Fetal Alcohol Spectrum Disorder and Adoption

Source: Photo by Kelly Sikkema on Unsplash

When I was in graduate school at the University of Rochester, I attended a colloquium by Marshall Schecter, a psychiatrist from nearby Syracuse. His topic involved the extraordinarily high rate of psychopathology in children and youth who had been adopted. His somewhat controversial explanation for the mental health problems of adopted persons was to blame it on the practice—promoted by the social work profession—of encouraging adoptive parents to tell the adopted child, literally from the first day in their new home, that they were adopted. While the recommended language was always positive (along the lines of “I love you, my adopted child”), Schecter’s position was that young children lack the cognitive and emotional capacity to process such potentially devastating information. The idea here was that knowledge of having been adopted creates identity issues for adoptees, and an attachment disorder, later termed “adopted child syndrome,” can pose significant mental health challenges.

One of the reasons cited by social workers for early notification is that, heaven forbid, a child might find out accidentally, such as from a playmate. Schecter’s response was, “So what? It is still better that the news come at a time when the child is better able to process it.” As a Piagetian aware of the invariant cognitive-developmental stage sequence, I found Schecter’s theory of adoptee psychopathology causation to be convincing. I subsequently made sure to tell anyone thinking of adopting a child to ignore any advice they received regarding the need for disclosure to the child at a very young age. Schecter eventually backed off from his insistence that adoptee psychopathology was caused by too early notification. Still, he wrote about adoptee identity issues, as in his co-edited book with David Brodzinsky and Robin Marantz Henig, Being Adopted: The Lifelong Search for Self.

An interesting research finding, which has contributed to a more differentiated understanding of the problem, is that children adopted in the first six months of life are much less likely to develop attachment-related emotional problems when compared to children adopted at an older age. That finding makes sense, given that secure attachment (and emotional distress when it is disrupted) is a phenomenon that does not manifest until around age seven months. But a problem with seeing adoptee mental health risk primarily in sociogenic and psychogenic terms is that it largely ignores a significant biological contributor to adoptee psychopathology, and that is the increased likelihood that the biological moms of children later given up for adoption binged on alcohol during pregnancy.

My interest in the teratogenic effects of prenatal alcohol consumption has been influenced by three experiences that I did not have at the time I encountered Marshall Schecter as a somewhat naïve graduate student: (a) I later became deeply immersed in the literature on Intellectual Disability (ID, formerly known as mental retardation), becoming aware that prenatal alcohol consumption is reputedly the most common known cause of ID, (b) I[ have done psychological assessments of many children and youth being considered for developmental services, noting that in a substantial percentage of these cases where the individual being evaluated turned out to have FASD, they also had been adopted, and (c) I have consulted in many criminal trials, and very commonly a defendant facing serious criminal charges was born to an alcoholic mother.

The disorder that results from prenatal alcohol exposure is today termed “Fetal Alcohol Spectrum Disorder” (FASD). It was first discovered in 1973 as “Fetal Alcohol Syndrome” (FAS). The talk by Marshall Schecter that I attended in Rochester took place around 1974, and it was thus unlikely that he knew about FAS and its high prevalence in adopted individuals. Even today, over four decades later, it is common for psychologists and psychiatrists to assign various mental health labels to individuals with likely FASD (which is associated with several comorbid disorders) and miss the signs that the individual has a damaged brain.

The brain damage in FASD stems from the fact that the liver is not fully formed until the third trimester and, thus, cannot adequately perform throughout most of the prenatal development its function of detoxifying alcohol or other poisonous substances. As a result, the fetal brain is being essentially pickled by the alcohol ingested by its mom. No level of prenatal alcohol consumption is considered safe in the US, unlike in the UK, where they are somewhat more accepting of light social drinking. However, it is undoubtedly true that binge drinking (for the purpose of getting drunk, defined operationally for a woman as four or more drinks in a two-hour period) is viewed in both countries as the type of alcohol ingestion most likely to damage a child’s brain permanently.

