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FETAL ALCOHOL SPECTRUM DISORDERS IN AFRICAN AMERICAN COMMUNITIES: CONTINUING THE QUEST FOR PREVENTION

CARL C. BELL, MD

For nearly 50 years, I have been trying to help children, boys and girls, who are in special education, foster care, and juvenile justice and who have difficulty learning, have been abused, and have explosive tempers along with poor judgment and poor people skills. I have been treading water in a sea of these children for years, so much so, seeing a child without these problems is like visiting a sunny island and being on dry land. Recently, it has become clear to me that many of the children I have been trying to help display behaviors consistent with a neuropsychiatric disorder the American Psychiatric Association is proposing to study by designating it as “Neurodevelopmental Disorder associated with Prenatal Alcohol Exposure” (APA, 2013). Since its scientific discovery in the United States in 1973 (Jones et al., 1973) and public health efforts by the Centers for Disease Control and Prevention, National Institute on Alcohol Abuse and Alcoholism, Substance Abuse and Mental Health Services Administration, and public health agencies, the knowledge that women should not drink during pregnancy is nearly ubiquitous. Unfortunately, too many women are drinking socially before they realize they are pregnant—nearly 50 percent of pregnancies are unplanned (Finer and Zolna, 2011)—only to heed the warning after they realize they are pregnant in a month or two. To understand how to address this public health issue, a little background in underserved population public health is necessary.

BACKGROUND

In 1967, African American physicians at Meharry Medical College in Nashville, Tennessee, were painfully aware of health disparities in the African American community. In turn, my medical training was entrenched in a public health and prevention model. The polio epidemic had provided a clear example of how prevention could eliminate health disparities, as the vaccine leveled the playing field between the haves and the have-nots. If one African American child presented with a rat bite, we were taught to treat the individual; if there were multiple such children, we were to treat the root cause, out in the community. We should get rid of the rats, or have our medical licenses revoked.

This concept of “getting rid of rats” has guided my career. In 1974, after completing a residency in psychiatry, I observed the common problem of African American children exposed to violence (Bell, 1987)—a potentially traumatic and preventable experience that I considered to be a “rat.” Later, our work with Dr. David Satcher (the 16th Surgeon General, whom I knew from his presidency at Meharry Medical College) on his Youth Violence report (HHS, 2001) and the Institute of Medicine’s Reducing Suicide report (IOM, 2002) highlighted the idea that there are protective factors in high-risk individuals and families that keep “risk factors from becoming predictive factors” (Griffin et al., 2011). Previously, several scientists (e.g., Garmezy et al., 1984; Luthar, 1991; Masten et al., 1988) had put forward the idea of resilience, but it had not yet received its due traction as a vital concept within the public health arena. In 2000, Dr. Satcher held his Children’s Mental Health Conference (U.S. Public Health Service, 2000), in which he advised the nation’s health care providers to focus on youth involved with child protective services, juvenile justice, and special education. These reports encouraged our public health systems to focus on strengthening protective factors, thus shifting our focus toward resiliency. After years of work, the issue of trauma, and resiliency in the face of trauma, has become an essential issue in public health—consider the impact our understanding of adverse childhood experiences has had on our nation (Felitti et al., 1998).

A STRONGER FOCUS ON PREVENTION IN THE 21ST CENTURY

I continued to follow the prevention path set out for me, and had success in violence prevention, suicide prevention, and HIV prevention in the United States and abroad. Consequently, I was given the honor of participating in the National Research Council and Institute of Medicine’s effort Preventing Mental,-

Emotional, and Behavioral Disorders Among Young People: Progress and Possibilities (NRC/IOM, 2009).

