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| Journal of the New Zealand Medical Association,
26-November-2004, Vol 117 No 1206
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Maternal methamphetamine use during pregnancy and child
outcome: what do we know?
Trecia Wouldes, Linda LaGasse, Janie Sheridan, Barry
Lester
‘P’, ‘Pure’, or ‘Burn’
are names that have become associated with potent forms of methamphetamine made
in illegal laboratories in New Zealand. The dramatic increase in the use of
these drugs in New Zealand has largely been associated with the young male
population. However, it has become apparent that a growing number of New Zealand
women are also using methamphetamine during their pregnancy. The objective of
this article was to review the literature that has associated
methamphetamine-use with adverse developmental outcomes.
What little we know about the effects of
‘methamphetamine-use during pregnancy on the developing child’ comes
from animal studies, a few human studies that have a number of methodological
problems, and the recent cocaine literature. Evidence from these studies suggest
there are likely to be adverse developmental effects for children exposed
prenatally to methamphetamine, either because of the drug
per se or because of the environment in
which these children are raised. At present, we do not know specifically what
those effects will be. Therefore, to avoid making unfounded judgements about the
development of infants born to mothers using these drugs during their pregnancy,
further research that considers the impact of other drug use as well as the
influence of the postnatal environment is needed.
Since the 1990s, there has been a dramatic increase in the
use of methamphetamine in a number of regions
worldwide.1 More recently, an increased use of
methamphetamine has emerged in the Asia Pacific
region,1–3 and in specific parts of New
Zealand.4–6 Although the greatest
increase in use has been associated with the young male population in New
Zealand,4,6 it is now apparent that a growing
number of women of child-bearing age are also using methamphetamine. This
widespread use has been reflected in the dramatic increase in referrals of women
who have used this drug during their current pregnancy to the Alcohol Drug and
Pregnancy Team (ADAPT) at National Women’s Hospital. In 2001, 10% (6/60)
of the total ADAPT referrals were due to methamphetamine use and associated
problems. This escalated to 59% (34/58) in 2003.
Women referred to ADAPT have a high rate of mental and
physical health problems that are often related to their drug use. Some of the
psychological, social, and health problems that we have already observed in
mothers referred to ADAPT for methamphetamine use or dependence over the past
year are reported in Table 1.
Further anecdotal reports from other antenatal departments
of hospitals in the Auckland region and community midwives suggest that a much
larger number of women are using or have used methamphetamine during their
current pregnancy that have not come to the attention of ADAPT. The purpose of
this commentary is to explore the evidence for the harm associated with
methamphetamine use in pregnancy, in order to avoid a “rush to
judgement” about the potential developmental outcomes of children born to
methamphetamine users.
Table 1. Psychological, social, and health problems
observed in mothers referred to ADAPT for methamphetamine use
ADAPT=Alcohol Drug and
Pregnancy Team; *Refer to numbers of mothers using that
substance.
‘A rush to judgement-the cocaine story’In the 1980s, prenatal drug use by
women in the United States became the focus of moral and public health debate
when a cheap, smokeable form of cocaine, ‘crack’, became widely
available. At that time, words such as ‘crisis’ and
‘epidemic’ were being used to describe the increased availability
and use of ‘crack cocaine’.
Driven by public and media interest, crack cocaine became
commonly associated with poor African Americans and Latinas and was often
portrayed as the cause of urban deterioration, increased gang violence, drive-by
shootings, the expanding underclass, and a proliferation of infants the media
dubbed ‘crack babies’. ‘Crack mothers’ were represented
as modern-day villains, and their substance-dependence resulted in a number of
punitive outcomes, including loss of parental rights to their children because
of charges of child neglect and/or abuse, loss or reduction in their welfare
benefits, and even imprisonment.7
Although there were valid concerns regarding the health and
developmental outcome of children exposed prenatally to crack cocaine, the media
often portrayed so-called ‘crack babies’ as ‘damaged for
life’. Media across the US ran headlines such as,
‘Crack babies turn 5 and Schools
Brace’8 and
‘Tragic end to adoption of crack baby:
Couldn’t take crying anymore mother
says’.9 These headlines were often
based on anecdotal reports and unsubstantiated findings from small and
methodologically compromised studies that suggested prenatal exposure to cocaine
caused brain damage and intellectual and social impairment.
Subsequent longitudinal studies that addressed the
methodological shortcomings of early investigations did not find evidence of
serious brain damage, nor major
impairment.10,11 However, what they did find
was a pattern of subtle, but significant neurobehavioural
effects.12,13 In a meta-analysis, Lester et
al10 found small effects of prenatal cocaine
exposure on school age IQ, but even these subtle effects resulted in a 1.5-fold
increase in the number of children who needed special education services at a
cost in excess of $352 million (US) per year.
