Effects of Methamphetamine Abuse Beyond Individual Users (Report‪)‬

Amphetamine (R,S-1-phenyl-2-propanamine) and methamphetamine (R,S -N-methyl-1 -phenyl-2-propanamine) are powerful stimulants that affect the central nervous system by acting as indirect sympathomimetic drugs (Kraemer & Maurer 2002). Methamphetamine (meth) was developed in the early twentieth century from amphetamine, its parent drug (McGuinness 2006; Anglin et al. 2000). Meth was first used medically in 1932 as a nasal decongestant and in bronchial inhalers (Lineberry & Bostwick 2006). Later, it was used in the treatment of many other conditions, including narcolepsy, mild depression, obesity, post-encephalitic Parkinson syndrome, chronic alcoholism, cerebral arteriosclerosis, and hay fever (McGuinness 2006; Anglin et al. 2000). In the United States, amphetamine and meth products were available without prescription until 1951 (Romanelli & Smith 2006). By the 1960s, amphetamines were available only by prescription but were widely used as recreational drugs; millions of amphetamine-containing prescriptions such as anorexiants were written in the mid-1960s (Ling et al. 2006; McGuinness 2006). By the 1970s, the dangers associated with the use of amphetamine and meth were better understood, which led to the classification in 1971 of all forms of amphetamine and meth as Drug Enforcement Agency Schedule II drugs (i.e., those that carry a high potential for abuse but are considered to have some medical uses) (McGuinness 2006; Anglin et al. 2000). The acute and long-term health effects of meth are integrally tied to its pharmacologic properties. Meth is easily absorbed through different bodily structures, including the gut, airways, and nasopharynx (Rawson, Gonzales & Brethen 2002). Two major actions of meth are (1) stimulation of the brain's synaptic sites, which produces a state of arousal, wakefulness, or mood elevation and (2) appetite suppression (Murray 1998). The drug gives users a "rush"--feelings of enhanced well-being, heightened libido, increased energy, and appetite suppression (Lineberry & Bostwick 2006). The immediate effects of meth are increased heart and respiratory rates, blood pressure, and body temperature (Anglin et al. 2000). The rush is reportedly often associated with euphoria and increased energy, which can last for several hours given the long half-life of the drug (Romanelli & Smith 2006). Acute ingestion of large doses of meth may lead to seizures, cerebrovascular hemorrhage, or vasospasm (Anglin et al. 2000). With long-term meth abuse, several distinct clinical effects may increase: confusion, paranoia, hallucinations, paranoid psychosis, depression, memory loss, cardiomyopathy, dermatologic lesions, poor dentition, and weight loss (Romanelli & Smith 2006; Cho & Melega 2002; Rawson, Gonzales & Brethen 2002; Cho et al. 2001; Wermuth 2000). Abrupt discontinuation of meth can result in withdrawal phenomenon characterized by severe depression (Rawson, Gonzales & Brethen 2002; Gygi et al. 1996), often accompanied by fatigue, anergia, and cognitive impairments, lasting from days to weeks (Rawson, Gonzales & Brethen 2002; Cho et al. 2001). Researchers have speculated that psychotic symptoms may persist even after a person abstains from use (Rawson, Gonzales & Brethen 2002; Cho et al. 2001; Wermuth 2000). Researchers have also raised concerns regarding the effect of long-term meth abuse on dopaminergic neurons and gray matter (Romanelli & Smith 2006; Cho & Melega 2002). In addition, prolonged meth use often results in tachyphylaxis, which requires the person to consume increasing doses of the drug to sustain the same clinical effects (Gygi et al. 1996). Tachyphylaxis is believed to result from depleted concentrations of neurotransmitters (Riviere, Gentry & Owens 2000; Gygi et al. 1996). Longterm use is also associated with dilated cardiomyopathy as a result of catecholamine-related toxicity (Lineberry & Bostwick 2006).