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NIH-funded (National Institutes of Health - USA) research shows that long-term marijuana is associated with impaired intellectual functioning, especially if usage starts during the teen years. Over 1,000 study participants were given neuropsychological tests in early adolescence, prior to initiation of marijuana use, and then re-tested in mid adulthood. Study members with more persistent marijuana dependence showed greater IQ decline and greater impairment across five different cognitive domains, especially executive function (The cognitive process that regulates an individual's ability to organize thoughts and activities, prioritize tasks, manage time efficiently, and make decisions and processing speed). This is the first long-term prospective study to test young people before their first use of marijuana and again after 20+ years of use. The study was thus able to rule out pre-existing differences in IQ between heavy marijuana users and others; it is also significant for including degree of cannabis exposure and age of onset as factors. Those who started use during the teen years showed greater IQ decline than those who began use as adults. These latter results are especially troubling, given recent data showing increased marijuana use among teens over the last five years, along with declines in perceived risk of harm associated with use. The results of this study are consistent with the notion that cannabis may actually cause some of the neuropsychological deficits seen in regular cannabis users.



NIDA is a Federal scientific research institute under the National Institutes of Health, United States Department of Health and Human Services. NIDA is the largest supporter of the world's research on drug abuse and addiction.

Heroin is an opiate drug that is synthesized from morphine, a naturally occurring substance extracted from the seed pod of the Asian opium poppy plant. Heroin usually appears as a white or brown powder or as a black sticky substance, known as "black tar heroin."

How Is Heroin Abused?

Heroin can be injected, snorted/sniffed, or smoked—routes of administration that rapidly deliver the drug to the brain. Injecting is the use of a needle to administer the drug directly into the bloodstream. Snorting is the process of inhaling heroin powder through the nose, where it is absorbed into the bloodstream through the nasal tissues. Smoking involves inhaling heroin smoke into the lungs. All three methods of administering heroin can lead to addiction and other severe health problems.

How Does Heroin Affect the Brain?

Heroin enters the brain, where it is converted to morphine and binds to receptors known as opioid receptors. These receptors are located in many areas of the brain (and in the body), especially those involved in the perception of pain and in reward. Opioid receptors are also located in the brain stem—important for automatic processes critical for life, such as breathing (respiration), blood pressure, and arousal. Heroin overdoses frequently involve a suppression of respiration.

After an intravenous injection of heroin, users report feeling a surge of euphoria ("rush") accompanied by dry mouth, a warm flushing of the skin, heaviness of the extremities, and clouded mental functioning. Following this initial euphoria, the user goes "on the nod," an alternately wakeful and drowsy state. Users who do not inject the drug may not experience the initial rush, but other effects are the same.

With regular heroin use, tolerance develops, in which the user's physiological (and psychological) response to the drug decreases, and more heroin is needed to achieve the same intensity of effect. Heroin users are at high risk for addiction—it is estimated that about 23 percent of individuals who use heroin become dependent on it.

What Other Adverse Effects Does Heroin Have on Health?

Heroin abuse is associated with serious health conditions, including fatal overdose, spontaneous abortion, and—particularly in users who inject the drug—infectious diseases, including HIV/AIDS and hepatitis. Chronic users may develop collapsed veins, infection of the heart lining and valves, abscesses, and liver or kidney disease. Pulmonary complications, including various types of pneumonia, may result from the poor health of the abuser as well as from heroin's depressing effects on respiration. In addition to the effects of the drug itself, street heroin often contains toxic contaminants or additives that can clog blood vessels leading to the lungs, liver, kidneys, or brain, causing permanent damage to vital organs.

Chronic use of heroin leads to physical dependence, a state in which the body has adapted to the presence of the drug. If a dependent user reduces or stops use of the drug abruptly, he or she may experience severe symptoms of withdrawal. These symptoms—which can begin as early as a few hours after the last drug administration—can include restlessness, muscle and bone pain, insomnia, diarrhea and vomiting, cold flashes with goose bumps ("cold turkey"), and kicking movements ("kicking the habit"). Users also experience severe craving for the drug during withdrawal, which can precipitate continued abuse and/or relapse. Major withdrawal symptoms peak between 48 and 72 hours after the last dose of the drug and typically subside after about 1 week. Some individuals, however, may show persistent withdrawal symptoms for months. Although heroin withdrawal is considered less dangerous than alcohol or barbiturate withdrawal, sudden withdrawal by heavily dependent users who are in poor health is occasionally fatal. In addition, heroin craving can persist years after drug cessation, particularly upon exposure to triggers such as stress or people, places, and things associated with drug use.

