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Methamphetamine Abuse and Impairment of Social Functioning: A Review
of the Underlying Neurophysiological Causes and Behavioral Implications
Bruce D. Homer, Todd M. Solomon, Robert W. Moeller, Amy Mascia, Lauren DeRaleau, and
Perry N. Halkitis
New York University
The highly addictive drug methamphetamine has been associated with impairments in social cognitions
as evidenced by changes in users’ behaviors. Physiological changes in brain structure and functioning,
particularly in the frontal lobe, have also been identified. The authors propose a biopsychosocial
approach to understanding the effects of methamphetamine addiction by relating the physiological effects
of the drug to the behaviors and social cognitions of its users, through the application of the theory of
mind paradigm. Although onset of methamphetamine use has been linked to the desire for socialization,
chronic use has been associated with an increase in depression, aggressiveness, and social isolation,
behaviors that also implicate involvement of the frontal lobe. The reviewed literature provides strong
circumstantial evidence that social-cognitive functioning is significantly impacted by methamphetamine
use and that the social isolation, depression, and aggressiveness associated with chronic use is due to
more than just the social withdrawal associated with addiction. Treatment considerations for metham-
phetamine must therefore consider the role of social cognition, and pharmacological responses must
address the documented impact of the drug on frontal lobe functioning.
Keywords: methamphetamine, addiction, social cognition, brain function, theory of mind
Methamphetamine (MA) is a highly addictive stimulant that has
significant effects on the CNS. In recent years, there has been a
marked increase in the use and abuse of MA. The 2003 MA/
amphetamine treatment admission rate in the United States was 56
admissions per 100,000 population (ages 12 or older), an increase
of over 400% from the 1993 rate of 13 admissions per 100,000
(Substance Abuse and Mental Health Services Administration
[SAMHSA], 2006). Both human and animal studies have found a
number of negative consequences to be associated with MA abuse,
including neurological damage and altered cognitive and behav-
ioral functioning.
The current article reviews both the short- and long-term phys-
iological and psychological effects of MA abuse, with a particular
emphasis on the neurophysiological damage caused by MA. Based
on these data, it is argued that abuse of MA causes neurological
damage of the specific brain regions associated with social cogni-
tion, leading to impairments in social-cognitive functioning, which
in turn contributes to a number of the observed behavioral changes
associated with chronic abuse of MA. The article concludes with
suggestions for future research and speculations on how social-
cognitive deficits may affect the treatment and rehabilitation of
MA abusers.
Physiological Effects of MA
MA is a cationic lipophilic molecule that has dramatic effects on
both the sympathetic nervous system and central nervous system
(CNS; Davidson, Gow, Lee, & Ellinwood, 2001). MA is more
potent than its parent compound amphetamine because its li-
pophilic nature allows greater penetration of the CNS (Meredith,
Jaffe, Ang-Lee, & Saxon, 2005). Similar to amphetamine, MA
stimulates the release of newly synthesized catecholamines in the
CNS and partially blocks the presynaptic reuptake of these neu-
rotransmitters (Cho & Melega, 2002). Animal studies have shown
that amphetamines, including MA, target the dopamine trans-
porter, which regulates dopaminergic transmission by facilitating
dopamine reuptake (Davidson et al., 2001). Amphetamines have
been shown to inhibit the reuptake of dopamine by reversing the
direction of the dopamine transporter, leading to an increased
dopamine release (Giros, Jaber, Jones, Wightman, & Caron, 1996).
Immediately after ingestion of MA, users experience a number
of highly desirable sensations, including a sense of euphoria
caused by an elevated level of dopamine. Other desirable sensa-
tions associated with MA include increased productivity, height-
ened attentiveness and curiosity, hypersexuality, decreased anxi-
ety, and increased energy (Cretzmeyer, Sarrazin, Huber, Block, &
Hall, 2003; Meredith et al., 2005). The euphoric feelings vary in
intensity and duration, depending on mode of administration, with
smoking or intravenous injecting leading to intense, but brief,
euphoria and with oral ingestion or snorting leading to a slightly
less intense, but more long-lasting, “high.” (National Institute on
Bruce D. Homer, Department of Applied Psychology, New York Uni-
versity; Todd M. Solomon, Center for Health, Identity, Behavior & Pre-
vention Studies (CHIBPS) and School of Medicine, New York University;
Robert W. Moeller and Perry N. Halkitis, CHIBPS and Department of
Applied Psychology, New York University; Amy Mascia and Lauren
DeRaleau, CHIBPS, New York University.
Bruce D. Homer is now at the PhD Program in Educational Psychology,
The Graduate Center, City University of New York (CUNY).
Correspondence concerning this article should be addressed to Bruce D.
