapse prevention therapy, relies on a general anesthetic to sedate the patient for several hours while an opiate blocker precipitates withdrawal.The method is not covered by insurance, which makes it difficult to determine how many patients have received anesthesia-assisted detox.

To compare anesthesia-assisted detox with other approaches, Dr. Collins and colleagues enrolled 106 people seeking heroin detox at Columbia University Medical Center's Clinical Research Center. The patients, aged 21 through 50, had abused heroin every day during the past month. All spent 3 days as Center inpatients during detox, then were scheduled for twice-weekly outpatient relapse prevention psychotherapy and naltrexone maintenance (50 mg/day) for 12 weeks.

The investigators randomly assigned the participants to one of three detox methods (see chart). The goal of each method was to minimize patients' discomfort during withdrawal. In the ultrarapid approach, physicians put patients under anesthesia for 4 to 6 hours while administering naltrexone, a medication that precipitates withdrawal by blocking opioid molecules from their receptors in the brain. In the second method, patients remained awake and took a single dose of buprenorphine, a medication that eases withdrawal symptoms by moderating and smoothing the rate of opioid clearance from the brain. In the third approach, patients also remained awake and received clonidine and other nonopioid medications as needed to counter symptoms for all 3 inpatient days. These medications were available to all groups as needed for the duration of the inpatient phase. Throughout detox, the researchers closely monitored patients for complications, assessed physical indications of withdrawal, and asked the participants to rate their subjective experiences.

Once awakened from anesthesia, patients in the ultrarapid detox group demonstrated and reported symptoms of discomfort comparable to those experienced by participants receiving the buprenorphine- and clonidine-assisted methods (see chart). Three patients receiving the anesthesia-assisted method experienced serious adverse events—pulmonary and psychiatric complications as well as a metabolic complication of diabetes, all of which required hospitalization. The complications were related to preexisting medical conditions that the patients had failed to reveal when they were screened for admission into the study. No adverse events occurred with the other detox methods.

Treatment outcomes among the three groups were similar. Following detox, the researchers offered all the patients relapse prevention therapy consisting of outpatient counseling and naltrexone, which counteracts the pleasurable effects of subsequently administered opioids. More than 90 percent of the patients who received the anesthesia- and buprenorphine-assisted detox completed naltrexone induction; only 21 percent of those receiving clonidine completed induction. By the third week, more than half the patients in all three groups had dropped out of the study; only 18 percent remained in treatment the full 12 weeks. The percentages of patients submitting opiatepositive urine samples during outpatient treatment also were comparable, roughly 63 percent, across the three detox methods.

Prescription Pain and Other Medications

Prescription medications such as pain relievers, tranquilizers, stimulants, and sedatives are very useful treatment tools, but sometimes people do not take them as directed and may become addicted. Pain relievers make surgery possible, and enable many individuals with chronic pain to lead productive lives. Most people who take prescription medications use them responsibly. However, the inappropriate or nonmedical use of prescription medications is a serious public health concern. Nonmedical use of prescription medications like opioids, central nervous system (CNS) depressants, and stimulants can lead to addiction, characterized by compulsive drug seeking and use.

Patients, healthcare professionals, and pharmacists all have roles in preventing misuse and addiction to prescription medications. For example, when a doctor prescribes a pain relief medication, CNS depressant, or stimulant, the patient should follow the directions for use carefully, learn what effects the medication could have, and determine any potential interactions with other medications. The patient should read all information provided by the pharmacist. Physicians and other healthcare providers should screen for any type of substance abuse during routine history-taking, with questions about which prescriptions and over-the-counter (OTC) medicines the patient is taking and why. Providers should note any rapid increases in the amount of a medication needed or frequent requests for refills before the quantity prescribed should have been used, as these may be indicators of abuse.

Commonly Abused Prescription Medications
While many prescription medications can be abused or misused, these three classes are most commonly abused:

Opioids - often prescribed to treat pain.

CNS Depressants - used to treat anxiety and sleep disorders.

Stimulants - prescribed to treat narcolepsy and attention deficit/hyperactivity disorder.

