METHAMPHETAMINE: FACT VS.

FICTION AND LESSONS FROM THE CRACK HYSTERIA

Carl L. Hart, Joanne Csete, Don Habibi

Department of Psychology, Columbia University,

Division on Substance Abuse, New York State Psychiatric Institute and
Department of Psychiatry, College of Physicians and Surgeons of Columbia University,
Institute for Research in African-American Studies, Columbia University,
Open Society Foundation
and
Department of Philosophy, University of North Carolina Wilmington

Address Correspondence to:

Carl L. Hart, Ph.D.

New York State Psychiatric Institute
1051 Riverside Dr., Unit 120
New York, NY 10032, U.S.A.
Voice (212) 543-5884
FAX (212) 543-5991
clh42@columbia.edu
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Executive Summary

The purpose of this report is to provide a critical examination of the available evidence on illicit
methamphetamine use and its consequences in the United States and internationally. It is the aim
of this report to dispel some of the myths about the effects of methamphetamine and other illicit
drugs using the best available scientific data. Further, it is our hope that this analysis will lead to
more rational policies for dealing with both legal and illegal amphetamine. The report begins
with an examination of the lessons learned from the “crack cocaine scare” in the 1980s. In this
way, the reader can draw parallels between society’s response to crack cocaine then, and
methamphetamine now. The report then describes distinctions and similarities between
methamphetamine and other amphetamine-type stimulants. Also examined is the prevalence of
methamphetamine use and public policies in response to the perceived increased use of the drug
and perceived drug-related problems. Finally, the report critically reviews the scientific literature
on the effects of methamphetamine on the brain, physiology, and behavior. The data show that
many of the immediate and long-term harmful effects caused by methamphetamine use have
been greatly exaggerated just as the dangers of crack cocaine were overstated nearly three
decades ago. Recommendations are made in an effort to remedy this situation and to enhance
public health and safety.

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Introduction

Lesson Learned from Crack in the United States

The emotional hysteria that stems from misinformation related to certain illegal drugs often leads
to more harm than the drugs themselves. In the United States during the mid-1980s, for example,
crack cocaine was believed to be so powerfully addictive that even first-time users would
become addicted. Even more worrisome was the perception that the drug produced unpredictable
and deadly effects. Despite the fact that there was virtually no real evidence supporting these
claims, in 1986, the United States Congress passed the now infamous Anti-Drug Abuse Act
setting penalties 100 times harsher for crack than for powder cocaine convictions. The law stated
that a person convicted of selling 5 grams of crack cocaine was required to serve a minimum
sentence of five years in prison; convictions involving 50 grams of crack carried a minimum
sentence of 10 years. To receive similar sentences for trafficking in powder cocaine, individuals
needed to have been caught selling (or intending to sell) 500 grams and 5 kilograms of cocaine,
respectively.

By 1988, concern about the drug had increased so much that penalties of the 1986 law
were extended to persons convicted of simple possession. Even first-time offenders faced such
stiff mandatory sentences. Simple possession by a first-time offender of any other illegal drug,
including powder cocaine or heroin, carried a maximum penalty of one year in prison.

The driving force behind passage of these anti-crack laws was the exaggerated claims
made in the media on a near-daily basis. Multiple stories warned of “crack-crazed” addicts. In
the months before the 1986 elections, more than 1,000 stories on cocaine appeared in the
national press, including five cover stories in Time and Newsweek. Time magazine called crack
cocaine the issue of the year. When the furor about crack had settled, two things were clear.
First, media accounts about the effects of the drug were inconsistent with the scientific data.
There are no pharmacological differences between crack and powder cocaine to justify their
differential treatment under the law. Figure 1 shows the chemical structures of cocaine
hydrochloride and cocaine base (crack). The structures are nearly identical.

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Figure 1 Chemical structure of cocaine hydrochloride (powder cocaine) and cocaine base
(crack)

The two forms of cocaine produce identical effects; these effects are predictable (Hatsukami and
Fischman, 1996). That is, as the dose is increased, so are the effects, whether they are blood
pressure and heart rate or subjective “high” and addictive potential. The way the drug is taken
differs based on its form, however. Crack is smoked, whereas powder is swallowed, snorted, or
injected. More intense effects are observed when the drug is smoked or injected intravenously,
but the drug itself remains the same. To punish crack users more harshly than powder users is
analogous to punishing those who are caught smoking marijuana more harshly than those caught
eating marijuana-laced brownies.

Another consequence that became apparent was that the differences between crack and
powder laws disproportionately targeted blacks. A whopping 85 percent of those sentenced for
crack cocaine offenses were black, despite the fact that the majority of users of the drug were
white (USSC 1995, 1997, 2002, 2007). Frustrated by the lack of willingness of lawmakers to
eliminate the disparity between crack and powder cocaine penalties, in 2007, even presidential
candidate Barack Obama voiced strong concerns: “…let's not make the punishment for crack
cocaine that much more severe than the punishment for powder cocaine when the real difference
between the two is the skin color of the people using them…That will end when I am President.”
On August 3, 2010, President Obama signed legislation that decreased, but did not eliminate, the
sentencing disparity between crack and powder cocaine offenses. The new law reduced the
sentencing disparity from 100:1 to 18:1.

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While we recognize the improvement this compromise represents, it remains an

inadequate solution because the scientific evidence does not support disparate penalties for crack
and powder cocaine violations. And when one considers the perception of the egregious racial
injustice that occurred in enforcing these laws, it is not difficult to draw a similar conclusion to
the one drawn by Malcolm X in 1964 when asked whether the U.S. had made sufficient progress
towards racial equality. He said “If you stick a knife in my back nine inches and pull it out six
inches, there is no progress… The progress is healing the wound.”

Methamphetamine: the new crack

There are multiple signs indicating that methamphetamine is the current drug about which
exaggerated media claims are made. As with the “crack scare” of the 1980s, many high-profile
stories about methamphetamine have appeared in the global press. On August 8, 2005, for
example, Newsweek ran a dramatic cover story called “The Meth Epidemic.” Use of this drug,
according to the magazine, had reached epidemic proportion. The evidence suggested otherwise.
At the height of methamphetamine’s popularity, there were never more than a million current
users of the drug in the United States. This number is considerably lower than the 2.5 million
cocaine users, the 4.4 million illegal prescription opioid users, or the 15 million marijuana
smokers during the same period. In the United States, the number of methamphetamine users has
never come close to exceeding the number of users of these other drugs (SAMHSA 2012).

