Mary McClure & Ally Satterlee
PSY 285
Dr. Jarcho
October 24, 2013
Understanding the Effects of Cocaine on Mothers and Infants
It is no surprise that an expecting mother’s cocaine use will have adverse effects on the
developing fetus. Such effects range from a smaller head size to delayed cognitive development
of the child later in life. These delays occur partly because cocaine is able to cross the placental
barrier and affect the fetus similarly to how it affects the mother. This paper explores the drug
itself, and more specifically its effects on the reproductive aged female population. It also
considers the consequences of prenatal exposure to cocaine and how stigma has developed
around the notion of “crack babies.” Recent research shows that much of these claims are not
well founded. While cocaine use is harmful to the developing fetus, other factors of the mother’s
use of the drug, such as her parenting style and socioeconomic status, are equally, if not more
significant.
Cocaine
Cocaine is derived from the leaves of Erythroxylon coca, which is native to South
America and has been used by natives since ancient times (Julien, 2001). Modern cocaine was
developed in 1855, when the active alkaloid from the leaf was isolated, and later in 1860,
purified (Julien, 2001). It was initially used for surgeries; doctors would use the drug as an
anesthesia until the early 1900’s (Julien, 2001).
Early in its conception, Sigmund Freud, the father of psychology, used, studied, and
prescribed cocaine (Julien, 2001). While he first touted its features and used it to treat his
personal depression, he ultimately identified its devastating consequences and side-effects, some
of which being “tolerance, dependence, a state of psychosis, and withdrawal depression.” He
even later referred to the substance as the “third scourge of humanity” (Julien, 2001). Around
the same time, no restrictions existed in the United States from selling or consuming cocaine, so
many medicines and products, such as Coca-Cola, included small doses of the drug (Julien,
2001). This was banned in 1914 by the Harrison Narcotic act, as many reports had surfaced
about deaths and intoxication (Julien, 2001). Use decreased as other cheaper drugs surfaced
(Julien, 2001).
Wide availability of “crack” cocaine resulted in the drug resurfacing in the late 1970s and
early 1980s (Julien, 2001). Today, it comes in water soluble cocaine hydrochloride which can be
“injected intravenously or absorbed through the nasal mucosa (snorted)”, or it can be inhaled
vapor called freebase or crack cocaine (Julien, 2001). When cocaine is snorted, the blood vessels
constrict and limit the absorption, so only 20-30 percent of the drug enters the bloodstream, but
the slow absorption prolongs the euphoric effect (Julien, 2001). Smoked cocaine has a rapid and
complete absorption with onset of effects within seconds, lasting for about 30 minutes (Julien,
2001). When entered intravenously, the entire dose enters the bloodstream and takes about 30- to
60-seconds to reach the brain (Julien, 2001). The biological half-life of cocaine in plasma is
about 30 to 90 minutes (Julien, 2001).
With 50 million Americans who have tried cocaine and 6 million who use it regularly,
cocaine is an extremely addictive and reinforcing drug (Julien, 2001). Another significant
demographic factor is that in 2010, nearly 4.6 million regular cocaine users were female, and
90% of drug-abusing women were at reproductive age (Srathearn and Mayes, 2010). This raises
concern about fetal exposure risks and the effects on parenting.
Cocaine and Pregnancy
In the United States, over 750,000 babies are born each year that have been exposed to
drugs (Srathearn and Mayes, 2010). Cocaine is especially pervasive to the unborn baby, as it is
able to cross the placental barrier, giving the baby equal levels of the drug that the mother intakes
(Julien, 2001). Furthermore, Boskovik et al. (2001) explained that when the drug enters the
fetus’s circulation, the drugs intermix with amniotic fluid. The fetus can swallow up to one liter
of fluid every day intensifying the drug exposure.
One method of assessment of babies suspected to have been exposed to drugs is to test
their hair for traces of the drug. Researchers in the Canary Islands also used this method, and
explained that due to unreliable maternal self-reports, testing the hair is a useful procedure. This
is because the drugs are permanently in the protein matrix of the baby’s hair and can be detected
months after drug use. (Cocaine use, 2012). Boskovik et al. notes that in 1988, newborn hair was
tested for cocaine, but also described one case in which a mother admitted to cocaine use but her
newborn’s hair showed no trace of the drug (2001). However, this method is useful for detecting
drugs in the infant’s system.