This probably explains why FASD is so prevalent among adopted children, as binge drinking is mainly a problem of young people (ages 18-24), and this is the age group most likely to have unwanted pregnancies resulting in adoption. There is an ethnicity/country-of-origin factor operating here as well, as alcoholism among young women is very prevalent in Eastern European countries such as Russia and Ukraine and relatively low in China (where consumption of alcohol is limited by a genetic phenomenon known as the “Asiatic flush,” which causes even a small intake of alcohol to be experienced as unpleasant). This explains why children adopted from China generally have good developmental outcomes while children adopted from Russia often end up having very tragic consequences. (Vladimir Putin may have thought he was punishing the US by cutting off adoptions to American parents, but he actually ended up sparing many of those parents decades of heartbreak).

Prenatal consumption of alcohol results in irreversible structural damage to the developing brain. Most often, the damage is found in the frontal and central structures such as the hippocampus and prefrontal cortex. This explains the fact that facial anomalies are often evident, as the face is being developed at the same time as the brain structures behind the face. The three most common facial anomalies associated with FASD are (a) a smooth philtrum (the indentation running down from the nose to the upper lip), (b) a thin vermillion (upper lip), and (c) a short palpedral fissure (horizontal distance between the corners of the eye), along with growth deficiencies. However, physical findings are not a requirement for diagnosing FASD, and for individuals with the most common form of FASD—“Alcohol-Related Neurodevelopmental Disorder” (ARND)—facial anomalies are not evident, even to a dysmorphologist (physician specializing in birth defects). It is for this reason, along with generally inadequate knowledge by clinicians, that FASD is usually not diagnosed, and primary diagnostic emphasis tends to focus on the very salient behavior problems manifested in almost all children and adults with FASD.

One behavioral area of difficulty in persons with FASD (as with people who have various other forms of brain damage) involves impulsivity and difficulty in focusing attention. For this reason, Attention Deficit Hyperactivity Disorder (ADHD) is typically the first diagnostic label affixed to people with FASD, even though they typically have a number of other problems that are not necessarily associated with ADHD. Among these other comorbid problems are extreme emotional reactivity, absence of risk-awareness, and deficiencies in social and practical judgment. This latter more cognitive problems are associated with severe difficulty in school achievement (especially math calculation), acting out behaviors, memory, language, etc. For this reason, FASD is a more severe disorder than ADHD and on a par with ID. However, the mean IQ level in FASD straddles the 70-75 cut-score most typically used to define ID and thus prevents many people with FASD from getting access to much-needed educational and adult services.

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Probably the most extensive area of deficiency associated with FASD is in the area of “Executive Functioning” (EF), which involves such things as cause-effect thinking, problem-solving, and understanding of consequences. For this reason, individuals with FASD are typically described as unable to learn from past mistakes and as very likely to behave (once they enter adolescence and young adulthood) in ways that get them in trouble with the law. This last problem is exacerbated by a lack of friends, which makes people with FASD very susceptible to bad influences from pretend friends, who exploit their lack of social judgment. In my practice as a consultant in death penalty cases, I have seen many cases in which someone with FASD (or ID generally) became sucked into participating in a homicide by a more competent co-defendant who exploited the gullibility of the brain-damaged peer.

Returning to the argument of Marshall Schecter and others who believed that the high rate of psychopathology in adopted individuals mainly reflected identity problems caused by attachment disruption, it is clear that there are two pathways to adoptee mental illness: (a) the relatively mild neurotic processes that affect individuals who have a hard time accepting their adoptee status, and (b) the relatively severe cognitive and behavioral difficulties of those who were affected in utero by the binge drinking of their biological mothers. It is also possible that for some individuals, both processes work in tandem. But the tragic outcomes stemming from FASD (and the high rates of alcohol consumption among pregnant women, often before they know they are pregnant) are to me a much bigger problem, not just limited, of course, to those who have been adopted. This problem ties in with the general tendency of psychologists and psychiatrists to fail to recognize various signs of brain damage, even when they are very salient and prominent.

Copyright Stephen Greenspan