The Institute of Medicine’s first prevention report (IOM, 1994) helped move the prevention agenda considerably. During the Clinton administration, a National Institute of Mental Health employee, Juan Ramos, first led this initiative. In a refreshingly nonpartisan manner, President Bush’s administration continued to focus on prevention through its New Freedom Commission on Mental Health (2003). Thanks to the efforts of A. Kathryn Power (Director, Center for Mental Health Services at the Substance Abuse and Mental Health Services Administration [SAMHSA]), in 2004, the New England Coalition for Health Promotion and Disease Prevention held an important conference: “Evidence-Based Programs for the Promotion of Mental Health and Prevention of Mental Health and Substance Abuse Disorders.” It was another stepping-stone to an even greater national focus on prevention. During the Bush administration, HHS supported the second National Research Council/Institute of Medicine prevention report (NRC/IOM, 2009), which provided the foundation for the Obama administration’s strong focus on prevention within the Affordable Care Act. It was also this report that led to the first U.S. National Prevention and Health Promotion Strategy (National Prevention Council, 2011).

THE MISSING PIECE

Despite the resounding success of the 2009 NRC/IOM prevention report, it is now exceedingly clear that we had overlooked a major piece of the prevention dialogue: fetal alcohol exposure (FAE). Depending on when it is classified and who is classifying it, several diagnoses fall under the category of fetal alcohol spectrum disorders (FASDs), the overarching diagnosis that is caused by FAE. Within the spectrum, SAMHSA (2014) lists the following:

The average layperson knows that when a woman is pregnant, she should not drink alcohol, because it has the potential to cause severe or subtle brain damage in the fetus. In turn, we generally associate FAE outcomes with newborns or young children. Moreover, FAE has long been considered an endemic problem within Native American communities (HHS, 2001). Although these medical and cultural rules of thumb may be accurate, the vast majority of workers in special education, child welfare, corrections, and mental health must now acknowledge how common and destructive this problem is for our nation as a whole. Like many clinicians, I have been seeing the impact of FAE for decades, but I did not know what I was seeing, nor did I understand its etiology. Additionally, all of the prevention efforts heretofore have brought health disparities and social determinants of health into the nation’s awareness, but the lack of flourishing that is endemic to low-income African Americans has not yet risen into its consciousness. As you will see, the journey to reach the intersection of these varied issues was a protracted one; after all, how does a fish recognize water?

THE JOURNEY TO AWARENESS OF FETAL ALCOHOL SPECTRUM DISORDERS

In 1968, as a medical student, I researched the nutritional status of 50 low-income African American children at the Children and Youth Clinic in Tennessee (Bell,

1971). In the research, 8 percent of subjects had been born prematurely, but their age- and sex-adjusted weight/height and head circumference were within normal limits, based on the European American norms at that time. Eleven years later, Schutte (1980) developed a weight-and-height-distribution graph that was normed on middle-class African American children, and reassessing the 1968 sample reveals that a little more than 40 percent of the children studied had signs of impaired growth—a sign of FAS. In 1967, public health surveillance revealed that African Americans were born prematurely at a rate that was two- to threefold higher than among European Americans (Buck, 1967), and a disproportionately high percentage of patients that Meharry served were thought to have “sociocultural mental retardation” or “minimal brain dysfunction” (Nelson, 1966). I was puzzled at the root causes of these health disparities.

While working for the Chicago Board of Education in 1977, I again observed mild “mental retardation” and “minimal brain dysfunction” in their special education youth. By then, our understanding of child psychiatry had improved, and it was possible to arrive at a more refined classification of these children’s symptoms. I categorized 274 children into 10 distinct categories: (1) organic brain syndrome/trainable mentally handicapped with explosive behavior, (2) educable mentally handicapped (EMH) with explosive behavior, (3) EMH with neurotic symptoms, (4) psychotic (autistic, childhood schizophrenia, adolescent schizophrenia), (5) borderline syndrome, (6) socially maladjusted behavior, (7) minimal brain dysfunction/learning disability with explosive and/or neurotic symptoms, (8) explosive behavior, (9) neurotic (anger/depressive) symptoms, and (10) psychophysiologic disorders. In retrospect, about two-thirds to three-quarters of these children exhibited multiple characteristics of FAE. This includes intellectual disability, speech and language difficulties, hyperactivity, high excitability, high distractibility with poor attention span, and poor frustration tolerance, all of which lead to poor impulse/affect control and can ultimately result in explosive or even violent behavior (Bell, 1979; Bell and Chimata, 2015). I wondered what was causing their affect dysregulation (Bell and McBride, 2010).