Homer, PhD Program in Educational Psychology, The Graduate Center,
CUNY, 365 5th Avenue, New York, NY 10016. E-mail:
Bhomer@gc.cuny.edu
Psychological Bulletin Copyright 2008 by the American Psychological Association
2008, Vol. 134, No. 2, 301–310 0033-2909/08/$12.00 DOI: 10.1037/0033-2909.134.2.301
301
Drug Abuse [NIDA], 2002; SAMHSA, 2004). The excessive stim-
ulation of the sympathetic nervous system also leads to a number
of undesirable physiological effects, including tachycardia, hyper-
tension, papillary dilation, diaphoresis, tachypnea, peripheral hy-
perthermia, and hyperpyrexia (Meredith et al., 2005). Repeated use
of MA results in a depletion of catecholamines and has been
shown to produce withdrawal symptoms marked by psychiatric
complaints (Meredith et al., 2005). Withdrawal from MA, also
known as “crashing,” can produce a constellation of symptoms
including anhedonia, irritability, fatigue, depressed mood, im-
paired social functioning, aggression, and an intense craving for
the drug (Cantwell & McBride, 1998; Meredith et al., 2005;
Newton, Kalechstein, Duran, Vansluis, & Ling, 2004).
A number of psychological and behavioral consequences have
been identified as being related to chronic MA use, including
euphoric disinhibition, impaired judgment, grandiosity, and psy-
chomotor agitation (Batki & Harris, 2004; Meredith et al., 2005;
Richards et al., 1999). Data from neuroimaging studies, neuropsy-
chological testing, and psychiatric evaluation indicate that heavy
use of MA contributes to a variety of psychiatric pathologies,
including psychosis (Batki & Harris, 2004), mood disturbance
(London et al., 2004), suicidal ideations (Zweben et al., 2004),
anxiety (Zweben et al., 2004), hostility (Zweben et al., 2004),
psychomotor dysfunction (Caligiuri & Buitenhuys, 2005), deficits
in cognitive skills (Gonzalez et al., 2004), and, in extreme cases,
paranoia, hallucinations, and delusion (Logan, 2002). There is
compelling evidence that the negative consequences of MA abuse
are due, at least in part, to damage to the brain caused by the
neurotoxicity of MA.
Neurotoxicity of MA
Evidence for the neurotoxicity of MA comes from studies with
a variety of mammalian species, including rodents and higher
primates. MA has been found to have neurotoxic effects on both
the dopaminergic and serotonergic transmitter systems, which can
lead to the irreversible loss of nerve terminals or neuron cell bodies
(Cho & Melega, 2002). Research on human MA abuse suggests a
typical abuse pattern of repeated dosing between 1 and 6 times a
day, which results in consumption of 0.5–1.0 grams during a 24
hour binge (Simon et al., 2002). Non-human primates treated with
an equivalent dosing regimen of MA have significantly reduced
dopamine axonal markers, significantly reduced serotonin axonal
markers, and decreased striatal dopamine transporter density as
measured by positron emission topography (PET) imaging (Ville-
magne et al., 1998). There is evidence from PET studies of damage
to dopamine nerve terminals or cell bodies in chronic abusers of
MA, even after a prolonged period of abstinence (McCann et al.,
1998). Although the degeneration of dopamine nerve terminals and
cell bodies associated with MA abuse may recover in younger
populations (Wilson et al., 1996), the evidence of medium- to
long-term neurotoxic effects of MA is quite conclusive.
Damage to the serotonin and dopamine systems caused by MA
abuse can have a number of effects. Serotonin plays an important
role in a wide range of physiological systems (e.g., cardiovascular
regulation, respiration, thermoregulation), as well as a number of
behavioral functions, including circadian rhythm entrainment,
sleep/wake cycle, appetite, aggression, sexual behavior, sensori-
motor reactivity, pain sensitivity, and learning (Meredith et al.,
2005). In the brain, dopamine plays a crucial role in a number of
functions, including control of movement, regulation of emotional
responses, and regulation of the reward system. Dopamine also
plays an important role in the cardiovascular system, hormonal
system, and CNS. Abuse of MA can cause disturbances in any of
these systems, which can affect behavior (Cho & Melega, 2002).
In addition to disturbance to the dopaminergic and serotonergic
transmitter systems, MA abuse also appears to cause localized
damage to the brain, thereby causing deficits in specific cognitive
functions. For example, in a proton MRS study, Ernst, Chang,
Leonido-Yee, and Speck (2000) found that MA users had signif-
icantly elevated levels of glial repair cells—a neurocellular index
of damage to the grey and white matter—in the basal ganglia and
the right frontal white matter, suggesting structural damage to the
frontostriatal areas. In an fMRI study, Paulus et al. (2002) exam-
ined neuronal activation in abstinent MA-dependent individuals
during decision making. They found that, compared with age and
education matched control participants, MA-dependent individuals
had less prefrontal cortex activation during decision making. These
and similar findings (e.g., Chang, Ernst, Speck, & Grob, 2005;
Chang et al., 2002; Fishbein et al., 2005) indicate that MA use can
lead to impaired brain functioning in ways that have significant
ramifications for certain cognitive abilities.