Heroin abuse during pregnancy, together with related factors like poor nutrition and inadequate prenatal care, has been associated with adverse consequences including low birthweight, an important risk factor for later developmental delay. If the mother is regularly abusing the drug, the infant may be born physically dependent on heroin and could suffer from serious medical complications requiring hospitalization.

What Treatment Options Exist?

A range of treatments exist for heroin addiction, including medications and behavioral therapies. Science has taught us that when medication treatment is combined with other supportive services, patients are often able to stop using heroin (or other opiates) and return to stable and productive lives.

Treatment usually begins with medically assisted detoxification to help patients withdraw from the drug safely. Medications such as clonidine and buprenorphine can be used to help minimize symptoms of withdrawal. However, detoxification alone is not treatment and has not been shown to be effective in preventing relapse—it is merely the first step.

Medications to help prevent relapse include the following:

Methadone has been used for more than 30 years to treat heroin addiction. It is a synthetic opiate medication that binds to the same receptors as heroin; but when taken orally, it has a gradual onset of action and sustained effects, reducing the desire for other opioid drugs while preventing withdrawal symptoms. Properly administered, methadone is not intoxicating or sedating, and its effects do not interfere with ordinary daily activities. Methadone maintenance treatment is usually conducted in specialized opiate treatment programs. The most effective methadone maintenance programs include individual and/or group counseling, as well as provision of or referral to other needed medical, psychological, and social services.

Buprenorphine is a more recently approved treatment for heroin addiction (and other opiates). Compared with methadone, buprenorphine produces less risk for overdose and withdrawal effects and produces a lower level of physical dependence, so patients who discontinue the medication generally have fewer withdrawal symptoms than those who stop taking methadone. The development of buprenorphine and its authorized use in physicians' offices give opiate-addicted patients more medical options and extend the reach of addiction medication. Its accessibility may even prompt attempts to obtain treatment earlier. However, not all patients respond to buprenorphine—some continue to require treatment with methadone.

Naltrexone is approved for treating heroin addiction but has not been widely utilized due to poor patient compliance. This medication blocks opioids from binding to their receptors and thus prevents an addicted individual from feeling the effects of the drug. Naltrexone as a treatment for opioid addiction is usually prescribed in outpatient medical settings, although initiation of the treatment often begins after medical detoxification in a residential setting. To prevent withdrawal symptoms, individuals must be medically detoxified and opioid-free for several days before taking naltrexone.Naloxone is a shorter-acting opioid receptor blocker, used to treat cases of overdose.

For pregnant heroin abusers, methadone maintenance combined with prenatal care and a comprehensive drug treatment program can improve many of the detrimental maternal and neonatal outcomes associated with untreated heroin abuse. Preliminary evidence suggests that buprenorphine may also be a safe and effective treatment during pregnancy, although infants exposed to either methadone or buprenorphine prenatally may still require treatment for withdrawal symptoms. For women who do not want or are not able to receive pharmacotherapy for their heroin addiction, detoxification from opiates during pregnancy can be accomplished with medical supervision, although potential risks to the fetus and the likelihood of relapse to heroin use should be considered.

There are many effective behavioral treatments available for heroin addiction—usually in combination with medication. These can be delivered in residential or outpatient settings. Examples are individual or group counseling; contingency management, which uses a voucher-based system where patients earn "points" based on negative drug tests—these points can be exchanged for items that encourage healthy living; and cognitive-behavioral therapy, designed to help modify a patient's expectations and behaviors related to drug abuse, and to increase skills in coping with various life stressors.

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 Cigarettes and Other Tobacco Products

NIDA is a Federal scientific research institute under the National Institutes of Health, United States Department of Health and Human Services. NIDA is the largest supporter of the world's research on drug abuse and addiction.

