Before We Know It
PRENATAL EXPOSURE
TO DRUGS AND MALNUTRITION
It was all very well to say “Drink me,” but the wise little Alice was not going to do that in a hurry, “No, I’ll look first,” she said, “and see whether it’s marked ‘poison’ or not”; for she had read several nice little stories about children who had got burnt, and eaten up by wild beasts, and other unpleasant things, all because they would not remember the simple rules their friends had taught them: such as, that a red-hot poker will burn you if you hold it too long; and that, if you cut your finger very deeply with a knife, it usually bleeds; and she had never forgotten that, if you drink much from a bottle marked “poison,” it is almost certain to disagree with you, sooner or later.
—LEWIS CARROLL,
Alice’s Adventures in Wonderland
My grandma grew dope in the basement, and everybody used to go down there on the weekends and clip buds off the dope plants and get high. And they loved to make love not war. She kind of brought the sixties into the seventies and the sixties into the eighties and then into the nineties. Outrageous! She had glaucoma, so she had a prescription for medicinal purposes to smoke marijuana . . . plus she could say she had a license to possess and grow marijuana for medicinal purposes. . . . My grandma got involved in drugs right after her first child was born. . . . She was fifteen. . . . My mom was smoking marijuana at age eleven. Alcohol and marijuana, a little heroin, a lot of prescription drugs. . . . Mom was fourteen when she got pregnant with my brother. My mom and dad knew each other because he was part of my grandma’s circle of friends. But they really met for the first time officially in church. He picked up my mother pregnant and took care of the baby even though it wasn’t his. I came along just a year and a month and a few days later. They never did get married. My dad started hitting my mom pretty early, especially when he was drinking. My mom was pretty depressed. She just laid on the couch some days and wouldn’t get up. She didn’t know what to do.
—JEFFREY, AUGUST 1996
Mom smoked cigarettes all the way through all her pregnancies. She smoked since she was a little kid and to this day. She probably did alcohol and marijuana—maybe white dope, too, I don’t know. She said she stopped as soon as she knew [she was pregnant], but I saw her with Julie [while pregnant]. They were all doing it, and maybe she stopped some time after she really knew. . . . They always fought and stuff—always fought. They fought all the time—screaming, yelling, grabbing stuff and throwing it. Always drugs. Always alcohol. I’m sure Mom was doing all of it during her pregnancy, including white dope—crack or cocaine.
—JOHN, BROTHER OF JEFFREY, AUGUST 1996
The incubation of violence happens quietly, subtly, out of sight and awareness. We don’t see it. We don’t expect it. It creeps up on little cat feet and catches us unaware, seeming to come out of nowhere. We look for its sources in all the obvious places. Fear drives our search. We are moved to think quickly, often narrowly—taking aim at the symptoms as they appear. As we move to contain one layer of problems, a new one unfolds. Old solutions don’t fit. Metal detectors replace jungle gyms as essential equipment in schools. But the tide keeps coming, its genesis unrecognized.
Ironically, babies in our culture are still commonly viewed as living in a twilight zone of unfinished wetness. Viewed as dewy-eyed and unseeing, moving only reflexively and preoccupied with little beyond eating, sleeping, and eliminating, infants have been routinely viewed as irrelevant to policy discussions concerning education, let alone the prevention of crime. But with new technology an amazing picture is emerging of the human infant. Far from the tabula rasa of John Locke’s view of the human baby, new graphic imaging reveals a riveting portrait of unmistakable complexity taking shape before we know it.
In America, we seem to think that intelligence, learning, and emotional responses suddenly kick in at birth or sometime after we are born. Graphic-imaging technology and the study of cognition and emotion in the fetus are so new that in-depth studies on fetal behavior and prebirth capacities are still sketchy chapters in the education of physicians and psychologists. Most of us have taken the period of gestation for granted as an unconscious and insensitive time of purely physical development. That assumption, based on an absence of information, has kept us believing that, beyond physical development, little about us is happening before birth. In Asian cultures, a child is considered one year old at birth, and the parent-child relationship begins nine months earlier. In contrast to most ancient cultures and many contemporary Eastern cultures, pregnancy in our country is seen as a time when only the physical structure of the brain is created. After birth, we assume that very slowly babies develop the hardware and gradually begin to develop the software for a system that has never before functioned. Even Western developmental psychologists generally refer to birth as marking the beginning of learning and feeling. Chapters in developmental textbooks on “the first year of life” begin with birth and continue to the child’s twelfth-month birthday. This belief that fetuses and babies are not sentient is a fundamental reason that we have not been successful in stemming the roots of violence.
