Prenatal substance abuse continues to be a significant problem in this country and poses important health risks for the developing fetus. The primary care pediatrician’s role in addressing prenatal substance exposure includes prevention, identification of exposure, recognition of medical issues for the exposed newborn infant, protection of the infant, and follow-up of the exposed infant. This report will provide information for the most common drugs involved in prenatal exposure: nicotine, alcohol, marijuana, opiates, cocaine, and methamphetamine.
- AAP —
- American Academy of Pediatrics
- THC —
Substance abuse has been a worldwide problem at all levels of society since ancient times. Attention has been directed toward the use of legal and illegal substances by pregnant women over the past several decades. Almost all drugs are known to cross the placenta and have some effect on the fetus. The effects on the human fetus of prenatal cigarette use have been identified and studied since the 1960s,1 the effects of alcohol and opiate use have been studied since the 1970s,2–4 and the effects a variety of other illicit drugs have been studied since the 1980s.5–7 This report reviews data regarding the prevalence of exposure and available technologies for identifying exposure as well as current information regarding short- and long-term outcomes of exposed infants, with the aim of facilitating pediatricians in fulfilling their role in the promotion and maintenance of infant and child health.
Prevalence estimates for prenatal substance use vary widely and have been difficult to establish. Differences are likely attributable to such things as the use of different sampling methods and drug-detection methods, screening women in different settings, and obtaining data at different points in time. For example, prevalence will vary depending on whether history or testing of biological specimens is used; whether the biological specimen is hair, urine, or meconium; and whether the specimens are merely screened for drugs or screened and confirmed with additional testing. There also will be differences depending on whether the sample being investigated is a community sample or a targeted sample, such as women who are in drug treatment or are incarcerated. Lastly, prevalence must be interpreted in light of the fact that the use of specific drugs waxes and wanes over time nationwide as the popularity of certain substances changes.
Although a variety of prevalence studies have been conducted over the past 2 decades, there is 1 national survey that regularly provides information on trends in substance abuse among pregnant women. The National Survey on Drug Use and Health (formerly called the National Household Survey on Drug Abuse), sponsored by the Substance Abuse and Mental Health Services Administration (http://www.oas.samhsa.gov/nhsda.htm), is an annual survey providing national and state level information on the use of alcohol, tobacco, and illicit drugs in a sample of more than 67 000 noninstitutionalized people older than 12 years. Data are combined into 2-year epochs and include reported drug use for pregnant women between the ages of 15 and 44 years. Current illegal drug use among pregnant women remained relatively stable from 2007–2008 (5.1%) to 2009–2010 (4.4%). These average prevalence rates are significantly lower than reported current illicit drug use rates for nonpregnant women (10.9%). Importantly, the rate of current drug use among the youngest and possibly the most vulnerable pregnant women was highest (16.2% for 15- to 17-year-olds, compared with 7.4% among 18- to 25-year-olds and 1.9% among 26- to 44-year-olds). Table 1 summarizes these data along with information regarding current alcohol use, binge drinking, and cigarette use by pregnant and nonpregnant women. An additional important finding from this survey was that the rate of cigarette smoking for those 15 to 17 years of age actually was higher for pregnant women than for nonpregnant women (22.7% vs 13.4%, respectively). This report details many sociodemographic variables related to drug use in the American population, and the reader is referred to the Substance Abuse and Mental Health Services Administration Web site for the full report (http://www.oas.samhsa.gov/nhsda.htm).
Comparison of Drug Use Among Women 15 to 44 Years of Age by Pregnancy Status: 2009–2010
Identification of Prenatal Exposure
Two basic methods are used to identify drug users: self-report or biological specimens. Although no single approach can accurately determine the presence or amount of drug used during pregnancy, it is more likely that fetal exposure will be identified if a biological specimen is collected along with a structured interview.8
Self-reported history is an inexpensive and practical method for identifying prenatal drug exposure and is the only method available in which information can be obtained regarding the timing of the drug use during pregnancy and the amount used. Unfortunately, self-report suffers from problems with the veracity of the informant and recall accuracy.9,10 Histories obtained by trusted, nonjudgmental individuals or via computerized survey forms; questions referring back to the previous trimester or prepregnancy usage, not current use; and pregnancy calendars used to assist recollection each improve the accuracy of the information obtained.11–13
Several biological specimens can be used to screen for drug exposure. Each specimen has its own individual variations with regard to the window of detection, the specific drug metabolites used for identification, methods of adulteration of the sample, and analytical techniques, thus altering the sensitivity and specificity for each drug of interest. The most common analytical method used for screening biological specimens is an immunoassay designed to screen out drug-free samples. Threshold values generally are set high to minimize false-positive test results but may be too high to detect low-dose or remote exposure. Because immunoassay is a relatively nonspecific test, positive results require confirmation by using gas chromatography/mass spectrometry. In addition, confirmation of the presence of a drug is not always associated with drug abuse. Alternative explanations include passive exposure to the drug, ingestion of other products contaminated with the drug, or use of prescription medications that either contain the drug or are metabolized to the drug.14 Thus, careful patient histories remain essential to the process of identification.