Media coverage has been filled with accounts of desperate users turning to crime to
support their use of the “dangerously addictive” drug. Many articles focused on the “littlest
victims.” The New York Times headlined one story, “Drug Scourge Creates Its Own Form of
Orphan,” describing an apparent rise in related foster care admissions and reports of addicted
biological parents who were impossible to rehabilitate. The paper quoted a police captain who
said methamphetamine “makes crack look like child's play, both in terms of what it does to the
body and how hard it is to get off” (Butterfield 2004). The paper also claimed: “Because users
are so highly sexualized, the children are often exposed to pornography or sexual abuse, or watch
their mothers prostitute themselves” (Zernike 2005).

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Then United States Attorney General Alberto Gonzales called it “the most dangerous
drug in America,” and President George W. Bush proclaimed November 30, 2006 National
Methamphetamine Awareness Day. Back in 1986, President Ronald Reagan proclaimed the
entire month of October Crack/Cocaine Awareness Month.

The parallels are clear enough to demonstrate that history is repeating itself—mistakes
and all. The emotional hysteria driving public policy on methamphetamine is causing great
harms that are avoidable. In an effort to avoid making many of the same mistakes that were made
with crack cocaine with regard to stigma, public policy and general misinformation, the purpose
of this report is to provide a critical examination of the available evidence on methamphetamine
use and its consequences in the United States and internationally. It is the aim of this report to
dispel some of the myths about the effects of methamphetamine and other illicit drugs using the
best available scientific data. Further, it is our hope that this analysis will lead to more rational
policies for dealing with both legal and illegal amphetamine.

What is methamphetamine?
Amphetamine is a class of chemical compounds that includes drugs used for both medical and
recreational purposes. Of this class, d-amphetamine and methamphetamine are approved in
several countries to treat a variety of disorders, including attention-deficit hyperactive disorder
(ADHD), narcolepsy, and obesity. These drugs as well as other amphetamines [e.g., 3,4-
methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA: as
known as ecstasy, Molly, or Mandy)] are used recreationally.

In recent years, a range of other substances has also been grouped with amphetamine to
comprise a class of drugs known as amphetamine-type stimulants (ATS). In addition to the
amphetamines mentioned, other ATS include, but are not limited to, methcathinone, fenetylline,
ephedrine, pseudoephedrine and methylphenidate. The major rationale for the inclusion of these
drugs as ATS is that they are synthetic stimulants. Cocaine is not an ATS because it is not
manufactured synthetically, although it is classified as a stimulant. From a behavioral or
neuropharmacological perspective, the grouping of ATS makes little sense. Methylphenidate
(Ritalin) and cocaine produce similar effects on human behavior and on monoamine
neurotransmitters, which modulate mood and other functions.

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Yet, only methylphenidate is included as an ATS. Hence, the ATS grouping seems
somewhat arbitrary. Another concern is that such grouping facilitates the exaggeration of the
extent of global amphetamine use because a large number of different drugs are all included in
one class.

For purposes of this report, the primary focus will be on methamphetamine. However,
because global ATS prevalence data include other compounds as well, an exclusive focus on
methamphetamine is nearly impossible. With this caveat in mind, our rationale for limiting the
focus on methamphetamine, where possible, is because it has generated the greatest amount of
concern. Indeed, periodically there are statements in the scientific and popular literature attesting
to methamphetamine’s greater potency and “addictive” potential, relative to other amphetamines.
Such statements, however, are inconsistent with the empirical evidence. In carefully controlled
laboratory studies of human research participants, d-amphetamine and methamphetamine
produce nearly identical physiological and behavioral effects (Martin et al. 1971; Sevak et al.
2009; Kirkpatrick et al. 2012). They both increase blood pressure, pulse, euphoria, and desire to
take the drug in a dose-dependent manner. Essentially, they are the same drug.

One reason for the unfounded beliefs about the drugs might be related to the fact that
methamphetamine is more readily available on the illicit market due to its apparent easier
synthesis. A quick search of the internet can provide the surfer with dozens of “How to make
meth” recipes. According to these recipes and law enforcement personnel, methamphetamine can
be ‘easily’ made from a few common products, the most important of which is the over-the-
counter cold medication, pseudoephedrine. This makes methamphetamine all the more accessible
to the poor, the marginalized, those wishing to avoid the medical establishment, and other
interested consumers. There is a large underclass of people who cannot afford to see a physician
in order to receive a referral to a psychiatrist to obtain a prescription for legal amphetamine.
Moreover, there are many people who are skeptical of psychiatrists, who consider it a stigma to
be under psychiatric care, or who, quite rationally, do not want any mental health issues to
appear on their medical records.

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Undoubtedly, there are also many people who have no medical or neurological condition
that would qualify them for a prescription, but who nonetheless seek stimulants for personal
reasons, be they work-related or recreational. As a result, it is not surprising that
methamphetamine is the most frequently abused amphetamine.1 But this has less to do with
pharmacology and more to do with access or availability.

Global extent of methamphetamine use

Nonetheless, over the past two decades excessive illicit amphetamine use has become a major
global concern. According to data from the United Nations Office on Drugs and Crime
(UNODC) in 2011, ATS were used at rates higher than any other drug class with the exception
of cannabis (UNODC, 2013). The number of cannabis users worldwide (on an annual basis) is
estimated to be about 180 million, ATS users about 34 million, opiate users 16.5 million, and
cocaine users about 17 million (UNODC 2013). These estimates are based on information
provided by individual governments to UNODC, and confidence intervals around them are wide.
The high side of the confidence interval for ATS use, for example, indicates that as many as 50
million people may use it during a year. Data from some governments distinguish
methamphetamines from other ATS, while others do not

In many countries, there are no population-based data on the extent of illicit drug use.
Since illicit drug use in many countries is subject to severe criminal sanctions, it is likely that a
substantial proportion of illicit drug users are unwilling to disclose information about their use,
especially to government-sponsored survey takers. Of course, these factors affect illicit drug use
estimates generally, but data collection on consumption of ATS is even more fraught with
difficulty than with respect to other drugs. This is because, unlike the processing of coca into
cocaine and of opium into heroin and other opiates, the manufacture of methamphetamine does
not rely on primary products that can be grown only in special locations. As noted by
Degenhardt and colleagues (2010), methamphetamine can be and is manufactured in a much
wider variety of locations and “under more clandestine conditions and for comparatively less
cost.”
1
The terms “abuse” and “dependence”, as they are used throughout this report, conform to the Diagnostic and
Statistical Manual of Mental Disorders 4th Edition (DSM-IV-TR) and International Statistical Classification of
Diseases and Related Health Problems (ICD-10) definitions of substance abuse and dependence. DSM-IV-TR and
ICD-10 terminology are used to avoid the use of pejorative words and terminology that have multiple meanings.

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A good illustration of this point is the production of homemade methamphetamine

(known as pervitin) in the Czech Republic. In the early 1970s, according to Zábranský (2007),
one individual perfected a simple process for producing pervitin from an ephedrine-containing
cough medicine available over the counter and the technique quickly spread, even at the risk of
harsh punishment during the period of Soviet control. Pervitin use and production are perceived
to be extensive in the Czech Republic even today (Mravcik et al. 2011), although data supporting
this perception are lacking.