JACK-IN-THE-BOX
The wall of the female belly has historically provided an effective shield against intrusive visual scrutiny of the developing fetus. But the advent of ultrasound gives us a new perspective through a relatively noninvasive window. As this technology has advanced, the clarity and precision of our observations have produced new information. Beginning at approximately two and a half weeks after the sperm has fused with the egg, neurons begin multiplying in the embryo at an unimaginable rate. Dr. Richard Restak, a neuroscientist and author of The Infant Mind, says:
Assuming that the adult human brain contains on the order of a hundred billion neurons and that no new neurons are added after birth, we can calculate that neurons must be generated in the developing brain at an average rate of more than two hundred and fifty thousand per minute. . . . An electrician delegated the task of wiring up a circuit as complex as that of the human brain and capable of soldering connections at a rate of one per second would take over thirty million years to complete the job.1
All of our senses are fully installed and are being test-driven prenatally. The first to develop is touch. But all will be employed before birth—which is why, to anyone paying attention, the infant is so capable of his or her incredible menu of skills and emotions upon arrival. Long before we are born, we are experiencing. Our early brain is hard at work recording sensual input, beginning with:2
Touch: By seventeen weeks of gestation, the infant can feel touch all over the body except for the back and top of the head, which have feeling by twenty weeks. At just two months the fetus will kick and jerk if poked, and by the fourth month will make facial expressions such as frowning, squinting, or grimacing if its scalp is tickled. He or she will kick violently if the mother drinks cold water.3
Taste: By fifteen weeks, taste buds are beginning to detect taste differences in the amniotic fluid due to the presence of varying chemicals.4
Hearing: By the twenty-fourth week, a baby hears the mother’s voice and the father’s, if he is close during gestation, and will distinguish them from others at birth.5 Several researchers have found that a fetus will quiet to Mozart, Vivaldi, and Bach.6 Dr. Anthony DeCasper demonstrated that French babies whose mothers repeated the same nursery rhyme while pregnant recognized it after birth. The mothers read the rhyme three times a day for a four-week period from the thirty-third to the thirty-seventh week of gestation. After birth the babies responded to the rhyme with rhythmic sucking and showed no sign of recognition of other rhymes.7
Vision: Dr. T. Berry Brazelton of Boston Children’s Hospital showed that fetuses are light sensitive from the sixteenth week. A direct light held to the mother’s abdomen will startle the fetus and cause it to move away. Some cover their eyes in response to light and their ears in response to ultrasound. By thirty-two weeks of gestation a fetus has the same capacity to see as that which is present at birth.8
In addition to development of the senses, the fetus is busy with:
Motor Development: Between ten and fifteen weeks, a cough from the mother will cause the fetus to move rapidly within seconds.9 Normal fetal functioning seems to include the practicing of reflexive movements that are necessary for later survival. New brain research indicates that the reflexive movements create sensations that provide early stimulation for the developing brain.10
Primitive Emotions and Memory: In 1994 researchers measured the impact on the fetus of a mother watching short clips of a violent movie. The fetus became agitated along with the mother as measured by heart rate and movement. And in another test, in 1981, using ultrasound, researchers observed fetuses who were experiencing amniocentesis. The fetuses responded fearfully—pulling away from the needle, defensively covering themselves—and sometimes aggressively by attempting to hit or kick at the needle.11 In light of the fact that their eyelids were still fused at the time of the testing, this is startling information. In reviewing all the evidence of the learning a baby engages in while still in the womb, Dr. David Chamberlain wrote in an article published in the British Journal of Psychotherapy in 1987:
There is mounting evidence for a theory of “cellular” memory which reaches back into the prenatal period. These memories are called cellular because they are usually behavioral rather than verbal memories and because specific parts of the body seem to hold and express these memory patterns.12
The reality is that there is no time in human development that equals fetal growth in the speed and complexity—and therefore vulnerability—of development. Long before birth, we have each developed all the basic brain cells (neurons) that we will ever have: The period of neuron proliferation begins within the first four weeks of development and is complete by twenty-four weeks. The process of neuronal migration to their intended location in the brain begins at about the same time and tapers off by about the thirtieth week. The process by which neurons differentiate to their specific functions begins at approximately fourteen weeks of gestation and continues through the first year of life. Before we know it, harmful agents or maternal experiences can have a huge impact at these crucial times, evidence of which may not appear until an affected system matures and begins to perform behaviorally. For example, early signs of an attention disorder may not become apparent until sometime after the child is walking and talking.
In summarizing the consequences of prenatal injuries to the brain, many of which may not be detectable until later development, Dr. Restak says:
If this complex process of migration is disturbed by genetic factors or toxins, the cells may not reach the proper position. If it is extreme, the fetus will be aborted. If it is milder, the pathologist would detect this malformation. However, if it is even milder, it will not come to the pathologist but to the psychiatrist.13
More likely, depending on the environment of the child, psychiatrists will share this role with judges. Research provides convincing evidence that violent criminals have poorly functioning brains. Low verbal IQs, attentional problems, impulsivity, poor school performance, inadequate processing of information, inflexibility, restlessness, agitation, and difficulty processing social cues are all characteristics commonly associated with criminal behavior. Adverse conditions during pregnancy are the seeds of significant distortions found in the brains of many violent criminals. The growing number of children who are surfacing at school age with attention deficits and other learning problems is compelling evidence that prenatal neurological damage is an escalating problem, a problem that may become more severe given the rise in drug use by children under eighteen.
While prenatal exposure to drugs in and of itself is probably not as strong a factor in producing violent children as later negative circumstances and experiences, the prenatal environment is a crucial protective opportunity. The quality of the prenatal environment can either maximize healthy development or create biological and behavioral vulnerabilities in a child’s brain. Children born already impaired are more likely to be the brunt of destructive parenting behaviors and abuse. They are less likely to do well with those consequences than a child with greater emotional and cognitive resources, such as an ability to recover quickly from frustration and to sort out relevant information from irrelevant distractions while learning a skill.
Witness the story of Eric Smith. Different from the beginning, Eric was born with protruding ears that curled inward, a minor physical anomaly that we now know often signals subtle neurological irregularities. As a toddler he was slow to walk and talk, and his mother enrolled him in an early intervention program for stimulation and therapy. Until he was four, Eric had frequent violent tantrums during which he would bang his head on the floor and hold his breath. Due to developmental delays, by school age he stood out from other children, who made fun of him. He had learning problems and was held back for two years in his grade school. By his mother’s accounts, given in court, he complained often that he was stupid and was “never going to be anybody.” When he was nine, Eric tried to choke a neighbor’s cat. He set fire to paper on the stove in the middle of the night. The mother of another child recommended to Eric’s mother that she get counseling for Eric concerning his school, behavioral, and self-image problems. Eric’s stepfather, Ted, who had adopted Eric, argued frequently with Eric’s mother, Tammy. He physically disciplined the children, including Eric’s older and younger sisters. According to Ted, by early adolescence, Eric was afraid of his own temper and had confided that “he wanted to hurt somebody.” He soon acted on his desire.