The 3 most commonly used specimens to establish drug exposure during the prenatal and perinatal period are urine, meconium, and hair; however, none is accepted as a “gold standard.” Urine has been the most frequently tested biological specimen because of its ease of collection. Urine testing identifies only recent drug use, because threshold levels of drug metabolites generally can be detected in urine only for several days. A notable exception to this is marijuana, the metabolites of which can be excreted for as long as 10 days in the urine of regular users15 or up to 30 days in chronic, heavy users. Urine is a good medium as well for the detection of nicotine, opiate, cocaine, and amphetamine exposure.16,17
Meconium is also easy to collect noninvasively. It is hypothesized that drugs accumulate in meconium throughout pregnancy, and thus, meconium is thought to reflect exposure during the second and third trimester of pregnancy when meconium forms. However, use of meconium to determine the timing or extent of exposure during pregnancy is controversial18 because of a lack of studies regarding the effects of the timing and quantity of the postpartum specimen collection as well as the effects of urine or transitional stool contamination of the meconium samples.19 Meconium has been used for the detection of nicotine, alcohol, marijuana, opiate, cocaine, and amphetamine exposure.16,20
Hair is easy to collect, although some people decline this sampling method because of cosmetic concerns and societal taboos. Drugs become trapped within the hair and, thus, can reflect drug use over a long period of time. Unfortunately, using hair to determine timing and quantity of exposure also is controversial. In addition, environmental contamination, natural hair colors and textures, cosmetic hair processing, and volume of the hair sample available all affect the rational interpretation of the results.21–24 Hair is useful for the detection of nicotine, opiate, cocaine, and amphetamine exposure.16,25
Other biological specimens have been studied for use in the detection of in utero drug exposure but are not commonly used in the clinical setting. These include such specimens as cord blood, human milk, amniotic fluid, and umbilical cord tissue.8,19,26 In the case of umbilical cord tissue, drug class-specific immunoassays for amphetamines, opiates, cocaine, and cannabinoids appear to be as reliable as meconium testing, with the additional benefit of availability of the tissue at the time of birth.27
Beginning in the early 1980s, states began to enact legislation in response to the increasingly popular use of “crack” cocaine in our society. Such laws required the reporting of women who used drugs during pregnancy to the legal system through states’ child abuse statutes. In 2003, the Keeping Children and Families Safe Act (Public Law 108-36) was passed by Congress, requiring physicians to notify their state child protective services agency of any infant identified as affected by illegal substances at birth or experiencing drug withdrawal. Currently, issues of whether to use biological specimens to screen for drug abuse; whether to screen the mother, her infant, or both; and which women and infants to screen are issues complicated by legal, ethical, social, and scientific concerns. Each of these concerns must be taken into account as obstetricians, neonatologists, and pediatricians work to develop protocols for identifying prenatal drug exposure. For example, there is no biological specimen that, when obtained randomly, identifies prenatal drug use with 100% accuracy; hence, a negative drug screening result does not ensure that the pregnancy was drug free. Targeted screening of high-risk women is problematic, because it can be biased toward women of racial or ethnic minorities and those who are economically disadvantaged or socially disenfranchised. Universal screening of pregnant women is impractical and not cost-effective.28–30 Finally, testing of biological specimens when the maternal history is positive for drug use increases medical costs and does not necessarily provide information that guides the medical care of the infant.31
Mechanisms of Action of Drugs on the Fetus
Drugs can affect the fetus in multiple ways. Early in gestation, during the embryonic stage, drugs can have significant teratogenic effects. However, during the fetal period, after major structural development is complete, drugs have more subtle effects, including abnormal growth and/or maturation, alterations in neurotransmitters and their receptors, and brain organization. These are considered to be the direct effects of drugs. However, drugs also can exert a pharmacologic effect on the mother and, thus, indirectly affect the fetus. For example, nicotine acts on nicotinic cholinergic receptors within the mesolimbic pathway, and neuropathways activated by alcohol enhance inhibitory γ-aminobutyric acid (GABA) receptors and reduce glutamate receptor activity. Drugs of abuse mimic naturally occurring neurotransmitters, such that marijuana acts as anandamides, opiates act as endorphins, and cocaine and stimulants act within the mesolimbic dopaminergic pathways to increase dopamine and serotonin within the synapses.32 Other indirect effects of drugs of abuse on the fetus include altered delivery of substrate to the fetus for nutritional purposes, either because of placental insufficiency or altered maternal health behaviors attributable to the mother’s addiction. These altered behaviors, which include poor nutrition, decreased access/compliance with health care, increased exposure to violence, and increased risk of mental illness and infection, may place the fetus at risk.33
Nicotine concentrations are higher in the fetal compartment (placenta, amniotic fluid, fetal serum) compared with maternal serum concentrations.34–36 Nicotine is only 1 of more than 4000 compounds to which the fetus is exposed through maternal smoking. Of these, ∼30 compounds have been associated with adverse health outcomes. Although the exact mechanisms by which nicotine produces adverse fetal effects are unknown, it is likely that hypoxia, undernourishment of the fetus, and direct vasoconstrictor effects on the placental and umbilical vessels all play a role.37,38 Nicotine also has been shown to have significant deleterious effects on brain development, including alterations in brain metabolism and neurotransmitter systems and abnormal brain development.39–43 Additional toxicity from compounds in smoke, such as cyanide and cadmium, contribute to toxicity.44–48
Ethanol easily crosses the placenta into the fetus, with a significant concentration of the drug identified in the amniotic fluid as well as in maternal and fetal blood.49,50 A variety of mechanisms explaining the effects of alcohol on the fetus have been hypothesized. These include direct teratogenic effects during the embryonic and fetal stage of development as well as toxic effects of alcohol on the placenta, altered prostaglandin and protein synthesis, hormonal alterations, nutritional effects, altered neurotransmitter levels in the brain, altered brain morphology and neuronal development, and hypoxia (thought to be attributable to decreased placental blood flow and alterations in vascular tone in the umbilical vessels).51–69
Although the main chemical compound in marijuana, δ-9-tetrahydrocannabinol (THC), crosses the placenta rapidly, its major metabolite, 11-nor-9-carboxy-THC, does not.70 Unlike other drugs, the placenta appears to limit fetal exposure to marijuana, as fetal THC concentrations have been documented to be lower than maternal concentrations in studies of various animal species.15,70–72 The deleterious effects of marijuana on the fetus are thought to be attributable to complex pharmacologic actions on developing biological systems, altered uterine blood flow, and altered maternal health behaviors.73–75 Similar to other drugs, marijuana has been shown to alter brain neurotransmitters as well as brain biochemistry, resulting in decreased protein, nucleic acid, and lipid synthesis.74,76–79 Marijuana can remain in the body for up to 30 days, thus prolonging fetal exposure. In addition, smoking marijuana produces as much as 5 times the amount of carbon monoxide as does cigarette smoking, perhaps altering fetal oxygenation.80
In humans, opiates rapidly cross the placenta, with drug equilibration between the mother and the fetus.81 Opiates have been shown to decrease brain growth and cell development in animals, but studies of their effects on neurotransmitter levels and opioid receptors have produced mixed results.82–89