Tobacco use is the leading preventable cause of disease, disability, and death in the United States. Between 1964 and 2004, cigarette smoking caused an estimated 12 million deaths, including 4.1 million deaths from cancer, 5.5 million deaths from cardiovascular diseases, 1.1 million deaths from respiratory diseases, and 94,000 infant deaths related to mothers smoking during pregnancy.1 According to the Centers for Disease Control and Prevention (CDC), cigarette smoking results in more than 443,000 premature deaths in the United States each year—about 1 in every 5 U.S. deaths2— and an additional 8.6 million people suffer with a serious illness caused by smoking.3 Thus, for every one person who dies from smoking, 20 more suffer from at least one serious tobacco-related illness.3

The harmful effects of smoking extend far beyond the smoker. Exposure to secondhand smoke can cause serious diseases and death. Each year, an estimated 126 million Americans are regularly exposed to secondhand smoke and almost 50 thousand nonsmokers die from diseases caused by secondhand smoke exposure.4

How Does Tobacco Affect the Brain?

Cigarettes and other forms of tobacco—including cigars, pipe tobacco, snuff, and chewing tobacco—contain the addictive drug nicotine. Nicotine is readily absorbed into the bloodstream when a tobacco product is chewed, inhaled, or smoked. A typical smoker will take 10 puffs on a cigarette over a period of 5 minutes that the cigarette is lit. Thus, a person who smokes about 1 1/2 packs (30 cigarettes) daily gets 300 "hits" of nicotine each day.

Upon entering the bloodstream, nicotine immediately stimulates the adrenal glands to release the hormone epinephrine (adrenaline). Epinephrine stimulates the central nervous system and increases blood pressure, respiration, and heart rate. Glucose is released into the blood while nicotine suppresses insulin output from the pancreas, which means that smokers have chronically elevated blood sugar levels.

Like cocaine, heroin, and marijuana, nicotine increases levels of the neurotransmitter dopamine, which affects the brain pathways that control reward and pleasure. For many tobacco users, long-term brain changes induced by continued nicotine exposure result in addiction—a condition of compulsive drug seeking and use, even in the face of negative consequences. Studies suggest that additional compounds in tobacco smoke, such as acetaldehyde, may enhance nicotine's effects on the brain.5 A number of studies indicate that adolescents are especially vulnerable to these effects and may be more likely than adults to develop an addiction to tobacco.

When an addicted user tries to quit, he or she experiences withdrawal symptoms including irritability, attention difficulties, sleep disturbances, increased appetite, and powerful cravings for tobacco. Treatments can help smokers manage these symptoms and improve the likelihood of successfully quitting.

What Other Adverse Effects Does Tobacco Have on Health?

Cigarette smoking accounts for about one-third of all cancers, including 90 percent of lung cancer cases. Smokeless tobacco (such as chewing tobacco and snuff) also increases the risk of cancer, especially oral cancers. In addition to cancer, smoking causes lung diseases such as chronic bronchitis and emphysema, and increases the risk of heart disease, including stroke, heart attack, vascular disease, and aneurysm. Smoking has also been linked to leukemia, cataracts, and pneumonia.1,2 On average, adults who smoke die 14 years earlier than nonsmokers.2

Although nicotine is addictive and can be toxic if ingested in high doses, it does not cause cancer—other chemicals are responsible for most of the severe health consequences of tobacco use. Tobacco smoke is a complex mixture of chemicals such as carbon monoxide, tar, formaldehyde, cyanide, and ammonia—many of which are known carcinogens. Carbon monoxide increases the chance of cardiovascular diseases. Tar exposes the user to an increased risk of lung cancer, emphysema, and bronchial disorders.

Pregnant women who smoke cigarettes run an increased risk of miscarriage, stillborn or premature infants, or infants with low birthweight.2 Maternal smoking may also be associated with learning and behavioral problems in children. Smoking more than one pack of cigarettes per day during pregnancy nearly doubles the risk that the affected child will become addicted to tobacco if that child starts smoking.6

While we often think of medical consequences that result from direct use of tobacco products, passive or secondary smoke also increases the risk for many diseases. Secondhand smoke, also known as environmental tobacco smoke, consists of exhaled smoke and smoke given off by the burning end of tobacco products. Nonsmokers exposed to secondhand smoke at home or work increase their risk of developing heart disease by 25 to 30 percent7 and lung cancer by 20 to 30 percent.2 In addition, secondhand smoke causes respiratory problems, such as coughing, overproduction of phlegm, and reduced lung function and respiratory infections, including pneumonia and bronchitis, in both adults and children. In fact, each year about 150,000 – 300,000 children younger than 18 months old experience respiratory tract infections caused by secondhand smoke.4 Children exposed to secondhand smoking are at an increased risk for sudden infant death syndrome, ear problems, and severe asthma. Furthermore, children who grow up with parents who smoke are more likely to become smokers, thus placing themselves (and their future families) at risk for the same health problems as their parents when they become adults.