On a summer morning in 1993, when Eric was thirteen, a neighbor living adjacent to a park said she heard what she thought was “a child’s scream.” When she went to check, her dog was barking at two cats, and she assumed they had made the noise. Before she left for work ten minutes later, she saw Eric ride by on his bike. Later that morning, a sudden rainstorm hastened the mother of four-year-old Derrick to the park to pick her son up from a summer recreation program. A counselor told her that Derrick had never arrived. Terrified, Derrick’s mother searched the school yard next door, checked neighbors’ houses and the church where her son went for day care. Soon a police search was under way. Neighbors joined with helicopters in looking for Derrick. Eric’s dad was one of the volunteers.
They found Derrick’s body that afternoon among the weeds on the property of the woman who had heard a child scream. The injuries inflicted on his small body were shocking in their brutality. Derrick had been bludgeoned repeatedly in the head and chest, choked, and sodomized with a stick. That night Eric stayed overnight at the home of the woman who had urged Tammy to get counseling for Eric. She recalled that he seemed frightened. What she didn’t know was that during the night Eric burned the nose of her teenage son with a cigarette while he slept. The following day the police still had not identified a suspect for Derrick’s savage death. Eric asked the neighbor what might happen if the killer “turned out to be a kid.” The neighbor once again went to Tammy out of concern for Eric, and at this point, Tammy took Eric to speak to the police who were investigating the crime. Under pressure from his mother, grandfather, and great-grandfather when his story proved to be inconsistent, Eric finally confessed.
Eric’s account to the police of what happened was straightforward. He told them he “wanted to take [Derrick] someplace and hurt him.” According to Eric’s account, on seeing the four-year-old walking alone the short distance to the park, Eric lured him into the weeds, choked him, stuffed a napkin and plastic bag from Derrick’s lunch into the little boy’s mouth, and struck him repeatedly with rocks, one weighing twenty-four pounds. He stuck a sharp twig up Derrick’s anus and poured Kool-Aid from Derrick’s lunch box into his wounds. He then pulled the little boy’s body into the weeds and rode away on his bike. But as he thought about what he had done, he worried that Derrick might still be alive and would tell someone, and so he went back to make sure that Derrick was dead.
At the trial, Eric appeared emotionless. Two psychiatrists testified as to the numerous social and biological factors contributing to Eric’s violent behavior. The complex recipe resulting in Eric’s impaired brain and antisocial behavior began with a family history of alcoholism and depression. The doctors testified that his strange ears and slow development were likely caused by his mother’s ingestion of trimethadione, which she took for epilepsy during the crucial first months of Eric’s gestation. Changes in Eric’s living situation and harsh physical discipline by his stepfather added to the problem. The medical testimony established that Eric had a mild attention-deficit/hyperactivity disorder. One psychiatrist diagnosed Eric as having an “intermittent explosive disorder.” In an account of Eric’s story published in the Ladies’ Home Journal, author Ronny Frishman wrote:
The psychiatrist cited other factors contributing to Eric’s mental illness: a family history of alcoholism and depression, his loneliness and the physical punishments he endured. He attributed Eric’s low self-esteem in part to his slow development and odd physical features, particularly his protruding ears. Physicians concluded that both abnormalities were caused by the anticonvulsant drug, trimethadione.14
At the time, Eric was the youngest person in the country ever to be tried for murder as an adult. He was tried and found guilty of second-degree murder. He was sentenced at age fourteen and is still serving his sentence (nine years to life). Since 2002, Eric Smith’s case has been reviewed six times. He was denied parole each time out of concern for public safety and the objections of the victim’s parents.
There are two areas of research that shed some light on the story of Eric Smith. The first of these focuses on teratogens, which are implicated in Eric’s mother’s testimony about the prescription drugs she took while pregnant with Eric. The second area, which we are just beginning to recognize, is the effect of prenatal stress. Particularly when such stress occurs simultaneously with exposure to teratogens, the effect on the developing brain may be profound.
PASSIVE POISONS
Until the 1950s, the development of the human fetus was commonly viewed as a genetically controlled operation. Sealed in the safety of the womb, fetal life seemed inviolate to outside influences. That was before thalidomide, a drug widely tested and commonly prescribed for anxiety and nausea, the bane of many pregnant women. In West Germany thalidomide was so widely used that it was released to nonregulated, “over-the-counter” consumption. Less known in the United States, it became a household word when it was linked with a wave of babies born with serious deformities, particularly in the limbs.
Since the 1960s, science has warned us of the risks posed by a wide array of drugs, both legal and illegal, to the physical development of the unborn. It is only in the last two decades, however, that we have begun to make the link between those drugs and behavioral risks, including later aggression and violence. Chemical or physical agents that cause fetal malformation are known as teratogens. The root of this term is the Greek word teraton, “monster.” Teratogens tend to selectively damage certain organs. The type and extent of the damage depends on the timing of the exposure, the quantity consumed, and the sensitivity of the developing organ to the teratogen. The exact processes whereby teratogens take their toll on the developing brain are still being researched. Fetal brain development may be directly affected by a particular toxin that kills developing cells. Or the damage may happen indirectly by the alteration of neurochemicals or impairment of the placental function.
Alcohol, nicotine, lead, and cocaine are teratogens, each of which has been associated with an array of later behavioral problems. Lead, in particular, has been directly linked in some children to violent behavioral patterns such as impulsive rage, aggression, and paranoia. Other teratogens, such as nicotine, while not directly linked to violent behavior, are linked to negative physiological and behavioral changes that can be the precursors of aggression. For example, nicotine is a cause of low birth weight and prematurity, which may later unfold into increased risks of learning disabilities, difficulty in connecting emotionally with others, and neurological impairments such as attention-deficit disorder. These characteristics may render children at greater risk for school failure, lowered self-esteem, and alienation, which in combination with environmental factors may place them at a higher risk of becoming violent. Any teratogen that renders a child relatively more vulnerable to subsequent environmental risks by weakening his or her basic physical, emotional, or cognitive capacities may be viewed as indirectly contributing to antisocial behavior. The vast majority of these precursors to aggression are preventable.