MA and Neurocognitive Impairments
Research with clinical populations has identified a number of
characteristic neurocognitive impairments associated with MA
abuse, with severity of symptoms linked to both dose and duration
of use (Meredith et al., 2005). For example, compared with age
matched control participants, MA abusers have severe grey matter
deficits in the cingulate, limbic, and paralimbic cortices as well as
significant shrinkage of hippocampal volume (8%) correlating
with impaired verbal memory performance (Thompson et al.,
2004). MA abusers also demonstrate deficits in tasks that involve
perceptual speed and information manipulation (Simon et al.,
2002). Much of the work on the neurocognitive deficits associated
with MA, however, has focused on decision making (e.g., Fishbein
et al., 2005; Paulus, Hozack, Frank, Brown, & Schuckit, 2003;
Paulus, Tapert, & Schuckit, 2005; Semple, Zians, Grant, & Patter-
son, 2005). In making decisions, MA abusers will tend to choose
an immediate reward at the expense of severe negative conse-
quences in the future (Verdejo-Garcia, Perez-Garcia, & Bechara,
2006). Paulus et al. (2005) found that these decision-making
deficits are predictive of subsequent relapse in recovering MA
addicts. Imaging studies have indicated that the impaired decision
making of MA users is associated with dysfunction in the orbito-
frontal cortex, dorsolateral prefrontal cortex, anterior cingulate,
and parietal cortex (Paulus et al., 2003). Functional deficits have
also been found in the anterior cingulum, which suggests that
attention deficits may contribute to impaired decision making
(Nordahl et al., 2002).
Given the scope of neurological damage associated with MA
abuse, it seems likely that there are other neurocognitive deficits in
addition to impaired decision making. Although, to date, no re-
search has explicitly examined the affects of MA abuse on the
neurocircuitry responsible for social-cognitive functioning, re-
search with other populations has indicated that several of the
brain regions affected by MA abuse are activated by tasks that
302 HOMER ET AL.
involve social cognition (Amodio & Frith, 2006; Frith & Frith,
2001). This suggests that MA abusers may also be suffering from
brain-based impairments in their social-cognitive functioning.
MA and Social Cognition
Compared with those of other species, human social interactions
are exceedingly complex. To navigate the complexities of these
interactions requires representing and processing a wide array of
information obtained from a variety sources. We use the term
social cognition (Fiske & Taylor, 1991) to refer to the broad set of
processes involved in assessing social situations. Essential to un-
derstanding social situations is being able to quickly and accu-
rately judge people’s mental states, such as beliefs and desires. The
ability to understand mental states in others as well as oneself has
been called a theory of mind (ToM; Premack and Woodruff, 1978).
ToM is first evident sometime around the age of 4 years, when
children realize that people can have beliefs about the world that
are false (Perner, Leekam, & Wimmer, 1987; Wimmer & Perner,
1983). The litmus test for possessing a ToM is being able to pass
a false-belief task. In this task, participants are told a story in
which a character has a false belief about the location of an object
and must then predict the character’s future action based on this
false belief. In a classic version of the story, the character Maxi
puts his chocolate into a cupboard and then leaves. While he is
gone, Maxi’s mother moves the chocolate from the cupboard to the
refrigerator. Participants are then asked, “Where will Maxi look
for his chocolate when he returns.” Answers based on reality or
participants’ own beliefs will result in an incorrect answer of
saying that Maxi will look in the refrigerator. To correctly predict
that Maxi will look in the cupboard, participants must answer
based on the understanding that Maxi’s actions depend on his false
belief about the location of the chocolate. Children under the age
of 4 typically fail this task as do many individuals with autism.
Although false-belief understanding occurs sometime around
the age of 4, ToM continues to develop and be refined throughout
childhood (Sullivan, Zaitchik, & Tager-Flusberg, 1994) and even
into late adulthood (Happe´, Winner, & Brownell, 1998). For
example, the understanding that preexisting biases or expectations
influence people’s interpretation of an ambiguous event does not
develop until around age 6 (Pillow & Henrichon, 1996). A few
factors have been identified as playing important roles for the
development of ToM, including language ability (Astington &
Jenkins, 1999; Hughes, 1998) and executive functions (Carlson,
Moses, & Breton, 2002; Hughes, 1998). In adult populations, only
executive functions have been found to relate significantly to ToM
(Rowe, Bullock, Polkey, & Morris, 2001), with inhibition appear-
ing to be of particular importance (Carlson et al., 2002).