Although quitting can be difficult, the health benefits of smoking cessation are immediate and substantial—including reduced risk for cancers, heart disease, and stroke. A 35-year-old man who quits smoking will, on average, increase his life expectancy by 5 years.8

Are There Effective Treatments for Tobacco Addiction?

Tobacco addiction is a chronic disease that often requires multiple attempts to quit. Although some smokers are able to quit without help, many others need assistance. Generally, rates of relapse for smoking cessation are highest in the first few weeks and months and diminish considerably after about 3 months. Both behavioral interventions (counseling) and medication can help smokers quit; but the combination of medication with counseling is more effective than either alone.

Behavioral Treatments

Behavioral treatments employ a variety of methods to assist smokers in quitting, ranging from self-help materials to individual counseling. These interventions teach individuals to recognize high-risk situations and develop coping strategies to deal with them.

Nicotine Replacement Treatments

Nicotine replacement therapies (NRTs), such as nicotine gum and the nicotine patch, were the first pharmacological treatments approved by the Food and Drug Administration (FDA) for use in smoking cessation therapy. NRTs deliver a controlled dose of nicotine to a smoker in order to relieve withdrawal symptoms during the smoking cessation process. They are most successful when used in combination with behavioral treatments. Current FDA-approved NRT products include nicotine chewing gum, the nicotine transdermal patch, nasal sprays, inhalers, and lozenges.

Other Medications

Bupropion and varenicline are two FDA-approved non-nicotine medications that effectively increase rates of long-term abstinence from smoking. Bupropion, a medication that goes by the trade name Zyban, was approved by the FDA in 1997 for use in smoking cessation. Varenicline tartrate (trade name: Chantix) targets nicotine receptors in the brain, easing withdrawal symptoms and blocking the effects of nicotine if people resume smoking.

Current Treatment Research

Scientists are currently pursuing many other avenues of research to develop new smoking cessation therapies. One promising intervention is a vaccine called NicVax that works by targeting nicotine in the bloodstream, blocking its access to the brain and thereby preventing its reinforcing effects. Preliminary trials of this vaccine have yielded promising results, with vaccinated smokers achieving higher quit rates and longer term abstinence compared to smokers given placebo. NicVax is now being evaluated in Phase III clinical trials; successful completion will bring NicVax closer to final approval by the FDA.

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1   Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Department of Health and Human Services. The Health Consequences of Smoking: What It Means to You, 2004. Available at:

2   Centers for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Department of Health and Human Services. Smoking and Tobacco Use—Fact Sheet: Health Effects of Cigarette Smoking. Updated January 2008. Available at:

3   Centers for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Department of Health and Human Services. Tobacco Use: Targeting the Nation's Leading Killer—At a Glance 2009. Available at:

4   Centers for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Department of Health and Human Services. Smoking & Tobacco Use, Fast Facts. Available at:

5   Belluzzi JD, Wang R, Leslie FM. Acetaldehyde enhances acquisition of nicotine self-administration in adolescent rats. Neuropsychopharmacology 30:705–712, 2005.

6   Buka SL, Shenassa ED, Niaura R. Elevated risk of tobacco dependence among offspring of mothers who smoked during pregnancy: A 30-year prospective study. Am J Psychiatry 160:1978–1984, 2003.

7   Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, Department of Health and Human Services, Smoking and Tobacco Use—Fact Sheet: Secondhand Smoke Causes Heart Disease. Updated May 2007. Available at:

8   Office of the Surgeon General, Office of Public Health and Science, Office of the Secretary, Public Health Service, Department of Health and Human Services. The Health Benefits of Smoking Cessation: A Report of the Surgeon General. Available at:


NIDA is a Federal scientific research institute under the National Institutes of Health, United States Department of Health and Human Services. NIDA is the largest supporter of the world's research on drug abuse and addiction.

Cocaine is a powerfully addictive stimulant drug. The powdered hydrochloride salt form of cocaine can be snorted or dissolved in water and then injected. Crack is the street name given to the form of cocaine that has been processed to make a rock crystal, which, when heated, produces vapors that are smoked. The term "crack" refers to the crackling sound produced by the rock as it is heated.

How Is Cocaine Abused?