The bridge between prenatal exposure to teratogens and later violent behavior occurs quietly in the recesses of the fetal brain. It is difficult to establish whether an individual fetus is affected and, if so, how and when the damage occurred. Scientists are just beginning to understand these complex processes. Generally speaking, that which enters the mother’s bloodstream also enters the baby’s. There is a “blood brain” barrier that serves to protect the central nervous system so that many toxins that easily enter into the cells of other soft tissues, such as muscle, do not enter the brain. The integrity of this barrier, however, varies with the age of the fetus or infant. An immature brain allows many more substances through. When a toxin crosses the barrier, not all areas of the brain are affected equally. There are considerable variations in the adverse consequences of a given toxin, which are based on the impact of neurochemistry on different vascular patterns and differing cell types.15
At the time of birth, approximately 3 percent of infants in the United States have observable physical defects.16 The subtle effects of toxins on certain regions of the brain may not be picked up until even later, when the development of the child reveals impairments to a part of the brain as it comes into play in the child’s development. Babies exposed to alcohol or cocaine may appear normal at birth. But tiny time bombs may be ticking away—waiting for the maturation of the affected system.
While the nature of the teratogen, factors in the mother, and perhaps even the fetus’s constitution may play a role, by far the greatest determinant of fetal damage is the timing of the developmental processes that are under way at the time of exposure. For example, thalidomide had an effect only on the babies of women who took the drug between the thirty-fourth and fiftieth days after their last menstrual period. The window of vulnerability was very specific. And the effects were even more so. If the drug was taken between the thirty-ninth and forty-fourth days, the baby’s arms were stunted or missing at birth. If the exposure was between the forty-second and forty-eighth days, the baby’s legs were shortened or absent. Exposure on days forty-one to forty-three affected the hands as well as the limbs of babies at birth. Babies of mothers who took thalidomide less than thirty-four or more than fifty days after the last menses showed no malformations.17
The same rule applies to other drugs that affect the fetus by interfering with and minutely altering brain development. The impact on the baby’s brain of drugs such as alcohol, nicotine, and cocaine depends on the specific neurological process under way at the time of exposure. There are similarities in the impact of several teratogens that are due to timing of the insult. It appears that there is a period of great vulnerability to many types of drugs and to alcohol during the embryonic period, which is defined as the first eight weeks of pregnancy. This period, which precedes the period of fetal growth (eight weeks to delivery), is the time of organogenesis, when cells are first dividing, proliferating, specializing, and then migrating to their permanent locations.
Unfortunately, this is a time when many women are unaware that they are pregnant. The subsequent detection of damage due to early drug consumption is often confounded by a mother’s pain in confronting her fears and guilt about the impact on her baby of her early, sometimes unwitting, use of drugs or alcohol. Her denial may reduce the likelihood of clear, early diagnosis. Fetal alcohol syndrome and its effects, for example, are often undetected in their earliest manifestations in infancy both because they are difficult to recognize and because physicians and mothers are uncomfortable with this conversation.
The impact of drugs on the fetus is now widely publicized. In the 1990s, most of us were aware of the potentially destructive effects of harmful substances like cocaine and alcohol. It is interesting to note, however, that in our culture when we think about “drug-affected babies,” crack—and, more recently, meth—comes immediately to mind. Beginning in the mid-1980s, crack-exposed babies had the media and American public on red alert: A wave of cocaine-exposed newborns would soon overrun the schools. Television news footage poignantly featured tiny newborns, small for the months of gestation or born prematurely. We watched their little bodies shake and startle with tremors and seizures as they endured the agony of withdrawal from the substances their mothers had taken to avoid their own pain. Apprehension approaching panic permeated our observations of these children, particularly among the child-focused professions.
But the wave of brain-damaged babies never materialized—at least not in the form ominously predicted. Some cocaine-exposed children did mature showing evidence of attention deficits, an increased rate of learning problems, and distractibility. But most “crack babies” who were placed in nurturing and stimulating foster care or adoptive homes now perform normally and are generally undistinguishable from their peers.
Studies indicate that prenatal exposure to cocaine does have serious consequences but not—as was previously feared—in physical growth, developmental test scores, or language outcomes. Cocaine exposure in utero can interrupt the flow of nutrients and oxygen to the fetus, which increases the risk of premature birth, low birth weight, and many other problems. By the time a cocaine-exposed baby goes to school, the effects are in subtle areas such as sustained attention and self-regulation. Newer research, however, shows little impairment directly attributable to cocaine in key areas such as growth, IQ, academic achievement, and language. While many of the children studied did have lowered IQ and poor academic and language achievement, it appeared that these difficulties may have been caused by the negative home factors that are associated with cocaine use, rather than from the cocaine itself.18
While the role of other addictive substances continues to capture our attention, alcohol is the most pervasively used and renders the most documented damage to babies. In January 1994, Alcohol Health and Research World revealed in a survey of drug use by women during their childbearing years that among women ages eighteen to twenty-five and twenty-six to thirty-four, 84.7 percent and 89.8 percent respectively reported lifetime alcohol use. Approximately 55 percent of the women reported use within the previous month. By contrast, only 9 percent of the women reported ever using cocaine, and less than 0.5 percent reported using it during the previous year. Less than 1 percent (0.8 percent) of the women reported ever using crack cocaine. Alcohol use by women is highest among young, unmarried Caucasian women who are better educated, with higher incomes, and who work outside the home.19 Crack use was highest among African American women. And most women who use crack also use alcohol and nicotine.20
From all that we currently understand, drawing on multiple studies, about the relative effects of cocaine versus alcohol, alcohol appears to have more enduring effects on the brains of far more children. Clear conclusions as to the long-term impact of cocaine are confounded by the fact that cocaine-abusing mothers may also be using alcohol and nicotine while dealing with other traumatic factors like domestic violence and depression. But we do know without a doubt that fetal alcohol syndrome from alcohol use alone is a major cause of retardation. Given the documented impact of alcohol versus cocaine, and the huge disparities between the numbers of women abusing alcohol or abusing cocaine, we appear to be pointing to the wrong drug and the wrong people in our concern about drug-exposed children. Many experts believe that fetal alcohol exposure, particularly because it may occur undetected and go untreated, may well be the single largest factor setting up physical and neurological conditions that predispose American babies to aggressive and violent behavior.21
TEETER-TOTTER, FIRE AND WATER
The ways in which teratogens affect the fetus, in addition to the current data on the scope of the problem, are summarized below. Each of these drugs is the subject of numerous studies. They appear in the order of their popularity and use among childbearing women. This summary is limited to variables that are linked to aggressive behavior.