Possessing a ToM enables representing and reasoning about
mental states. It provides a conceptual framework for understand-
ing social situations, in which people’s behaviors are understood as
being intentional and based on their desires and beliefs (Malle,
2005). The conceptual framework provided by ToM is essential for
competent social functioning, and performance on ToM tasks is
correlated with measures of social competence. For example,
scores on advanced ToM tasks positively predict social compe-
tence in adolescents (Bosacki & Astington, 1999), and, conversely,
deficits in ToM have been found to co-occur with problems in
social functioning (Langdon, 2003).
The most well-documented example of deficits in ToM relating
to impaired social functioning comes from research on autism.
Baron-Cohen, Leslie, and Frith (1985) were the first to demon-
strate that individuals with autism fail tests for understanding
beliefs and other mental states, such as the false-belief task. Even
if individuals with autism are able to pass a simple false-belief
task, they often fail more advanced tasks such as the Faux Pas
Recognition Task (Baron-Cohen, O’Riordan, Jones, Stone, &
Plaisted, 1999). This task assesses the ability to understand a faux
pas, which is an awkward social situation that occurs when some-
one says something that they should not have said without realiz-
ing that they should not have said it. Understanding a faux pas
requires a person to represent the mental states of both the speaker
and hearer of the faux pas, as it requires an understanding that the
speaker does not realize they should not have said something and
that the person on the receiving end of the faux pas will feel hurt
or insulted.
Numerous studies have found that individuals with autism have
difficulty in making mental-state-based explanations of behavior,
establishing ToM deficit as one of the core cognitive impairments
associated with autism (Baron-Cohen, 1995). Furthermore, several
studies have found that, in individuals with autism, deficits in ToM
are associated with impaired frontal lobe functioning (e.g., Happe´,
1994; Hughes, Soares-Boucaud, Hochmann, & Frith, 1997; Ozo-
noff & McEvoy, 1994). These studies and research with other
populations have begun to identify the neurophysiological under-
pinnings of ToM and social cognition.
Neurophysiological Correlates of ToM
Broadly speaking, research on the neurophysiological correlates
of ToM has implicated the frontal lobes. Evidence supporting
frontal lobe involvement has come from a number of sources,
including studies of individuals diagnosed with an autistic spec-
trum disorder, neuropsychological lesion studies with adult brain
injured patients, and functional neuroimaging studies with normal
adults (e.g., Baron-Cohen et al., 1994; Fletcher et al., 1995; Goel,
Grafman, Sadato, & Hallett, 1995; Stone, 1998). For example, data
from PET studies have indicated a relationship between the frontal
lobes and deficits associated with the ToM. For example, Happe´et
al. (1996) found structural and metabolic abnormalities in the
brains of individuals diagnosed with Asperger’s syndrome (a vari-
ant of autism). In their PET study, Happe´ et al. (1996) found
abnormal metabolic activity in a highly specific brain region
adjacent to the left medial prefrontal cortex, a region that has
previously been found to show increased activation during ToM
tasks (Fletcher et al., 1995). In a recent review, Sabbagh (2004)
concluded that deficits in the orbitofrontal and medial temporal
circuits may be at the root of abnormal social-cognitive function-
ing associated with autism.
Neuroimaging studies in normally functioning adults have also
implicated regions of the frontal lobes as playing a vital role in
social cognition. Baron-Cohen et al. (1994) found that the right
frontal cortex was activated when participants were asked to
distinguish different actions of “mind.” Fletcher et al. (1995) found
that the left medial prefrontal cortex was activated when partici-
pants performed ToM tasks, a finding that has since been repli-
cated (Gallagher et al., 2000). In addition to activation of the left
medial prefrontal cortex, Gallagher et al. (2000) also found sec-
303
METHAMPHETAMINE AND SOCIAL COGNITION
ondary activation in the temporal parietal regions of the brain
during ToM tasks. Finally, Frith and Frith (2003) in their review of
ToM-related neuroimaging studies identified three regions that
show selective activation during tasks that involve reasoning about
mental states: the medial prefrontal cortex, the temporal poles, and
the posterior superior temporal sulcus. The authors suggest that the
medial prefrontal cortex region is of particular importance for
distinguishing mental state representations from physical state
representations.
The literature cited above and related studies have clearly es-
tablished the importance of the frontal lobes for ToM; however,
data specifying the lateralization of brain region for ToM have
been inconclusive. Much of this work has been with individuals
who have experienced some form of brain injury. Overall, studies
have found that injury to either the left or right frontal lobe is
detrimental to ToM performance. Winner, Brownell, Happe´,
Blum, and Pincus (1998), for example, found that individuals with
acquired right frontal brain damage had difficulty with ToM-like
tests. Sabbagh and Taylor (2000) found that evoked potential
activation in participants performing the false-belief test was stron-
gest in the left frontal region. Stuss, Gallup, and Alexander (2001)
and Rowe et al. (2001) found that lesions in either the left or right
frontal lobe lead to ToM impairment. Similarly, Homer, Ramsay,
and McFadden (2001) found that injury to either the left or right
frontal lobe during childhood resulted in impaired ToM and pre-
dicted maladaptive social functioning.
