Methamphetamine: The Basics
Introduction and Basic Description
Methamphetamine, also known as desoxyephedrine, N,a-dimethylphenethylamine and N,a-dimethylbenzeneethanamine, is a highly-potent central nervous system (CNS) stimulant. Methamphetamine is a member of the amphetamine group of sympathomimetic amines.
Methamphetamine is one of the most commonly abused drugs worldwide, second only to Cannabis, with an estimated prevalence of 0.4 percent of the world’s population consuming it.  It is used recreationally to induce feelings of increased sociability, euphoria, vigilance, energy/reduction of fatigue and increased confidence. Methamphetamine is also recognized for its ability to heighten sexual pleasure and increase sexual stamina.
In the medical communities of many countries, methamphetamine hydrochloride (marketed under the trade name Desoxyn) is indicated for the pharmacotherapeutic treatment of Attention-Deficit Hyperactivity Disorder (ADHD) and as an anorectic for the short-term treatment of exogenous obesity. Methamphetamine may also be prescribed as an “off-label” treatment for narcolepsy. Desoxyn preparations are presently restricted to immediate-release tablets containing 5mg of the dextratory isomer of methamphetamine hydrochloride.
Timeline of Experience
The timeline of the methamphetamine experience is heavily influenced by dosage and route-of-administration. Below are approximated timeline values for methamphetamine with regard to varying types of drug administration for non-tolerant users:
Methamphetamine produces a wide variety of physiological and behavioral/psychological effects in humans. It is important to be mindful of the fact that the incidence and prevalence of methamphetamine’s individual physiological, behavioral and psychological effects are dose-dependant and can differ significantly from one person to the next in a given population of users.
- Anorexia (Loss of appetite)
- Insomnia (Inability to sleep, disrupted sleep architecture)
- Mydriasis (dilated pupils)
- Diaphoresis (excessive sweating)
- Tachycardia (dangerously rapid heart rate)
- Bradycardia (dangerously slow heart rate)
- Trismus (jaw-clenching)
- Bruxia (teeth-grinding)
- Increased energy
- Sexual arousal
- Xerostomia (dry mouth) 
At higher doses, or in individuals predisposed to cardiovascular conditions, the physiological effects of methamphetamine may become much more severe, and may include: 
- Arrhythmias (irregular heartbeat)
- Heart attack
Behavioral & Psychological
- Increased confidence/sociability
- Increased reaction time
- Increase in compulsive behaviors
- Lowered inhibitions
- Increase in selective attention
- Increase in motivation
- Improved reflexes
- Empathy, feelings of openness
Long-term, continuous use of methamphetamine can result in a debilitating mental state known as “amphetamine psychosis” that closely mimics the symptoms of paranoid schizophrenia. The incidence of psychosis produced my chronic methamphetamine use is generally higher than that produced by amphetamine. Symptoms of amphetamine psychosis include megalomania (inflated ego, sense of power), paranoid delusions, sensory hallucinations (generally auditory and tactile, but can include visual and olfactory hallucinations), depersonalization, violence and homicidal/suicidal ideations. 
In order to avoid complications and minimize the incidence of negative side effects, it is important to emphasize that dosages for methamphetamine can vary due to many factors, not the least of which is accumulated tolerance to the drug from past exposure. The lowest dose possible should always be attempted first. The following dosages represent approximations for non-tolerant users classified according to route of administration under the assumption of pure methamphetamine:
Methods of Administration
Methamphetamine is most frequently insufflated (snorted), vaporized or injected intravenously. The hydrochloride salt of methamphetamine readily melts and vaporizes without combusting, thus making this route of administration (ROA) not only simple, but efficient. Many users, however, prefer to inject methamphetamine. The user typically experiences a "rush" following injection that is experientially more significant than intravenous amphetamine due to methamphetamine's additional methyl group which allows the drug to cross the blood-brain barrier more thoroughly.
Other viable ROA for methamphetamine include buccal, oral (swallowed), sublingual and rectal (known as "plugging"). Buccal and sublingual administration are generally discouraged due to the extent that methamphetamine irritates the body's mucous membranes. Similarly, even short-term insufflation of methamphetamine may result in profound nasal tissue irritation and bleeding, with long-term insufflation causing potentially irreversible damage to the septum (that which divides your left from your right nostril).