Alcohol: Exposure to alcohol during fetal development causes a continuum of effects, the most extreme of which is fetal alcohol syndrome (FAS). Fetal alcohol syndrome is characterized by abnormal facial features, including a smooth ridge between the nose and the upper lip, a thin upper lip, and a short distance between the inner and outer corners of the eyes, giving the eyes a wide-spaced appearance. These babies are often born prematurely. Abnormal growth issues are also common—the children are generally small, often below the tenth percentile for height and weight. They often have smaller than normal head size and can have poor coordination and muscle control, indicating the devastating impact of the drug on the brain. As the child develops, cognitive deficits (e.g., low IQ) or developmental delays—including learning disabilities as well as executive function deficits like poor organization and planning, lack of inhibition, difficulty comprehending cause and effect, poor judgment, and inability to apply knowledge to new situations—are common characteristics of FAS. Attention problems and social skill impairments are frequent challenges for these children. They have difficulty learning from their own mistakes and “common sense” is often outside their grasp.22
Over the last two decades we have begun to realize that prenatal exposure to alcohol can have a range of subtler effects on a child’s development. Many affected children do not have the physical anomalies associated with FAS and they may look normal at birth and for a year or two. Though they are often small for their ages, recognition of the effect of their prenatal experience is often not discerned until later in their development when the part of the brain that was affected comes into play—often in subtle cognitive differences that affect learning, following and remembering directions, consistent poor judgment, and impulsivity. Once referred to as “fetal alcohol effects” (FAE), this broader range of subtler effects stemming from alcohol exposure is now viewed as a spectrum ranging from mild to severe with FAS at the extreme end of the spectrum and including all the varied manifestations of FAE, ARBD (alcohol-related birth defects), and ARND (alcohol-related neurodevelopmental disorder) along the continuum. The entire spectrum of disorders taken together is referred to as “fetal alcohol spectrum disorders” (FASD), which include physical and behavioral as well as motoric and learning differences.
There is growing recognition that many adults as well as children have historically been overlooked or mislabeled, as they evidenced varying pathologies that effect the cortical brain but did not fit into the earlier FAS or FAE diagnostics. Now that is changing. The research in this area is burgeoning and there is growing clarity regarding the brain and how and when it is built—all are hopeful. But more and more evidence points to prenatal exposure to alcohol as the major—and insidiously common—culprit in the rising rates of learning and behavioral difficulties that can set children up for later aggression and violence, for school failure, for relational and social problems of all kinds.
Alcohol (ethanol) ingested by the mother crosses the placenta and can alter the development of the fetal nervous system by interfering with cell migration, the production of neurotransmitters, and brain growth. Even before the mother is aware of her pregnancy, alcohol may have caused significant damage. The placenta operates like a sieve, and the immature liver cannot process alcohol, so the mother’s liver is functioning for both of them. When the mother is drinking, so is the fetus.
Immature neurons first appear around the eleventh day after conception, when the embryo is no larger than a grain of rice. If at this time a mother is drinking to the point of intoxication, alcohol may affect the growth and differentiation of the neural cells. Early and excessive alcohol consumption causes chromosomal aberrations, impedes the transfer of essential nutrients through the placenta, and impairs the baby’s immune system. The possible damage to a fetus associated with intrauterine exposure covers a wide range of systems such as heart, kidneys, limbs, lungs, skin, and connective tissue. But the effects of alcohol that play the greatest role in setting up later violent behavior are those that affect the brain. Cognitive deficits, learning disabilities, and behavior problems, including attention deficits, hyperactivity, and high distractibility, are all strongly associated with fetal alcohol syndrome and fetal alcohol effects.
Many studies confirm the long-term teratogenic effects of prenatal alcohol exposure on infants, children, adolescents, and adults. The symptoms evolve with maturation. A baby can be born with visible distortions of the face that are hard to recognize in the newborn. As the baby progresses through the first months, damage to the central nervous system may gradually become detectable when he or she is slow to walk and talk and has difficulty learning and remembering new skills.