Three routes of administration are commonly used for cocaine: snorting, injecting, and smoking. Snorting is the process of inhaling cocaine powder through the nose, where it is absorbed into the bloodstream through the nasal tissues. Injecting is the use of a needle to insert the drug directly into the bloodstream. Smoking involves inhaling cocaine vapor or smoke into the lungs, where absorption into the bloodstream is as rapid as it is by injection. All three methods of cocaine abuse can lead to addiction and other severe health problems, including increasing the risk of contracting HIV/AIDS and other infectious diseases.

The intensity and duration of cocaine's effects—which include increased energy, reduced fatigue, and mental alertness—depend on the route of drug administration. The faster cocaine is absorbed into the bloodstream and delivered to the brain, the more intense the high. Injecting or smoking cocaine produces a quicker, stronger high than snorting. On the other hand, faster absorption usually means shorter duration of action: the high from snorting cocaine may last 15 to 30 minutes, but the high from smoking may last only 5 to 10 minutes. In order to sustain the high, a cocaine abuser has to administer the drug again. For this reason, cocaine is sometimes abused in binges—taken repeatedly within a relatively short period of time, at increasingly higher doses.

How Does Cocaine Affect the Brain?

Cocaine is a strong central nervous system stimulant that increases levels of dopamine, a brain chemical (or neurotransmitter) associated with pleasure and movement, in the brain's reward circuit. Certain brain cells, or neurons, use dopamine to communicate. Normally, dopamine is released by a neuron in response to a pleasurable signal (e.g., the smell of good food), and then recycled back into the cell that released it, thus shutting off the signal between neurons. Cocaine acts by preventing the dopamine from being recycled, causing excessive amounts of the neurotransmitter to build up, amplifying the message to and response of the receiving neuron, and ultimately disrupting normal communication. It is this excess of dopamine that is responsible for cocaine's euphoric effects. With repeated use, cocaine can cause long-term changes in the brain's reward system and in other brain systems as well, which may eventually lead to addiction. With repeated use, tolerance to the cocaine high also often develops. Many cocaine abusers report that they seek but fail to achieve as much pleasure as they did from their first exposure. Some users will increase their dose in an attempt to intensify and prolong the euphoria, but this can also increase the risk of adverse psychological or physiological effects.

What Adverse Effects Does Cocaine Have on Health?

Abusing cocaine has a variety of adverse effects on the body. For example, cocaine constricts blood vessels, dilates pupils, and increases body temperature, heart rate, and blood pressure. It can also cause headaches and gastrointestinal complications such as abdominal pain and nausea. Because cocaine tends to decrease appetite, chronic users can become malnourished as well.

Different methods of taking cocaine can produce different adverse effects. Regular intranasal use (snorting) of cocaine, for example, can lead to loss of the sense of smell; nosebleeds; problems with swallowing; hoarseness; and a chronically runny nose. Ingesting cocaine can cause severe bowel gangrene as a result of reduced blood flow. Injecting cocaine can bring about severe allergic reactions and increased risk for contracting HIV/AIDS and other blood-borne diseases. Binge-patterned cocaine use may lead to irritability, restlessness, and anxiety. Cocaine abusers can also experience severe paranoia—a temporary state of full-blown paranoid psychosis—in which they lose touch with reality and experience auditory hallucinations.

Regardless of the route or frequency of use, cocaine abusers can experience acute cardiovascular or cerebrovascular emergencies, such as a heart attack or stroke, which may cause sudden death. Cocaine-related deaths are often a result of cardiac arrest or seizure followed by respiratory arrest.

Added Danger: Cocaethylene

Polydrug use—use of more than one drug—is common among substance abusers. When people consume two or more psychoactive drugs together, such as cocaine and alcohol, they compound the danger each drug poses and unknowingly perform a complex chemical experiment within their bodies. Researchers have found that the human liver combines cocaine and alcohol to produce a third substance, cocaethylene, which intensifies cocaine's euphoric effects. Cocaethylene is associated with a greater risk of sudden death than cocaine alone.1

What Treatment Options Exist?

Behavioral interventions—particularly, cognitive-behavioral therapy—have been shown to be effective for decreasing cocaine use and preventing relapse. Treatment must be tailored to the individual patient's needs in order to optimize outcomes—this often involves a combination of treatment, social supports, and other services.