Methamphetamine has many common street names, sometimes causing confusion arising from geographic and procedural differences in clandestine production. Some common colloquial terms referring to methamphetamine are listed below:
Contraindications and Overdose
Possible Drug Interactions
- Sympathomimetics eg: MAOIs (isocarboxazid, linezolid, methylene blue, moclobemide,
phenelzine, procarbazine, rasagiline, selegiline, tranylcypromine, chlorgyline, nialamide, pargyline, befloxatone, brofaromine, moclobemide) If taken within 2 weeks before, during, and after treatment with this medication, in some cases a serious and possibly life threatening drug interaction may occur. Very high blood pressure can occour. DO NOT COMBINE ANY MAOI WITH METHAMPHETAMINE!!
- Tricyclic antidepressants (e.g. amitriptyline, amoxapine, clomipramine, doxepin, imipramine, desipramine,
nortriptyline, protriptyline, trimipramine) Taking methamphetime with tricyclics can change the way the brain reacts to methamphetamine, possibly causing more side effects.
- SSRIs (e.g. fluoxetine, citalopram, fluvoxamine, paroxetine, sertraline)
Serotonin reuptake inhibitors may potentiate the pharmacologic response to sympathomimetic agents.
- NARIs/Noradrenaline Reuptake Inhibitors (e.g. mianserin)
Stimulant effects felt by methamphetamine are almost completely blocked by NARIs.
If taken with methamphetamine, insulin can increase the risk of low blood sugar (hypoglycemia) because you may eat less while taking methamphetamine (it is an appetite suppressant).
- Medications for high blood pressure (guanethidine)
Since psychotstimulants can increase blood pressure, they may counteract the effectiveness of antihypertensives
- Beta-blockers (e.g. paropranolol, atenolol)
- Medications that affect the acid level of the urine (e.g. sodium bicarbonate, acetazolamide)
Alkalinization of the urine can decrease the renal elimination of methamphetamines. Methamphetamine effects may be prolonged, and the risk of toxicity may be increased.
- Other stimulant medications (e.g. dextroamphetamine, methylphenidate, lisdexamfetamine)
Combining other stimulants with methamphetamine may decrease the effects of methamphetamine.
- Phenothiazines (e.g. chlorpromazine, thioridazine, fluphenazine, perphenazine, promethazine,
trifluoperazine) If taken with methamphetamine, this may decrease the effectiveness of methamphetamine.
- Cough & Cold Products (Containing Dextromethorpan HBr/Polistirex)
Mixing cold medicines with methamphetamine may cause blood pressure to become dangerously high or lead to irregular heart rythyms
- Isoniazid (INH)
- Ioflupane (eg: dopamine transporter bin)
Drugs that bind to the dopamine transporter with high affinity may interfere with the image obtained using ioflupane I-123, which also binds to the dopamine transporter.
- SNRIs (e.g. venlafaxine)
Possibly causes seizures when combined with methamphetamine. Can cause dangerous fluctuations in blood pressure and possible serotonin syndrome.
- Serotonergics (MDMA, St. Johns Wort, tramadol, pethidine, triptans)
These drugs have the potential to produce symptoms of serotonin toxicity
- Antipsychotics (e.g. colazapine)
These drugs antagonize the effects of dopamine at D2 receptor. Using methamphetamine with any of these drugs can greatly reduce the efficacy of each drug. May also induce a meth-related psychosis or psychotic symptoms, or antipsychotic-induced acute dystonias.
Pre-Existing Conditions That Should Not be Mixed With Methamphetamine
- Allergy to methamphetamine hydrochloride, Desoxyn, or any inactive component in the drug
- Heart conditions including heart disease, atherosclerosis, congestive heart failure, recent heart
attack, certain irregular heart rhythyms (arrhythmias)
- Have moderate to severe hypertension (high blood pressure)
- Severe agitation
- Overactive thyroid (hyperthyroidism)
- If you have used a monoamine oxidase inhibitor (MAOI) within fourteen days
- Tourette's Syndrome (methamphetamine can exacerbate tics)
- Pregnant or could be pregnant, or breastfeeding (methamphetamine is passed through breast milk and may effect an unborn baby resulting in low birth
Negative Short-Term Side Effects
- Increased blood pressure
- Increased respiration
- Emotional lability
- Repetitive, obsessive-compulsive behaviors
- Mydriasis (dilated pupils)
- Diaphoresis (excessive sweating)
- Dry mouth
- Poor oral hygiene
- Bruxism (jaw clenching)
- Sudden death (cardiac arrest)
Negative Long-Term Side Effects
Addiction and Withdrawal Issues
Methamphetamine is widely considered the most powerful, and arguably the most reinforcing, of the stimulant drugs-of-abuse. Studies whose participants had sought treatment for methamphetamine addiction show relapse rates of as high as 92%, although more conservative estimates place the relapse rate of those who have undergone treatment at just above 60% at 12 months post-treatment.