Opioids
Opioids are commonly prescribed because of their effective analgesic, or pain relieving, properties. Studies have shown that properly managed medical use of opioid analgesic compounds is safe and rarely causes addiction. Taken exactly as prescribed, opioids can be used to manage pain effectively.

Among the compounds that fall within this class-sometimes referred to as narcotics-are morphine, codeine, and related medications. Morphine is often used before or after surgery to alleviate severe pain. Codeine is used for milder pain. Other examples of opioids that can be prescribed to alleviate pain include oxycodone (OxyContin-an oral, controlled release form of the drug); propoxyphene (Darvon); hydrocodone (Vicodin); hydromorphone (Dilaudid); and meperidine (Demerol), which is used less often because of its side effects. In addition to their effective pain relieving properties, some of these medications can be used to relieve severe diarrhea (Lomotil, for example, which is diphenoxylate) or severe coughs (codeine).

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.

In addition, opioid medications can affect regions of the brain that mediate what we perceive as pleasure, resulting in the initial euphoria that many opioids produce. They can also produce drowsiness, cause constipation, and, depending upon the amount taken, depress breathing. Taking a large single dose could cause severe respiratory depression or death.

Opioids may interact with other medications and are only safe to use with other medications under a physician's supervision. Typically, they should not be used with substances such as alcohol, antihistamines, barbiturates, or benzodiazepines. Since these substances slow breathing, their combined effects could lead to life-threatening respiratory depression.

Long-term use also can lead to physical dependence-the body adapts to the presence of the substance and withdrawal symptoms occur if use is reduced abruptly. This can also include tolerance, which means that higher doses of a medication must be taken to obtain the same initial effects. Note that physical dependence is not the same as addiction-physical dependence can occur even with appropriate long-term use of opioid and other medications. Addiction, as noted earlier, is defined as compulsive, often uncontrollable drug use in spite of negative consequences.

Individuals taking prescribed opioid medications should not only be given these medications under appropriate medical supervision, but also should be medically supervised when stopping use in order to reduce or avoid withdrawal symptoms. Symptoms of withdrawal can include restlessness, muscle and bone pain, insomnia, diarrhea, vomiting, cold flashes with goose bumps ("cold turkey"), and involuntary leg movements.

Individuals who become addicted to prescription medications can be treated. Options for effectively treating addiction to prescription opioids are drawn from research on treating heroin addiction. Some pharmacological examples of available treatments follow:

Methadone, a synthetic opioid that blocks the effects of heroin and other opioids, eliminates withdrawal symptoms and relieves craving. It has been used for over 30 years to successfully treat people addicted to opioids.

Buprenorphine, another synthetic opioid, is a recent addition to the arsenal of medications for treating addiction to heroin and other opiates.

Naltrexone is a long-acting opioid blocker often used with highly motivated individuals in treatment programs promoting complete abstinence. Naltrexone also is used to prevent relapse.

Naloxone counteracts the effects of opioids and is used to treat overdoses.

Central Nervous System (CNS) Depressants
CNS depressants slow normal brain function. In higher doses, some CNS depressants can become general anesthetics. Tranquilizers and sedatives are examples of CNS depressants.

CNS depressants can be divided into two groups, based on their chemistry and pharmacology:

Barbiturates, such as mephobarbital (Mebaral) and pentobarbitalsodium (Nembutal), which are used to treat anxiety, tension, and sleep disorders.

Benzodiazepines, such as diazepam (Valium), chlordiazepoxide HCl (Librium), and alprazolam (Xanax), which can be prescribed to treat anxiety, acute stress reactions, and panic attacks. Benzodiazepines that have a more sedating effect, such as estazolam (ProSom), can be prescribed for short-term treatment of sleep disorders.

There are many CNS depressants, and most act on the brain similarly-they affect the neurotransmitter gamma-aminobutyric acid (GABA). Neurotransmitters are brain chemicals that facilitate communication between brain cells. GABA works by decreasing brain activity. Although different classes of CNS depressants work in unique ways, ultimately it is their ability to increase GABA activity that produces a drowsy or calming effect. Despite these beneficial effects for people suffering from anxiety or sleep disorders, barbiturates and benzodiazepines can be addictive and should be used only as prescribed.

