Methamphetamine

What is Methamphetamine?

 Methamphetamine is a powerful, highly addictive stimulant that affects the central nervous system. Also known as meth, chalk, ice, and crystal, among many other terms, it is a white, odorless, bitter-tasting crystalline powder that easily dissolves in water or alcohol.

  Methamphetamine was developed early in the 20th century from its parent drug, amphetamine, and was used originally in nasal decongestants and bronchial inhalers. Like amphetamine, Methamphetamine causes increased activity and talkativeness, decreased appetite, and a pleasurable sense of well-being or euphoria. However, Methamphetamine differs from amphetamine in that, at comparable doses, much more significant amounts of the drug get into the brain, making it a more potent stimulant. It also has longer-lasting and more harmful effects on the central nervous system. These characteristics make it a drug with a high potential for widespread abuse.

  The U.S. Drug Enforcement Administration has classified Methamphetamine as a Schedule II stimulant, which makes it legally available only through a non-refillable prescription. Medically it may be indicated for treating attention deficit hyperactivity disorder (ADHD) and as a short-term component of weight-loss treatments. However, these uses are limited and rarely prescribed; the prescribed doses are far lower than those typically abused.

How is Methamphetamine Abused?

 Methamphetamine comes in several forms and can be smoked, inhaled (snorted), injected, or orally ingested. The preferred drug abuse method varies by geographical region and has changed over time. Smoking methamphetamine is currently the most common way of consuming it, according to CEWG data.
Smoking or injecting Methamphetamine puts the drug very quickly into the bloodstream and brain, causing an immediate, intense “rush” and amplifying the drug’s addiction potential and adverse health consequences. The rush, or “flash,” lasts only a few minutes and is highly pleasurable. Snorting or oral ingestion produces euphoria—a high but not an intense rush. Snorting produces effects within 3 to 5 minutes, and oral ingestion has effects within 15 to 20 minutes.
As with many stimulants, Methamphetamine is most often abused in a “binge and crash” pattern. Because the pleasurable effects of Methamphetamine disappear even before the drug concentration in the blood falls significantly, users try to maintain the high by taking more of the drug. In some cases, abusers indulge in a form of binging known as a “run,” foregoing food and sleep while taking the drug for up to several days.

How is Methamphetamine Manufactured?

Most of the Methamphetamine abused in this country is manufactured in “superlabs” here or, usually, in Mexico. But the drug is also easily made in small clandestine laboratories, with relatively inexpensive over-the-counter ingredients such as pseudoephedrine, a common ingredient in cold medications. To curb the production of Methamphetamine, Congress passed the Combat Methamphetamine Epidemic Act in 2005, which requires that pharmacies and other retail stores keep logs of products containing pseudoephedrine and limits the amount of those products an individual can purchase per day. A few States have even made pseudoephedrine available only with a prescription. Mexico has also tightened its restrictions on this and other methamphetamine precursor chemicals. But manufacturers adapt to these restrictions via small- or large-scale “smurfing” operations: obtaining pseudoephedrine from multiple sources below the legal thresholds, using numerous false identifications. Manufacturers in Mexico are also increasingly using a different production process (P2P, from the precursor chemical phenyl-2-propanone) that does not require pseudoephedrine.
Methamphetamine production also involves many other easily obtained chemicals that are hazardous, such as acetone, anhydrous ammonia (fertilizer), ether, red phosphorus, and lithium. Toxicity from these chemicals can remain in the environment around a methamphetamine production lab long after the lab has been shut down, causing a wide range of damaging effects on health. Because of these dangers, the U.S. Environmental Protection Agency has guided the cleanup and remediation of methamphetamine labs.

How is Methamphetamine Different from Other Stimulants, such as cocaine?

