Substance Abuse During Pregnancy and Childhood (Drug and Alcohol Abuse Reviews)

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Illicit drugs are the most often targeted drugs in the fight against maternal substance abuse, because they are perceived to produce the most harmful side effects in both the mothers and the children. Whether this is true or not is a topic that is certainly up for debate.

As mentioned earlier, it is hard to pinpoint the exact prevalence of illegal drug use among pregnant women because figures are derived from self-reporting by the women or reporting by a physician. Figures on the frequency of illegal drug use among pregnant women range from , to , [ 85 , 86 ]. There are numerous birth complications attributed to illegal drug use, including pre-term delivery, low birth weight, smaller-than-normal head size, miscarriages, genital and urinary tract deformities, and nervous system damage [ 87 ].

For cocaine, we now know that early scientific reports were exaggerated, and portrayed children who were exposed to cocaine in utero as irreparably doomed and damaged [ 29 , 88 - 90 ]. Published studies on cocaine-exposed children suggest a pattern of small deficits in intelligence and moderate deficits in language [ 91 ]. Further, cocaine-exposed children at 6 years show deficits in academic skills including poor sustained attention, more disorganization, and less abstract thinking [ 92 - 94 ].

Research on prenatal marijuana exposure started slightly before the explosion of cocaine research in the s. Developmental effects on executive function have been reported in a study of 9—12 year olds [ 78 ].

Pregnant women with substance use disorders need treatment, not prison

However, despite the fact that marijuana is the most frequently abused illegal drug, it has not received the attention, as have other drugs, and there are calls for legalization and approval for medicinal use. Longitudinal studies of development in methamphetamine-exposed children are just beginning [ 95 ]. A lingering puzzle, especially with the cocaine literature, is the discrepancy between preclinical animal and clinical human studies.

There is substantial preclinical evidence that cocaine and other drugs of abuse are neuroteratogens that can produce serious abnormalities in brain development. More recent findings [ 96 ] suggest that the behavioral impact of such neural abnormalities that might occur in humans depends on other complex pre- and postnatal factors, which may also include genetic vulnerability.

Substance Abuse During Pregnancy and Beyond Conference 2013

We have seen how public understanding of the impact of prenatal exposure has lurched from an initial over-reaction in which drug-exposed children were characterized as irrevocably and irreversibly damaged to a perhaps equally premature excessive "sigh of relief" that drugs such as cocaine do not have lasting effects, especially if children are raised in appropriate environments. Exaggerated statements about the benign effects of cocaine as found in Frank et al. Infants exposed to drugs in utero may have a milder phenotype with appropriate environment input.

We need to understand combinations of biological including genetic predispositions and environmental conditions that result in normal development and what specific factors might promote resilience. The goal is to isolate the unique effects of the drug, typically by controlling other variables that could also explain child outcome [ 98 , 99 ]. This approach is based on our understanding of the mechanisms of action of ATID, as well as on preclinical and clinical studies, and enables us to study the potential pharmacological and toxic effects of the drugs per se.

The limitation of this approach is that it does not lend itself to study drug exposure as part of a developmental model in which the goal is to predict child outcome with ATID as one of many contributing factors. This is because behavioral teratology research designs typically treat environmental variables as potential confounding factors rather than as a primary focus for investigation [ ]. Developmental-ecological models have shown that many, if not most, child outcomes are due to multiple antecedent variables [ ].

Developmental models should also take into account the effects of polydrug exposure. Adverse MATID effects are thought to be due to mechanisms by which the drugs disrupt programs for brain development associated with alterations in brain structure and neuronal function that have unique behavioral consequences.

ATID freely cross the placenta and the developing fetal brain. However, in addition to these mechanisms specific to each drug, recent literature suggests a mechanism of action common to all drugs of abuse. Every drug of abuse appears to increase the levels of the neurotransmitter dopamine in the brain pathways that control pleasure.

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This explanation centers on activation of specific neural pathways that project from the pons and midbrain to more rostral forebrain regions, including the amygdala, medial prefrontal cortex, anterior cingulate cortex, ventral palladium, and subdivisions of the striatum, particularity the nucleus accumbens [ ]. This model of a final common pathway for all drugs of abuse is critical because, as documented earlier, most prenatal drug use is polydrug use.