While absolute numbers of users of ATS at a given moment is difficult to estimate, better
trend estimates of use can be discerned when prevalence data are combined with government
seizure statistics over time. Based on such data, UNODC’s most recent report concluded that
markets for methamphetamine are growing faster than for other ATS, fueled in part by
significant increases in East and Southeast Asia, the United States and Mexico in the last five or
six years (UNODC 2012). Figure 2 illustrates the dramatic increase in seizures in East and
Southeast Asia since 2008. Methamphetamine markets in Europe, while small relative to those of
North America, have also expanded since 2009 based on seizure data, especially in Scandinavia
and Turkey (UNODC 2012). Seizure data alone may be misleading in that increases in seizures
may reflect better investments in policing rather than real increases in production, and declines in
seizures may reflect producers’ improved ability to evade capture rather than a real decline in
production. This point highlights the importance of combining multiple types of data to shed
light on drug use prevalence rates.

On behalf of the United Nations Reference Group on HIV and Injecting Drug Use,
Degenhardt et al. (2010) conducted an extensive review of the literature on the extent of
methamphetamine and ATS use and means of consumption around the world. They observed
that all regions of the world have some documented illicit ATS use, including methamphetamine
use. While production was highest in the Middle East, Southeast Asia and North America
(including Mexico), production in Africa, especially South Africa, was increasing (Degenhardt et
al. 2010). Some have suggested that stringent measures taken in the United States to limit access
to methamphetamine precursors (e.g., pseudoephedrine) have decreased United States production
but have increased production in Mexico (Colfax et al. 2010).

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Figure 2. Methamphetamine tablets seized in East and South-East Asia, 2008-2010

Source: UNODC, World Drug Report 2012, p 53.

Data from drug treatment centers that track the preferred drugs among those seeking
treatment can also aid in determining ATS prevalence rates. But, as is the case with seizure data,
this information should be used in combination with other information such as drug use
prevalence data because it too, when used alone, has serious limitations. For example, it is likely
that many marginalized drug abusers are under-represented in such data because drug treatment
may not be available to them for a variety of reasons ranging from an inability to pay for services
to a lack of treatment facilities. On the other hand, some individuals may be encouraged to
exaggerate the extent of their drug use in order to receive drug treatment in lieu of receiving a
prison sentence. So, it is conceivable that a large proportion of ATS users are excluded from this
type of data or the drug use rates of treatment-seekers may be less than accurate. These caveats
notwithstanding, Figure 3 shows that the percentage of individuals seeking treatment for
methamphetamine use dramatically increased in the Western Cape Province of South Africa
between 2002 and 2011 (SACENDU 2012). Based on the available information, it might be
supposed that the number of clandestine amphetamine laboratories has risen along with the
number of people seeking treatment for amphetamine use problems. As we noted above, the
increased number of amphetamine seizures could simply reflect a greater focus, in terms of
resources and attention, by various law enforcement agencies to this problem. Similarly, in
recent years the presence of more treatment facilities may also have increased the number of
people seeking amphetamine-related treatments.

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Even with these caveats, it seems clear that the extent of illicit methamphetamine use deserves
of the attention of public health officials. The strategies for addressing problems related to illicit
amphetamine use and abuse, however, should be mindful of the strengths and limitations of our
current data.

Figure 3 Methamphetamine as primary and secondary drug of use among people seeking
treatment in Western Cape Province, South Africa

Source: SACENDU Research Brief 15(1), 2012

Policy, law and programs: national and multinational responses to methamphetamines

Methamphetamine scare: Scare tactics sold as drug prevention
Like crack cocaine, methamphetamine in North America has been the object of sensational
“scare” campaigns in the media, fed by nearly everyone -- from scientists to healthcare
professionals to law enforcement personnel to politicians. Jenkins (1994) describes an early such
flood of media reports on “ice” or smokable methamphetamine, which resulted in Congressional
hearings and a national panic, though consumption of ice was largely confined to Hawaii. Media
reports suggested that the whole of the US would be deluged by “epidemic” levels of use of ice
in a short time, ushering in an “ice age” (Jenkins 1994). Jenkins concluded that the demonization
of crack versus powder cocaine paved the way for the demonization of ice versus other
amphetamines, and that the ice scare served a particular political purpose for certain politicians
in Hawaii and beyond who needed to portray themselves as “tough on drugs.” Indeed, as
discussed above, a similar situation occurred with crack cocaine in the late 1980s.

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Both liberal and conservative politicians added their voice to the cacophony that blamed crack
for everything from premature death to child abandonment and neglect to high crime and
unemployment rates.

A decade later – in the late 1990s – the methamphetamine hysteria in the United States
began to generate considerable interest among public officials; some were even making explicit
connections with crack cocaine in their demonizing of the drug. Then Oklahoma Governor Frank
Keating characterized methamphetamine in this way: “It’s a white trash drug --
methamphetamines largely are consumed by the lower socio-economic element of white people
and I think we need to shame it. “Just like crack cocaine was a black trash drug and is a black
trash drug” (Senate Communications Division, 1999).

Since 2000, concerns about methamphetamine have further intensified. Most media
portrayals of methamphetamine use emphasized unrealistic effects and exaggerated the harms
associated with the drug. For example, in January 2010, National Public Radio (NPR) ran a story
entitled, “This is your face on meth, kids” (NPR, 2010). The story described a California sheriff
who was trying to stop young people from experimenting with methamphetamine. With the help
of a programmer, he developed a computer program that digitally altered teenagers’ faces to
show them what they would look like after using methamphetamine for 6, 12, and 36 months.
These young people watched their images change from those of healthy, vibrant individuals to
faces marred by open scabs, droopy skin, and hair loss. They were told that these were the direct
physiological effects of using methamphetamine. Ninety percent of individuals who tried
methamphetamine once, they were also told, would become “addicted.”

There is no empirical evidence to support the claim that methamphetamine causes

physical deformities. Of course, there have been the pictures of unattractive methamphetamine
users in media accounts about how the drug is ravaging some rural town. The infamous “meth
mouth” images (extreme tooth decay) have been widely disseminated. But, consider this:
methamphetamine and Adderall are essentially the same drug. Both drugs restrict salivary flow
leading to xerostomia (dry mouth), one proposed cause of “meth mouth.” Adderall and generic
versions are used daily and frequently prescribed – each year they are among the top 100 most
prescribed drugs in the United States – yet there are no published reports of unattractiveness or
dental problems associated with their use. The physical changes that occurred in the dramatic

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depictions of individuals before and after their methamphetamine use are more likely related to
poor sleep habits, poor dental hygiene, poor nutrition and dietary practices, and media
sensationalism. With regard to the addictiveness of methamphetamine, the best available
information clearly shows that the overwhelmingly majority of people who try
methamphetamine will not become addicted (O'Brien and Anthony 2009). Less than 15 percent
of those who have ever used the drug will become addicted. The bottom line is that the
overwhelming majority of methamphetamine users use the drug without problems.