One study conducted in 1993 followed 382 inner-city mothers and their babies prenatally and throughout the child’s first year. Based on bimonthly prenatal interviews of the mothers, the researchers calculated the amount of alcohol consumed during pregnancy. At birth, the infants were divided into groups reflecting the timing and amount of the mother’s alcohol consumption. The infants were followed at regular intervals for a year to assess their cognitive development. The study found that there were clinically significant effects on mental performance even in infants prenatally exposed to as little as .5 ounce of alcohol per day, less than the amount in a single drink. The number of children with discernible mental handicaps more than doubled with exposure to one drink per day. Another study of fifty-three eighteen- to nineteen-month-old toddlers corroborated these findings. The children exposed to alcohol during the first two trimesters or throughout pregnancy scored significantly lower on later assessments of language and other cognitive tasks. Continuous exposure to alcohol throughout gestation resulted in impairments to both gross- and fine-motor skills such as walking and self-feeding.23
As with thalidomide, specific birth defects from alcohol exposure are related to the quantity and timing of the mother’s consumption relative to the specific developmental processes under way in the fetus, irrespective of other factors such as family history or the nutrition of the mother. Pregnant women who consume between one and two drinks per day are twice as likely as nondrinkers to have low-birth-weight babies and are at increased risk of miscarrying during the second trimester of pregnancy.24 Chronic heavy alcohol consumption, which is defined as three or more drinks a day, throughout pregnancy usually results in retarded physical growth and impaired brain functioning together with the classical facial indications of fetal alcohol syndrome. Facial malformations are linked to alcohol exposure during the first eight weeks. The effects on head circumference and brain growth appear to be linked to exposure in both the first and the third trimesters. One study has connected minor physical anomalies in children to heavy drinking (defined as one drink per day) at or around the time of conception. Defects in learning and motor skills are associated with exposure in the third trimester.25
Episodic binge drinking, which is defined as six or more drinks in one day, or regular consumption in just the first and second trimesters increases the probability of general developmental deficits, delayed speech acquisition, and skeletal abnormalities. Alcohol abuse limited to the third trimester can have a negative impact on future cognitive and behavioral functioning. Moderate social drinking anytime during pregnancy, especially in the first eight weeks, may result in more subtle neurological deficits such as attention difficulties or memory problems.26
Every year, approximately 40,000 babies are born with symptoms of prenatal alcohol exposure. A 2011 report from the U.S. Department of Health and Human Services Substance Abuse and Mental Health Services Administration (SAMHSA) states:
Among pregnant women aged 15 to 44, an estimated 10.8 percent reported current alcohol use, 3.7 percent reported binge drinking, and 1.0 percent reported heavy drinking. These rates were significantly lower than the rates for nonpregnant women in the same age group (54.7, 24.6, and 5.4 percent, respectively). Binge drinking during the first trimester of pregnancy was reported by 10.1 percent of pregnant women aged 15 to 44. All of these estimates by pregnancy status are based on data averaged over 2009 and 2010.27
Perhaps the most damaging combination of all to a baby is prenatal alcohol exposure in conjunction with maternal stress. Dr. Mary Schneider, of the Harlow Primate Laboratory at the University of Wisconsin at Madison, believes that this is the worst possible combination for producing aggression in offspring, particularly when it occurs early in the pregnancy. In discussing her research on the long-term impact on rhesus monkeys of prenatal exposure to alcohol combined with maternal stress, Dr. Schneider says:
These animals look sort of ADD [attention-deficit disordered] when they’re younger. Later, they are the most aggressive in their peer groups, especially when those groups are just forming. It appears that early gestational stress is more harmful than mid- or later-term stress.28
When the same monkeys were tested for learning and memory tasks at twelve to eighteen months, which is equivalent to about five years of age in humans, they were highly destructible, were delayed in their motor development, and had lower than average muscle tone and activity levels. But then they would unpredictably flip into high intensity and become very impulsive in their learning tasks.
Taken together, the studies indicate that there is no safe time or safe level for fetal exposure to alcohol. Dr. Paul Lemoine, the French physician who first discovered FAS in 1968, found that it appears that tobacco further facilitates the damaging effect of alcohol on the fetus. Lemoine says that in even “moderately alcoholic” mothers, heavy smoking greatly increases the chance of FAS.29
Alcohol consumption by the father may also be a factor affecting fetal intellectual development. While the researchers theorize that there may be a genetic link, none has yet been confirmed.30 There is general agreement, however, that the sons of alcoholics, regardless of how they were raised (e.g., adoption by nonalcoholic parents), have a higher incidence of alcoholism. The heritability of alcoholism is currently being studied. It also appears that alcohol abuse by a male may affect his ability to produce normal offspring. Studies done on rodents show that delayed sexual maturation and onset of puberty are consistent outcomes of paternal alcoholism.31 Researchers postulate that alcohol and other drugs may impair the sperm directly, or that the chemical composition of semen is altered so that the ejaculated sperm may be affected, or that certain sperm may be selected for survival following prolonged exposure to alcohol. Questions have also been raised as to the impact on the ovum or embryo of semen that has been negatively affected by alcohol. Further research on these theories is currently under way.32
Fetal alcohol syndrome is the leading cause of mental retardation in the Western world, surpassing even Down syndrome, cerebral palsy, and spina bifida. Difficult to estimate, the rate of FAS ranges between 0.5 to 2.0 cases out of every 1,000 live births, with costs to the nation estimated at more than $4 billion annually. In 2002, the lifetime cost for one individual with FAS was estimated to be at least $2 million.33 The incidence of FASD is three times that of FAS. These exceptionally high costs—in both human and economic terms—are clear justification for major prevention efforts.
In children adversely affected by prenatal exposure to alcohol, we see the entire spectrum of educational, social, and behavioral problems that compromise their future. With measurable deficits in IQ ranging from profoundly retarded to low normal, these children perform very differently in school than their nonexposed peers. They have problems with short-term memory on both verbal and visual tasks, difficulty in processing information, very low comprehension in mathematics, and inflexibility when solving everyday problems. In addition to these cognitive impairments, 85 percent of FAS children have attention deficits combined with hyperactivity (ADHD). Because the ADHD percentage holds true regardless of wide environmental differences among these children, this outcome provides clear evidence of the permanent damage alcohol wreaks on the central nervous system during fetal development.
FAS children also show a variety of social deficits. One longitudinal study found that parent ratings of 158 of these children placed them at the ninety-first percentile on a mean ranking of social problems.34 They were stubborn and hard to discipline and had extreme difficulty in respecting their own and other people’s boundaries. The FAS children inappropriately sought affection and demanded attention and were overly tactile with other people. Other children avoided them.35
The tragedy of FAS children and their parents is poignantly told by Michael Dorris in his book The Broken Cord. Dorris describes the anguish of learning that his adopted son, Adam, is permanently “learning disabled” at the time Adam is in kindergarten:
My son, however, was not destined to follow in my musical or medicine ball footsteps, nor was he likely to become, according to his WPPSI scores, a star in any other field. The psychologist’s summation of Adam’s performance was less than encouraging. His overall IQ fell into the “borderline” category, and his skills ranged from approximately a year below his age level in some visual tasks to considerably greater disparities from the norm in “areas requiring attention to auditory input.” This translated to mean that Adam had trouble concentrating, particularly when dealing with abstractions. Furthermore, he was found to be more active than expected for his age level, impulsive in his approach to tasks, and highly destructible (“both auditorily and visually”).