CNS depressants should not be combined with any medication or substance that causes drowsiness, including prescription pain medicines, certain OTC cold and allergy medications, or alcohol. If combined, they can slow breathing, or slow both the heart and respiration, which can be fatal.

Discontinuing prolonged use of high doses of CNS depressants can lead to withdrawal. Because they work by slowing the brain's activity, a potential consequence of abuse is that when one stops taking a CNS depressant, the brain's activity can rebound to the point that seizures can occur. Someone thinking about ending their use of a CNS depressant, or who has stopped and is suffering withdrawal, should speak with a physician and seek medical treatment.

In addition to medical supervision, counseling in an in-patient or out-patient setting can help people who are overcoming addiction to CNS depressants. For example, cognitive-behavioral therapy has been used successfully to help individuals in treatment for abuse of benzodiazepines. This type of therapy focuses on modifying a patient's thinking, expectations, and behaviors while simultaneously increasing their skills for coping with various life stressors.

Often the abuse of CNS depressants occurs in conjunction with the abuse of another substance or drug, such as alcohol or cocaine. In these cases of polydrug abuse, the treatment approach should address the multiple addictions.

Stimulants
Stimulants increase alertness, attention, and energy, which are accompanied by increases in blood pressure, heart rate, and respiration.

Historically, stimulants were used to treat asthma and other respiratory problems, obesity, neurological disorders, and a variety of other ailments. As their potential for abuse and addiction became apparent, the use of stimulants began to wane. Now, stimulants are prescribed for treating only a few health conditions, including narcolepsy, attention-deficit hyperactivity disorder (ADHD), and depression that has not responded to other treatments. Stimulants may also be used for short-term treatment of obesity and for patients with asthma.

Stimulants such as dextroamphetamine (Dexedrine) and methylphenidate (Ritalin) have chemical structures that are similar to key brain neurotransmitters called monoamines, which include norepinephrine and dopamine. Stimulants increase the levels of these chemicals in the brain and body. This, in turn, increases blood pressure and heart rate, constricts blood vessels, increases blood glucose, and opens up the pathways of the respiratory system. In addition, the increase in dopamine is associated with a sense of euphoria that can accompany the use of stimulants.

Research indicates that people with ADHD do not become addicted to stimulant medications, such as Ritalin, when taken in the form and dosage prescribed. However, when misused, stimulants can be addictive.

The consequences of stimulant abuse can be extremely dangerous. Taking high doses of a stimulant can result in an irregular heartbeat, dangerously high body temperatures, and/or the potential for cardiovascular failure or seizures. Taking high doses of some stimulants repeatedly over a short period of time can lead to hostility or feelings of paranoia in some individuals.

Stimulants should not be mixed with antidepressants or OTC cold medicines containing decongestants. Antidepressants may enhance the effects of a stimulant, and stimulants in combination with decongestants may cause blood pressure to become dangerously high or lead to irregular heart rhythms.

Treatment of addiction to prescription stimulants, such as methylphenidate and amphetamines, is based on behavioral therapies proven effective for treating cocaine or methamphetamine addiction. At this time, there are no proven medications for the treatment of stimulant addiction. Antidepressants, however, may be used to manage the symptoms of depression that can accompany early abstinence from stimulants.

Depending on the patient's situation, the first step in treating prescription stimulant addiction may be to slowly decrease the drug's dose and attempt to treat withdrawal symptoms. This process of detoxification could then be followed with one of many behavioral therapies. Contingency management, for example, improves treatment outcomes by enabling patients to earn vouchers for drug-free urine tests; the vouchers can be exchanged for items that promote healthy living. Cognitive-behavioral therapies, which teach patients skills to recognize risky situations, avoid drug use, and cope more effectively with problems, are proving beneficial. Recovery support groups may also be effective in conjunction with a behavioral therapy.

Source: National Institute on Drug Abuse (NIDA)

What are hallucinogens?

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Hallucinogens are drugs that cause hallucinations - profound distortions in a person's perceptions of reality. Under the influence of hallucinogens, people see images, hear sounds, and feel sensations that seem real but do not exist. Some hallucinogens also produce rapid, intense emotional swings.