Although the hysteria about methamphetamine and crack cocaine use shared many
similarities, the perceived users of the respective drugs differed, as indicated above by former
governor Keating. Crack users were believed to be black and urban, whereas methamphetamine
users were seen as white and rural. As a result, at the start of the new millennium an intense
electronic media campaign was initiated targeting many rural communities in the western United
States. The stated goal was to prevent young people from experimenting with methamphetamine.
In 2005, the state of Montana adopted a graphic advertising campaign called the Montana Meth
Project. The advertisements show in horrifying details a young person who uses
methamphetamine for the first time, and then ends up engaging in some unthinkable act such as
prostitution or assaulting strangers for money to buy methamphetamine. At the end of the
advertisement, printed on the screen is the message: “Meth, not even once.” A year after its
inception, the Montana Meth Project was recognized by the White House for its innovative
approach to drug prevention. Indeed, preliminary findings from a report by the Montana
Department of Justice suggested that the campaign was successful at decreasing
methamphetamine use among teens. This apparent success led several other states to join the
“Meth Project” and adopt identical advertising strategies.

Is it true that scare tactic campaigns decrease drug use? More complete evidence would
suggest not. A recent critical review of the impact of the Montana Meth Project on
methamphetamine use indicated that the advertisement campaign had no effect when preexisting
downward trends in methamphetamine use were taken into account (Anderson 2009).

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One potential reason for the lack of success is that the population most likely to use
methamphetamine finds the advertisements laughable because they exaggerate
methamphetamine-related harmful effects. These individuals most likely know people who have
used the drug, and the information presented in the advertisements is inconsistent with their own
knowledge. Here, the parallel is to early propaganda about marijuana and the film “Reefer
Madness.” The film is now a ‘cult classic’ because it is widely regarded as a comedy as well as a
cautionary tale of official propaganda.

This raises the question, what are the potential negative consequences of presenting
exaggerated or misleading information about drugs to young people? Some educators and
healthcare professionals have expressed concern that the types of embellishment used by the
Montana Meth Project decrease their credibility and relevance and lead many young people to
reject other drug-related information from “official” sources, even when the information is
accurate. Despite these concerns and no evidence of preventing drug use, the Meth Project
remains popular with some officials and continues to use these types of scare tactics (see,
http://www.methproject.org/).

Laws and policies

Veracity aside, the anti-methamphetamine media campaign and incredible statements made
about the drug has led to considerable concern by the general public, which, in turn, inspired
policy-makers to pass new legislation. In Canada, for example, a particularly concerted media
“scare” campaign on methamphetamine was followed quickly by the legal reclassification of
both methamphetamine and its constituent ingredients or precursors, as noted by Boyd and
Carter (2010):

Substances commonly used in the production of methamphetamine, such as red

phosphorus and hydriodic acid, were added to the list of Class A [i.e. most highly
criminalized] precursors….In August 2005, methamphetamine was rescheduled from a
Schedule II to a Schedule I drug under the Controlled Drugs and Substances Act. Thus
the maximum penalties now apply to methamphetamine, including the possibility of life
sentences for trafficking, and production and possession can garner sentences of up to
seven years.

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Since Boyd and Carter’s analysis was published, the government of Canada passed into law a
wide-ranging crime bill that imposes mandatory minimum sentences for many categories of drug
crimes (Cohen 2012). This measure will likely mean that for minor methamphetamine
convictions, for example, a judge inclined to give a lighter sentence will not be able to do so.

In some countries, the perception of problems associated with the abuse of amphetamine
has become so worrisome that even more drastic measures have been taken. Topping the list is
Iran, which has a mandatory death penalty for possession of 30 grams of methamphetamine in a
regime with extremely harsh penalties for all drug offenses. Moreover, the executions can be
drawn out and extremely painful (Mogelson, 2012). In response to reports of precipitous
increases in methamphetamine abuse, in 1996 the government of Thailand banned all uses of
amphetamine, including those for medical purposes (Pilley and Perngpam, 1998). Other
governments have also taken steps to restrict legal uses of amphetamine, although most have not
been as extreme as those taken in Iran and Thailand. For example, in the United Kingdom and
New Zealand, while d-amphetamine remains available for medical purposes, any use of
methamphetamine (including medical use) has been banned. Recall that d-amphetamine and
methamphetamine are essentially the same drug (e.g., Kirkpatrick et al. 2012).

In the United States, new laws have also been implemented in response to the increased
negative advertising campaign waged against the drug. These laws focus on both
methamphetamine and compounds used to make the drug illicitly (i.e., precursors).
Amphetamine tablets were available over the counter in the United States until the early 1950s
(Maxwell and Rutkowski 2008). In 1970, in response to perceived abuses of the drug in the
1960s, amphetamine was placed under Schedule II of the newly passed Controlled Substances
Act. This meant that all amphetamines were classified under the most restrictive category for
drugs available by prescription. Other Schedule II drugs include cocaine and morphine. More
recently, the Comprehensive Methamphetamine Control Act of 1996 increased criminal penalties
for trafficking and producing methamphetamines. The law also restricted access to precursors,
including ephedrine and pseudoephedrine, which were key ingredients in over-the-counter cold
medicines (Franco 2005).

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Another change in the United States -- the Methamphetamine Penalty Enhancement Act
of 1998 -- lowered the cut-off that would trigger mandatory sentences for methamphetamine
trafficking. The Methamphetamine Anti-Proliferation Act of 2000 imposed restrictions on access
to precursors, including blister packs for over-the-counter ephedrine and pseudoephedrine. The
Combat Methamphetamine Epidemic Act of 2005 increased restrictions on pseudoephedrine.
Pharmacists and sellers of medications containing pseudoephedrine were required to place these
medications behind the counter and buyers were required to show a state-issued identification
card and sign a log that could be used to track their purchases (Gonzales et al. 2010). Fearing that
this inconvenience would decrease sales, many pharmaceutical companies simply replaced
pseudoephedrine with phenylephrine. Unfortunately, compared with pseudoephrine,
phenylephrine is a less effective nasal decongestant, the condition for which these medications
are most often used (Eccles 2007). This important unintended consequence is rarely discussed
among supporters of these laws.