Currently, there are no FDA-approved medications for treating cocaine addiction; thus, developing a medication to treat cocaine and other forms of addiction remains one of NIDA's top research priorities. Researchers are seeking to develop medications that help alleviate the severe craving associated with cocaine addiction, as well as medications that counteract cocaine-related relapse triggers, such as stress. Several compounds are currently being investigated for their safety and efficacy, including a vaccine that would sequester cocaine in the bloodstream and prevent it from reaching the brain. Current research suggests that while medications are effective in treating addiction, combining them with a comprehensive behavioral therapy program is the most effective method to reduce drug use in the long term.

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Harris DS, et al. The pharmacology of cocaethylene in humans following cocaine and ethanol administration. Drug Alcohol Depend 72(2):169–182, 2003.


NIDA is a Federal scientific research institute under the National Institutes of Health, United States Department of Health and Human Services. NIDA is the largest supporter of the world's research on drug abuse and addiction.

Marijuana is the most commonly abused illicit drug in the United States. It is a dry, shredded green and brown mix of flowers, stems, seeds, and leaves derived from the hemp plant Cannabis sativa. The main active chemical in marijuana is delta-9-tetrahydrocannabinol, or THC for short.

How is Marijuana Abused?
Marijuana is usually smoked as a cigarette (joint) or in a pipe. It is also smoked in blunts, which are cigars that have been emptied of tobacco and refilled with a mixture of marijuana and tobacco. This mode of delivery combines marijuana's active ingredients with nicotine and other harmful chemicals. Marijuana can 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-and-sour odor.

How Does Marijuana Affect 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 the brain and other organs throughout the body.
THC acts upon specific sites in the brain, called cannabinoid receptors, kicking off a series of cellular reactions that ultimately lead to the "high" that users experience when they smoke marijuana. Some brain areas have many cannabinoid receptors; others have few or none. The highest density of cannabinoid receptors are found in parts of the brain that influence pleasure, memory, thinking, concentrating, sensory and time perception, and coordinated movement.Not surprisingly, marijuana intoxication can cause distorted perceptions, impaired coordination, difficulty with thinking and problem solving, and problems with learning and memory. Research has shown that, in chronic users, marijuana's adverse impact on learning and memory can last for days or weeks after the acute effects of the drug wear off.2 As a result, someone who smokes marijuana every day may be functioning at a suboptimal intellectual level all of the time.
Research into the effects of long-term cannabis use on the structure of the brain has yielded inconsistent results. It may be that the effects are too subtle for reliable detection by current techniques. A similar challenge arises in studies of the effects of chronic marijuana use on brain function. Brain imaging studies in chronic users tend to show some consistent alterations, but their connection to impaired cognitive functioning is far from clear. This uncertainty may stem from confounding factors such as other drug use, residual drug effects, or withdrawal symptoms in long-term chronic users.

Addictive Potential
Long-term marijuana abuse can lead to addiction; that is, compulsive drug seeking and abuse despite the known harmful effects upon functioning in the context of family, school, work, and recreational activities. Estimates from research suggest that about 9 percent of users become addicted to marijuana; this number increases among those who start young (to about 17 percent) and among daily users (25-50 percent).
Long-term marijuana abusers trying to quit report withdrawal symptoms including: irritability, sleeplessness, decreased appetite, anxiety, and drug craving, all of which can make it difficult to remain abstinent. These symptoms begin within about 1 day following abstinence, peak at 2-3 days, and subside within 1 or 2 weeks following drug cessation.3

Marijuana and Mental Health
A number of studies have shown an association between chronic marijuana use and increased rates of anxiety, depression, and schizophrenia. Some of these studies have shown age at first use to be an important risk factor, where early use is a marker of increased vulnerability to later problems. However, at this time, it is not clear whether marijuana use causes mental problems, exacerbates them, or reflects an attempt to self-medicate symptoms already in existence.
Chronic marijuana use, especially in a very young person, may also be a marker of risk for mental illnesses - including addiction - stemming from genetic or environmental vulnerabilities, such as early exposure to stress or violence. Currently, the strongest evidence links marijuana use and schizophrenia and/or related disorders.4 High doses of marijuana can produce an acute psychotic reaction; in addition, use of the drug may trigger the onset or relapse of schizophrenia in vulnerable individuals.

What Other Adverse Effect Does Marijuana Have on Health?