Therefore, understanding these potential pathways will give us one model for understanding the developmental effects of polydrug use. Immediate drug effects are direct teratogenic consequences of MATID exposure and emerge during the first year before postnatal environmental effects become salient.

These effects may be transient, such as catch-up in physical growth or more long lasting, such as behavioral disregulation that is observed in infancy and persists through school age. Latent drug effects are also direct teratogenic effects but reflect brain function that becomes relevant later in development. There are two kinds of latent effects. First, MATID can affect brain function that does not manifest until children are older, including cognitive processes I.

By "predisposition" we mean an increase in risk that requires other conditions to be met. These conditions would be activated during school age when opportunities to use drugs arise, leading to early substance use onset. There is also evidence from the nicotine and alcohol literature for the biological basis of drug use in children, such that adolescent or childhood onset of substance use is related to prenatal exposure. Adolescents are more likely to smoke if their mothers smoked during pregnancy even after controlling for later maternal smoking [ - ].

Similar results have been reported for alcohol [ ]. In two cohorts Kandel [ ] found that adolescent girls are more likely to smoke if their mothers smoked during pregnancy even after controlling for postnatal maternal smoking.

Substance use during pregnancy

It was suggested that nicotine input to the dopaminergic system could predispose the brain to later addictive behavior. Therefore, prenatal exposure may be related to increased risk of substance abuse in the offspring. More recently, Weissman [ ] found a 4-fold increase of prepubertal-onset CD in boys and a 5-fold increased risk of adolescent onset drug dependence in girls whose mothers smoked during pregnancy, also unrelated to postnatal maternal smoking.

In a year follow-up, [ ] prenatal alcohol exposure was more predictive of adolescent alcohol use and its negative consequences than was family history of alcohol problems. Moderate to heavy maternal drinking during pregnancy was related to current drinking in daughters after controlling for current maternal drinking and child rearing practices.

Prenatal maternal smoking was also related to elevated rates of adolescent drinking [ ]. Therefore, drug exposure in utero may alter the brain in ways that increase the risk for later addiction. Postnatal environment effects include general environmental factors socio-demographics, care giving context and style, and caregiver characteristics that include both risk and protective factors.

Environmental risk factors are well established correlates of a variety of poor child outcomes including cognitive, social, psychological, school, and health problems that occur in both drug-using and non-drug using populations. MATID is associated with general psychosocial risk factors that compromise child outcome apart from substance abuse issues including poverty, [ , ] chaotic and dangerous lifestyles, [ , ] symptoms of psychopathology, [ - ] history of childhood sexual abuse, [ , ] and involvement in difficult or abusive relationships with male partners [ , ].

Pregnant women in substance abuse treatment show a high incidence of psychopathology [ ] including affective and personality disorders [ , ] and depressive symptoms [ , ]. Pregnant cocaine using women showed elevated levels of depression, general mental distress and more psychological symptoms postpartum [ ]. There are also specific aspects of the caregiving environment unique to AOD using mothers analogous to the well-documented literature on "children of alcoholics" COAs. Passive exposure to smoke is also a direct teratogenic effect that is also part of the environment [ 78 ].

Another problem with the behavioral teratology model is that as a deficit model it does not include protective or resiliency factors that buffer the child against adverse child outcome. Connectedness to others and intolerance of attitudes toward deviance were also highlighted by the Surgeon General Report [ ] on youth violence. Finally, the model includes the "development" arrow to indicate that development is a dynamic process.

Parental substance misuse and child abuse and neglect

Rather there are reciprocal causal relations between intra- and extra-individual factors that change over the course of development. We can say unequivocally that some children exposed to drugs in utero have learning and behavioral problems. Clearly in the case of cocaine the problem is not as severe as was once feared. We also know that environmental factors play a large role in determining the development of drug-exposed children. There is increasing evidence that amount of exposure makes a difference.

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This is well established for alcohol, for tobacco with respect to effects on birthweight, and the cocaine literature is just starting to study level of exposure. There is also some evidence that timing of exposure makes a difference, again especially for alcohol. Not all children who are exposed to drugs in utero show neurobehavioral deficits and those who are affected display a wide range of neurobehavioral effects.

The same drug, even at the same dose does not appear to produce the same deficits in all children. It is almost superfluous to say that advances over the coming years will provide a much clearer picture and deeper understanding of the long-term effects of prenatal drug exposure.