Given the fact that new laws in the United States restrict availability of an effective cold
and flu medication (pseudoephedrine), it is of interest to know whether this approach is effective
at decreasing the availability of methamphetamine. Dobkin and Nicosia (2009) studied this
question by focusing on two major seizures of pseudoephedrine in the United States in 1995.
They concluded that this intervention substantially disrupted the supply of methamphetamine,
but that the effect was only temporary. Within four to 18 months, the methamphetamine market
had returned to pre-intervention levels. This result suggests that legislation aimed at restricting
precursors such as pseudoephedrine may have only short-term effects on illicit drug markets,
while it permanently reduces the ability of the whole population to obtain effective cold
medications.

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Methamphetamine effects on the brain

The intense focus on restricting access to methamphetamine suggests that it must be one of the
most dangerous drugs with respect to the potential damage to the brain and behavior. Over the
past several decades, data from basic research have contributed to an increased understanding of
methamphetamine-related effects on cells in the brain.

A comprehensive review of the effects of methamphetamine on the brain is beyond the scope of
the current report, and excellent reviews already exist (e.g., Sulzer et al. 2005; Fleckenstein et al.
2007). Here, we present a brief overview because we think it will be useful for the reader to have
some understanding of the neurotransmitters involved in the actions of methamphetamine. In this
way, we hope to provide the reader with tools to evaluate more accurately “brain statements”
made about methamphetamine in the popular media and scientific literature.

As Figure 4 indicates, amphetamine-related drugs bear a striking resemblance to the

catecholamine neurotransmitters dopamine and norepinephrine. Catecholamine neurotransmitters
are known to play an important role in several behaviors, including movement and mood
regulation. They are also known to be involved in malfunctions that lead to disease states. For
example, a prominent theory guiding the treatment of clinical depression proposes that too little
activity of the neurotransmitters dopamine, norepinephrine, and/or serotonin (together known as
monoamine neurotransmitters) can cause depression and too much can cause a manic state. This
theory also postulates that drugs such as methamphetamine lead to abuse because they stimulate
the “dopamine reward system,” which is responsible for telling the rest of the brain “that’s
good—do that again.” Thus, the structural similarities between amphetamine and catecholamine
neurotransmitters provide clues about the drugs’ mechanisms of action.

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Figure 4 Chemical structures of neurotransmitters and amphetamines

Multiple lines of evidence demonstrate that amphetamine causes a release of

monoamines from brain cells. Behaviorally, this can have the effect of elevating mood,
increasing alertness and vigilance, while decreasing tiredness and sleepiness (e.g., Hart et al.
2003, 2005). These effects can be beneficial for individuals required to work extended hours or
workers who have to perform at the circadian nadir of alertness. Undoubtedly, this is the reason
that several nations’ militaries have used (and continue to use) amphetamine since World War II
(Caldwell and Caldwell 2005). The drug helps soldiers fight better and longer. The performance
enhancing benefits are widely recognized by students and professionals in most every field from
athletics to zoology.

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A downside to amphetamine effects on monoamine neurotransmitters is that the drug

may also produce toxicity to cells containing these neurotransmitters. An accumulating amount
of evidence shows that amphetamine, when administered repeatedly in large doses, promotes the
formation of free radicals that damage brain cells. Following release of dopamine, for example,
certain enzymes inactivate the neurotransmitter. But, abnormally enhanced dopamine activity –
caused by repeated administration of large amphetamine dopamine - may produce an increased
formation of free radicals and thereby cause cell injury (Cadet and Krasnova 2009). This, in turn,
could lead to persistent deficits in the functioning of dopamine-containing cells.

This knowledge has raised concerns about the potential harmful consequences of
methamphetamine abuse on the human brain and behavior. Dopamine-rich areas serve a wide
range of important human functions ranging from mood to movement to learning and memory.
Indeed, a substantial database collected in laboratory animals suggests that acute and long-term
administration of amphetamine produces disruptive effects in several cognitive domains,
including learning and memory (for review, see Marshall et al. 2007). There is, however, an
important limitation associated with many of these studies when extrapolating the findings to
humans: the dosing regimens used did not capture key elements of human recreational
amphetamine use, specifically gradual dose escalation. Typically, investigators administered
large doses of methamphetamine repeatedly for one or more consecutive days to drug-naïve
animals, whereas human recreational drug users usually start with smaller amounts and increase
their doses gradually as their drug use progresses. This difference is not trivial because the
harmful neurobiological and behavioral changes that occur in response to repeated large doses of
methamphetamine can be prevented with prior exposure to several days of escalating doses
(Segal et al. 2003; O’Neil et al. 2006; Belcher et al. 2008). Given this situation, it is critically
important to employ more ecologically relevant models in future animal studies investigating the
impact of amphetamine use on cognitive functioning. These issues underscore the importance of
carefully assessing behaviors of interest in humans under rigorous conditions.

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Methamphetamine effects on human physiology and behavior

Immediate effects

There is now a large database investigating the direct effects of methamphetamine on human
physiology and behavior (for review, see Hart et al. 2012). These laboratory studies are designed
to document the immediate and short-term effects of the drug on measures of cognitive
functioning, mood, sleep, blood pressure, heart rate and the drug’s addictiveness. These studies
employ carefully controlled, within-participant designs, during which participants: (1) complete
a baseline battery of tests, which includes the measures of interest; (2) are administered a
methamphetamine dose (ranging from placebo to 50 mg); and (3) are reassessed on the battery at
predetermined time points for several hours after drug administration. Also, all of the drug doses
are given in a double-blind manner – the research participants don’t know whether they are
getting a placebo or real methamphetamine, nor do the medical staff monitoring the sessions.

The findings to date can be summarized in the following way. After methamphetamine
administration, participants reported feeling more euphoric and their cognitive functioning was
improved. These effects lasted about four hours. The drug also caused significant increases in
blood pressure (BP) and heart rate that lasted for up to 24 hours. The maximum levels were
about 150/90 (BP) and 100 (beats per min.). While these elevations were statistically significant,
they were well below levels obtained when engaged in a rigorous physical exercise, for example.
Another finding was that the drug reduced the amount of time participants slept (Perez et al.
2008). For example, when they took placebo, participants got about eight hours of sleep, but
when the 50 mg dose was given, they got only about six hours. Together, the results indicate that
a large dose of methamphetamine produced expected effects. The drug didn’t keep people up for
consecutive days, it didn’t dangerously elevate their vital signs, nor did it impair their judgment.