Pharmacologic studies of cocaine in animal models using a variety of species have demonstrated that cocaine easily crosses both the placenta and the blood-brain barrier and can have significant teratogenic effects on the developing fetus, directly and indirectly.90 Cocaine’s teratogenic effects most likely result from interference with the neurotrophic roles of monoaminergic transmitters during brain development,91–94 which can significantly affect cortical neuronal development and may lead to morphologic abnormalities in several brain structures, including the frontal cingulate cortex.94 It also appears that the development of areas of the brain that regulate attention and executive functioning are particularly vulnerable to cocaine. Thus, functions such as arousal, attention, and memory may be adversely affected by prenatal cocaine exposure.89,91,95–97 Furthermore, insults to the nervous system during neurogenesis, before homeostatic regulatory mechanisms are fully developed, differ from those on mature systems. Thus, cocaine exposure occurring during development of the nervous system might be expected to result in permanent changes in brain structure and function, which can produce altered responsiveness to environmental or pharmacologic challenges later in life.98
Methamphetamine is a member of a group of sympathomimetic drugs that stimulate the central nervous system. It readily passes through the placenta and the blood-brain barrier and can have significant effects on the fetus.99–101 After a single dose of methamphetamine to pregnant mice, levels of substance in the fetal brain were found to be similar to those found in human infants after prenatal methamphetamine exposure, with accumulation and distribution of the drug most likely dependent on the monoaminergic transport system. It is possible that the mechanism of action of methamphetamine is an interaction with and alteration of these neurotransmitter systems in the developing fetal brain100 as well as alterations in brain morphogenesis.102
Medical Issues in the Newborn Period
Fetal tobacco exposure has been a known risk factor for low birth weight and intrauterine growth restriction for more than 50 years,103 with decreasing birth weight shown to be related to the number of cigarettes smoked.104–107 Importantly, by 24 months of age, most studies no longer demonstrate an effect of fetal tobacco exposure on somatic growth parameters of prenatally exposed infants.108-114 Growth restriction is 1 of the hallmarks of prenatal alcohol exposure and must be present to establish a diagnosis of fetal alcohol syndrome.3,115 However, even moderate amounts of alcohol use during pregnancy is associated with a decrease in size at birth.116–119 In general, marijuana has not been associated with fetal growth restriction, particularly after controlling for other prenatal drug exposures.109,120-122 Fetal growth effects are reported in studies of prenatal opiate exposure; however, confounding variables known to be associated with poor growth, such as multiple drug use and low socioeconomic status, were not well controlled in many of the studies.123 Using data from the Maternal Lifestyle Study, Bada et al124 reported lower birth weight in opiate-exposed newborn infants born at ≥33 weeks’ gestation, independent of use of other drugs, prenatal care, or other medical risk factors. An independent effect of prenatal cocaine exposure on intrauterine growth has been the most consistent finding across studies of prenatally exposed infants.122,125-130 Early studies on prenatal methamphetamine exposure131 as well as recent studies132 reveal independent effects of the drug on fetal growth. However, the literature available is limited at this time. Several reviews on the effects of prenatal drug exposure on growth contain additional details.133–135
Nicotine has been associated with oral facial clefts in exposed newborn infants,136–140 although the data are relatively weak. There is a vast literature on the teratogenic effects of prenatal alcohol exposure after the first description of fetal alcohol syndrome in 1973.3 The American Academy of Pediatrics (AAP) policy statement “Fetal Alcohol Syndrome and Alcohol-Related Neurodevelopmental Disorders” contains more information.141 No clear teratogenic effect of marijuana or opiates is documented in exposed newborn infants.142 Original reports regarding cocaine teratogenicity have not been further documented.133,143 Studies of fetal methamphetamine exposure in humans are limited. However, Little et al131 reported no increase in the frequency of major anomalies in a small sample of exposed infants when compared with nonexposed infants.
No convincing studies are available that document a neonatal withdrawal syndrome for prenatal nicotine exposure. Although several authors describe abnormal newborn behavior of exposed infants immediately after delivery, the findings are more consistent with drug toxicity, which steadily improves over time,144,145 as opposed to an abstinence syndrome, in which clinical signs would escalate over time as the drug is metabolized and eliminated from the body. There is 1 report of withdrawal from prenatal alcohol exposure in infants with fetal alcohol syndrome born to mothers who drank heavily during pregnancy,146 but withdrawal symptoms have not been reported in longitudinal studies available in the extant literature. Neonatal abstinence symptoms have not been observed in marijuana-exposed infants, although abnormal newborn behavior has been reported with some similarities to that associated with narcotic exposure.147 An opiate withdrawal syndrome was first described by Finnegan et al148 in 1975. Neonatal abstinence syndrome includes a combination of physiologic and neurobehavioral signs that include such things as sweating, irritability, increased muscle tone and activity, feeding problems, diarrhea, and seizures. Infants with neonatal abstinence syndrome often require prolonged hospitalization and treatment with medication. Methadone exposure has been associated with more severe withdrawal than has exposure to heroin.149 Early reports regarding buprenorphine, a more recent alternative to methadone, suggest minimal to mild withdrawal in exposed neonates. A large multicenter trial evaluating buprenorphine’s effect on exposed infants documented decreased morphine dose, hospital length of stay, and length of treatment.150–152 There has been no substantiation of early reports regarding cocaine withdrawal.153 Currently, no prospective studies of withdrawal in methamphetamine-exposed infants are available. A retrospective study by Smith et al154 reported withdrawal symptoms in 49% of their sample of 294 methamphetamine-exposed newborn infants. However, only 4% required pharmacologic intervention. The AAP clinical report on neonatal drug withdrawal contains in-depth information on neonatal drug withdrawal, including treatment options.155
Abnormalities of newborn neurobehavior, including impaired orientation and autonomic regulation156 and abnormalities of muscle tone,144,147,157 have been identified in a number of prenatal nicotine exposure studies. Poor habituation and low levels of arousal along with motor abnormalities have been identified in women who drank alcohol heavily during their pregnancy.80,158 Prenatal marijuana exposure is associated with increased startles and tremors in the newborn.120 Abnormal neurobehavior in opiate-exposed newborn infants is related to neonatal abstinence (see earlier section on Withdrawal). Using the Brazelton Newborn Behavioral Assessment Scale,159 reported effects of prenatal cocaine exposure on infants have included irritability and lability of state, decreased behavioral and autonomic regulation, and poor alertness and orientation.160 Recent data from the Infant Development, Environment, and Lifestyle multicenter study on the effects of prenatal methamphetamine exposure documented abnormal neurobehavioral patterns in exposed newborn infants consisting of poor movement quality, decreased arousal, and increased stress.161
Few sources are available documenting the prevalence of drug use during breastfeeding. Lacking recent data, the 1988 National Maternal and Infant Health Survey (http://www.cdc.gov/nchs/about/major/nmihs/abnmihs.htm) revealed that the prevalence of drug use during pregnancy was comparable to the prevalence of use among women who breastfed their infants. Women who used various amounts of alcohol or marijuana and moderate amounts of cocaine during their pregnancy were not deterred from breastfeeding their infants. Thus, the pediatrician is faced with weighing the risks of exposing an infant to drugs during breastfeeding against the many known benefits of breastfeeding.162 For women who are abstinent at the time of delivery or who are participating in a supervised treatment program and choose to breastfeed, close postpartum follow-up of the mother and infant are essential.