Hallucinogens cause their effects by disrupting the interaction of nerve cells and the neurotransmitter serotonin. Distributed throughout the brain and spinal cord, the serotonin system is involved in the control of behavioral, perceptual, and regulatory systems, including mood, hunger, body temperature, sexual behavior, muscle control, and sensory perception.

LSD (an abbreviation of the German words for "lysergic acid diethylamide") is the drug most commonly identified with the term "hallucinogen" and the most widely used in this class of drugs. It is considered the typical hallucinogen, and the characteristics of its action and effects described in this Research Report apply to the other hallucinogens, including mescaline, psilocybin, and ibogaine.

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What are dissociative drugs?

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Drugs such as PCP (phencyclidine) and ketamine, which were initially developed as general anesthetics for surgery, distort perceptions of sight and sound and produce feelings of detachment - dissociation - from the environment and self. But these mind-altering effects are not hallucinations. PCP and ketamine are therefore more properly known as "dissociative anesthetics." Dextromethorphan, a widely available cough suppressant, when taken in high doses can produce effects similar to those of PCP and ketamine.

The dissociative drugs act by altering distribution of the neurotransmitter glutamate throughout the brain. Glutamate is involved in perception of pain, responses to the environment, and memory. PCP is considered the typical dissociative drug, and the description of PCP's actions and effects in this Research Report largely applies to ketamine and dextromethorphan as well.

People who abuse drugs are also likely to be cigarette smokers. More than two-thirds of drug abusers are regular tobacco smokers, a rate more than double that of the rest of the population. NIDA researchers have found that craving for nicotine appears to increase craving for illicit drugs among drug abusers who also smoke tobacco, and this relationship suggests that smokers in drug treatment programs may be less successful than nonsmokers in staying off drugs.

At NIDA's Intramural Research Program in Baltimore, Dr. Stephen Heishman and his colleagues examined the interaction of craving for nicotine and craving for other drugs and found that situations that increased desire to smoke also increased desire to use drugs. The study involved male and female adult smokers who were not trying to stop smoking and had histories of abusing alcohol, cocaine, heroin, marijuana, and/or other substances.

The researchers asked participants to listen to recorded scripts describing scenes and then to rate their urge to smoke and their desire to use other drugs. In the first part of the study, which involved 18 participants, the scripts had content that was generally pleasant (watching children on a sunny beach), unpleasant (a friend asking to borrow money), or neutral (doing household chores). Some scripts also included people expressing a desire to smoke, while others did not mention smoking at all (see "Cues Trigger Craving"). Both the scripts including a mention of smoking and those containing negative emotional content increased the participants' craving for drugs, as well as for smoking.

Among patients in a methadone treatment program for opiate addiction, levels of cocaine or opiate use were directly related to levels of cigarette smoking.

In the second part of the study, 24 participants heard scripts with only pleasant content (enjoying the beach, talking on the phone with an old acquaintance, or visiting friends). These scripts also contained descriptions of tobacco craving that increased in intensity from no mention of smoking to asking the question, "How could you really enjoy yourself fully unless you were smoking?" Participants reported that craving for both drugs and tobacco increased as the intensity of the tobacco craving messages in the scripts increased.

"One of our more interesting findings was that scripts that elicited craving for tobacco also elicited craving for the subject's drug of choice. This suggests that real-world situations that produce tobacco craving also may result in craving for drugs of abuse," Dr. Heishman says. The findings also suggest that treatment for heroin, cocaine, or alcohol addiction might be more effective if it included concurrent treatment of tobacco addiction, he says.

In a NIDA-supported study at the University of California, San Diego, doctoral candidate Dominick Frosch and his colleagues at the Integrated Substance Abuse Program at the University of California, Los Angeles, investigated the relationship between levels of cigarette smoking and levels of cocaine and heroin use among 32 individuals who had been in a methadone treatment program for at least 4 months. The participants included 10 nonsmokers (6 female, 4 male) and 22 smokers (16 female, 6 male). The smokers were equally divided among heavy smokers (20 to 40 cigarettes per day) and "chippers" who smoked 5 or fewer cigarettes per day. "Compared with heavy smokers, chippers have less intense craving for their first cigarette of the day and can more comfortably avoid smoking in situations where it is not permitted," Mr. Frosch explains.