In 1996, the Institute of Medicine published its report Fetal Alcohol Syndrome (IOM, 1996), but I still had not connected the likelihood of the high prevalence of FASD cases in African American communities to their disproportionately high number of liquor stores (Altman et al., 1991; Hackbarth et al., 1995; LaVeist and Wallace, 2000). The previously mentioned association of FAE with Native Americans as well as with the pediatric population also impeded my ability to connect the dots. As such, the clinical actuality that FAS/FASD could persist into adulthood was simply not on my radar as a community psychiatrist. Moreover, I was oblivious to the fact that the overabundance of liquor stores in the African

American community could serve as a social determinant of health that produced an acquired biological disability of subtle brain damage. My judgment was clouded: I did not recognize that this subtle brain damage could masquerade as a whole host of educational, criminal, and psychiatric disorders.

For years, I continued to practice community psychiatry on Chicago’s South Side and consult with the Special Education Services of the Chicago Board of Education, the Illinois Department of Children and Family Services, and the Cook County Temporary Detention Center. I continued to see low-income African American children, many of whom displayed what I considered an odd cluster of symptoms: a peculiar form of ADHD; various learning disabilities; intellectual disability; soft neurological signs; affect dysregulation mainly characterized by explosive, short-lived tempers; and naïve, childlike social interactions. Additionally, many of these patients had been victimized and/or exposed to violence in childhood. At that time, I attributed these symptoms to the high rates of prematurity (which I hypothesized could cause a subtle form of brain damage at birth from intracerebral bleeding that preemies have that would persist into childhood and adolescence) and/or exposure to violence, along with poor parenting, but it still did not add up. Though I did not pin down FAE as a culprit, I began to write extensively on the issue of children exposed to violence. In a short period, through our and others’ efforts, our nation became acutely aware of this problem.

In 1985, as a member of the National Commission on Correctional Health Care’s survey team reviewing the entire Texas Department of Corrections’ (TDC) prisons, I learned from TDC that 20 percent of the approximately 20,000 mostly African American inmates had “mental retardation.” It was clear to me that something was going on in the African American community that generated a large number of intellectually challenged individuals, and contrary to prevailing theories of the genetic inferiority of African Americans (Thomas and Sillen, 1972), I doubted that it was genetic inferiority. In later years, as the nation’s public health infrastructure was trying to fully crystallize its efforts on prevention and resiliency, the criminal justice system was struggling with the disproportionate number of African American youth and adults who were being incarcerated.

The Children’s Defense Fund (CDF), shepherded by Marion Wright Edelman, began to take advantage of the increasing amount of information about the health and well-being of the nation’s African American citizens. There was a looming question that was raised at the CDF’s Black Community Crusade for Children Juvenile and Family Court Judges’ Leadership Council Fall Symposium in 2000: “Why Are So Many African American Children Diagnosed with Attention

Deficit Hyperactivity Disorder?” By 2007, the CDF had congealed its focus on the early processes that caused so many African Americans to wind up in corrections, and a conference on promising approaches to end violence and strengthen communities in dismantling the cradle-to-prison pipeline was held at Howard University (September 25–26, 2007).