For most street drugs, including marijuana, opiates, cocaine, and methamphetamine, the risks to the infant of ongoing, active use by the mother outweigh the benefits of breastfeeding, because most street drugs have been shown to have some effect on the breastfeeding infant.163–166 In addition, the dose of drug being used and the contaminants within the drug are unknown for most street drugs. Nicotine is secreted into human milk167,168 and has been associated with decreased milk production, decreased weight gain of the infant, and exposure of the infant to environmental tobacco smoke.169–171 Alcohol is concentrated in human milk. Heavy alcohol use has been shown to be associated with decreased milk supply and neurobehavioral effects on the infant.172–174 However, for nicotine and alcohol, the benefits of breastfeeding in the face of limited use of these drugs outweigh the potential risks. Marijuana has an affinity for lipids and accumulates in human milk,175 as can cocaine26 and amphetamines.101,165 Although the AAP considers the use of marijuana, opiates, cocaine, and methamphetamine to be a contraindication to breastfeeding, supervised methadone use not only is considered to be compatible with breastfeeding, with no effect on the infant or on lactation, but also is a potential benefit in reducing the symptoms associated with neonatal abstinence syndrome. Several available reviews provide more detailed information with regard to breastfeeding and substance abuse.162,176 The reader is also referred to the AAP policy statement “Breastfeeding and the Use of Human Milk.”177
Long-term Effects Related to Prenatal Drug Exposure
The effects of prenatal tobacco exposure on long-term growth are not clear-cut. Reports in the literature of effects on height and weight178–181 have not been substantiated by research teams able to control for other drug use in the sample.109,117,182,183 Recent studies, some of which include adolescents, have suggested that the effect on growth might be attributable to a disproportionate weight for height, such that prenatally exposed children were more likely to be obese as evidenced by a higher BMI, increased Ponderal index, and increased skinfold thickness.113,183,184 A robust and extensive literature is available documenting the effects of prenatal alcohol exposure on long-term growth. Although poor growth is 1 of the hallmarks of fetal alcohol syndrome, it is the least sensitive of the diagnostic criteria.185 No independent effect of prenatal marijuana exposure on growth has been documented throughout early childhood and adolescence.109,182,184 Long-term effects on growth have not been documented in the opiate-exposed child.186 The available literature on the effect of prenatal cocaine exposure on growth throughout childhood is not conclusive. Although several studies document the negative effects of prenatal cocaine exposure on postnatal growth,187–189 others do not.126,190,191 No studies are available linking prenatal methamphetamine exposure to postnatal growth problems. However, 1 study of unspecified amphetamine use suggests that in utero exposure may be associated with poor growth throughout early childhood.192
After controlling for a variety of potentially confounding socioeconomic, psychosocial, family, and health variables, a number of studies have identified independent effects of prenatal tobacco exposure on long-term behavioral outcomes extending from early childhood into adulthood. For example, impulsivity and attention problems have been identified in children prenatally exposed to nicotine.193–195 In addition, prenatal tobacco exposure has been associated with hyperactivity196 and negative197 and externalizing behaviors in children,198–200 which appear to continue through adolescence and into adulthood in the form of higher rates of delinquency, criminal behavior, and substance abuse.201–206 Prenatal alcohol exposure is linked with significant attention problems in offspring207–210 as well as adaptive behavior problems spanning early childhood to adulthood.211 Problems identified included disrupted school experiences, delinquent and criminal behavior, and substance abuse. Kelly et al212 published an in-depth review of the effects of prenatal alcohol exposure on social behavior. Inattention and impulsivity at 10 years of age have been associated with prenatal marijuana exposure.213 Hyperactivity and short attention span have been noted in toddlers prenatally exposed to opiates,214 and older exposed children have demonstrated memory and perceptual problems.215 Caregiver reports of child behavior problems in preschool-aged216 and elementary school-aged children217,218 have not been related to cocaine exposure, except in combination with other risk factors.219–221 However, in longitudinal modeling of caregiver reports at 3, 5, and 7 years of age, the multisite Maternal Lifestyles Study revealed that prenatal cocaine exposure had an independent negative effect on trajectories of behavior problems.222 There have been teacher reports of behavior problems in prenatally exposed children,223 although again, findings have not been consistent across studies,190 and some have been moderated by other risks.224 There also have been reports in this age group of deficits in attention processing190 and an increase in symptoms of attention-deficit/hyperactivity disorder and oppositional defiant disorder self-reported by the exposed children.217,218 To date, no studies are available that link prenatal methamphetamine exposure with long-term behavioral problems. However, 1 study of unspecified amphetamine use during pregnancy suggests a possible association with externalizing behaviors and peer problems.225,226
The link between prenatal nicotine exposure and impaired cognition is not nearly as strong as the link with behavioral problems. However, studies of both young and older children prenatally exposed to nicotine have revealed abnormalities in learning and memory227,228 and slightly lower IQ scores.201,229–231 Prenatal alcohol exposure frequently is cited as the most common, preventable cause of nongenetic intellectual disability. Although IQ scores are lower in alcohol-exposed offspring,207,232 they can be variable. Additionally, prenatal alcohol exposure has been associated with poorer memory and executive functioning skills.233 Marijuana has not been shown to affect general IQ, but it has been associated with deficits in problem-solving skills that require sustained attention and visual memory, analysis, and integration230,231,234–236 and with subtle deficits in learning and memory.237 Longitudinal studies of prenatal opiate exposure have not produced consistent findings with regard to developmental sequelae. Although developmental scores tend to be lower in exposed infants, these differences no longer exist when appropriate medical and environmental controls are included in the analyses.238–240 With little exception,241 prenatal cocaine exposure has not predicted overall development, IQ, or school readiness among toddlers, elementary school-aged children, or middle school-aged children.190,242–250 However, several studies have revealed alterations in various aspects of executive functioning,221,241 including visual-motor ability,244 attention,251–253 and working memory.254 To date, limited data are available revealing an association between prenatal methamphetamine exposure and IQ.255
Poor language development in early childhood after prenatal nicotine exposure has been reported,227,256,257 as have poor language and reading abilities in 9- to 12-year-olds.258 Prenatal alcohol exposure has been shown to interfere with the development and use of language,259 possibly leading to long-term problems in social interaction.260 No effect of prenatal marijuana exposure on language development has been identified in children through 12 years of age.227,258 Subtle language delays have been associated with prenatal cocaine exposure.256,261,262 Currently, no data are available relating the prenatal use of opiates or methamphetamine to language development in exposed offspring.