In summary, there is clear evidence that the frontal lobes,
particularly the prefrontal cortex, play a vital role in ToM. Im-
paired functioning in this brain region can affect ToM, thereby
impairing social-cognitive functioning. In the case of autism, im-
pairments to frontal lobe functioning are most likely due to genetic
factors leading to abnormal brain development, which means that
a proper ToM may never develop. In the case of individuals who
have suffered strokes or brain injury, trauma to the brain leads to
impaired functioning. This means that these individuals who were
once functioning normally have an impaired ToM and altered
social-cognitive functioning. We are proposing that abuse of MA
may have a similar effect.
MA and Social Interactions
The neurological damage caused by MA is known to affect
frontal lobe functioning that, we suggest, can result in impairments
in ToM. As reviewed above, MA abuse has been shown to cause
damage to the frontal lobes, including regions of the prefrontal
cortex. Impairments of certain cognitive functions in MA abusers
have been associated with damage to these regions of the brain.
This suggests that MA abuse can lead to impaired social-cognitive
functioning as a result of damage to the frontal lobes. Although no
study has explicitly examined the link between the neurological
damage caused by MA abuse and impairments in social cognition,
there is evidence from many studies indicating that MA abuse can
lead to impairments in social functioning.
Evidence for the effects of MA on social functioning comes
from studies that have noted changes in social behavior associated
with chronic MA exposure (e.g., Clemens et al., 2004; Semple et
al., 2005). Furthermore, many of the behavioral changes associated
with MA abuse, such as depression and aggression, are linked to
impaired social functioning. One of the paradoxes associated with
MA use and abuse is that MA is widely used as a means of
increasing the desire and ability to have social interactions. De-
creased social or sexual inhibitions, increased energy, and the
desire to lengthen social interactions or to socialize with others
using the drug as a means of achieving a similar mental state are
behaviors that have all been associated with MA use (Halkitis,
Parsons, & Wilton, 2003; Halkitis, Shrem, & Martin, 2005; Kurtz,
2005; Semple, Patterson, & Grant, 2004). MA use and abuse has
also been highly correlated with social venues such as bars, clubs,
and sex and circuit parties (Halkitis et al., 2003, 2005; Semple et
al., 2004). Other studies have indicated that negative side effects,
such as paranoia, depression, and increased aggressiveness (Gor-
man, Nelson, Applegate, & Scrol, 2004), as well as the need to
hide increased usage, eventually lead to social isolation for users
(Gorman et al., 2004; Kurtz, 2005). Thus, despite the original
intention to use MA to facilitate and enhance social interactions,
MA abuse often erodes social connection.
Altered social functioning has also been found in animals ex-
posed to MA. A number of studies have found that rats injected
with MA make significantly less body contact with other rats
compared with that of control rats (Clemens et al., 2004; Syme &
Syme, 1974). Similarly, Schio¨rring (1977) found that both acute
and chronic MA exposure lead to extreme social withdrawal in
monkeys. More recently, Clemens et al. (2004) found that even
several weeks after being injected with a dose of MA, rats were
significantly less social than rats that had not been exposed to MA.
Because animals are free of the social stigma of addiction, but still
become socially withdrawn, it is most likely that desire to hide
excessive MA usage is not the only factor in the eventual self-
isolation of some MA users. Instead, these findings suggest that
changes in social behavior (e.g., social withdrawal, aggression,
depression) associated with chronic MA abuse have a physiolog-
ical basis and may, in part, be explained by impairments in
social-cognitive functioning.
If social-cognitive deficits do develop as a result of MA abuse,
then there should be additional psychological and behavioral con-
sequences of impaired social-cognitive functioning. The research
reviewed above indicates that MA use can cause physiological
changes that results in altered social behavior and possible social
isolation. Research on the consequences of impaired social cogni-
tion indicates two primary psychological consequences of having
impairments in social-cognitive functioning: depression and in-
creased aggression. In the sections below, each of these symptoms
is described in detail and the underlying causes are discussed, with
attention being given to the possible role that impaired social
cognitions may play.
MA and Depression
By far the most common psychiatric symptom associated with
chronic MA use is depression. In a study with one of the largest
samples of MA users (N⫽1,016), Zweben et al. (2004) examined
co-occurring psychiatric symptoms and found particularly high
scores on depression scales for MA users. Specifically, 68% of the
women and 50% of the men reported feeling depressed at some
point in their lives, and 28% of the women and 13% of the men
reported at least one suicide attempt. Frequency of use and injec-
tion were both associated with higher reported BDI scores and
304 HOMER ET AL.
users who injected also reported more suicide attempts and sui-
cidal thoughts.