In 2009, a serendipitous consultation with the Temporary Juvenile Detention Center revealed that between two-thirds and three-fourths of the youth in the Cook County Temporary Juvenile Detention Center had problems with mild intellectual disability, speech and language disorders, ADHD, and specific learning disorders (Bell, 2015b). Accordingly, it was clear that something was still driving the problem of subtle brain damage in African Americans that had been evident over the years. The cradle-to-prison pipeline hypothesis was that African American children were being shaped and seasoned to become correctional inmates within their formative years. In addition, a 2011 random-sample chart audit on 20 percent (162) of the children in four Chicago public school clinics revealed that 39 percent also had possibly been exposed to alcohol when they were in utero (Bell, 2014). Biology and environment together influenced these children’s early educational outcomes, which served as a driving force in their being slated for the juvenile justice system. The youth in the school clinics evidenced a palpable pattern in their medical records, progressing from diagnoses of ADHD, speech and language disorders, specific learning disorders, and intellectual disability (all possible indicators of being exposed to prenatal alcohol) to a diagnosis of conduct disorder. The latter diagnosis set them up for incarceration when their affect dysregulation led to behaviors that were interpreted as intentional, criminal activities, without any acknowledgment of the possibility that untreated and undiagnosed subtle brain damage was driving their behavior.

After nearly half a century of not “getting it,” I was seeing a young African American woman who had been a ward of the Illinois Department of Children and Family Services (Illinois DCFS) and whose three children were currently wards of the State of Illinois. While I was evaluating her for whether she should be able to see her children and potentially regain custody, I noticed her extremely obvious epicanthal folds, flat midface, and strabismus. When I asked her why she had come, she not only a reported a history of ADHD, speech and language disorders, specific learning disorders, and intellectual disability, she also stated, “I have bipolar disorder, schizophrenia, and depression.” When she was 8 years old, she had been given a diagnosis of bipolar disorder because she would have emotional outbursts related to frustration she felt within situations that she did not understand, for example while trying to learn reading or math. As a result, she had several psychiatric hospitalizations as a child and,

despite her “mood swings” lasting only 30 minutes to an hour, she was placed on mood stabilizers; and despite their lack of efficacy in modulating her affect dysregulation, she was maintained on these medications for years. In addition, she began to “hear voices” in her late teens. Upon closer examination, these voices were coming from inside of her head; she referred to them as her conscience. These “voices” were clearly a manifestation of her “inner dialogue” or “inner voice” that every human being experiences within his/her mind. Because no one had bothered to get the details of what she “heard,” she was thought to be schizophrenic and was accordingly placed on high doses of antipsychotic medications. When she was emancipated from the Illinois DCFS, she could not successfully adapt to life as a young adult and became “depressed”—she was assigned this diagnosis despite her obvious capacity for humor and her strong desire to do well in life.

Thanks to pediatrics training in medical school, it hit me like a ton of bricks—fetal alcohol exposure. Although I was certainly not taught to look for FAE in adolescents and adults or in psychiatric patients, I knew what I was looking at was that same picture. I quickly obtained a history of her mother being a teenager when she had the patient—poor women 18–24 years old have unintended pregnancy rates two to three times higher than the national average (Finer and Zolna, 2011). Her grandmother had told her that her mother had been drinking before she realized she was pregnant; but once she learned she was pregnant, the patient’s mother stopped drinking.

The following week, I was consulting with the government of Manitoba, Canada (Healthy Living, Seniors and Consumer Affairs, 2012) on the work we had done for the Institute of Medicine’s 2009 prevention report (NRC/IOM, 2009). I learned that 19 out of 20 youth in the Canadian detention centers had FASD (Popova et al., 2011). As an aside, this illustrated the principle that “culture protects” and the absence of culture places youth at risk. Individuals with intact cultural proscriptions are less likely to engage in risky behaviors such as drinking, unsafe sex, drug use, and so on, because their culture informs and guides them (Bell, 2011, 2013b). Because of this insight about FASD, Clinical Psychiatry News graciously published an Advisor’s Viewpoint to inform the psychiatrists across the country about the problem of FASD that had been hiding within psychiatric populations (Bell, 2012a). In spring 2012, the correctional health care workforce was made aware of the problem of FASD in the inmates within the correctional system (Bell, 2012b). Again, part of the obfuscation in recognizing FASD stems from our basic medical training: We were taught to look for fetal alcohol facies in infants. However, FAE leads to so much more than our basic understanding of FAS or FASD; it causes children, adolescents,

and adults to have difficulty with learning, controlling their affect, remembering important things, and adapting to social situations.