The literature available evaluating academic achievement is limited. In nicotine-exposed children, Batstra et al200 identified poorer performance on arithmetic and spelling tasks that were part of standardized Dutch achievement tests. Howell et al232 reported poorer performance in mathematics on achievement tests in adolescents who had been exposed prenatally to alcohol. Streissguth et al263 describe a variety of significant academic and school problems related to prenatal alcohol exposure, primarily associated with deficits in reading and math skills throughout the school years.263–266 Prenatal marijuana exposure has been associated with academic underachievement, particularly in the areas of reading and spelling.267 School achievement is not an area that has been studied adequately with regard to prenatal opiate exposure. Reported effects of cocaine exposure on school achievement are variable. In the longitudinal Maternal Lifestyle Study, 7-year-old children with prenatal cocaine exposure had a 79% increased odds of having an individualized educational plan (adjusted for IQ),268 and Morrow et al249 found 2.8 times the risk of learning disabilities among children with prenatal cocaine exposure compared with their peers who were not exposed to drugs prenatally. However, other studies do not support significant cocaine effects on school achievement.190,269 No data are available for the effects of methamphetamine on school achievement. Cernerud et al270 reported on 65 children prenatally exposed to amphetamines. At 14 to 15 years of age, the children in their cohort scored significantly lower on mathematics tests than did their classmates who were not exposed to amphetamines prenatally and had a higher rate of grade retention than the Swedish norm.
Predisposed to Own Drug Use
A limited number of studies are available that have investigated the association between prenatal substance exposure and subsequent drug abuse in exposed offspring. These studies did not document cause and effect, and it remains to be determined how much of the association can be linked to prenatal exposure versus socioeconomic, environmental, and genetic influences. Studies available for prenatal nicotine exposure suggest an increased risk of early experimentation271 and abuse of nicotine in exposed offspring.272,273 Brennan et al274 reported an association of prenatal nicotine exposure with higher rates of hospitalization for substance abuse in adult offspring. Mounting clinical data support an increased risk of ethanol abuse later in life after prenatal exposure.275,277 Prenatal marijuana exposure has been associated with an increased risk for marijuana and cigarette use in exposed offspring.273 Insufficient data are available to draw any conclusions relative to the affects of prenatal opiate, cocaine, or methamphetamine exposure on the risk for tobacco, problem alcohol, or illicit drug use later in life.
Although methodologic differences between studies and limited data in the extant literature make generalization of the results for several of the drugs difficult, some summary statements can be made by using the current knowledge base (Table 2).
The negative effect of prenatal nicotine exposure on fetal growth has been known for decades; however, longitudinal studies do not reveal a consistent effect on long-term growth. Clinical studies have failed to reach a consensus regarding congenital anomalies, and there is no evidence of a withdrawal syndrome in the newborn infant. Recent studies document a negative effect of prenatal exposure on infant neurobehavior as well as on long-term behavior, cognition, language, and achievement.
Alcohol remains the most widely studied prenatal drug of abuse, and the evidence is strong for fetal growth problems, congenital anomalies, and abnormal infant neurobehavior. There has been no convincing evidence of a neonatal withdrawal syndrome. Ongoing longitudinal studies continue to document long-term effects on growth, behavior, cognition, language, and achievement, and alcohol is the most common identifiable teratogen associated with intellectual disability.
Although there have been studies revealing subtle abnormalities in infant neurobehavior related to prenatal marijuana exposure, there have been no significant effects documented for fetal growth, congenital anomalies, or withdrawal. Long-term studies reveal effects of prenatal exposure on behavior, cognition, and achievement but not on language or growth.
The most significant effect of prenatal opiate exposure is neonatal abstinence syndrome. There have been documented effects on fetal growth (but not on long-term growth) and infant neurobehavior as well as long-term effects on behavior. There is not a consensus as to the effects of prenatal opiate exposure on cognition, and few data are available regarding language and achievement.
Prenatal cocaine exposure has a negative effect on fetal growth and subtle effects on infant neurobehavior. However, there is little evidence to support an association with congenital anomalies or withdrawal. There is not a consensus regarding the effects of prenatal cocaine exposure on either long-term growth or achievement; however, there are documented long-term effects on behavior and subtle effects on language. Although there is little evidence to support an effect on overall cognition, a number of studies have documented effects on specific areas of executive function.
Studies on prenatal methamphetamine exposure are still in their infancy. Early studies have documented an effect of prenatal exposure on fetal growth and infant neurobehavior but no association with congenital anomalies and no data regarding infant withdrawal or any long-term effects.
Summary of Effects of Prenatal Drug Exposure
Marylou Behnke, MD
Vincent C. Smith, MD
Committee on Substance Abuse, 2012–2013
Sharon Levy, MD, Chairperson
Seth D. Ammerman, MD
Pamela Kathern Gonzalez, MD
Sheryl Ann Ryan, MD
Lorena M. Siqueira, MD, MSPH
Vincent C. Smith, MD
Past Committee Members
Marylou Behnke, MD
Patricia K. Kokotailo, MD, MPH
Janet F. Williams, MD, Immediate Past Chairperson
Vivian B. Faden, PhD – National Institute on Alcohol Abuse and Alcoholism
Deborah Simkin, MD – American Academy of Child and Adolescent Psychiatry
Committee on Fetus and Newborn, 2012–2013
Lu-Ann Papile, MD, Chairperson
Jill E. Baley, MD
William Benitz, MD
Waldemar A. Carlo, MD
James J. Cummings, MD
Eric Eichenwald, MD
Praveen Kumar, MD
Richard A. Polin, MD
Rosemarie C. Tan, MD, PhD
Kasper S. Wang, MD
FORMER COMMITTEE MEMBER
Kristi L. Watterberg, MD
CAPT Wanda D. Barfield, MD, MPH – Centers for Disease Control and Prevention
Ann L. Jefferies, MD – Canadian Pediatric Society
George A. Macones, MD – American College of Obstetricians and Gynecologists
Erin L. Keels APRN, MS, NNP-BC – National Association of Neonatal Nurses
Tonse N. K. Raju, MD, DCH – National Institutes of Health
This document is copyrighted and is property of the American Academy of Pediatrics and its Board of Directors. All authors have filed conflict of interest statements with the American Academy of Pediatrics. Any conflicts have been resolved through a process approved by the Board of Directors. The American Academy of Pediatrics has neither solicited nor accepted any commercial involvement in the development of the content of this publication.
The guidance in this report does not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.
All technical reports from the American Academy of Pediatrics automatically expire 5 years after publication unless reaffirmed, revised, or retired at or before that time.
My cocaine addiction left me deranged, delusional and on the brink of death. It took 10 years and four stints in rehab before I got sober
The author at home with her husband, Colin Hubley; her nine-month old daughter, Nolah; and her dog, Jean-Jacques Rousseau
The author at home with her husband, Colin Hubley; her nine-month old daughter; Nolah; and her dog, Jean-Jacques Rousseau
I was always an anxious kid. My earliest memories involve hopping over cracks on the sidewalk, counting out steps, tapping my foot quietly so that no one could hear and pulling the corners of my pillowcase several times before I could go to bed. Eventually I’d fall asleep and dream of death, destruction, kidnappings and roving gangs of thugs trying to hurt my family. I often awoke drenched in sweat.