 The methamphetamine molecule is structurally similar to amphetamine and to the neurotransmitter dopamine. This brain chemical is vital in regulating reward, but it differs from cocaine. Although these stimulants have similar behavioral and physiological effects, there are some significant differences in the basic mechanisms of how they work.
In contrast to cocaine, which is quickly removed from and almost completely metabolized in the body, methamphetamine has a much longer duration of action, and a more significant percentage of the drug remains unchanged. Methamphetamine, therefore, remains in the brain longer, leading to prolonged stimulant effects. Although both methamphetamine and cocaine increase levels of dopamine, the administration of methamphetamine in animal studies leads to much higher levels of dopamine because nerve cells respond differently to the two drugs. Cocaine prolongs dopamine actions in the brain by blocking the re-absorption (reuptake) of the neurotransmitter by signaling nerve cells. At low doses, methamphetamine also blocks the reuptake of dopamine. However, it also increases the release of dopamine, leading to much higher concentrations in the synapse (the gap between neurons), which can be toxic to nerve terminals.

  Figure 1. Methamphetamine versus Cocaine 
                                 Methamphetamine                           Cocaine
Stimulant   Stimulant and local anesthetic
Man-madePlant-derived
Smoking produces a long-lasting highSmoking produces a brief high
50% of the drug is removed from the body in 12 hours50% of the drug is removed from the body in 1 hour
Increases dopamine release and blocks dopamine re-uptakeBlocks dopamine re-uptake
Limited medical use for ADHD, narcolepsy, and weight loss Limited medical use as a local anesthetic in some surgical procedures

What Are the Immediate (short-term) Effects of Methamphetamine Abuse?

 As a powerful stimulant, methamphetamine, even in small doses, can increase wakefulness and physical activity and decrease appetite. Methamphetamine can also cause cardiovascular problems, including rapid heart rate, irregular heartbeat, and increased blood pressure. Hyperthermia (elevated body temperature) and convulsions may occur with methamphetamine overdose and, if not treated immediately, can result in death.

  Most of the pleasurable effects of methamphetamine are believed to result from the release of very high levels of the neurotransmitter dopamine. Dopamine is involved in motivation, the experience of pleasure, and motor function and is a common mechanism of action for most drugs of abuse. The elevated release of dopamine produced by methamphetamine is also thought to contribute to the drug’s deleterious effects on nerve terminals in the brain.

Short-term effects may include:

What Are the Long-Term Effects of Methamphetamine Abuse?

 Long-term methamphetamine abuse has many negative consequences, including addiction. Addiction is a chronic, relapsing disease characterized by compulsive drug seeking and use accompanied by functional and molecular changes in the brain.
As is the case with many drugs, tolerance to methamphetamine’s pleasurable effects develops when it is taken repeatedly. Abusers often need to take higher doses of the drug, take it more frequently, or change how they take it to get the desired effect. Chronic methamphetamine abusers may develop difficulty feeling any pleasure other than that provided by the drug, fueling further abuse. Withdrawal from methamphetamine occurs when a chronic abuser stops using the drug; withdrawal symptoms include depression, anxiety, fatigue, and an intense craving for the drug.
In addition to being addicted to methamphetamine, chronic abusers may exhibit symptoms that can include significant anxiety, confusion, insomnia, mood disturbances, and violent behavior. They also may display several psychotic features, including paranoia, visual and auditory hallucinations, and delusions (for example, the sensation of insects creeping under the skin). Psychotic symptoms can sometimes last for months or years after a person has quit abusing methamphetamine, and stress has been shown to precipitate spontaneous recurrence of methamphetamine psychosis in formerly psychotic methamphetamine abusers.
These and other problems reflect significant changes in the brain caused by the abuse of methamphetamine. Neuroimaging studies have demonstrated alterations in the dopamine system’s activity associated with reduced motor speed and impaired verbal learning. 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.