In September 2012, I was communicating with Dr. Renato D. Alarcon, MD, who was working diligently on the issue of cultural issues within the DSM-5 Personality Work Group, of which I was a member. At the time, I was developing my own criteria for diagnosing FASD in adolescents and adults who lacked the fetal alcohol facies, as I did not know that the American Psychiatric Association (APA) was considering a diagnosis of ND-PAE for DSM-5 (APA, 2013). In a communication regarding cultural issues as they related to personality diagnoses, I had raised the issue of FASD as a significant problem for African Americans. Although the intellectual and behavioral sequelae of FASD have been attributed to culture in African Americans (Nelson, 1966), the reality is that these behaviors are caused by the social determinants of health that put them at risk for subtle brain damage (Bell, 2016). With my new understanding of FAE, I underlined a significant concern about how DSM-5 would address this phenomenon that was largely due to social determinants of health, that is, the large number of liquor stores within African American ghettos. When the APA finally gave their work groups the completed DSM-5, I was heartened to see that neurobehavioral disorder associated with prenatal alcohol exposure matched my criteria exactly. There is nothing sweeter in science than the moment when two distinct processes lead to the same conclusion—the validation is unquestionable.

Although I was extremely late to the FASD dance, I felt strongly that this problem had been largely overlooked in the African American community. Science and advocacy were the only ways to bring light to this hidden epidemic, but the path was fraught with danger, as history has shown that attempts to address issues of African American public health have often backfired. Consider the efforts to address the issue of black-on-black violence (Bell and Jenkins, 1990). After Surgeon General Koop declared some forms of black-on-black violence a public health problem, several public health advocates successfully put this issue on the public health agenda. Shortly after this public health initiative, the problem was attributed to the drug trade, and the rates of incarceration soared within the United States (Bell, 2015a). Despite the danger, the 2010 publication of The New Jim Crow (Alexander, 2010) fueled the urgency to address the issue of FASD in corrections and society at large. We had to follow Albert Einstein’s admonition, displayed outside of the National Academy of Sciences’ Keck Building in Washington, DC: “The right to search for truth implies also a duty; one must not conceal any part of what one has recognized to be true.”

Accordingly, proponents started to push the conversation. The National Center for Youth in Confinement was informed about the problem of FASD for the youth within their walls (Bell, 2013a). Abram and colleagues (2004) highlighted the high levels of comorbidity of attention deficit and hyperactivity disorder (ADHD) or behavioral disorders and affective, substance use, anxiety, ADHD, and behavioral disorders among juvenile detainees. In this vein, FASD was touted as a major cause of ADHD and behavioral disorders. It was hypothesized that the most common problems occurring in all youth—(1) speech and language disorders, (2) specific learning disorders, (3) ADHD, and (4) mild intellectual deficiency—possibly originated with FASD (IOM, 1996). Unfortunately, because confined individuals are a protected population, conducting research on these problems has been difficult.

In 2012, the State of Illinois halted funding for the organization that I had helped to build: the Community Mental Health Council, Inc., which took me out of leadership and the isolation from the wellspring of researchable ideas, that is, clinical service. I was forced back into direct service—the best thing that could have ever happened to me and the public health mission bestowed on me by Meharry Medical College. After all, our motto at Meharry was “Worship of God through Service to Mankind.”