There was no obvious reason for my perpetual unease. I grew up in a beautiful Forest Hill home, the second youngest of four siblings. My dad was a financial whiz who published a book on quantitative marketing when he was 26 (I can barely understand a word of it) and then ran his own marketing firm. My mum stayed at home; she later got a PhD in sociology and worked as a consultant. For most of my childhood I attended private school at TFS and Branksome Hall. When I was 12, I switched to Deer Park Public School. I remember telling a friend that the rules of private school were suffocating me. Really, I was just sad. I always felt uncomfortable in my own skin.
At Deer Park, my academic performance slid but my confidence grew. To my classmates, I was exotic: a private school refugee. My parents had recently divorced, and I started acting out. I began drinking and smoking pot every weekend, getting blitzed and messing around with random guys. When I started high school at North Toronto Collegiate the next year, it quickly devolved into something else entirely. My friends and I would drop acid all weekend. Soon I was cutting weeks of school and committing petty crimes—I’d shoplift, steal subway signs, and pocket CDs, clothes and books from house parties. My parents were stressed and exhausted. They would have done anything to help, although it didn’t feel that way to me. I told them I hated them on a regular basis. When they sent me to therapists, I told them I hated them, too.
I was having the time of my life. I was cool. I was outrageous. Every time I’d drink, I’d lose chunks of time: two hours here, an hour there. Booze and drugs did something to me that I couldn’t do for myself. They changed me, if only for a moment, and the promise of that moment was too alluring to resist.
I started dating my friend Adam in the summer before Grade 12. He gave me all the love, attention, kindness and understanding I’d been craving. After high school I started at McGill. We rented a place together in Montreal, on Avenue des Pins. I introduced him to Woody Allen movies. He taught me about jazz, literature and how to wear a black baseball hat with every outfit. My parents thought Adam was a stabilizing influence. They were grateful.
But they didn’t know we were doing drugs every weekend: coke, E and most of all speed. I don’t know what was in it, but the dealers called it “peaches.” We partied at Sona, one of Montreal’s first mega–dance clubs. The dealers were always sporty-looking dudes in Tommy Hilfiger, leaning casually against the walls. They’d throw me a pill for $30, and then I’d dance for the next 14 hours straight, drenched in sweat, biting my lips and chewing the inside of my cheek. After each peaches binge, I’d spend three days huddled in withdrawal—but I’d still go back for more. My weight dropped from 125 pounds to a gamine 110, and everyone told me I looked great. I never went to class, just crammed for exams, and somehow I secured a B+ average. (I’ve always had a strange talent for bullshitting my way through school.) To everyone else, my life looked manageable.
A year and a half later, Adam and I broke up. I wanted to go clubbing all the time. I wanted to wear skimpy clothes and do lines off toilets in black-lit washrooms. I wanted powerful men to want me. I wanted to feel alive. Adam wanted something I couldn’t give him: purpose and direction. He wanted to settle down. It didn’t work—six months later, he killed himself. I had spoken to him a few days before, and we were planning to get together for my birthday on October 5 in Toronto. I arrived at my mum’s to see all the lights on, despite the fact that it was 10 p.m. I thought, selfishly, They’re throwing me a surprise party. It turns out my friends had gathered at my house to tell me about Adam.
After his death, I stayed in Toronto and transferred to U of T. My dad rented me a ground-floor apartment in a house in the Annex. I would sit by candlelight reading and rereading the torn, tear-stained letters Adam had written me over the years. I started using coke more frequently. I didn’t have a regular dealer yet—my friends always had a connection, so I’d throw them some cash and take whatever I needed. I was kicked out of every bar on College Street for harassing patrons. Once, at the Midtown, I tried to request a song and the bartender told me to step back or else. Provoked, I pivoted my foot into his space, tapping it in and out again, taunting him. “Out!” he screamed. Two bouncers had to toss me on my backside. I shook it off and bounced on to another bar down the street.
My last functional period came in my early 20s, when I got a job as an assistant editor at a fashion magazine. By this time I had access to a trust fund my dad had set up. I’d used some of it to buy myself a Yorkville condo, and my dad invested the rest for me. I wasn’t supposed to touch it, but of course I did: I liquidated shares like other people take out 20s from an ATM. I was bingeing on cocaine every few nights, yet somehow I was able to get to work on time and focus. I’d cap the night at 1 a.m. and sink myself to sleep with a couple of shots of Jack and a tab or two of Ativan. In the morning, I’d drink a few Red Bulls and I was good to go.
As my drug use skyrocketed, I began to get paranoid. Every night at the bar, I’d wonder if people were talking about me. Did my colleagues at the magazine know what was going on? Did the police know about the drugs I had on me? As the sweat crept up my neck, I’d drown it with more shots.
I began to think about leaving the magazine and going back to school. In retrospect, I was probably worried, if only subconsciously, that my bingeing would catch up to me at a 9-to-5 job. I became convinced I belonged in academia, and, in September 2005, I began a master’s degree in political theory at U of T. In the academic world I was on terra firma—I was writing papers, reading Rousseau and even attending half my classes, which was a big improvement from my undergrad days. The rest of the time, I was partying.
It was during this period that I first met Javier. (I’ve changed his name and a few others, to protect their identities.) He was my age and portly, with a sibilant Spanish accent. We would see each other at parties and I’d buy a gram of coke from him, sometimes two. Most users make two grams last a couple of days. I went through it in a few hours. I started buying two eight balls at a time, or seven grams of powder, for around $400, which I would snort in a 24-hour period. I used compulsively and immoderately, and I wore it on my face like a clown mask. My skin was pale grey, my pupils perpetually dilated. I was jittery, my mannerisms were spastic, my dialogue was jumpy and curse-laden. I was calling Javier all the time. And finally, after a month, he told me I was too high maintenance and never to bother him again. I had been fired by my drug dealer.
But he’d introduced me to a number of other dealers—and, because addicts always find a way, I soon had a regular roster, so that there was a steady supply and no one dealer would ever know how much I was using. I don’t know exactly what that amount was. I just know I never bought less than an eight ball, and often I would re-up several times over the course of a binge. I was snorting so much coke that I burned holes in my nose.