The researchers evaluated the connection between tobacco smoking and illicit drug use among the smokers and nonsmokers by using breath and urine samples from the participants over a 7-day period. They found that the amount of cocaine and heroin use was closely related to the level of tobacco use. "The more cigarettes smoked, the more likely the person was to use illegal drugs," Mr. Frosch says. "These findings provide compelling reasons for implementing smoking cessation programs for patients in methadone treatment, as the benefits of smoking cessation may extend to opiate addiction as well."

Sources
Taylor, R.C.; Harris, N.A.; Singleton, E.G.; Moolchan, E.T.; and Heishman, S.J. Tobacco craving: intensity-related effects of imagery scripts in drug abusers. Experimental and Clinical Psychopharmacology 8(1):75-87, 2000.

Frosch, D.L.; Shoptaw, S.; Nahom, D.; and Jarvik, M.E. Associations between tobacco smoking and illicit drug use among methadone-maintained opiate-dependent individuals. Experimental and Clinical Psychopharmacology 8(1):97-103, 2000.

What are the immediate (short-term) effects of heroin use?
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Soon after injection (or inhalation), heroin crosses the blood-brain barrier. In the brain, heroin is converted to morphine and binds rapidly to opioid receptors. Abusers typically report feeling a surge of pleasurable sensation - a "rush." The intensity of the rush is a function of how much drug is taken and how rapidly the drug enters the brain and binds to the natural opioid receptors. Heroin is particularly addictive because it enters the brain so rapidly. With heroin, the rush is usually accompanied by a warm flushing of the skin, dry mouth, and a heavy feeling in the extremities, which may be accompanied by nausea, vomiting, and severe itching.

Opiates Act on Many Places in the Brain and Nervous System

After the initial effects, abusers usually will be drowsy for several hours. Mental function is clouded by heroin's effect on the central nervous system. Cardiac function slows. Breathing is also severely slowed, sometimes to the point of death. Heroin overdose is a particular risk on the street, where the amount and purity of the drug cannot be accurately known.

What are the long-term effects of heroin use?
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One of the most detrimental long-term effects of heroin use is addiction itself.

Addiction is a chronic, relapsing disease, characterized by compulsive drug seeking and use, and by neurochemical and molecular changes in the brain. Heroin also produces profound degrees of tolerance and physical dependence, which are also powerful motivating factors for compulsive use and abuse. As with abusers of any addictive drug, heroin abusers gradually spend more and more time and energy obtaining and using the drug. Once they are addicted, the heroin abusers' primary purpose in life becomes seeking and using drugs. The drugs literally change their brains and their behavior.

Physical dependence develops with higher doses of the drug. With physical dependence, the body adapts to the presence of the drug and withdrawal symptoms occur if use is reduced abruptly. Withdrawal may occur within a few hours after the last time the drug is taken. Symptoms of withdrawal include restlessness, muscle and bone pain, insomnia, diarrhea, vomiting, cold flashes with goose bumps ("cold turkey"), and leg movements. Major withdrawal symptoms peak between 24 and 48 hours after the last dose of heroin and subside after about a week. However, some people have shown persistent withdrawal signs for many months. Heroin withdrawal is never fatal to otherwise healthy adults, but it can cause death to the fetus of a pregnant addict.

At some point during continuous heroin use, a person can become addicted to the drug. Sometimes addicted individuals will endure many of the withdrawal symptoms to reduce their tolerance for the drug so that they can again experience the rush.