The relationship between depression and MA use appears to be
bidirectional. A number of studies have found that depression is a
risk factor for subsequent abuse of drugs, including MA. For
example, Grant (1995) found that lifetime risk of amphetamine
abuse or dependence was 6.19 times more likely for individuals
with major depression than among those without major depression.
The risk decreased to 4.04 times for amphetamine abuse only and
increased to 8.89 times for dependence (Grant, 1995). Similarly, in
a study of young club-drug users, Clatts, Goldsamt, and Yi (2005)
found high rates of prior suicide attempts (34%) and clinically
significant depressive symptoms in over half (58%) of all users.
Other studies have found that MA abuse is a risk factor for
subsequent depression. Semple et al. (2005) found that 40% of
their sample of MA users met criteria for moderate to severe
depression and that greater intensity of use was associated with
higher levels of depressive symptoms, even controlling for demo-
graphic characteristics, stigma, and social and health problems.
They also found that perceived stigma had a significant positive
direct effect on depressive symptoms, whereas social and health
problems did not. Multivariate analyses indicated that MA use
uniquely accounted for 11% of the explained variance in depres-
sive symptoms. In a retrospective study, Kalechstein et al. (2000)
found that in the 12 months prior to assessment, MA-dependent
individuals were more likely to report depressive symptoms and
suicidal ideation than were non-dependent individuals, even after
controlling for demographic profile and dependence on other sub-
stances. They also found that MA-dependent participants were
more likely to report a need for psychiatric assistance.
A number of factors seem to contribute to the development of
depression in MA abusers. Altered brain metabolism appears to be
one important factor. For example, London et al. (2004) found
that, compared with non-users, abusers of MA had higher self-
ratings of depression and showed lower regional glucose metabo-
lism in the anterior cingulate and insula and higher glucose me-
tabolism in the lateral orbitofrontal area, middle and posterior
cingulate, amygdala, ventral striatum, and cerebellum. Depressive
symptoms in MA abusers were found to correlate significantly
with glucose metabolism in the perigenual anterior cingulate gyrus
and amygdala, both of which are part of the limbic system. The
researchers also found that in MA abusers self-reports of depres-
sive symptoms co-varied positively with relative glucose metabo-
lism in limbic regions (e.g., perigenual anterior cingulated gyrus
and amygdale), and ratings of state and trait anxiety co-varied
negatively with relative activity in the anterior cingulated cortex
and left insula. London et al. concluded that MA abusers have
abnormalities in brain regions that can result in mood disorders,
including depression and anxiety. They suggest that the resulting
affective deficits may have implications for addiction recovery
during MA abusers’ initial periods of abstinence.
In addition to altered affect regulation, the social isolation
associated with chronic MA abuse is also likely to play a causal
role in the development or the heightening of depression. Lack of
social connection is a well-established risk factor for depression
(e.g., Costello, 1982; George, Blazer, Hughes, & Fowler, 1989),
and impairments in social cognition may be partially to blame for
the social isolation associated with depression. A number of stud-
ies have found a link between impairments in social cognition and
depression (e.g., Inoue, Tonooka, Yamada, & Kanba, 2004; Mc-
Clure et al., 2005). For example, Kerr, Dunbar, and Bentall (2003)
found that patients with bipolar depression demonstrated impair-
ments in ToM performance. Similarly, Lee, Harkness, Sabbagh,
and Jacobson (2005) found that women diagnosed with clinical
depression had significant impairments in their ability to identify
mental states compared with that of control participants. The
authors suggest that these impairments in social cognition contrib-
ute to depression by causing a breakdown in depressed individu-
als’ everyday social interactions. These and related findings sug-
gest that impairment in social cognition makes an important
contribution to the depression that is associated with MA abuse.
MA and Aggression
Substance abuse in general has been linked to violence and
aggression, and this link is particularly strong for abuse of am-
phetamine and MA (Boles & Miotto, 2003). Studies of amphet-
amine and MA users have indicated elevated levels of violent
behaviors as well as problems controlling aggression and aggres-
sive outbursts (Hall, Hando, Darke, & Ross, 1996; Vincent, Schoo-
bridge, Ask, Allsop, & Ali, 1998; Wright & Klee, 2001). For
example, Makusa, Nakamura, Yamada, Inoue, and Nakazawa
(1990) found that MA-dependent individuals were significantly
more impulsive and less able to inhibit aggression than were
control participants and had significantly more verbal and physical
aggression than did alcohol dependents. Similarly, Brecht,
O’Brien, von Mayrhause, and Anglin (2004) found that violent
behaviors were reported by 57% of MA users, and Zweben et al.
(2004) found that 43% of MA users reported having problems
controlling their angry or violent behavior. These problems exist
even for MA abusers who are not abusing any other substances,
indicating that MA abuse alone can contribute to increases in
violent behavior (Sekine et al., 2006).