One similar factor among fetal cocaine exposure incidents is poverty. Zuckerman and
Frank (1992) note that poor children are prenatally exposed to cocaine more often than their nonpoor counterpants. Boskovik et al. (2001) list nutrition, alcohol and cigarette use, and poor
prenatal care as factors that can also explain adverse outcomes for these children. The disparities
between what is considered a healthy lifestyle and the lives of these children, which are
categorized by inadequate nutrition, healthcare, education and the culture of poverty show that
cocaine use is not the only factor at play. (Zuckerman & Frank, 1992).
When solely cocaine use is considered and these other significant factors are ignored,
mother-blaming is a probably outcome (Zuckerman & Frank, 1992). Furthermore, mothers with
drug addictions often face emotional challenges while parenting. The developmental delays that
some children whose mothers abused cocaine demonstrate may be partly due to a lack of nurture,
rather than chemical harm done by the actual drug. Mothers who abused cocaine expressed an
undecided attitude towards raising children and did not know much in regard to basic childcare
(Strathearn & Mayes, 2010). They also displayed disengagement in relation to responding to
their child’s needs, as well as being less likely to interact with the child. This might allude to an
issue of parenting tactics rather than a chemical imbalance.
One study found that expectant mothers who abuse cocaine display lower levels of
plasma oxytocin (Strathearn & Mayes 2010). This is relevant because for other species of
mammals, such as rats and sheep, a higher level of plasma oxytocin is necessary to activate
maternal behaviors. This could signify that mothers are chemically unable to create a maternal
bond with the child. Another study researched the levels of cortisol in infants that were exposed
to cocaine while in the womb (Eiden, Veira, & Granger 2009). The study found evidence that
supported the theory that this group of infants would have higher levels of cortisol, the stress
hormone. This may be responsible for some of the negative affect and susceptibility to stress that
they often experience.
Women who abuse cocaine during pregnancy are very likely to suffer from psychological
distress, such as paranoia, depression, anxiety, and many other mental health related concerns
(Minnes et al., 2008). Furthermore, cocaine activates the hypothalamic-pituitary-adrenal axis
stress response; this is intensified by female sex hormones which are increased during pregnancy
(Williams et al., 2012). Not only is the health of developing fetus impacted by cocaine use, but
also the mother’s ability to parent, which will affect the child throughout his or her lifetime.
Cocaine use can also physically affect the mother during pregnancy, which is evidenced
by research conducted by Hulse and Milne (1997). Their research shows that abruptio placentae,
or the separation of the placenta from the uterus before the baby is delivered, is common with
cocaine use. By studying available data, they found a strong correlation between maternal
cocaine use and abruptio placentae, but noted that the analysis did not take cigarette smoking
into consideration (Hulse & Milne, 1997). They identified that other confounding variables could
include factors present in poverty, such as poor nutrition and lack of prenatal care, along with the
use of multiple drugs (Hulse & Milne, 1997).
The Notion of “Crack Babies”
There are a fair amount of misconceptions surrounding the public’s understanding of the
long term effects of cocaine on a baby. Boskovik et al. (2001) found that fetal cocaine exposure
often has negative effects including low birth weight, intrauterine growth retardation, congenital
anomalies, and cerebrovascular accidents. This became particularly of interest during the late
1980’s and early 1990’s when the media was flooded with reports about the negative long term
negative effects of prenatal cocaine exposure. The infants that resulted were referred to as “crack
babies” and many people predicted that their development would be severely delayed. This is
evidenced through Zuckerman and Frank (1992), who referenced a quote from a 1990 Rolling
Stone Magazine article, which described children who had been prenatally exposed to cocaine as
“brain damaged in ways yet unknown” and “oblivious to any affection.” They also reference a
New York Times article that reported that children who had been prenatally exposed to drugs
were unable to make friends, control impulses, concentrate, feel and return love, and make
friends due to brain damage (Zuckerman & Frank, 1992). Articles from popular publications
such as these likely influenced the public perception.
Discrediting the Perception of “Crack Babies”
The notion of “crack babies” was revisited in a New York Times article, which explained
that limited research and uncritical evaluations led to the public belief that cocaine would
seriously impair the infants’ lives (Winerip, 2013). It stated that in essence, alcohol use during
pregnancy is a much more serious problem. The current research supports the notion that cocaine
is not a primary cause for an epidemic response.
Current research supports this claim, such as a study by Bandstra et al. (2004), which
reviewed the cases of nearly 500 infants. The infants included in this study were all of African
American origins, of a low socioeconomic status, and were from the inner city. This longitudinal
study followed the participants through age 7. The researchers assessed the abilities of each of
these children and found that children whose mothers did not abuse cocaine had higher speech
abilities than their counterparts. Although interesting, the researchers found that the differences
between the two groups’ development were very subtle. This is notable because it alleviates
some of the assumptions that people hold about “crack babies” and their development.