Methamphetamine abuse also has been shown to have adverse effects on non-neural brain cells called microglia. These cells support brain health by defending the brain against infectious agents and removing damaged neurons. Too much activity of the microglial cells, however, can assault healthy neurons. A study using brain imaging found more than double the levels of microglial cells in former methamphetamine abusers compared to people with no history of methamphetamine abuse, which could explain some of the neurotoxic effects of methamphetamine.
Some neurobiological effects of chronic methamphetamine abuse appear to be at least partially reversible. As the study mentions below, abstinence from methamphetamine resulted in less excess microglial activation over time, and abusers who had remained methamphetamine- free for two years exhibited microglial activation levels similar to the study’s control subjects. Another neuroimaging study showed neuronal recovery in some brain regions following prolonged abstinence (14 but not six months). This recovery was associated with improved performance on motor and verbal memory tests. But function in other brain regions did not recover after 14 months of abstinence, indicating that some methamphetamine-induced changes are long-lasting. Moreover, methamphetamine use can increase one’s risk of stroke, which can cause irreversible damage to the brain. A recent study even showed a higher incidence of Parkinson’s disease among past users of methamphetamine.
In addition to the neurological and behavioral consequences of methamphetamine abuse, long-term users also suffer physical effects, including weight loss, severe tooth decay and loss (“meth mouth”), and skin sores. The dental problems may be caused by poor nutrition and dental hygiene and dry mouth and teeth grinding caused by the drug. Skin sores result from picking and scratching the skin to eliminate insects imagined to be crawling under it.

Recovery of Brain Dopamine Transporters in
Chronic Methamphetamine (METH) Abusers


    Methamphetamine abuse greatly reduces dopamine binding to dopamine transporters (highlighted in red and green) in the striatum, a brain area important in memory and movement. With prolonged abstinence, dopamine transporters in this area can be restored.

Long-Term Effects Include:

What Are the Risks of Methamphetamine Abuse During Pregnancy?

Our knowledge of the effects of methamphetamine abuse during pregnancy is limited because studies on this issue have used small samples and cannot account for the possibility that mothers used other drugs besides methamphetamine. But the available research points to increased rates of premature delivery, placental abruption (separation of the placental lining from the uterus), and various effects on babies prenatally exposed to methamphetamine, including small size, lethargy, and heart and brain abnormalities. A large ongoing NIDA-funded study examines developmental outcomes in children born to mothers who abused methamphetamine. Thus far, researchers have found neurobehavioral problems such as decreased arousal, increased stress, and subtle but significant attention impairments in these children.

Are People Who Abuse Methamphetamine at Risk for Contracting HIV/AIDS and Hepatitis B and C?

 Methamphetamine abuse raises the risk of contracting or transmitting HIV and hepatitis B and C—not only for individuals who inject the drug but also for non-injecting methamphetamine abusers. Among injecting drug users, HIV and other infectious diseases are spread primarily through reusing or sharing contaminated syringes, needles, or related paraphernalia. But regardless of how methamphetamine is taken, its intoxicating effects can alter judgment and inhibition and lead people to engage in unsafe behaviors like unprotected sex.
Methamphetamine abuse is associated with a culture of risky sexual behavior, both among men who have sex with men and in heterosexual populations, a link that may be attributed to the fact that methamphetamine and related stimulants can increase libido. (Although paradoxically, long-term methamphetamine abuse may be associated with decreased sexual functioning, at least in men.) The combination of injection practices and sexual risk-taking may result in HIV becoming a more significant problem among methamphetamine abusers than among other drug abusers, and some epidemiologic reports are already showing this trend. For example, while the link between HIV infection and methamphetamine abuse has not yet been established for heterosexuals, data show an association between methamphetamine abuse and the spread of HIV among men who have sex with men.
Methamphetamine abuse may also worsen the progression of HIV disease and its consequences. In animal studies, methamphetamine has been shown to increase viral replication. Clinical studies in humans suggest that methamphetamine users taking highly active antiretroviral therapy (HAART) to treat HIV may be at greater risk of developing AIDS than non-users, possibly due to poor medication adherence. Methamphetamine abusers with HIV also have shown more significant neuronal injury and cognitive impairment due to HIV compared with those who do not abuse the drug.
NIDA-funded research has found that, through drug abuse treatment, prevention, and community-based outreach programs, drug abusers can change their HIV risk behaviors. Drug abuse and drug-related risk behaviors, such as needle sharing and unsafe sexual practices, can be reduced significantly, thus decreasing the risk of exposure to HIV and other infectious diseases. Therefore, drug abuse treatment is HIV prevention.