It is apparent from current reports by the media, the police
and substance abuse agencies, that we are at risk of ‘a rush to
judgement’ regarding the effects of prenatal methamphetamine
exposure.5,14 However, despite the widespread
use of methamphetamine worldwide, little is known about its potential neurotoxic
effects on the developing child.
Prenatal methamphetamine exposure and child developmentMethamphetamine is a highly
addictive central-nervous-system (CNS) stimulant, and the most potent member of
the amphetamine group of synthetic drugs. Methamphetamine can be injected,
smoked, snorted, or ingested orally or administered anally. These drugs have
acquired a number of street names such as ‘P’, ‘Pure’,
‘Burn’, ‘Ice’, and ‘Crystal’ that are quite
often related to their purity and psychostimulant properties.
‘P’, ‘Pure’, or ‘Burn’
are the names given to potent forms of methamphetamine made in New Zealand in
illegal laboratories.5,6 ‘Crystal’
and ‘Ice’ resemble tiny chunks of translucent glass or ice which can
be heated and the resulting vapour inhaled. In adults, chronic high-dose use has
been shown to cause a number of adverse physiological, psychological and
behavioural effects including damage to cardiac, vascular and neurological
systems, hostility, violence, hallucinations and paranoid psychosis resembling
schizophrenia.15
All illicit drugs taken during pregnancy cross the placenta
and reach the fetus.16,17 The effects of drugs
in the fetus can be caused directly through placental transfer of the drug, or
can be secondary to changes in the fetal environment. For instance,
methamphetamine has been shown to have vasoconstrictive effects resulting in
decreased uteroplacental blood flow and fetal hypoxia, and anorexic effects on
the mother which may result in intrauterine growth
retardation.18 In addition, psychoactive drugs
are quite often used in different combinations. For instance, mothers receiving
daily methadone maintenance in an Auckland programme continued to use large
quantities of benzodiazepines, smoked more than 10 cigarettes per day and smoked
cannabis regularly during their pregnancy.19
Most (33/34) of the women referred to ADAPT in 2003 were
polydrug users (Table 1). Therefore, in addition to understanding the effect of
prenatal exposure to methamphetamine on child development there is also a need
to understand the combined impact of these drugs on physical, cognitive and
emotional development.
Evidence of adverse developmental effects from animal studiesWhat little we know about the
effects of methamphetamine-use during pregnancy on the developing fetus and
child comes from three areas: animal studies, a limited number of human studies
of prenatal methamphetamine exposure, and studies of prenatal exposure to other
stimulants such as ‘crack’ cocaine.
Animal studies have found a range of physical, motor,
neurotransmitter, and behavioural effects in methamphetamine exposed rats and
their offspring.20–25 These results have
shown that prenatal exposure to methamphetamine may cause effects such as
increased maternal and offspring mortality, retinal
defects,20–22 cleft palate and rib
malformations, decreased rate of physical growth, and delayed motor
development.21,23 Neurotoxic effects of
prenatal methamphetamine exposure on serotoninergic neurons produce
neurochemical alterations in the CNS20,23,25,26
thought to be associated with learning
impairment,20 behavioural
deficits,25 increased motor
activity,21 and enhanced conditioned avoidance
responses.23
Evidence
of potential adverse developmental effects from human studies of prenatal
exposure to methamphetamines
There are a few human studies but as with the early cocaine
reports, these have a number of methodological problems including small sample
size and results that are often confounded by maternal use of a variety of other
drugs. In these studies methamphetamine use during pregnancy has been associated
with an increased rate of premature delivery and placental
abruption.27,28 Some of the methamphetamine
effects reported in animal studies have also been found in methamphetamine
exposed human infants. These include clefting, cardiac anomalies and fetal
growth retardation.18
A high rate (35%) of cranial abnormalities was reported in a
group of infants prenatally exposed to methamphetamine and
cocaine.29 Oro and
Dixon30 found that in comparison to narcotic
exposed infants, methamphetamine/cocaine-exposed infants were more likely to be
preterm, lower birth weight, intrauterine growth retarded, and have a smaller
head circumference. In addition, they reported more fetal distress, and more
neurologic and physiologic alterations in methamphetamine/cocaine exposed
infants. These effects remained when maternal factors were controlled. Decreased
fetal-growth related to methamphetamine exposure was also reported by Little et
al.31 However, they did not find congenital
anomalies were significantly increased in their sample of 52 women who
self-reported frequent use of methamphetamines.