Another article that references research from Boston University about “crack babies”
attempts to discredit much of the stigma directed towards this population. (Huston, McLoyd &
Cull 2001). The article compared the findings of various studies that explore elements such as
the cognitive functioning, language skills, and physical growth of infants whose mothers were
exposed to crack cocaine during the time of their pregnancy. It notes that the findings of such
studies’ have results that do not often agree. For example, of nine studies conducted to measure
cognitive abilities of infants with and without prenatal exposure to cocaine, only four of the
studies found a significant effect produced by cocaine usage. In another case, researchers
examined ties between neonatal cocaine exposure and physical growth of infants. Two of the
three studies that the article assessed found that cocaine exposed infants had a head that was
smaller in size and a lower weight, while one other study showed little to no difference. Once
again public perception and scientific findings fail to reach a consensus.
Cocaine is a powerful, addicting, and widespread drug in American society. Because its
relevance to women of reproductive age and the drug’s high permeability of the placenta, its
effects on prenatal development must be considered. While prenatal cocaine exposure is
developmentally harmful to the child, it does not warrant the stigma that lingers from the
negative media attention that the concept of “crack babies” previously received. Recent research
discredits many of the exaggerated claims made in the past. It is important to not only consider
prenatal cocaine exposure in these cases, but also the factors of poverty, inadequate nourishment,
other drug use, and mother-child relationships. It would be worthwhile to continue the
longitudinal studies to examine if fetal cocaine exposure makes an adult more likely to become
addicted to cocaine or other drugs
References
Bandstra, E. S., Vogel, A. L., Morrow, C. E., Anthony, J. C., & Lihua Xue, J. C. (2004). Severity
of Prenatal Cocaine Exposure and Child Language Functioning Through Age Seven
Years: A Longitudinal Latent Growth Curve Analysis. Substance Use & Misuse, 39(1),
25-59. doi:10.1081/JA-120027765
Boskovic, R., Klein, J., Woodland, C., Karaskov, T., & Koren, G. (2001). The role of the
placenta in variability of fetal exposure to cocaine and cannabinoids: A twin study.
Canadian Journal Of Physiology & Pharmacology, 79(11), 942-945.
Cocaine use during pregnancy assessed by hair analysis in a Canary Islands cohort. (2012). BMC
Pregnancy & Childbirth, 12(1), 2-9. doi:10.1186/1471-2393-12-2
Eiden, R. D., Veira, Y., & Granger, D. A. (2009). Prenatal Cocaine Exposure and Infant Cortisol
Reactivity. Child Development, 80(2), 528-543. doi:10.1111/j.1467-8624.2009.01277.x
Hulse, G. K., & Milne, E. E. (1997). Assessing the relationship between maternal cocaine use
and abruptio placentae. Addiction, 92(11), 1547-1551.
Julien, Robert M. A Primer of Drug Action. New York: Holt, 2001. Print.
Minnes, S., Singer, L. T., Kirchner, H. H., Satayathum, S., Short, E. J., Min, M., & ... Mack, J. P.
(2008). The association of prenatal cocaine use and childhood trauma with psychological
symptoms over 6 years. Archives Of Women's Mental Health, 11(3), 181-192.
doi:10.1007/s00737-008-0011-z
Researchers debunk stigma of 'crack babies'. (Cover story). (2001). DATA: The Brown
University Digest of Addiction Theory & Application, 20(6), 1.
Strathearn, L., & Mayes, L. C. (2010). Cocaine addiction in mothers. Annals Of The New York
Academy Of Sciences, 1187(1), 172-183. doi:10.1111/j.1749-6632.2009.05142.x
Williams, S. K., Barber, J. S., Jamieson-Drake, A. W., Enns, J. A., Townsend, L. B., Walker, C.
H., & Johns, J. M. (2012). Chronic Cocaine Exposure During Pregnancy Increases
Postpartum Neuroendocrine Stress Responses. Journal Of Neuroendocrinology, 24(4),
701-711. doi:10.1111/j.1365-2826.2012.02291.x
Winerip, M. (2013, May 20). Revisiting the 'crack babies' epidemic that was not. New York
Times, Retrieved from http://www.nytimes.com/2013/05/20/booming/revisiting-thecrack-babies-epidemic-that-was-not.html?_r=0
Zuckerman, B., & Frank, D. A. (1992). 'Crack Kids': Not Broken. Pediatrics, 89(2), 337.