Physical dependence and the emergence of withdrawal symptoms were once believed to be the key features of heroin addiction. We now know this may not be the case entirely, since craving and relapse can occur weeks and months after withdrawal symptoms are long gone. We also know that patients with chronic pain who need opiates to function (sometimes over extended periods) have few if any problems leaving opiates after their pain is resolved by other means. This may be because the patient in pain is simply seeking relief of pain and not the rush sought by the addict.
Short- and Long-Term Effects of Heroin Use

• Short-Term Effects
• Long-Term Effects
• "Rush"
• Depressed respiration
• Clouded mental functioning
• Nausea and vomiting
• Suppression of pain
• Spontaneous abortion
• Addiction
• Infectious diseases, for example, HIV/AIDS and hepatitis B and C Collapsed veins Bacterial infections Abscesses
• Infection of heart lining and valves Arthritis and other rheumatologic problems

What are the medical complications of chronic heroin use?
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Medical consequences of chronic heroin injection use include scarred and/or collapsed veins, bacterial infections of the blood vessels and heart valves, abscesses (boils) and other soft-tissue infections, and liver or kidney disease. Lung complications (including various types of pneumonia and tuberculosis) may result from the poor health condition of the abuser as well as from heroin's depressing effects on respiration. Many of the additives in street heroin may include substances that do not readily 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. Immune reactions to these or other contaminants can cause arthritis or other rheumatologic problems.

Of course, sharing of injection equipment or fluids can lead to some of the most severe consequences of heroin abuse- infections with hepatitis B and C, HIV, and a host of other bloodborne viruses, which drug abusers can then pass on to their sexual partners and children.

What is Panic Disorder?
Panic disorder is an anxiety disorder and is characterized by unexpected and repeated episodes of intense fear accompanied by physical symptoms that may include chest pain, heart palpitations, shortness of breath, dizziness, or abdominal distress.

Signs & Symptoms
People with panic disorder have feelings of terror that strike suddenly and repeatedly with no warning. During a panic attack, most likely your heart will pound and you may feel sweaty, weak, faint, or dizzy. Your hands may tingle or feel numb, and you might feel flushed or chilled. You may have nausea, chest pain or smothering sensations, a sense of unreality, or fear of impending doom or loss of control.

What is Generalized Anxiety Disorder?
Generalized Anxiety Disorder, GAD, is an anxiety disorder characterized by chronic anxiety, exaggerated worry and tension, even when there is little or nothing to provoke it.

Signs & Symptoms
People with generalized anxiety disorder can't seem to shake their concerns. Their worries are accompanied by physical symptoms, especially fatigue, headaches, muscle tension, muscle aches, difficulty swallowing, trembling, twitching, irritability, sweating, and hot flashes.

What is Obsessive-Compulsive Disorder?
Obsessive-Compulsive Disorder, OCD, is an anxiety disorder and is characterized by recurrent, unwanted thoughts (obsessions) and/or repetitive behaviors (compulsions). Repetitive behaviors such as handwashing, counting, checking, or cleaning are often performed with the hope of preventing obsessive thoughts or making them go away. Performing these so-called "rituals," however, provides only temporary relief, and not performing them markedly increases anxiety.

Signs & Symptoms
People with OCD may be plagued by persistent, unwelcome thoughts or images, or by the urgent need to engage in certain rituals. They may be obsessed with germs or dirt, and wash their hands over and over. They may be filled with doubt and feel the need to check things repeatedly.

Post-Traumatic Stress Disorder, PTSD, is an anxiety disorder that can develop after exposure to a terrifying event or ordeal in which grave physical harm occurred or was threatened. Traumatic events that may trigger PTSD include violent personal assaults, natural or human-caused disasters, accidents, or military combat.

Signs & Symptoms
People with PTSD have persistent frightening thoughts and memories of their ordeal and feel emotionally numb, especially with people they were once close to. They may experience sleep problems, feel detached or numb, or be easily startled.

What is Social Phobia?
Social Phobia, or Social Anxiety Disorder, is an anxiety disorder characterized by overwhelming anxiety and excessive self-consciousness in everyday social situations. Social phobia can be limited to only one type of situation ? such as a fear of speaking in formal or informal situations, or eating or drinking in front of others ? or, in its most severe form, may be so broad that a person experiences symptoms almost anytime they are around other people.

Signs & Symptoms
People with social phobia have a persistent, intense, and chronic fear of being watched and judged by others and being embarrassed or humiliated by their own actions. Their fear may be so severe that it interferes with work or school, and other ordinary activities. Physical symptoms often accompany the intense anxiety of social phobia and include blushing, profuse sweating, trembling, nausea, and difficulty talking.