I listened, stunned with disappointment and worry, as she outlined a recommended educational program for “children like Adam.” If he were to be in a regular school, he would require lots of external structure and would have to avoid “overstimulation.” A teacher might want to provide him with a “study booth” set apart from his classmates to ensure a distraction-free environment. The main body of the psychologist’s eventual written report concluded with the sentence: “In the same sense, monitoring of TV programs and movies would be even more important to a child like Adam, as he is highly stimuable and unable to inhibit the excitement once the wheels are set in motion.”36
As FAS children mature, these characteristics may become more pronounced. Long-term follow-up typically shows an increase in attention deficit and hyperactive behaviors when children’s scores in grade school are compared with their earlier preschool scores. As the children become adolescents, they often show an increase in distractibility, impulsivity, inattentiveness, disorganization, restlessness, and agitation, and they become less cooperative.37 Lack of judgment, poor decision making, high frustration, impulsivity, and difficulty in perceiving social cues render these children at high risk for aggressive behavior and of being co-opted by negative role models during adolescence. When Lemoine went back to find 124 of the 127 FAS patients who first brought the FAS diagnosis to public knowledge, he found 106 of them in institutions.
Michael Dorris’s account of his personal journey with Adam is testimony to the fact that, even with loving parents and exceptional resources, the damage is not reversible. In the foreword, Dorris’s wife, noted author Louise Erdrich, writes:
Yet, in loving Adam, we bow to fate. Few of his problems can be solved or ultimately changed. So instead, Michael and I concentrate on only what we can control—our own reactions. If we can muster grace, joy, or happiness in helping him confront and conquer the difficulties life presents . . . then we have received gifts. Adam has been deprived of giving so much else. . . . Everyone agrees that the best answer is not to lock up pregnant women, but to treat them. However, this problem is now generations in the making. Women who themselves suffer from Fetal Alcohol Syndrome or Effect are extremely difficult to counsel because one of the most damaging aspects of FAS is the inability to make cause-effect connections, or to “think ahead.”38
Tobacco/Nicotine: Among women of childbearing age, cigarette use occurs as frequently as alcohol use. But women are less likely to decrease tobacco use than the use of other drugs while pregnant. Women who smoke are most likely to be Caucasian, married, less educated, and users of alcohol and illicit drugs. Tobacco exposure correlates with low birth weight, prematurity, lung disorders, and sudden infant death syndrome.39 Nicotine-exposed children may experience delays and difficulties in performing the basic tasks of infancy such as eye contact, sucking, and head turning. Dr. David Olds and his colleagues found that by ages four and eight, children born to mothers who smoked had IQs that were four to five points lower than the comparison group of children born to nonsmoking mothers. At school age, children of mothers who smoke may be at risk of poor reading skills, attention deficits, and hyperactivity.40
Prenatal exposure to nicotine may also directly affect the developing brain.41 Data from the Ottawa Prenatal Prospective Study done in Canada in 1992 show that prenatal exposure to nicotine, as to alcohol, is related to impulsiveness and attention deficits in six-year-olds.42 Another report, using a national sample in the United States, found that prenatal exposure to tobacco predicted an increased rate of behavior problems in children ages four through eleven.43 Numerous studies have found small deficits in intellectual development and higher rates of hyperactivity attributable to smoking during pregnancy.44
Smoking seems to do the most damage during the last four months of pregnancy. Birth weight does not appear to be affected by smoking before the end of the fifth month. The implication of these findings is that reduction in smoking even as late as mid-gestation may be enough to effectively protect the developing fetal brain. By supplying the fetus with greater nutrients and oxygen and by reducing the cerebral cortex’s exposure to nicotine, many potential problems can be averted.45 In 1995 Brigham and Women’s Hospital in Boston reported that smoking by pregnant women was linked to the deaths of 5,600 babies, 115,000 miscarriages, 53,000 low-birth-weight babies, and 22,000 babies who needed intensive care at birth each year in the United States. The study stated that 18 percent to 19 percent of all pregnant women smoke. Another 3,700 children die each year by the age of one month from complications caused by tobacco smoke during the mother’s pregnancy, many because they were too tiny to survive. Also attributed to smoking by pregnant women are 1,900 cases of SIDS (sudden infant death syndrome) annually. Tobacco has been implicated as an exacerbating factor in increased impairments to the fetuses of women who drink alcohol. Yet in 2008, approximately 13 percent of women reported smoking during the last three months of pregnancy. Of women who smoked three months before pregnancy, 45 percent quit during pregnancy, with 50 percent of those relapsing within six months after delivery.46
Lead: Lead has long been linked with a capacity to induce abortion, a use to which it was commonly put at the turn of the century to terminate unwanted pregnancies. In high doses, lead will cross the placenta and accumulate in the fetal bones and liver. Contaminating pregnant women through water from old pipes, old paint, improperly glazed dishes, and gasoline emissions, this toxin appears to be showing up more, particularly in the blood of urban children.47 Lead’s most invasive impact is on the nervous system, whether prenatally or postnatally absorbed. Studies show that lead absorption by children can lead to a lowering of IQ and a significant increase of impulsivity, distractibility, and learning disabilities.