Dopamine Pathways

 In the brain, dopamine plays a vital role in regulating reward and movement. As a primary chemical messenger in the reward pathway, dopamine is manufactured in nerve cell bodies located within a group of neurons called the ventral tegmental area and is released in the nucleus accumbens, sometimes called the “pleasure center” because of its role in producing rewarding feelings, as well as in the prefrontal cortex, which is responsible for higher cognitive functions like decision-making and self-control. Dopamine’s regulation of motor functions links to a separate pathway: Cell bodies in the substantia nigra manufacture and release dopamine into the striatum, which is involved in executing and inhibiting movements and reward-seeking behavior.

What Treatments are Effective for People Who Abuse Methamphetamine?

 The most effective treatments for methamphetamine addiction are behavioral therapies, such as cognitive-behavioral and contingency-management interventions. For example, the Matrix Model, a 16-week comprehensive behavioral treatment approach that combines behavioral therapy, family education, individual counseling, 12-Step support, drug testing, and encouragement for non-drug-related activities, effectively reduces methamphetamine abuse. Contingency management interventions, which provide tangible incentives in exchange for engaging in treatment and maintaining abstinence, have also been shown to be effective. Motivational Incentives for Enhancing Drug Abuse Recovery (MIEDAR), an incentive-based method for promoting cocaine and methamphetamine abstinence, has demonstrated efficacy in methamphetamine abusers through NIDA’s National Drug Abuse Clinical Trials Network.
Although medications have proven effective in treating some substance use disorders, there are currently no medications that counteract the specific effects of methamphetamine or prolong abstinence from and reduce the abuse of methamphetamine by an individual addicted to the drug. However, NIDA has made research in the development of medications to treat addiction to stimulants and other drugs a priority. One approach being tried is to target the activity of glial cells. A drug called AV411 (ibudilast) that suppresses the neuro-inflammatory actions of glial cells has been shown to inhibit methamphetamine self-administration in rats and is now being fast-tracked in clinical trials to establish its safety and effectiveness in humans with methamphetamine addiction. Also under study are approaches that use the body’s immune system to neutralize the drug in the bloodstream before it reaches the brain. These approaches include injecting a user with anti-methamphetamine antibodies or vaccines that would stimulate the body to produce such antibodies. Researchers have begun a clinical study to establish the safety of an anti-methamphetamine monoclonal antibody known as mAb7F9 in human methamphetamine users.

Where Can I Get Further Information About Methamphetamine?

 To learn more about methamphetamine and other drugs of abuse, visit the NIDA Web site at www.drugabuse.gov or contact the DrugPubs Research Dissemination Center at 877-NIDA-NIH (877-643-2644; TTY/TDD: 240-645-0228) or online at drugpubs.drugabuse.gov.
What’s on the NIDA Web Site:

  • Information on drug abuse and related health consequences
  • NIDA publications, news, and events
  • Resources for healthcare professionals
  • Funding information (including program announcements and deadlines)
  • International activities
  • Links to related Web sites (access to Web sites of many other organizations in the field)

NIDA Web Sites:
www.drugabuse.gov
www.teens.drugabuse.gov
Other Web Sites
Information on drug abuse and other mental illnesses is also available through these other Web sites:
National Institute of Mental Health: www.nimh.nih.gov
National Institute on Alcohol Abuse and Alcoholism:www.niaaa.nih.gov
Substance Abuse and Mental Health Services Administration Publications Ordering:www.store.samhsa.gov/home

References:

References
Chang, L.; Alicata, D.; Ernst, T.; and Volkow, N. Structural and metabolic brain changes in the striatum associated with methamphetamine abuse. Addiction 102(Suppl 1):16–32, 2007.

Chang, L.; Ernst, T.; Speck, O.; and Grob, C.S. Additive effects of HIV and chronic methamphetamine use on brain metabolite abnormalities. Am J Psychiatry 162:361–369, 2005.