Methamphetamine Withdrawal Syndrome
Suddenly stopping chronic methamphetamine use may cause an array of withdrawal-related psychological and behavioral symptoms such as disrupted sleep architecture/insomnia, significant depression, anxiety and intense cravings for the drug. Another hallmark of methamphetamine withdrawal is impairment on a battery of cognitive functions; these include memory, divided and directed attention, motivation and planning. Other common effects of withdrawal include “…hyperphagia [excessive eating], agitation, vivid and unpleasant dreams, [and] reduced energy…”
The syndrome is formally classified by the American Psychiatric Association as “amphetamine-type stimulant withdrawal syndrome.” Research currently suggests that the syndrome’s etiology results “…from the depletion of presynaptic monoamine stores, down-regulation of receptors and neurotoxicity.”
Content forthcoming ~ vaya
In the United States, methamphetamine is classified as a Schedule II substance - a substance with established medical and clinical applications and with a high liability for abuse. It is illegal to possess without a prescription or government-issued license. It is currently sold by Abbot Pharmaceuticals under the trade name Desoxyn, and generically by Mylan Pharmaceuticals as “methamphetamine HCl” in the form of 5mg instant-release tablets.
Sanctions against the possession of materials considered precursors in the manufacture of methamphetamine were instituted in 1983, and the United States government began to aggressively pursue the elimination of clandestine methamphetamine laboratories that had become driving forces behind the rapid spread and rising popularity of methamphetamine in America. Over time, progressively more restrictions were placed on over-the-counter cold and sinus remedies that included the ingredient pseudoephedrine, a critical component in the methamphetamine production process. The U.S. Combat Methamphetamine Act of 2005 imposed federally-regulated laws stating that pseudoephedrine-containing products were to be sold behind the counter of nationwide drug stores. The law made it a requirement that consumers present photo identification and sign a register when purchasing these products, and that a limit be placed on the amount of product one could buy at a given time. As a sub-division of the USA Patriot Act, consumers' transactions at various stores are able to be electronically monitored in order to identify illegal diversion.
In 1996, Canada’s federal government passed the Controlled Drugs and Substances Act, establishing firmer guidelines for the regulation of licit and illicit substances within the country.[SUP][/SUP] In August of 2005, Canada moved methamphetamine into its most restrictive class of controlled substances, Schedule I, alongside cocaine and heroin. Canada currently does not recognize methamphetamine as a drug with medical value.
Placing methamphetamine apart from other amphetamines (Schedule III) imposes harsher legal consequences for those illicitly involved with the substance: Possession of methamphetamine carries a maximum penalty of $5,000 and/or up to three years in prison, and the maximum penalty for production/distribution of the drug rose from a maximum of 10 years in prison to life imprisonment in 2005.
Unlike Canada, the Australian government recognizes methamphetamine as a substance with medical value. It is listed in Schedule 8 of the Australian Standard for the Uniform Scheduling of Drugs and Poisons. This indicates that methamphetamine is a federally controlled substance “…which should be available for use but require[s] restriction of manufacture, supply, distribution, possession and use to reduce abuse, misuse and physical or psychological dependence.”
On January 18th, 2007, the United Kingdom complied with a June 2006 recommendation made by the Advisory Council on the Misuse of Drugs to reclassify methamphetamine. Whilst previously classified in Class B (except in injectable ampoule or liquid vial forms) , methamphetamine became a Class A drug under the Misuse of Drugs Act of 1971, the UK’s most restrictive controlled drug class.