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Tellingly, the above human laboratory data are at odds with anecdotal reports and
conventional wisdom. Perhaps researchers had not asked the right question. One of the most
popular beliefs about methamphetamine is that it is highly addictive, more so than any other
drug. So, in another set of experiments, Hart and colleagues set out to address this issue. Under
one condition, methamphetamine-dependent individuals were given a choice between taking a
big hit of methamphetamine (50 mg) or $5 in cash. They chose the drug on about half of the
opportunities. But, when we increased the amount of money to $20, they almost never chose the
drug (Kirkpatrick et al. 2012). Similar results were observed among crack cocaine addicts in an
earlier study (Hart et al. 2000). Thus, the addictive potential of methamphetamine was not as had
been claimed; its addictiveness was not extraordinary. These results also showed that
methamphetamine addicts, just like crack addicts, can and do make rationale decisions, even
when faced with a choice to take the drug or not. This was consistent with the literature assessing
cognitive functioning of methamphetamine users, but as noted below, only if one looked
carefully and guarded against much of the biased information that influences public perceptions
about methamphetamine users (Hart et al. 2012).

While the above results suggest that many of the immediate harmful effects caused by
methamphetamine use may have been greatly exaggerated, there are real documented potential
negative consequences associated with this drug. For instance, methamphetamine abuse is
associated with multiple deleterious medical consequences, including paranoia mimicking full-
blown psychosis (Grelotti et al. 2010) and hypertensive crisis leading to stroke (Ho et al. 2009).
While serious, such cases are rare, and entail the long-term use of extremely large doses. Still, in
order to better understand the potential consequences of long-term use of methamphetamine, in
the next section we review the literature on methamphetamine-related brain and cognitive effects
by examining individuals who have used the drug illicitly for several years.

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Long-term effects

What are the long-term effects of methamphetamine on intelligence and brain functioning of
addicts? These are people who had used the drugs for many years. In these studies, abstinent
methamphetamine addicts and a control group (usually non-drug users) completed a
comprehensive set of cognitive tests over the course of several hours, and the results were
compared to determine whether or not the cognitive functioning of the methamphetamine addicts
was normal. Of course, normality is a relative concept that is determined not only by comparing
performance of the methamphetamine group with the performance of a control group, but also by
comparing the methamphetamine group’s scores with those from a normative dataset, taking into
consideration each individual’s age and level of education. These requirements are important
because they allow us to take into account the relative contribution of age and education in terms
of the individual’s score and adjust the score accordingly. Simply stated, it would be
inappropriate to compare the vocabulary scores of a 16-year-old high school dropout with those
of a 22-year-old college graduate. The older college graduate would be expected to outperform
the younger high school dropout.

A biased and less than careful reading of the scientific literature might lead one to
conclude that methamphetamine addicts have severe cognitive impairment. In one study by Sara
Simon and colleagues, the apparent impairments observed among methamphetamine users were
so bad that it led the researchers to warn: “The national campaign against drugs should
incorporate information about the cognitive deficits associated with methamphetamine…Law
enforcement officers and treatment providers should be aware that impairments in memory and
in the ability to manipulate information and change points of view (set) underlie
comprehension… methamphetamine abusers will not only have difficulty with inferences… but
that they also may have comprehension deficits… the cognitive impairment associated with
[methamphetamine abuse] should be publicized…” (Simon et al. 2002). But, as one reads this
and similar papers more critically there are strong grounds for skepticism. While the data showed
that the control participants outperformed methamphetamine users on a few tests, the
performance of the two groups was not different on the majority of tests.

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More importantly, when the cognitive scores of the methamphetamine addicts in the Simon study
are compared against scores in a larger normative dataset, none of the methamphetamine users’
scores fall outside the normal range (Hart et al. 2012). Based on all of the data, this indicates that
the cognitive functioning of the methamphetamine users is normal. This should have tempered
the researchers’ conclusions and prevented them from stating such dire warnings. Unfortunately,
the inappropriate conclusions drawn by Simon and colleagues are not atypical. The
methamphetamine literature is filled with similar unwarranted conclusions. As a result, the
apparent methamphetamine addiction-cognitive impairment link has been widely publicized -
numerous articles have appeared in scientific journals and the popular press. We contend that
this has helped shape an environment in which there is an unwarranted and unrealistic goal of
eliminating methamphetamine use at any cost to amphetamine users and to the public.

The reporting of brain imaging findings has been especially misleading. On July 20,
2004, for example, The New York Times printed an article entitled, “This Is Your Brain on Meth:
A ‘Forest Fire’ of Damage.” It stated: “People who do not want to wait for old age to shrink their
brains and bring on memory loss now have a quicker alternative—abuse methamphetamine . . .
and watch the brain cells vanish into the night.” This conclusion was based on a study that used
magnetic resonance imaging (MRI) to compare brain sizes of methamphetamine addicts with
those of non-drug-using healthy individuals (Thompson et al. 2004). The researchers also
assessed the correlation between memory performance and several brain structural sizes. They
found that methamphetamine users’ right cingulate gyrus and hippocampus were smaller than
controls by 11 and 8 percent, respectively. Memory performance on only one of four tests was
correlated with hippocampal size (i.e., individuals with larger hippocampal volume performed
better). As a result, the researchers concluded, “chronic methamphetamine abuse causes a
selective pattern of cerebral deterioration that contributes to impaired memory performance.”
This interpretation, as well as the one printed in The New York Times article, is inappropriate for
several reasons.

First, brain images were collected at only one time point for both groups of participants.
This makes it virtually impossible to determine whether methamphetamine use caused “cerebral
deterioration,” because there might have been differences between the groups even before
methamphetamine was ever used. Second, the non-drug users had significantly higher levels of
education than methamphetamine users (15.2 vs. 12.8 years, respectively);

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it is well established that higher levels of education lead to better memory performance. Third,
there were no data comparing methamphetamine users with controls on any memory task. This,
in itself, precludes the researchers from making statements regarding impaired memory
performance caused by methamphetamine. Nonetheless, the only statistically significant
cognitive finding was a correlation of hippocampal volume and performance on one of the four
tasks. This finding is the basis for the claim that methamphetamine users had memory
impairments, because the hippocampus is known to play a role in some long-term memory; but
other brain areas are also involved in processing long-term memory (e.g., overlying temporal
neocortex). The size of these other areas was not different between the groups. Finally, the
importance for everyday functioning of the brain differences is unclear because an 11 percent
difference between individuals, for example, is still most likely within the normal range of
human brain structure sizes.

This example is not unique. The brain imaging literature is replete with a general
tendency to characterize any brain differences as dysfunction caused by methamphetamine (as
well as other drugs), even if differences are within the normal range of human variability (Hart et
al. 2012). It would be like comparing the brains of police officers who only completed high
school with those of college professors who had obtained a Ph.D. and, then concluding that the
officers are cognitively impaired as a result of any differences that might be noted. This
simplistic thinking is the main thrust behind the notion that drug addiction is a brain disease. It
certainly isn’t a brain disease like Parkinson’s disease or Alzheimer’s disease. In the case of
these illnesses, one can look at the brains of affected individuals and make good predictions
about the illness involved. We are nowhere near being able to distinguish the brain of a drug
addict from that of non-drug addict.