Evidence also suggests that the aggression and violence associ-
ated with MA abuse is somewhat context dependent. In a study
that analyzed life histories of MA users, Sommers and Baskin
(2006) found that 26.8% had committed violence while under the
influence of MA. More than half of the reported violent events
occurred in domestic relationships, and more than two-thirds of
incidents occurred in private homes. MA-related violence, there-
fore, seems more likely to occur in private, domestic settings rather
than the public, street settings associated with other drugs. Som-
mers and Baskin (2006) supported this claim with their finding that
although the use of alcohol and MA were both significantly
correlated with reported partner violence in college students, only
alcohol use correlated with assault. These data again suggest that
MA is more likely to increase the risk of private, domestic violence
rather than violence or aggression committed in public.
Although the association between MA and violence is well
supported, violence is not a certain outcome of even chronic use of
MA. A number of factors have been found to influence the
MA–violence link. Austin (2004) identified several factors as
predictive of the age at which MA abusers first committed vio-
lence against another person. These included age at first MA use,
current use, frequency of use in last month, and age at which
person became a regular user. Hall et al. (1996) found that mode
of MA use also made a difference, with users who injected being
significantly more likely to exhibit violent behavior. Sommers and
305
METHAMPHETAMINE AND SOCIAL COGNITION
Baskin (2006) found that the main predictors of MA-related vio-
lence were exposure to family deviance, such as arrests and child
abuse, previous substance-related violence, age at first MA use,
childhood fighting, and social functioning problems. Other studies
have found a number of psychosocial factors, such as family
violence, loose parental supervision, early exposure to violence,
early exposure to substance abuse, and an individual history of
aggressive behavior, are linked to subsequent MA-related violence
(Cohen et al., 2003; Semple et al., 2005; Zweben et al., 2004),
possibly via changes in early behavioral patterns (Boles & Miotto,
2003).
There is also evidence that altered brain function caused by MA
abuse is related to increased aggression and violence. In a study on
the neurophysiology of aggression, Amen, Stubblefield, Car-
michael, and Thisted (1996) found that, compared with control
participants, aggressive participants had decreased activity in the
prefrontal cortex as well as increased activity in the medial frontal
lobes and left basal ganglia and/or limbic system. Buffenstein,
Heaster, and Ko (1999) found that MA abusers who experience
psychotic symptoms after the onset of MA use have a pattern of
altered brain function similar to the altered brain patterns associ-
ated with aggression in the Amen et al. (1996) study, with 76% of
patients showing localized blood flow deficits in the frontal, pa-
rietal, and temporal lobes. The overlap between neural deficits
seen in aggressive participants and MA abusers suggests a strong
relation between the two.
One likely cause of increased aggression in MA abusers is a
decrease in the ability to inhibit impulsive behavior. A strong
association exists between impulsivity and aggression (e.g., Trem-
blay, Pihl, Vitaro, & Dobkin, 1994). In a sample of MA abusers
who had been abstinent for an average of 19 months, Kim et al.
(2005) found decreased cerebral metabolic rate of glucose (CM-
Rglc) in frontal white matter that correlated with impairments in
executive functioning as measured by the Wisconsin Card Sorting
Test, including the inability to inhibit impulsive acts.
Impaired social cognition is another factor that is likely to play
a role in the increase in aggression associated with MA abuse.
Several studies have found deficits in social-cognitive functioning
to be associated with aggression (e.g., Holmes-Lonergan, 2003;
Johoda, Pert, & Trower, 2006; Weimer & Guajardo, 2005; Yiwen,
Chongde, & Wenxin, 2004), and many chronic MA users report
disorganized cognitions and distorted perception such as paranoia
and psychotic episodes (Cretzmeyer et al., 2003). This means that
deficits in social-cognitive functioning could result in harmless
situations being misinterpreted as threatening by MA users, mak-
ing it more likely that they would resort to violence or aggressive
behavior.
In sum, research on the relation between MA abuse and aggres-
sion suggests a complex interaction. Although MA abuse is a risk
factor for aggression and violence, not every abuser becomes
violent. Sommers and Baskin (2006) suggest a path from youth
aggression to adult violence, with various long-term factors lead-
ing to individual tendencies toward violence and additional short-
term factors leading to variations in these tendencies. The link
between impaired social cognition and aggression suggests that
one of the ways in which MA is responsible for increased aggres-
sion and violence is by altering they way in which MA abusers are
able in interpret social situations. For those individuals whose life
history puts them at higher risk, this frustration may be expressed
by violent acts.