After some time on an inpatient psychiatric unit at St. Bernard Hospital in the heart of Englewood—one of the poorest African American communities in Chicago (Bell, 2014)—my work revealed that among 93 consecutively admitted patients, 32 percent met the DSM-5 “condition for further study,” ND-PAE (APA, 2013). Around the same time, the National Academy of Sciences (NAS) Committee on Law and Justice decided to tackle the problem of harsh disciplinary practices within juvenile justice. The issue of FASD was briefly mentioned, but there is still a great deal more work to be done to document the high rates of FASD in juvenile justice facilities around the nation (NRC, 2013). In 2014, the Committee on Law and Justice also addressed causes and consequences of high rates of incarceration, but the issue of FASD in corrections did not make the cut, because there was not enough solid research in corrections to document this phenomenon (NRC, 2014).

Finally, during the 30th Annual Rosalynn Carter Symposium on Mental Health Policy in 2014, the findings from the research at Jackson Park Hospital’s Family Practice Clinic came to the fore. In a family medicine clinic on Chicago’s South Side, serving a population of 143,000 (96 percent African American with a median household income of $33,809), 297 of 611 (49 percent) of the adults and youth had neurodevelopmental disorders with 237 (39 percent) having clinical profiles consistent with ND-PAE (Bell and Chimata, 2015). Because

of the Carter Center presentation, the January 2015 Newsletter to the National Association of County Behavioral Health and Developmental Disability Directors carried a front-page article on the prevalence of FAE in low-income African Americans (Bell, 2015c).

LATE TO THE FETAL ALCOHOL DANCE

Despite all of the progress in public health, there remains a glaring oversight: Since the late 1960s and early 1970s, the disorders associated with FAE were being observed in infants and children, but it was not fully clear how prevalent this problem was in society at large. There have been a great many luminaries who have been at the FASD dance long before I ever heard the music. They have come from SAMHSA-funded FASD centers of excellence: the Center for Behavioral Teratology, San Diego; the North Dakota Fetal Alcohol Syndrome Center; University of Minnesota, Child Psychiatry Department, Minneapolis; Center on Human Development and Disability, University of Washington, Seattle; Fetal Alcohol Spectrum Disorders Regional Training Center, Nashville, Tennessee; Centers for Disease Control and Prevention (CDC); and the National Organization of Fetal Alcohol Syndrome in the United States and the United Kingdom. They have been doing outstanding work. For example, Astley et al. (2002) documented that the rates of FASD in Washington State’s foster care population were 10–15 per 1,000,¹ and the CDC even has an FASD app. In addition, neuroimaging of the effects PAE on the developing human brain is well established as strong science (Donald et al., 2015). However, considering the tremendous impact this problem has on public health, and although there has been some traction within the nation on this issue, there has not been nearly enough. Tragically, despite nearly 20 years of good FAE research, child welfare organizations, corrections, mental health, and special education are still not cognizant of its significance. Perhaps they have been deterred because they would not know what to do about it if they found it in the people whom they serve. Certainly, the proposed diagnosis in APA’s DSM-5 of ND-PAE will strengthen the conversation, because there is now a label for what we have been seeing in juvenile justice, special education, child protective services, adult unemployment services, and adult corrections, among others, for years.

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¹ Although the CDC admits it does not know exactly how many people have FASD, it has studies that have identified 0.2 to 1.5 infants with FAS for every 1,000 live births in certain areas of the United States, and studies using in-person assessment of school-age children in several U.S. communities report FAS at 6–9 of 1,000 children (http://www.cdc.gov/ncbddd/fasd/data.html).

GATHERING MOMENTUM AND HEADING TOWARD A TIPPING POINT

Momentum is gathering. May and colleagues (2014) published a paper on the prevalence of FASD in a predominately European American, middle-class, midwestern city and illustrated that the prevalence of FASD was much higher than expected—as high as 5 percent in this population-based sample. Then, a wonderful thing happened that determined the size of the problems for children in child protective services. Chasnoff and colleagues (2014) published a paper on 547 children referred to their facility from the Illinois DCFS for behavior problems and observed that 28.5 percent had FASD, but had never been properly diagnosed. We discovered a FAE rate of 388 per 1,000 patients in a low-income family medicine clinic on Chicago’s South Side (Bell and Chimata, 2015), and we suspect equally high rates in African American ghettos throughout the United States. Another recent paper by Rojmahamongkol and colleagues (2014) documented that pediatricians in New Haven County, Connecticut, were more able to diagnose Williams syndrome (estimated to occur at rates of 1 per 7,500) than they were able to diagnose FASD, which has been reported at rates of 2–388 per 1,000, depending on the population being studied (Bell and Chimata, 2015). Thus, it seems that interest in this issue is burgeoning. However, there is not enough attention to this issue.