Background and Chemistry
History of Methamphetamine
The discovery of methamphetamine followed shortly after amphetamine was created in Germany in 1897. Methamphetamine was first synthesized in Japan in 1919, but remained obscure and without practical use for some time afterwards. The first widespread use of methamphetamine was during World War II by soldiers in the German, American and Japanese militaries. The drug was dispensed to soldiers by heir commanding officers in order to increase bravery, aggression and resiliency when sleep and food were not abundant. It is rumored that Japanese fighter pilots utilized methamphetamine to help spur enthusiasm for kamikaze attacks, such as those enacted on Pearl Harbor. The very first human methamphetamine epidemic was a direct result of wartime manufacture of methamphetamine; following the final days of World War II, Japan discovered itself with an abundant supply of the drug and its high solubility in water made it an ideal stimulant for intravenous abuse. In 1951, the Japanese government responded by banning methamphetamine.
On December 31st, 1943, Ovation Pharmaceuticals received FDA approval to begin marketing d-methamphetamine hydrochloride in the United States. In the U.S., the 1950’s marked a cultural explosion of amphetamine (Dexedrine, Benzedrine) and methamphetamine (Desoxyn, Methedrine) misuse by college students, truck drivers, athletes and professionals. The 1960’s marked a substantial increase in IV methamphetamine abuse, and the United States government responded with the 1970 Controlled Substances Act that drastically reduced the production of injectable meth. Methamphetamine was formally classified as a Schedule II substance according to the Controlled Substances Act on July 7th, 1971.
The abuse of methamphetamine experienced a resurgence in the late 1980's as illicit chemists discovered that the drug was easily made via the reduction of two legal stimulant compounds, ephedrine and pseudoephedrine, using legal and easily obtainable chemical precursors to accomplish the intermediary steps required for synthesis. Methamphetamine became favored amongst truck drivers, western motorcycle gangs and the homosexual community, and clandestine production within the United States has seen a tremendous increase since 1991.
Methamphetamine continues to be one of the most popular and widely used drugs of abuse, especially in North America, where its availability and distribution has spread from the west coast of the United States to its eastern coast. Regional anti-methamphetamine campaigns and sensationalist press coverage of the present methamphetamine “epidemic” have caused meth to become one of the most stigmatized substances in America’s War on Drugs.
In late April of 2010, Mylan Pharmaceuticals introduced the first generic form of Desoxyn, methamphetamine hydrochloride tablets USP, 5mg.
Pharmacology & Mechanism of Action
Methamphetamine is derived from amphetamine (a-methylphenethylamine) and is synonymous withN-methyl-1-phenylpropan-2-amine, the N-methyl derivative of amphetamine. Methamphetamine is also known as methylamphetamine, metamfetamine, methyl-beta-phenylisopropylamine, 1-phenyl-2-methylaminopropane and N,a-Dimethylbenzeneethanamine.
Owing largely to its structural similarity with monoamine neurotransmitters, including dopamine and norepinephrine, methamphetamine substitutes for these monoamines at their respective transporters. These predominately include the dopamine transporter (DAT), the norepinephrine transporter (NET), and the serotonin transporter (SERT). Methamphetamine also exerts its action by reversing the action of the vesicular monoamine tranporter-2 (VMAT-2), and thus expelling dopamine (DA), serotonin (SER) and norepinephrine (NE) into the cytosol between neurons. Methamphetamine's action on VMAT-2 alters the neuronal roles of DAT, NET and SERT with the result that these monoamines are transported from the cytosol into nerve synapses and increasing levels of these neurotransmitters in many parts of the brain. The brain areas affected most predominately by methamphetamine-induced neurotransmitter release are the pre-frontal cortex (PFC), striatum and areas of the mesolimbic system such as the ventral tegmental area (VTA) and substantia nigra. The activity of DA, the neurotransmitter most heavily affected by methamphetamine, is increased most significantly in the "...mesolimbic, mesocortical circuit and nigrostantial pathways." Additionally, "in vitro studies indicate that methamphetamine is twice as potent at releasing noradrenaline as dopamine, and its effect is 60-fold greater on noradrenaline than serotonin release."
Methamphetamine undergoes hepatic metabolism via several mechanisms. When catalysed by cytochrome P450 2D6, methamphetamine undergoes N-demethylation (producing amphetamine) and aromatic hydroxylation (producing 4-hydroxymethamphetamine). Beta-hydroxylation produces norephedrine. The various metabolites resulting from the metabolism of methamphetamine do not significantly contribute to its effects on the human body.