The only study that has examined the long-term effects of
prenatal amphetamine exposure is of a sample of 65 children born to mothers who
had abused amphetamines during their pregnancy in Sweden. Developmental
assessments of these children have been carried out at regular intervals from
birth to 14 years of age.27,32,33 As there was
no control group in this study, comparisons were made with Swedish peers born in
1976. At birth, 1, and 4 years of age, the mean weight, height, and head
circumference of the amphetamine-exposed children were below the means of their
peers.
Females, but not males, were significantly shorter and
lighter than their peers and remained smaller at age
10.27,32 At age 8, there was a significant
correlation between amount and duration of amphetamine exposure prenatally and
aggressive behaviour and social adjustment.33
At age 14–15 years, their achievement in mathematics, Swedish language,
and sports were statistically below those of their
classmates.32 However, impaired growth and the
behavioural and academic outcomes were also associated with a number of
psychosocial factors related to their environment—such as stress, number
of siblings, maternal alcohol abuse, and a higher number of foster care
placements.
These human studies are limited in several ways, most
notably by small numbers, a reliance solely on maternal self-reporting to
confirm drug use, lack of control groups, and confounding with other maternal
drug use and environmental factors that were associated with the developmental
outcomes. However, these findings do suggest that these children may be at risk
developmentally due to both the direct effects of prenatal drug exposure and the
caregiving environment associated with that drug use.
Evidence of adverse developmental effects from human studies of prenatal exposure to “crack” cocaineAnother area of research that may
provide some insight into the effects of prenatal methamphetamine exposure is
the cocaine literature. The pharmacological properties of cocaine and
methamphetamine are similar; therefore, findings from the cocaine literature may
be useful in suggesting possible developmental effects. At the same time, it is
important to appreciate that methamphetamine has a longer half-life and more
sympathomimetic effects than cocaine. In addition, it is likely that the
demographics of methamphetamine users will be different than cocaine users. For
instance, there are likely to be differences in self-identified ethnicity, the
kinds and combinations of other drug use, and the socioeconomic status of the
mothers.
Evidence from recent studies investigating the developmental
outcomes of infants exposed prenatally to cocaine may also suggest specific
domains of behaviour that are likely to be affected by methamphetamine. In the
neonate, research has found effects of prenatal exposure to cocaine on infant
neurobehaviour.34,35 The most consistent
findings from these studies is the effect of cocaine on state
regulation.34,36–38 State regulation is
the newborn infant’s ability to regulate his level of arousal in the face
of internal and external stimulation and serves as a marker of nervous system
integrity.
The infant regularly cycles through six
‘states’, quiet (deep) sleep, active (rapid-eye-movement ) sleep,
drowsy, alert, fussy (active), and crying. In the alert state, infants are best
able to focus attention on a source of stimulation such as auditory and visual
stimuli. Therefore, the infant’s availability for interpersonal
interaction and learning are at their maximum in the alert state.
DiPietro et al38 found that
cocaine infants displayed significantly greater state transitions and shorter
sleep bouts, and fussed or cried more often. Acoustic cry characteristics that
reflect reactivity, respiratory, and neural control of the cry sound were also
compromised by prenatal cocaine exposure.39
Karmel and Garner40 found that
cocaine-exposed infants at 1 month of age did not modulate attention relative to
their arousal, preferring faster frequencies of stimulation regardless of
arousal condition.
Lower arousal regulation has also been observed at 3 and 4
months of age in cocaine-exposed infants.41, 42
Effects of cocaine have also been found on
attention.43, 44 Furthermore, Jacobson et
al43 found lower scores related to heavy
cocaine exposure on tests of recognition memory at 6 and 12 months, and
suggested that these infants had difficulty modulating their arousal and
attention. Several studies have also reported cocaine effects on standardised
measures of motor development. Across time, cocaine-exposed infants and toddlers
to 36 months have shown a general decline in motor
performance.45 At 5 and 6 years of age,
cocaine-exposed children have been shown to perform more poorly than controls on
tasks that require inhibitory motor control under changing
circumstances.46 The ability to inhibit such a
response may be related to memory deficits, and has been related to
teacher-assessed externalising behaviours in school-aged
children.47
Drug-use in context—psychosocial risk factorsThere is also evidence that maternal
drug use is associated with general psychosocial risk factors that may
compromise child outcome apart from substance dependence issues. Research shows
a number of these factors may be more pronounced in drug-using populations and
include poverty, chaotic and dangerous lifestyles, symptoms of psychopathology,
history of childhood sexual abuse, and involvement in difficult or abusive
relationships with male
partners.19,43,48–52
Pregnant women receiving treatment for drug-dependence show
a high incidence of psychopathology, including affective and personality
disorders, and depressive symptoms.19 For
instance, a recent New Zealand study that compared the parental characteristics
of infants (whose mothers were receiving methadone-maintenance treatment for
their opiate dependence) with infants born to non-opiate-dependent parents found
methadone mothers and fathers reported significantly more symptoms of
depression, were more likely to be living on a Government benefit, had fewer
years of education, and had a self-reported history of criminal behaviour that
often included (paternal) arrests for violent behaviour. In addition,
opiate-dependence was associated with a self-reported history of sexual and/or
physical abuse and personality characteristics of sensation-seeking, with less
desire to conform to societal norms.