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Other Health Concerns

Methamphetamine abuse has been shown to exacerbate AIDS pathology, including cognitive
deficits (Cherner et al. 2005; Carey et al. 2006), and is associated with reduced immunological
response to secondary infections such as hepatitis C (Gonzales et al. 2006).
In addition, concerns about methamphetamine users contracting blood-borne illnesses such as
HIV and hepatitis C as a result of their drug use have increased interest in determining the extent
to which methamphetamines are injected intravenously. Relative to heroin and cocaine,
methamphetamine is injected less frequently (Colfax 2010), but injection rates vary widely from
region to region. Degenhardt et al. (2010) observed higher methamphetamine injection rates in
parts of East and Southeast Asia, North America, northern and central Europe, the former Soviet
states, Australia and New Zealand than in Thailand and the United States.

One factor that may influence whether methamphetamine is injected or consumed by

other routes is the purity of the drug. If a drug is less pure, containing only 5-10 percent of the
desired compound, for example, then, of course, there is less of it to waste. Moreover, taking a
drug by mouth can lead to only 10 to 20 percent bioavailability of the ingested dose.
Bioavailability is the proportion of the dose of the drug that reaches its target -- in this case, the
brain. One reason that a drug’s bioavailability is lower following oral administration is because
enzymes in the liver specialize in breaking down chemicals, including methamphetamine, in
order to protect the brain and to make any poisons we eat less destructive. This process is called
first-pass metabolism. It can significantly reduce the effective dose of a drug taken orally. First-
pass metabolism can be circumvented by injecting or smoking a drug. In general, illicit
methamphetamine purity is high (greater than 80 percent: USDOJ, 2011) compared to drugs such
as heroin and cocaine. This might be one reason that intravenous use of the drug has been
consistently lower than that of these other drugs. Thus, as public health officials consider
consequences for various measures taken to limit illicit amphetamine use, they should also be
mindful of the fact that their interventions might alter the route by which methamphetamine
users take the drug. And a new route might be potentially more dangerous not only to the user,
but also to the general public because of blood-borne diseases.

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Treatment with a focus on agonist replacement therapies

While several behavioral/psychosocial therapies have been demonstrated to reduce illicit
amphetamine abuse, a substantial proportion of individuals do not benefit from these
interventions (Lee and Rawson 2008).
This suggests the importance of developing pharmacotherapies for those individuals who may be
less responsive to behavioral treatments alone. Pharmacotherapies may be used alone, in
combination with behavioral/psychosocial therapies, or in a staged manner following inadequate
response to behavioral/psychosocial therapies. Most researchers/clinicians recognize that
pharmacotherapies alone will not cure a chronic, relapsing disorder such as substance
dependence, in part because the problem of substance dependence is expressed behaviorally.
Hence, a major goal is that pharmacotherapies will provide a window of opportunity by relieving
withdrawal symptoms, for example, so behavioral/psychosocial interventions can be more
effectively implemented.

A key argument for the development of effective methamphetamine abuse treatment

medications is that they would reduce illicit drug use in HIV-infected individuals in an effort to
slow the progression of the disease or reduce the likelihood of HIV-negative individuals
engaging in behaviors that might increase the chances of contracting the disease. The underlying
theoretical assumption guiding the use of agonist therapies is that maintenance on a
pharmacologically similar medication will induce cross-tolerance to the abused drug.
Methadone, a long-acting µ-opioid agonist for opioid dependence and nicotine replacement
medications for tobacco dependence have been used as agonist maintenance treatments to
prevent relapse and cravings in individuals attempting to maintain abstinence. Agonist
maintenance medications typically use safer routes of administration (e.g., oral or transdermal)
and produce diminished psychoactive effects.

In contrast to medication development efforts for opioid and nicotine dependence, in

which the neurobiological mechanisms mediating reinforcement are fairly well understood, the
neuronal mechanisms of action for amphetamine are more complicated. As stated above,
amphetamine increases the activity of monoamine neurotransmitters. Accordingly, it has been
reasoned that medications that more closely mimic the actions of the methamphetamine on
monoaminergic activity may be useful in treating methamphetamine abuse.

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A number of published single-blind studies and case reports indicate that maintenance on
oral amphetamines may be helpful in the treatment of methamphetamine abuse (Fleming and
Roberts 1994; 1994; Pates et al. 1996; Bradbeer et al. 1998; Shearer et al. 2001). These studies
have reported that amphetamine maintenance has many positive outcomes, including reductions
in illicit amphetamine use and in injecting as well as improvements in general health. Such
programs increase treatment retention and the number of users presenting for healthcare services.
Importantly, reported incidence of adverse effects during amphetamine maintenance has been
extremely low. However, it is important to note that most data were collected under non-blind
conditions, which increase the likelihood of positive results. To address this concern, Longo et
al. (2009) completed a randomized, double-blind placebo-controlled trial assessing the
effectiveness of sustained-release d-amphetamine (average dose 80 mg/d) for treating
amphetamine dependence. Positive results were obtained on two of the three outcome measures:
the amphetamine maintenance group had significantly better treatment retention and a lower
degree of methamphetamine dependence compared with the placebo group. On the third
outcome measure (self-reported drug use), there was a trend toward reduced amphetamine use in
the amphetamine maintenance group, but it did not reach statistical significance.

The above observations suggest that carefully controlled, double-blind investigations of

long-acting oral amphetamine should be expanded. Such therapies may not only be important for
curtailing illicit methamphetamine use, but may also be critical for reducing public health risk
associated with contraction, progression, and transmission of HIV. It is important to note that
prior to initiating such therapies, clinicians should be cognizant of the fact that our knowledge is
incomplete and should be prepared to alter their actions as new, more complete knowledge
dictates.

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Harm reduction

As described in this report, we have learned a great deal about the conditions under which either
positive or negative effects are more likely to occur with amphetamine use. Low to moderate
doses of amphetamine can improve mood, enhance performance, and delay the need for sleep.
Repeated administration of large doses of the drug can severely disrupt sleep and lead to
psychological disturbances, including paranoia. Unfortunately, this knowledge is rarely
disseminated to the public in an unbiased manner, primarily because of the irrational belief that it
might lead one to engage in drug use. In light of the fact that there may be as many as 50 million
people who use illegal ATS on an annual basis, it seems that a rational approach – one that aims
to reduce drug-related harms – would be to share what we have learned with drug users and
those in positions to help keep them safe. Otherwise, we may do society a major disservice.

If more amphetamine users were aware of a few simple facts that we have learned, this
would substantially enhance public health and safety. First, inexperienced amphetamine users
should be discouraged from taking these drugs in the manner in which experienced users do.
Experienced users tend to take drugs in ways that get them to the brain quickly, i.e., smoking or
intravenous injections. Because smoking and injecting produce more potent effects, the
likelihood of harmful consequences is increased with these methods. Alternatively, taking a drug
by mouth is usually safer than other ways of consuming drugs for two reasons: 1) the stomach
can be pumped in case of an overdose; and 2) some of the drug will be broken down before
reaching the brain, resulting in a muted effect.