WHAT NEEDS TO BE DONE?

The problem is now squarely before us. Consider the traction that the IOM received when it revisited the 1994 prevention report and published a second version in 2009. After all, there has been an explosion in prevention knowledge since 1994, and a similar explosion in FASD knowledge since 1996. Now, the provocative question is, “What needs to be done?”

First, NAS should convene a meeting of the experts to examine the current state of FASD knowledge. If there is sufficient new knowledge, NAS needs to develop a new report on FASD. It has been 21 years since the first FAS report from the Institute of Medicine (IOM, 1996). It needs to be revisited, but it appears that the correctional, child protective services, special education, and mental health fields are not aware of the breadth of available research and its importance to the nation’s public health. I believe that we are at a pre–“tipping point” moment and it would help to finally give the attention to what the second NRC/IOM report failed to highlight—the issue of FAE.

Maybe the awareness of the problem of FASD is hampered by the lack of understanding about what can be done about it. I have seen this dynamic once

before when I suggested that children be screened for witnessing violence. The response was, “What do we do with them once they are identified?” Fortunately, in terms of FASD, there are animal studies showing that, when rats are given alcohol during pregnancy, and are given choline while they are still pregnant, the damage done to their fetuses is reduced and their birth outcomes are better (Thomas et al., 2007). Unfortunately, I know of only one study, done on humans in Russia, that supports this strategy, but that study has not yet been published. Of course, this strategy would be easy to implement, as choline is an over-the-counter nutrient, and the daily requirement for this quasi vitamin has been well established and shown to be safe. Unfortunately, choline supplements are relatively difficult to obtain, as most drug stores do not carry them, and there are only small amounts present in prenatal vitamins.

There is some indication from animal research that giving animals with FASD choline, folate, omega-3, and vitamin A postnatally helps to correct the damage that alcohol does to the fetus (Ballard et al., 2012; Thomas et al., 2007). This might work for humans, as well. Unfortunately, there is very little choline in infant formula. If an infant is born prematurely or with low birth weight, it is bound to be choline deficient. The infant leaves the womb early, is usually fed formula, and does not get the benefit of the choline that is shunted through the mother’s breast milk. In this vein, Wozniak and coworkers (2013) suggest that giving 2.5- to 5-year-old children choline postnatally can improve outcomes for children with FASD. Ross et al. (2016) has recently published exciting work on CHRNA7, the alpha-7 nicotinic acetylcholine receptor gene that has been shown to play a role in the etiology of ADHD and autism spectrum disorders, showing that its expression is positively altered by perinatal phosphatidylcholine supplementation.

It is fascinating how much animal research has been done with choline and other substances (e.g., thyroxin), but human clinical trials have been lagging behind. We must explore the reparative capacity of choline, and other supplements, both prenatally and postnatally. We need to confirm that this strategy is empirically sound if we want to have a true impact. Because the problem of FAE is so rampant in the community I serve, until the research pans out, there are some ideas for addressing the problems related to FAE. I have been suggesting that some patients take choline, folate, omega-3, and vitamin A and I have seen some positive results.