A typical day went like this: I’d wake up from a binge, sometimes in the morning and sometimes at night, and call one of my dealers—D’Angelo, for example. In the hour it took him to get to my place, I’d go to the LCBO and buy a couple of 26ers of vodka, a few bottles of prosecco, maybe some Jack Daniel’s. D’Angelo would arrive, we’d slam back some drinks, do some coke, play some music, joke around and have a few other people over. He nicknamed me Hollywood because of my appetite for massive lines. Eventually, D’Angelo would leave to go sell to other customers, and, if I ran out (which I always did), I’d call the next guy on my list. And so, for a while, everything was great—a shallow and reckless parade of party people. I thought I was Holly Golightly and that my life was Breakfast at Tiffany’s. Some days I wanted to stop, but I didn’t think I could.
I finished my degree, just barely. And that’s when the partying ceased. My paranoia got so bad that I was convinced the police were coming for me. I shut everyone out of my life and refused to speak to my parents for months at a time. The only people I talked to were my dealers, and even they were desperate to get away from me right after selling me the blow. I was alone most of the time, except for the pigeons that used to fly into my apartment when I left the balcony door open. And so I just used—all day and all night. It was all I could think about.
My body started to deteriorate. My skin bruised easily from lack of sleep and I had deep circles under my eyes. My hands and feet swelled to the size of balloons. Once, I mistakenly applied pink nail polish under my eyes thinking it was concealer. I chopped my hair off into a white-blonde pixie faux-hawk, and wore tank tops with men’s ties, booty shorts and Vans. I’d stay awake for days at a time, sometimes for a full week. I never ate when I was using, and I drank only alcohol—water, juice and pop made me sick. I guzzled olive oil for calories, and sometimes, to clear my clogged sinuses, I would drink Frank’s RedHot straight out of the bottle. It burned my mouth and eyes, but the shock would do the trick: I could stop blowing my nose and blow lines instead. By this time I weighed 102 pounds. I kept thinking that I would spontaneously return to my previous self—when I was using less, when I felt validated and happy, when my life seemed exciting and glamorous.
My paranoia descended into full-fledged psychosis. I suspected that everyone was on drugs—my neighbours, the concierge in my building, the barista at Starbucks. I saw men pointing machine guns at me from the shadows in the corner of my living room. When I watched TV, I thought the shows were trying to tell me something: characters on a kids’ cartoon would say “Jump!” and I would jump; they would say “Touch your nose,” and I’d touch my nose. One day, a dealer I was seeing told me to go out on the balcony of my condo, that a plane was coming to save me from this hell I was living. I gingerly made my way to the balcony and slid open the door, wanting to make him happy. I stepped into the cool night air and tried to climb over the railing. As I started my descent, he screamed, and rushed outside and grabbed me: he’d told me no such thing. I had hallucinated the conversation.
Seasons floated by. Over the winter of 2006, I only emerged from my condo a few times. When I left one day in the spring, I was shocked to discover the steel skeleton of the Michael Lee-Chin Crystal at the ROM. It seemed to have appeared out of nowhere. My parents were hysterical—they were constantly calling me and dropping by, but I ignored them. I still had some of the money my father had given me, and as long as I did, who needed them?
When I was 26, I met a guy I’ll call Jesse at the Comfort Zone, a thumping after-hours club at College and Spadina. After one night, we were inseparable. Whatever I thought I knew about drug use, it was nothing compared to him. He introduced me to GHB and taught me how to do coke in ways I would never have imagined, like dissolving the powder in shots of Jack Daniel’s and drinking until we went into convulsions. Or snorting an entire gram in a single line. Or swallowing so much GHB that we were crawling around the club, salivating like animals.
Jesse moved into my condo just a few weeks after we met. When we’d fight, he’d smash mirrors and throw vases at my head, then scream at me to clean up the mess. We travelled to Costa Rica, Mexico, Israel, Italy, Hungary, desperately trying to escape ourselves. At the end of 2006, we spent a sombre Christmas night at the Comfort Zone. It was my first real moment of clarity. The whole time I was sullen and depressed, thinking about my family. I loved them, but it was buried so far beneath piles of lies and years of equivocation that sometimes I hardly remembered they existed.
Two weeks later, Jesse and I went over to his parents’ house for his birthday dinner. As soon as the door opened, I knew something was up. His dad was standing in front of us, and beyond him I saw his family waiting; my family was there too. It was a double intervention. Jesse was willing to stay, but I was furious. I gave my family members 15 minutes to read letters, then freaked out: I wasn’t going to be judged by them or anyone. I demanded that they stay out of my life and bolted out the front door. When I got outside, I took out my phone and called one of my dealers.
I knew then that I was really alone. My dealers wouldn’t go near my place, which looked more like a crack den than a luxury Yorkville condo. They made me come to them, and I had to mentally prepare for hours before I could get up the courage to go outside. It was like training for the Olympics. I once got lost walking around the old Four Seasons, trying to find the room my dealer had said he was in. A guest called security, and two thick guards had to toss me out of the hotel. Apparently guests were disturbed that this emaciated waif-like creature was walking around unsupervised, either completely high or completely mad.
My family still called every week; they tried to find out what was going on with me by asking the concierge or people in my building. Once, after holing up for days in my apartment, I found my way to my dad’s and banged on his door, wailing that I needed help. But when he tried to get me to talk, I brushed him off. I said it wasn’t serious.
I finally agreed to go to rehab in the summer of 2007. I flew to L.A. and checked into Promises, a high-end treatment centre that cost my dad $90,000 for a month-long stay. He was thrilled that I was seeking help. I hoped I might find a career as an actress—who knows who I would meet at a treatment centre in California? My capacity for self-deception would have been funny if it weren’t so tragic. There I was in Malibu, wearing a bloodstained Ralph Lauren sweater, my bleached blonde hair in an overgrown faux-hawk, hoping to be “discovered.” I had no idea how delusional I was.
The treatment centre was a sprawling set of lodges overlooking the Pacific Ocean. It housed roughly two dozen patients at a time. The first thing I did was collapse on my bed and sleep for three days straight. When I finally woke up, I saw two sets of eyes peering at me. “I’m Lydia,” one girl said. “And I’m Jen,” said the other. “And you’re in Lindsay Lohan’s old bed. She just left.” At Promises, I went to every meeting, talked earnestly to my counsellor, exercised, learned to meditate, and took part in group therapy and psychodrama, a technique where addicts use role-play to work through their issues. Still, I wasn’t getting better. All I could think about was getting home and getting high. Which I promptly did, the moment I landed.
The next few years were a dizzying sea of hallucinations, loneliness and desperate attempts at detox. I sold my condo to pay for drugs and went through the proceeds in nine months. My dad, ever supportive, rented me an apartment. Anytime I asked for help, my parents would intervene and send me to another treatment centre, hoping something would stick. I was at Women’s Own in Toronto, on Dundas, where I slept on a cot. Then came Bellwood, in Scarborough, where I lasted three days before they kicked me out for fooling around with another patient. I went to treatment in Minnesota, where I dismissed the notion of addiction to such a point that I was asked to leave after 10 days because I was undermining the recovery of other people. They told me they had never seen someone so deep in denial. One time, I was so high that I sat cross-legged in the middle of the intersection at Bay and Bloor, stopping traffic. The police took me to Mount Sinai, and later I was sent to CAMH. I checked myself out after a few days.