70% of a dose of methamphetamine is excreted in urine within 24 hours. “The terminal plasma half-life of methamphetamine of approximately 10 hours is similar across administration routes, but with substantial inter-individual variability. Acute effects persist for up to 8 hours following a single moderate dose of 30 mg… via vapour inhalation (smoking), methamphetamine bioavailability ranges from 67% to 90%... [and] is 79% bioavailable via the intranasal route.”
Methamphetamine is prepared via the reduction of ephedrine or pseudoephedrine into desoxyephedrine. For educational purposes, that is all you need to know.
Content forthcoming ~ vaya
(1) ChemSpider (2009). “Methamphetamine Names and Identifiers.” The Royal Society of Chemistry. http://www.ChemSpider.com/Chemical-Structure.10379.html. Retrieved 14 January 2012.
(2) Hanson, G.R., Venturelli, P.J. & Fleckenstein, A.E. (2005). "Drugs and Society (Ninth Edition)". Jones and Bartlett Publishers. ISBN 9780763737320. Retrieved 19 April 2011.
(3)“ATS: second most commonl abused drug type worldwide,” (2011). United Nations Office on Drugs and Crime. http://www.unodc.org/unodc/en/frontpage/2011/September/ats-second-most-used-drug-type-in-the-world.html. Retrieved 17 January 2012.
(4)Cruickshank, C.C. & Dyer, K.R. (2009). A review of the clinical pharmacology of methamphetamine. Addiction, 2009; 104: 1085-1099.
(5)EMCDDA Drug Profiles (2011). “Methamphetamine.” European Monitoring Centre for Drugs and Drug Addiction. http://www.emcdda.europa.eu/publications/drug-profiles/methamphetamine. Retrieved 16 January 2012.
(6) Monson, K., Schoenstadt, A. (2010). “What Is Methamphetamine Used For?” e-MedTV. http://mental-health.emedtv.com/methamphetamine/what-is-methamphetamine-used-for-p2.html. Retrieved 16 January 2012.
(7) Ovation Pharmaceuticals Medication Guide: Desoxyn (2007). Food and Drug Administration. http://www.fda.gov/downloads/Drugs/DrugSafety/ucm088582.pdf. Retrieved 14 January 2012.
(8) Erowid (2003). “Methamphetamine Dosage V1.0.” Erowid.org. http://www.erowid.org/chemicals/meth/meth_dose.shtml. Retrieved 15 January 2012.
(9) http://www.Montana.edu (2011). "Physiological Effects of a Methamphetamine Overdose.” Montana State University. Retrieved 9 January 2011.
(10) Angrist, B. M. & Gershon, S. The phenomenology of experimentally induced amphetamine psychosis - Preliminary observations. Journal of Biological Psychiatry, 1970; 2: 95–107.
(11)Center for Substance Abuse Research (CESAR) (2005). “Methamphetamine.” University of Maryland. http://www.cesar.umd.edu/cesar/drugs/meth.asp. Retrieved on 27 January 2012.
(12) Otero, C., Boles, S., Young, N. K. and Dennis, K. Methamphetamine Addiction, Treatment, and Outcomes: Implications for Child Welfare Workers. Substance Abuse and Mental Health Services Administration, Center for Substance Abuse Treatment, 2006. http://www.ncsacw.samhsa.gov/files/Meth%20and%20Child%20Safety.pdf. Retrieved 20 January 2012.
(13) Kalechstein, A. D., Newton, T. F. & Green, M. Methamphetamine dependence is associated with neurocognitive impairment in the initial phases of abstinence. Journal of Neuropsychiatry and Clinical Neuroscience, 2003; 15: 215–20.
(14) Meredith, C. W., Jaffe, C., Ang-Lee, K. and Saxon, A. J. Implications of chronic methamphetamine use: a literature review. Harvard Review of Psychiatry, 2005; 13: 141–54.
(15) Joseph, Richard (2009). “History of Meth.” Albuquerque Breaking Bad “The Book.” http://www.albuquerquebreakingbad.com/history-of-meth. Retrieved 15 January 2012.
(16) “Controlled Drugs and Substances Act.” Isomer Design, 2012. http://isomerdesign.com/Cdsa/. Retrieved on 19 January 2012.