Risk factors related to maternal psychosocial functioning
and the home environment have been found to adversely affect child development
independent of the mother’s use of substances during
pregnancy.13,19,53 In an intergenerational
study, drug users reported having less control over their children, and those
children, in turn, were seen by their parents as being more aggressive and
having more behaviour problems.54 This link
between drug-using parents and disruptive behaviour in their children has
important long-term consequences, as behavioural-conduct problems in childhood
and early adolescence have been shown to be important precursors of adolescent
drug use, delinquency, and teenage
pregnancy.56–57 Thus, converging evidence
from New Zealand as well as other countries suggest that there may be a double
jeopardy in which these children are at risk due to the combination of prenatal
exposure effects and postnatal environmental effects.
ConclusionThere is no doubt that there has
been an increase in methamphetamine-use in New Zealand, and that this increase
is being noted among pregnant women. Three lines of evidence (animal studies,
human methamphetamine studies, and cocaine studies) suggest that there are
likely to be direct effects of prenatal methamphetamine use on neonatal and
early child development. The effects at birth are likely to include preterm
birth, growth retardation, and (depending on the extent and combination of drugs
used) there may also be neurobehavioural outcomes that reflect neurotoxic
effects on the CNS.
Based on the cocaine literature, the specific developmental
domains that are likely to be affected during infancy and early childhood
include state regulation, arousal, attention, and psychomotor development.
Finally, these children may be born to parents who are at a high risk of
parenting failure due to a range of issues beyond drug-dependence that include
psychological problems, low socioeconomic status, fewer years of education, a
history of criminal activity, and an intergenerational history of physical and
sexual abuse.
The literature reviewed in this commentary, together with
the problems we are currently observing in mothers referred to ADAPT, suggest
there are likely to be adverse developmental effects for children exposed
prenatally to methamphetamine in New Zealand, either because of the drug
per se or because of the environment in
which these children are raised. At present, we do not know specifically what
those effects will be. However, for those healthcare providers who are
responsible for the care of these infants and for those workers in special
education services, identification of the specific physical, cognitive, and
social-emotional needs of these children is paramount.
This will require a two-staged approach. First, to avoid a
second ‘rush to judgement’ we need well-designed studies to
determine if there are effects of methamphetamine on child outcome. Second, if
there are effects, we need to develop effective intervention programs for the
infants and their families to reduce methamphetamine-related deficits. The cost
savings alone from preventing the need for special education services in school
would more than pay for early intervention programs.
However, while the ‘jury is still out’ on the
effects of methamphetamine, the courts may be faced with more immediate problems
in protecting the safety of these children. In Rhode Island (USA), the Women and
Infants Hospital established ‘VIP’—the Vulnerable Infants
Program to help the court with placement decisions and treatment for
drug-exposed infants and their families so that they can remain together, where
appropriate. VIP is an example of how our understanding of drug abuse (as a
mental health/medical illness) translates into new collaborative efforts between
the healthcare community and the criminal justice system to provide treatment as
well as sanctions and act in the best interest of the child.
Author information:
Trecia Wouldes, Developmental Psychologist and Lecturer, Health Psychology
– Faculty of Medical and Health Sciences, University of Auckland,
Auckland; Linda LaGasse, Assistant Professor of Pediatrics, Brown University
(and Director of Research, Infant Development Center, Bradley Hospital and Women
& Infants Hospital), Providence, Rhode Island, United States;
Janie Sheridan, Associate Professor, School of Pharmacy, University of
Auckland, Auckland; Barry Lester, Professor, Psychiatry and Human Behaviour (and
Pediatrics), Brown University (and Director, Infant Development Center, Bradley
Hospital and Women & Infants Hospital), Providence, Rhode Island, United
States
Correspondence: Dr
Trecia Wouldes, Health Psychology, Faculty of Medical and Health Sciences,
University of Auckland, PO Box 92019. Fax: (09) 373 7013; email: t.wouldes@auckland.ac.nz
References:
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