This is the idea behind an innovative harm reduction program for methamphetamine
users in the Czech Republic, which takes its cue from users’ own practices (Mravčík et al. 2011).
Some people who use methamphetamines in the Czech Republic engage in what they call
“parachuting” or swallowing a bolus of pervitin wrapped in a piece of plastic. The main
practitioners of this method were people who wanted to inject less or who had trouble injecting
because of damaged veins. Service providers in low-threshold facilities are facilitating this
process by making available gelatin capsules, which are superior to an improvised plastic
wrapper as something to swallow (Mravčík et al. 2011). Czech service providers hope that this
method will encourage some people who use methamphetamines to shift from injection to oral
use.

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Second, healthy sleep habits should be stressed for all drug users because prolonged sleep
loss can cause deterioration of mental functioning. In severe cases of sleep deprivation, even
without drugs, hallucinations and paranoia may also occur. Because amphetamines reliably
reduce fatigue and offset performance decrements, some may repeatedly take these drugs to
lessen problems associated with sleep loss. This is a less than ideal approach. One of the most
consistent effects of stimulants is the disruption of sleep, which means that repeated use could
exacerbate problems related to sleep loss. Given the vital role that sleep plays in healthy
functioning, regular users of amphetamine should be mindful of their sleep durations and avoid
drug use near the sleep period. In cases of severe sleep disruptions caused by amphetamine,
medical healthcare professionals should be consulted to determine whether a sleeping aid is
appropriate.

Third, people who inject methamphetamine should be provided access to clean injection
equipment. The effectiveness of needle exchange programs for HIV prevention among people
who inject other drugs is supported by a large database (Wodak and Cooney 2004). There is little
available information on needle exchange programs targeting amphetamine users, despite the
fact that UNODC recommends needle and syringe programs as a central element of HIV
prevention (UNODC 2012).

Alternatively, for individuals who smoke amphetamine, harm reduction services should
include access to clean pipes, plastic tips, filters, lip balm and smoking foil. Presumably, these
measures will decrease the likelihood of exchanging bodily fluids and encourage other health
promoting behaviors. For example, researchers in Ottawa, Canada, found that cocaine users --
who used the drug via both smoking and injection -- tended to inject less when smoking
equipment was readily available; they also engaged in less sharing of potentially contaminated
smoking equipment (Leonard et al. 2008).

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Conclusions and Recommendations for Policy and Research

Evidence presented in this report suggests that illicit ATS use, primarily methamphetamine use,
has become the new crack cocaine with respect to sensational media reporting about the extent of
ATS use and hyperbolic description of the disastrous consequences of methamphetamine
addiction. It has taken nearly three decades for the public to come to a superficial understanding
that the deleterious effects of crack cocaine were greatly exaggerated in mass media and
government statements. The monetary and human costs of our earlier misunderstandings about
crack cocaine are incalculable. Today, unfortunately, much of the public information about
methamphetamine has little foundation in evidence. Overblown worst-case anecdotes are usually
disseminated uncritically by the popular press and accepted as sound evidence by an
undiscerning public.

Recent implementation of laws and policies aimed at curtailing methamphetamine use in several
countries, including the United States, are based on less than accurate assumptions. For example,
major themes in anti-methamphetamine advertisements are that the drug is instantly addictive
and that use of methamphetamine leads to extreme tooth decay. There is no evidence to support
either of these myths. Another common lore is that illicit methamphetamine use leads to
neuroanatomical pathologies that cause cognitive impairments. This supposition is also not
supported by evidence.

These campaigns have reached the point where they undermine themselves perhaps because
methamphetamine users and their acquaintances know that the information is unfounded in all
but the rarest cases, as happened for decades with public education materials that suggested that
marijuana was a direct route to harmful addiction to hard drugs.

There is an urgent need to revisit policies and information programs related to

methamphetamines both nationally and with respect to international norms. In particular:

 Countries that apply harsh criminal sanctions to methamphetamine use and possession should
urgently revisit those laws and policies. There is no empirical evidence that suggests that
even long-term users of methamphetamines pose a threat to those around them. Nor is there
evidence to suggest that methamphetamine users should be incarcerated in order to deal with
the “threat” they pose.

 Growing evidence suggests that treatment and harm reduction measures in the health sector
may be helpful for some persons who are methamphetamine-dependent, though science and
best practices are evolving. Specialized health services and social support informed as much
as possible by the best science, rather than criminal sanctions, should be the dominant
response to methamphetamine addiction in national policy. Cognitive-behavioral therapies
should not be denied to people who need them based on the flawed idea that
methamphetamine users are too cognitively compromised to benefit from these interventions.

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There is an urgent need for national authorities and donors to invest in development of
affordable, accessible and scientifically appropriate health and social services in this area.

 National regulatory authorities and the World Health Organization should restudy the costs
and benefits of suppressing access to amphetamine used for legitimate medical purposes in
the name of methamphetamine control. Blanket bans on amphetamine for all purposes are
unjustified and may have high costs in terms of disease burden in the population. Moreover,
these restrictions provide the impetus for the illicit proliferation of “meth labs,” which pose
hazards to public safety.

 Precursor control may hold some promise for short-term supply reduction of
methamphetamine, but is unlikely to be effective beyond the short run. Like eradication of
coca in the Andes, precursor markets made illicit are likely to manifest a “balloon effect”
whereby they may be shut down in the short term in one location, but they will pop up
quickly in another location. As suggested by the expert Global Commission on Drug Policy
(2011) based on evaluation of decades of supply-control efforts in many parts of the world, it
is unlikely that illicit precursor markets will be controlled in the long term without some
level of state regulation that eschews criminal sanctions.

 National and international institutions and civil society organizations should stop supporting
wasteful and ineffective campaigns of misinformation on methamphetamine that use
exaggerations and fabricated data as scare tactics. These campaigns are not effective, and
their dishonesty renders them counter-productive. There is an urgent need for correcting
misinformation on methamphetamine in formats that both policy-makers and the public can
understand and use.

 Where injection of methamphetamines is prevalent, access to sterile injection equipment for

all who need it must be a policy and program priority. Needle and syringe programs continue
to be undermined by paraphernalia laws in many countries and by tolerance of disruption of
these services by the police. Denial of the reality of drug injection in prisons and refusal to
provide sterile injecting equipment in prisons and other detention facilities undermine HIV
and hepatitis control in many countries (Lines et al. 2005). Investment in ensuring access to
sterile injection equipment remains a lagging element of national and international HIV
programs in spite of decades of evidence demonstrating the effectiveness of these programs.

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