Ellis, R.J.; Childers, M.E.; Cherner, M.; Lazzaretto, D.; Letendre, S.; and the HIV Neurobehavioral Research Center Group. Increased human immunodeficiency virus loads in active methamphetamine users are explained by reduced effectiveness of antiretroviral therapy. J Infect Dis188(12):1820–1826, 2003.

Fairbairn, N.; Kerr, T.; Milloy, M.-J.; Zhang, R.; Montaner, J.; and Wood, E. Crystal methamphetamine injection predicts slower HIV RNA suppression among injection drug users. Addict Beh 36(7):762–763, 2011.

Gavrilin, M.A.; Mathes, L.E.; and Podell, M. Methamphetamine enhances cell-associated feline immunodeficiency virus replication in astrocytes. J Neurovirol 8:240–249, 2002.
Huber, A.; Ling, W.; Shoptaw, S.; Gulati, V.; Brethen, P.; and Rawson, R. Integrating treatments for methamphetamine abuse: A psychosocial perspective. J Addict Dis 16(4):41–50, 1997.

Johnston, L.D.; O’Malley, P.M.; Bachman, J.G.; and Schulenberg, J.E. Monitoring the future: National results on drug use: 2012 overview, key findings on adolescent drug use. Ann Arbor: Institute for Social Research, The University of Michigan, 2013. Available at: http://www.monitoringthefuture.org/pubs/monographs/mtf-overview2012.pdf. Last accessed March 18, 2013.

Kiblawi, Z.N.; Smith, L.M.; LaGasse, L.L.; Derauf, C.; Newman, E.; Shah, R.; Arria, A.; Huestis, M.; DellaGrotta, S.; Dansereau, L.M.; Neal, C.; and Lester, B. The effect of prenatal methamphetamine exposure on attention as assessed by continuous performance tests: Results from the Infant Development, Environment, and Lifestyle study. J Dev Behav Pediatr 34(1):31–37, 2013.

Kuehn, B.M. Meth use linked to risk of Parkinson disease.JAMA 306:814, 2011.

London, E.D.; Simon, S.L.; Berman, S.M.; Mandelkern, M.A.; Lichtman, A.M.; Bramen, J.; Shinn, A.K.; Miotto, K.; Learn, J.; Dong, Y.; Matochik, J.A.; Kurian, V.; Newton, T.; Woods, R.; Rawson, R.; and Ling, W. Mood disturbances and regional cerebral metabolic abnormalities in recently abstinent methamphetamine abusers. Arch Gen Psychiatry61:73–84, 2004.

Morgenthaler, T.I.; Kapur, V.K.; Brown, T.; Swick, T.J.; Alessi, C.; Aurora, R.N.; Boehlecke, B.; Chesson, A.L.; Friedman, L.; Maganti, R.; Owens, J.; Pancer, J.; and Zak, R. Practice parameters for the treatment of narcolepsy and other hypersomnias of central origin. An American Academy of Sleep Medicine Report. Sleep 30(12):1705–1711, 2007.

National Institute on Drug Abuse. Drugs of Abuse and Related Topics: Methamphetamine. Available at: www.drugabuse.gov/DrugPages/Methamphetamine.html. Last accessed March 18, 2013.

National Institute on Drug Abuse. Epidemiologic Trends in Drug Abuse: Proceedings of the Community Epidemiology Work Group, Highlights and Executive Summary, June 2012. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health, 2012. Available at: www.drugabuse.gov/sites/default/files/cewg_june_2012_vol1_508.pdf. Last accessed September 9, 2013.

National Institute on Drug Abuse. Methamphetamine abuse linked to impaired cognitive and motor skills despite recovery of dopamine transporters. NIDA Notes 17(1), 2002. Available at: http://archives.drugabuse.gov/NIDA_Notes/NNVol17N1/Methamphetamine.html. Last accessed March 22, 2013.

National Institute on Drug Abuse. Methamphetamine abusers show increased distractibility. NIDA Notes 22(3), 2009. Available at: www.drugabuse.gov/news-events/nida-notes/2009/04/methamphetamine-abusers-show-increased-distractibility. Last accessed March 22, 2013.