Of course, everyone is aware that women should not drink when they are pregnant—we get that. Nevertheless, admonishing women not to drink while they are pregnant only works if they know they are pregnant. The problem is that half of pregnancies are unplanned (Finer and Zolna, 2011): Most of the women I talked to, whose children have FASD, report that they did not know they were pregnant. Accordingly, primary prevention misses so many women

who do not know they are pregnant. There could be an opportunity to intervene by screening pregnant women for mistakenly drinking in the first trimester and giving them high doses of choline, if it proves efficacious. For example, about 10 percent of women going into corrections are pregnant and probably represent a high-risk group. Why not screen them for drinking before they knew they were pregnant and give them high doses of choline? Of course, you could give all childbearing women prophylactic vitamins and omega-3; screen all recently pregnant females for a history of prenatal alcohol use; and, if such a history exists, give those vitamins and omega-3 to mitigate the effects of FAE. Such a plan would involve educating obstetricians about FAE and the potential benefits of choline supplementation. In this regard, their political voice could help put pressure on the Food and Drug Administration to add choline into prenatal vitamins. Fortunately, I have it on good authority that the obstetricians are starting to pay more attention to this public blight.

If the postnatal choline strategy works, we could do public service announcements to grandmothers who are caregiving for grandchildren who have learning disorders, intellectual disability, ADHD, speech and language disorders, explosive tempers, and who know that their daughters or daughters-in-law were drinking during pregnancy. Naturally, there could be collaboration with public schools to identify children in special education who have the characteristic histories of FAE, and a parallel conversation with juvenile detention centers and child welfare services. The identified children could be given choline, folate, and vitamin A. Of course, the possibilities are endless and, accordingly, it will take a diverse, multidisciplinary committee to flush them all out.

ONE SIMPLE CONCLUSION

Clearly, there is a great deal to be done regarding the huge problem of FAE. Without the leadership of the NAS and the National Academy of Medicine to create some synergy between all of the spaces where FAE shows up, I am afraid our nation will continue to flounder in this regard, and our public health will continue to suffer tremendously. By illustrating my own ignorance, I hope I have given others the courage to become aware and more involved in solving this national scourge.

REFERENCES

Alexander, M. 2010. The new Jim Crow—mass incarceration in the age of colorblindness. New York: New Press.

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APA (American Psychiatric Association). 2013. Diagnostic and statistical manual, 5th edition. Washington, DC: Author.

Astley, S. J., J. Stachowiak, S. K. Clarren, and C. Clausen. 2002. Application of the fetal alcohol syndrome facial photographic screening tool in a foster care population. Journal of Pediatrics 141(5):712–717.

Ballard, M. S., M. Sun, and J. Ko. 2012. Vitamin A, folate, and choline as a possible preventive intervention to fetal alcohol syndrome. Medical Hypotheses 78: 489–493.

Bell, C. C. 1971. A social and nutritional survey on the population of the Children and Youth Center of Meharry College of north Nashville, TN. Journal of the National Medical Association 63(5):397–398.

Bell, C. C. 1979. Preventive psychiatry in the board of education. Journal of the National Medical Association 71(9):881–886.

Bell, C. C. 1987. Preventive strategies for dealing with violence among blacks. Community Mental Health Journal 23(3):217–228.

Bell, C. C. 2011. Trauma, culture, and resiliency. In Resiliency in psychiatric clinical practice, edited by S. Southwick, D. Charney, B. Litz, and M. Friedman. Cambridge, UK: Cambridge University Press. Pp. 176–188.

Bell, C. C. 2012a. Preventing fetal alcohol syndrome. Clinical Psychiatry News 40(5):8.

Bell, C. C. 2012b. An ethical conundrum in correctional health care. Correct Care 26(2):3–4.

Bell, C. C. 2013a. Common mental health problems experienced by youth in confinement—action steps. National Center for Youth in Confinement. Available from http://nc4yc.cloudaccess.net/list-all-resources/mental-health/192-common-mental-health-problems-experienced-by-youth-in-confinement-action-steps.html; http://nc4yc.cloudaccess.net/images/resources/nc4yc_mental_health.pdf.

Bell, C. C. 2013b. Culture: A key touchstone for treatment. Clinical Psychiatry News 41(2):10.

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