Discussion
Although no study to date has explicitly examined social-
cognitive functioning in MA abusers, the research presented above
provides strong circumstantial evidence that social-cognitive func-
tioning may be significantly impacted by MA use. MA users report
increased social isolation, which seems to be due to more than just
the social withdrawal associated with addiction. Difficulties with
social cognition also appear to make significant contributions to
the depression that is associated with MA abuse. Finally, impaired
social-cognitive functioning seems to be one of the factors in-
volved in the tendency for the increased aggression and violence
associated with MA use.
Research is needed to first establish that, as argued above, MA
users do demonstrate deficits in social-cognitive functioning. Em-
pirical data are needed to determine if MA use is associated with
impaired performance on ToM tasks, particularly on the more
advanced ToM tests such as the Eyes Task (Baron-Cohen, Jolliffe,
Mortimore, & Robertson, 1997), which requires participants to
identify mental states based solely on viewing the eyes, and the
Faux Pas Recognition Task (Baron-Cohen et al., 1999), which
requires participants to reason about mental states embedded in a
social context. If the hypothesized cognitive deficits are found,
then structural and functional neuroimaging studies should be
conducted to determine the specific brain regions that are involved.
Social-cognitive deficits would also have implications for treat-
ment.
Treatment Considerations
The multiple effects of MA abuse clearly suggest that treatment
models be holistic in their approach and consider the interplay
between psychological, biological, and social factors. As of yet,
studies from community-based, clinical, and research settings have
not found any single treatment for MA addiction to be completely
effective (Halkitis, in press). Furthermore, although certain medi-
cations show signs of reducing the “high” associated with MA and
reducing cravings during withdrawal, pharmaceutical therapies
remain relatively elusive (NIDA, 2002). Several treatment ap-
proaches have been tried with varying degrees of success, includ-
ing cognitive behavioral therapy, motivational interviewing, and
contingency management, 12-step/12-step facilitation, aversion
therapy, and psychoeducational approaches (Halkitis, in press). In
general, treatment models that are directed by social-cognitive
theory and principles of cognitive behavioral therapy (CBT), such
as the matrix model (Anglin & Rawson, 2000), appear to be the
most effective in treating MA abuse (NIDA, 2002). Central to this
theoretical approach is the attempt to increase knowledge, moti-
vation, and behavioral skills in an attempt to reduce MA use and
provide mechanisms that address the link between MA use and
faulty decision making in social situations while under the influ-
ence. As Fisher and Fisher (1993) suggest, information alone is
insufficient for behavior change; motivation and skills building
must also be included. Thus, to accomplish this, a program based
on CBT and informed by the principles of motivational interview-
ing (Miller & Rollnick, 1991) serves to both increase individuals’
306 HOMER ET AL.
motivations to reduce their MA use as well as to promote skills
necessary to achieve behavioral change with regard to use and
social malfunctioning. In the substance abuse treatment field, the
integration of motivational interviewing and CBT has been viewed
as an approach providing maximum flexibility to meet the needs of
clients (Baer, Kivlahan, & Donovan, 1999). It has been further
argued that relapse prevention (which is critical when addressing
MA use) requires both support for pursuing change (motivational
interviewing) and behavioral techniques to be successful (CBT).
Such integrated interventions are effective in cognitive– behavioral
outpatient counseling programs for substance abuse (Annis,
Schober, & Kelly, 1996) and in relapse prevention programs for
problem drinkers (Allsop, Saunders, Phillips, & Carr, 1997).
If, as we have argued, MA abuse results in impaired social
functioning, then treatments must consider social interactions and
social settings, including but not limited to sexual contexts and
interactions that are associated with MA use. Moreover, the asso-
ciation of MA abuse with depression and aggression further im-
plies that MA treatments must consider the psychological dynam-
ics which act as precursors to abuse of the substance and which are
exacerbated by use of the drug itself (Shrem & Halkitis, in press).
In this view, “re-learning” social interactions and behaviors must
be central to the treatment of MA abuse. At the same time, the
effects of MA abuse on brain functioning, as indicated by reduced
cellular activity in the frontal cortex, suggest that treatments must
not neglect the biological elements of addiction.
Conclusions
The research reviewed above points to a fundamental problem
for the social functioning of MA abusers as the drug itself may be
causing damage to regions of the brain responsible for social
cognition. Therefore, even users who eventually become abstinent
from MA may face irreversible neurological deficits resulting in
long-term difficulties with social cognition. The deficits in social-
cognitive functioning may contribute to a number of related psy-
chological and behavioral problems that are associated with MA
use. The extent to which duration of use, amount used, and mode
of administration may affect social-cognitive functioning or the
extent to which such deficits can be overcome through various
types of therapy remains to be seen. However, if MA use and
abuse truly do produce permanent and neurophysiologic and
social-cognitive deficits, this may change the way that both the
medical and psychological communities view and treat the use of
MA.
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Received January 16, 2007
Revision received August 7, 2007
Accepted October 12, 2007 䡲
310 HOMER ET AL.