National Institute on Drug Abuse. Methamphetamine turns helper cells into destroyers. NIDA Notes 22(5), 2009. Available at: www.drugabuse.gov/news-events/nida-notes/2009/11/methamphetamine-turns-helper-cells-destroyers. Last accessed March 22, 2013.

Petry, N.M.; Peirce, J.M.; Stitzer, M.L.; Blaine, J.; Roll, J.M.; Cohen, A.; Obert, J.; Killeen, T.; Saladin, M.E.; Cowell, M.; Kirby, K.C.; Sterling, R.; Royer- Malvestuto, C.; Hamilton, J.; Booth, R.E.; Macdonald, M.; Liebert, M.; Rader, L.; Burns, R.; DiMaria, J.; Copersino, M.; Stabile, P.Q.; Kolodner, K.; and Li, R. Effect of prize-based incentives on outcomes in stimulant abusers in outpatient psychosocial treatment programs: A National Drug Abuse Treatment Clinical Trials Network study. Arch Gen Psychiatry62(10):1148–1156, 2005.

The RAND Corporation. The economic cost of methamphetamine use in the United States, 2005. The RAND Corporation, 2009. Available at: http://www.rand.org/content/dam/rand/pubs/monographs/2009/RAND_MG829.pdf. Last accessed March 22, 2013.

Rawson, R.A.; Marinelli-Casey, P.; Anglin, M.D.; Dickow, A.; Frazier, Y.; Gallagher, C.; Galloway, G.P.; Herrell, J.; Huber, A.; McCann, M.J.; Obert, J.; Pennell, S.; Reiber, C.; Vandersloot, D.; and Zweben, J. A multi-site comparison of psychosocial approaches for the treatment of methamphetamine dependence. Addiction 99:708–717, 2003.

Rippeth, J.D.; Heaton, R.K.; Carey, C.L.; Marcotte, T.D.; Moore, D.J.; Gonzalez, R.; Wolfson, T.; and Grant, I. Methamphetamine dependence increases risk of neuropsychological impairment in HIV infected persons. J Int Neuropsychol Soc 10:1–14, 2004.

Sekine, Y.; Ouchi, Y.; Sugihara, G.; Takei, N.; Yoshikawa, E.; Nakamura, K.; Iwata, Y.; Tsuchiya, K.J.; Suda, S.; Suzuki, K.; Kawai, M.; Takebayashi, K.; Yamamoto, S.; Matsuzaki, H.; Ueki, T.; Mori, N.; Gold, M.S.; and Cadet, J.L. Methamphetamine causes microglial activation in the brains of human abusers. J Neurosci 28(22):5756–5761, 2008.

Smith, L.M.: LaGasse, L.L.; Derauf, C.; Grant, P.; Shah, R.; Arria, A.; Huestis, M.; Haning, W.; Strauss, A.; Della Grotta, S.; Fallone, M.; Liu, J.; and Lester, B.M. Prenatal methamphetamine use and neonatal neurobehavioral outcome. Neurotoxicol Teratol 30(1):20–28, 2008. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2358984/. Last accessed April 9, 2013.

Smith, L.M.; LaGasse, L.L.; Derauf, C.; Grant, P.; Shah, R.; Arria, A., Huestis, M.; Haning, W.; Strauss, A.; Della Grotta, S.; Liu, J.; and Lester, B.M. The Infant Development, Environment, and Lifestyle Study: Effects of prenatal methamphetamine exposure, polydrug exposure, and poverty on intrauterine growth. Pediatrics118(3):1149–1156, 2006.

Snider, S.E.; Hendrick, E.S.; and Beardsley, P.M. Glial cell modulators attenuate methamphetamine self-administration in the rat. Eur J Pharmacol 701(1–3):124–130, 2013.

Substance Abuse and Mental Health Services Administration. Results from the 2012 National Survey on Drug Use and Health: Summary of National Findings, NSDUH Series H-46, HHS Publication No. (SMA) 13-4795. Rockville, MD: U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, 2013. Available at: http://www.samhsa.gov/data/NSDUH/2012SummNatFindDetTables/NationalFindings/NSDUHresults2012.htm. Last accessed September 9, 2013.