(17) Legal status of methamphetamine. (n.d.). Retrieved January 18th, 2012 from Wikipedia: http://en.wikipedia.org/wiki/Legal_status_of_methamphetamine#Canada
(18) CTV.ca News Staff (2005, August 12). Ottawa Toughens Methamphetamine Penalties. CTV News. Retrieved from http://www.ctv.ca/CTVNews/TopStories/20050812/crystal_meth_050811/
(19) Australian Government Department of Health and Aging (2008). Therapeutic Goods Administration: Standard for the uniform scheduling of drugs and poisons no. 23. Canberra: Commonwealth of Australia. ISBN 1741865964. Retrieved 4 June 2009.
(20) BBC News Staff (2006, June 14). Crystal Meth to be Class A Drug. BBC News. Retrieved from http://news.bbc.co.uk/2/hi/uk_news/politics/5079266.stm
(21) “Desoxyn.” Prescription Drug-Info. http://www.prescriptiondrug-info.com/Drugs/Desoxyn/. Retrieved 15 January 2012.
(22) United States Office of Diversion Control (2005). “Code of Federal Regulations, Section 1308: Schedules of Controlled Substances.” United States Department of Justice. http://www.deadiversion.usdoj.gov/21cfr/cfr/2108cfrt.htm. Retrieved 14 January 2012.
(23) “History of Methamphetamine.” Montgomery County Sheriff’s Office. http://www.montgomerycountytn.org/County/sheriff/meth/methHistory.aspx. Retrieved 10 January 2012.
(24) Mylan Inc. (2010). “Mylan Begins Marketing First Generic Version of Desoxyn.” PR Newswire. http://investor.mylan.com/releasedetail.cfm?ReleaseID=463277. Retrieved 14 January 2012.
(24) “3-D Methamphetamine Molecule.” Erowid.org. http://www.erowid.org/chemicals/meth/images/archive/methamphetamine_3d.jpg. Retrieved 14 January 2012.
(25) Various (1996). “Methamphetamine Frequently Asked Questions.” Amphetamines.com. http://amphetamines.com/methamphetamine-faq/index.html. Retrieved 14 January 2012.
(26) RnCeus (2007). “Pharmacological Action of Meth.” RnCeus Interactive. http://www.rnceus.com/meth/methpharm.html. Retrieved 20 January 2012.
(27) Wise R. A. (2004). Dopamine, learning and motivation. Nature Reviews Neuroscience, 2004; 5: 483–94.
(28) Kraemer T. & Maurer H. H. Toxicokinetics of amphetamines: metabolism and toxicokinetic data of designer drugs, amphetamine, methamphetamine, and their N-alkyl derivatives. Journal of Therapeutic Drug Monitoring, 2002; 24: 277–89.
(29) Lin, L. Y., Di Stefano, E. W., Schmitz, D. A., Hsu, L., Ellis, S. W., Lennard, M. S. et al (1997). Oxidation of methamphetamine and methylenedioxymethamphetamine by CYP2D6. Journal of Drug Metabolism and Disposition, 1997; 25: 1059–64.
(30) Kim, I., Oyler, J. M., Moolchan, E. T., Cone, E. J. and Huestis, M. A. Urinary pharmacokinetics of methamphetamine and its metabolite, amphetamine following controlled oral administration to humans. Journal of Therapeutic Drug Monitoring, 2004; 26: 664– 72.
(31) Mohler & Townsend (2006). “Advanced Therapy In Hypertension And Vascular Disease.” PMPH-USA. p. 469. ISBN 978-1550093186.
(32) Center for Substance Abuse Research (CESAR). "Methamphetamine.” Cesar.umd.edu. Retrieved 9 January 2011.
(33) "Erowid Methamphetamines Vault: Effects." www.Erowid.org. Retrieved 1 September 2011.
(34) http://www.Montana.edu (2011). "Physiological Effects of a Methamphetamine Overdose.” Montana State University. Retrieved 9 January 2011.
(35) American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text revision edn. Washington DC: American Psychiatric Association; 2000.
Additional Resources/External Links
- A Key to Methamphetamine-Related Literature
- Erowid Methamphetamines Vault
- U.S. National Library of Medicine: Drug Information Portal - Methamphetamine
- Poison Information Monograph 334: Methamphetamine