By the time I was 30, in 2010, I was on my fourth stint in rehab, this time on an island off the coast of Vancouver. It was beautiful and forlorn, with winding streets that climbed up long hills dotted with little cabins. The treatment didn’t take. With each passing day, I was getting noticeably worse—edgier, angrier, agitated and frustrated. After 30 days, I willingly and optimistically moved into “extended” care, which was the midway point between primary care and sober living in society. My family came and we went to group therapy together, but I could tell that whatever was supposed to be happening wasn’t.
I had always assumed that drugs and alcohol were my problem, and that everything would be okay as soon as I got sober. By then, I’d realized that the crux of my addiction was bigger than bad behaviour. It was my thinking: the way I made the world completely about me and my sadness and my hate and my anger, to the point that anything good was completely obscured by my narcissism. Instead of realizing I was hurting my family, I could only complain that if it weren’t for their interventions, we would have a good relationship—that they should let me do what I wanted. It didn’t matter that half the time I begged them to intervene. I couldn’t see it.
I was even more miserable sober than I was when I used. I couldn’t sit still. I was feverish all the time. Without drugs, I became addicted to controlling my weight, and developed a form of exercise bulimia, where I’d eat entire boxes of cookies and run for hours to burn off the calories. I told the counsellors I was getting worse. They encouraged me to stop focusing on the negative—that I was giving new patients the impression that their program didn’t work.
A few days before my treatment was over, I relapsed. I went to a bar in Vancouver, downed a few shots of JD and found a coke dealer within minutes. I snorted a ton that night. I missed curfew, and bought clean urine from the dealer’s mom so I could pass the drug test at rehab. The counsellors busted me the next morning, and, three days later, my dad put me on a plane home to Toronto. I thought there was no saving me.
The turning point came in January 2011. On New Year’s Eve, I got so high on booze and coke that I ran into oncoming traffic on Eglinton. A taxi slammed the brakes but still hit me, and when the driver rushed out to check on me, I punched him and blacked out. Apparently, he called the police. I woke up hours later in a hospital room, handcuffed to a gurney, my legs in iron cuffs, surrounded by my father and a few police officers. I had no idea what had happened, but they filled me in. I passed out again after a few minutes and woke up in my apartment. The police had released me from custody, and my dad had driven me home. The next day he came to my place and gave me two options: I could either live sober in the apartment he paid for, or I could sleep on the streets.
A couple of weeks later, I was lying on the floor of my apartment, staring at the popcorn ceiling. My experience in that last treatment centre in Vancouver had made me realize that I was as sick sober as I was when using. I didn’t move for hours. I knew there might be enough change in my couch to buy a mickey, but I’d just down it in one go. At that moment, something strange happened to me. I’d never been a religious person, but I was flooded with a sense of serenity. I had no idea who I was or who I’d been, but suddenly I was convinced that God was there with me. I knew that no substance on earth could change me permanently. At some point I would always come back to being myself. It felt like the choice was simple. I called someone I knew was sober, who had tried to help me before. Her name was Margot. “I’m ready to quit,” I told her. My sober life began on that day.
Margot and I met three to four times a week to work on the 12 steps. I followed every direction she gave me. I prayed, I meditated, and if she had told me to stand naked on the 401, I would have done it. I joined her recovery group, arriving before each meeting to set up chairs and make coffee. I greeted people at the door and gave out my number to those women who were coming into recovery with even less clean time than me. I would call them and listen—if selfishness was my problem, compassion would be my solution.
I felt like I was 13 again, the person I was before I started using. I had to relearn everything—how to eat, how to sit at a table, how to have conversations without interrupting, how to speak without swearing. I slowly started to come back to life. I walked the city, often going out for two-, sometimes three-hour jaunts. My feet felt lighter. I was excited to go to sleep at night because it brought me eight hours closer to waking up again. Gone were the crippling paranoia, the self-loathing, the destructive impulses that had plagued me all my life. The LCBO seemed like a foggy memory, a distant place I used to go to for stuff I no longer wanted. I worked with other addicts and alcoholics, taking them through the steps. It wasn’t easy. They’d yell at me and sometimes steal money from me; they’d beg me to help them get sober so that they wouldn’t kill themselves. I took them to detoxes, and talked to their desperate mothers and friends in an effort to shed light on this debilitating illness.
Along the way I made amends to my family. It was a brutal experience—I can’t imagine the sleepless nights I caused my parents and siblings during my teens and 20s. To them, it was as though an alien had abducted me when I was 14 and never brought me back. Most of my relatives accepted my apologies, and were relieved and excited to see how much I’d changed. Now I have a great relationship with my parents. But to some of my family members, I’ll always be a drug addict.
A year and a half after getting sober, I applied to the Schulich School of Law at Dalhousie University. For my entrance essay, I wrote about my addiction—and I was accepted in September 2012. One of the professors even came to my yearly celebration of sobriety. During law school, I was open about my addiction, and people were curious but kind and encouraging. I was able to demonstrate to myself and others that someone can live in recovery and still have a gratifying professional and personal life.
While in Halifax, I met a hilarious, thoughtful man at a recovery meeting named Colin Hubley. We quickly fell in love. We married on August 20, 2014, and, nine months ago, I gave birth to our daughter, Nolah. She is the happiest baby I’ve ever seen. Colin and I spend our free time walking our dog, Jean-Jacques Rousseau, having dinner with our families and seeing our close friends, all of whom are in recovery.
I’ve lost a lot of friends in the past few years, people who weren’t able to overcome their addiction. Jamie, a good friend I’d met at CAMH, overdosed and died in the summer of 2014. My friends Danny and Jenn also passed away last year from drug and alcohol overdoses; both of them left small children and grieving families. And this fall I was buying a coffee at Queen and Jarvis when I ran into an ex-boyfriend who was panhandling at the corner for his next high. Most people think addiction is a series of progressively bad choices. That’s a myth: it’s an illness. In our society, we value people who can march forward and self-correct. Addiction is a stain on our ability to improve.
Last year, I finished law school and secured an articling position at a firm that specializes in social justice and advocacy work. My employer is not just accepting of my past but supportive of my decision to write about it. I want to go into criminal law. It won’t be easy or particularly lucrative, but everybody deserves a second chance. And a third, and a fourth. I believe that with a lot of work, anyone can turn their life around. Even me.