Substance Abuse and Mental Health Services Administration. Office of Applied Studies. Drug Abuse Warning Network: 2011. National estimates of drug-related emergency department visits, HHS Publication No. SMA 13-4760, DAWN Series D-39. Rockville, MD: U.S Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, 2013 Available at: http://www.samhsa.gov/data/2k13/DAWN2k11ED/DAWN2k11ED.htm. Last accessed September 09, 2013.

Substance Abuse and Mental Health Services Administration. Office of Applied Studies. Drug Abuse Warning Network: 2012. DAWN 2010 Emergency Department Excel Files–National Tables. Rockville, MD: U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, 2012. Available at: http://www.samhsa.gov/data/DAWN.aspx. Last accessed March 18, 2013.

Substance Abuse and Mental Health Services Administration. Office of Applied Studies. Treatment Episode Data Set (TEDS): 2001–2011. National Admissions to Substance Abuse Treatment Services, BHSIS Series S-65, HHS Publication No. (SMA) 13-4772 Rockville, MD: U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, 2013. Available at: http://www.samhsa.gov/data/2k13/TEDS2011/TEDS2011NAck.htm. Last accessed September 9, 2013.

Thompson, P.M.; Hayashi, K.M.; Simon, S.L.; Geaga, J.A.; Hong, M.S.; Sui, Y.; Lee, J.Y.; Toga, A.W.; Ling, W.; and London, E.D. Structural abnormalities in the brains of human subjects who use methamphetamine. J Neurosci24:6028–6036, 2004.

Toussi, S.S.; Joseph, A.; Zheng, J.H.; Dutta, M.; Santambrogio, L.; and Goldstein, H. Short communication: Methamphetamine treatment increases in vitro and in vivo HIV replication. AIDS Res Hum Retroviruses 25(11):1117–1121, 2009.

U.S. Environmental Protection Agency. Voluntary guidelines for methamphetamine laboratory cleanup, August 2009. Available at: http://www.epa.gov/osweroe1/meth_lab_guidelines.pdf. Last accessed March 22, 2013.

U.S. Food and Drug Administration. Post-market Drug Safety Information for Patients and Providers. FDA asks attention-deficit hyperactivity disorder (ADHD) drug manufacturers to develop patient medication guides. Available at:http://www.fda.gov/drugs/drugsafety/postmarketdrugsafetyinformationforpatientsandproviders/ucm107918.htm. Last accessed March 22, 2013.

Volkow, N.D.; Chang, L.; Wang, G-J.; Fowler, J.S.; Franceschi, D.; Sedler, M.; Gatley, S.J.; Miller, E.; Hitzemann, R.; Ding, Y-S.; and Logan, J. Loss of dopamine transporters in methamphetamine abusers recovers with protracted abstinence. J Neurosci 21(23):9414–9418, 2001.

Volkow, N.D.; Chang, L.; Wang G-J.; Fowler, J.S.; Leonido-Yee, M.; Franceschi, D.; Sedler, M.J; Gatley, S.J.; Hitzemann, R.; Ding, Y-S.; Logan, J.; Wong, C.; and Miller, E.N. Association of dopamine transporter reduction with psychomotor impairment in methamphetamine abusers. Am J Psychiatry 158(3):377– 382, 2001.

Wang G-J; Volkow, N.D.; Chang, L.; Miller, E.; Sedler, M.; Hitzemann, R.; Zhu, W.; Logan, J.; Ma, Y.; and Fowler, J.S. Partial recovery of brain metabolism in methamphetamine abusers after protracted abstinence. Am J Psychiatry161(2):242–248, 2004.

Wouldes, T.; LaGasse, L.; Sheridan, J.; and Lester, B. Maternal methamphetamine use during pregnancy and child outcome: What do we know? N Z Med J 117: U1180, 2004.

Source: National Institute on Drug Abuse; National Institutes of Health; U.S. Department of Health and Human Services.