Effects on the Heart
Marijuana increases heart rate by 20-100 percent shortly after smoking; this effect can last up to 3 hours. In one study, it was estimated that marijuana users have a 4.8-fold increase in the risk of heart attack in the first hour after smoking the drug.5 This may be due to increased heart rate as well as the effects of marijuana on heart rhythms, causing palpitations and arrhythmias. This risk may be greater in aging populations or in those with cardiac vulnerabilities.

Effects on the Lungs
Numerous studies have shown marijuana smoke to contain carcinogens and to be an irritant to the lungs. In fact, marijuana smoke contains 50-70 percent more carcinogenic hydrocarbons than tobacco smoke. Marijuana users usually inhale more deeply and hold their breath longer than tobacco smokers do, which further increase the lungs' exposure to carcinogenic smoke. Marijuana smokers show dysregulated growth of epithelial cells in their lung tissue, which could lead to cancer;6 however, a recent case-controlled study found no positive associations between marijuana use and lung, upper respiratory, or upper digestive tract cancers.7 Thus, the link between marijuana smoking and these cancers remains unsubstantiated at this time.
Nonetheless, marijuana smokers can have many of the same respiratory problems as tobacco smokers, such as daily cough and phlegm production, more frequent acute chest illness, and a heightened risk of lung infections. 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.

Effects on Daily Life
Research clearly demonstrates that marijuana has the potential to cause problems in daily life or make a person's existing problems worse. In one study, heavy marijuana abusers reported that the drug impaired several important measures of life achievement, including physical and mental health, cognitive abilities, social life, and career status.9 Several studies associate workers' marijuana smoking with increased absences, tardiness, accidents, workers' compensation claims, and job turnover.

What Treatment Options Exist?
Behavioral interventions, including cognitive-behavioral therapy and motivational incentives (i.e., providing vouchers for goods or services to patients who remain abstinent) have shown efficacy in treating marijuana dependence. Although no medications are currently available, recent discoveries about the workings of the cannabinoid system offer promise for the development of medications to ease withdrawal, block the intoxicating effects of marijuana, and prevent relapse.
The latest treatment data indicate that in 2008 marijuana accounted for 17 percent of admissions (322,000) to treatment facilities in the United States, second only to opiates among illicit substances. Marijuana admissions were primarily male (74 percent), White (49 percent), and young (30 percent were in the 12-17 age range). Those in treatment for primary marijuana abuse had begun use at an early age: 56 percent by age 14.**

Is Marijuana Medicine?
The potential medicinal properties of marijuana have been the subject of substantive research and heated debate. Scientists have confirmed that the cannabis plant contains active ingredients with therapeutic potential for relieving pain, controlling nausea, stimulating appetite, and decreasing ocular pressure. Cannabinoid-based medications include synthetic compounds, such as dronabinol (Marinol®) and nabilone (Cesamet®), which are FDA approved, and a new, chemically pure mixture of plant-derived THC and cannabidiol called Sativex®, formulated as a mouth spray and approved in Canada and parts of Europe for the relief of cancer-associated pain and spasticity and neuropathic pain in multiple sclerosis.
Scientists continue to investigate the medicinal properties of THC and other cannabinoids to better evaluate and harness their ability to help patients suffering from a broad range of conditions, while avoiding the adverse effects of smoked marijuana.

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

2 Pope HG, Gruber AJ, Hudson JI, Huestis MA, Yurgelun-Todd D. Neuropsychological performance in long-term cannabis users. Arch Gen Psychiatry 58(10):909–915, 2001.

3 Budney AJ, Vandrey RG, Hughes JR, Thostenson JD, Bursac Z. Comparison of cannabis and tobacco withdrawal: Severity and contribution to relapse. J Subst Abuse Treat, e-publication ahead of print, March 12, 2008.

4 Moore TH, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: A systematic review. Lancet 370 (9584):319–328, 2007.

5 Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering myocardial infarction by marijuana. Circulation 103(23):2805–2809, 2001.

6 Tashkin DP. Smoked marijuana as a cause of lung injury. Monaldi Arch Chest Dis 63(2):92–100, 2005.

7 Hashibe M, Morgenstern H, Cui Y, et al. Marijuana use and the risk of lung and upper aerodigestive tract cancers: Results of a population-based case-control study. Cancer Epidemiol Biomarkers Prev 15(10):1829–1834, 2006.

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

9 Gruber AJ, Pope HG, Hudson JI, Yurgelun-Todd D. Attributes of long-term heavy cannabis users: A case control study. Psychological Med 33(8):1415–1422, 2003.