A 1996 study by Dr. Herbert Needleman, professor of psychiatry and pediatrics at the University of Pittsburgh Medical School, found that even when race, poverty, and family stability are taken into account, low levels of lead significantly increase the rate of attention problems, aggression, and delinquency. Children who had been exposed to lead showed no external physical differences from normal children; the effects were entirely behavioral. Needleman believes that lead acts on the neocortex in such a way as to block its ability to limit impulsive behavior. He estimates that 1 in 12 children are affected, primarily boys growing up in urban communities where old pipes, old paint, and auto emissions are concentrated. In February 1996 during an interview on National Public Radio, Needleman stated that 5 percent to 20 percent of criminality could be prevented by “removing lead from old housing stock before it gets into children rather than removing it from children once it gets into their bodies.”
The connection between later criminality and the early poisoning of brain tissue triggered a study by Deborah Denno, a law professor at Fordham University in New York. Denno looked at a group of nearly five hundred boys from birth to age twenty-three. To her surprise, rather than the family factors, which she expected to be the largest contributing factor to delinquency, she found that lead poisoning is the single best predictor of boys’ disciplinary problems in school. These problems are in turn associated with later adult crime.48
Cocaine: Cocaine-exposed babies show clear signs of addiction at birth. Researchers have found that babies exposed prenatally to cocaine, as to alcohol, have a lower weight at birth, are shorter, and have a smaller head. They cry (often piercingly), shake, show erratic sleep-wake cycles, have trouble feeding, and are difficult to comfort. Due to its effect of raising blood pressure and restricting blood flow to the placenta, cocaine increases complications during pregnancy, including prematurity, preterm labor, precipitous labor, and premature detachment of the placenta.49
Despite the initial press and public hysteria, the long-term impact of prenatal exposure to cocaine is not yet clear. During the late 1980s and early 1990s a series of studies measuring intelligence and motor skills failed to find significant differences between cocaine-exposed babies and nonexposed babies. The tests used in these studies, however, did not directly measure the babies’ abilities to regulate emotional states or their attentional capabilities. More recent research, on both other animals and infants, suggests that cocaine may damage the areas of the brain that regulate the capacities for arousal and attention—areas that may not show up except on more finely tuned assessments, which are typically not performed until later in life when some affected children show attentional or emotional differences in a classroom setting. Cocaine-affected children are frequently more reactive to stimuli, have a reduced ability to modulate their level of arousal, and have more difficulty focusing and attending to specific stimuli. Researchers believe that the most serious damage occurs during the first trimester of gestation. Cocaine exposure at that time may irreversibly alter the development and function of neurotransmitters that are key to assuring that the embryonic brain cells migrate to their proper place in the cortex. This process, which is completed during the first 120–125 days of life, has a profound impact on synaptic development, which begins during the third trimester of gestation and continues for the first few years after birth. These interruptions of cell migration due to cocaine exposure may result in minute differences in brain wiring, later causing children to become more agitated in the face of novelty or stress, and more destructible and less persistent in completing structured tasks.50
In one study done at Yale University by Dr. Linda Mayes, three-month-old infants who had been exposed to cocaine in utero had a more difficult time processing novel information than nonexposed babies. For example, rather than becoming alert and showing interest in a picture of a new face, they became overaroused and irritable more quickly, showed more negative facial expressions, and cried for longer periods of time. Researchers have also reported significant differences between cocaine exposed and nonexposed preschool children in individual developmental domains such as speech and language.51 Mayes warns, however, that most cocaine-abusing mothers may use one or more additional drugs and that not all babies are affected: “It’s very hard to separate out these effects in a human study. Most of these children are also growing up in complicated and tragic worlds where many of the effects of prenatal drug exposure, including cocaine, are combined with environmental neglect due to the mother’s illness.”52
While the worst of the anticipated effects of prenatal cocaine exposure have failed to appear, children who have had such exposure remain at high risk. During the initial withdrawal from cocaine dependency following birth, they are difficult babies to care for, even in supportive and loving environments. But when these infants are entrusted to parents who are themselves addicted to drugs, child neglect and abuse rather than prenatal toxicity may be the real threat to the developing child. Addicted parents leave their babies with multiple, often unskilled caregivers; the children are often malnourished, poorly housed, and deprived of the experiences and opportunities for play necessary for normal cognitive development.53 Cocaine-abusing parents also tend to be agitated and inconsistent in their responses to their babies. Capacities for trust, self-esteem, focused learning, and problem-solving skills may be diminished by lack of competent adult attention. In addition, parents who use illegal drugs are also frequently involved in the criminal justice system. As a result, cocaine-exposed children often grow up without a consistent adult to teach prosocial values. In an environment where antisocial behaviors may be the norm, aggressive, even violent, behavior may be an everyday response to minor irritations.
Dr. Mayes, who has spent much of her career studying the long-range impact of teratogens on children, believes that the real poverty such children face goes well beyond a lack of dollars. Rather, it is a deeper emotional impoverishment caused by such factors as the absence of adult time and consistent loving attention, or the presence of parental depression or chronic medical problems that push the child’s needs into the background. “Too often with these children there is a poverty of attention, consistency, safety, health, stimulation, and basic attention to the child’s needs,” Dr. Mayes says. “And, when we lose one generation, we really lose several.”54
The number of children born exposed to cocaine in utero has not significantly changed in the last decade; it exceeds 100,000 children annually.55 While hundreds of thousands of such children remain in the care of drug-addicted parents, the number in foster care continues to rise. Because children in foster care are often moved from one home to another and not provided with the therapy necessary for children to deal with the loss of parents, placing the children of drug-abusing parents in foster care does not generally offset the early risks associated with later violent behavior.
Marijuana: Marijuana seems to have its strongest impact on the verbal and memory domains of learning. Children who were prenatally exposed to marijuana were tested at age four as part of the Ottawa Prenatal Prospective Study. On cognitive tests, marijuana-exposed children showed lower scores on both the verbal and the memory tasks. Another study focusing on six-year-olds exposed to marijuana found that they performed poorly on tasks requiring attention. The mothers of these children described them as being impulsive and hyperactive.56 While these studies are far less numerous and less conclusive than those done on alcohol, tobacco, and cocaine, they are of interest due to their relevance to both cognitive and behavioral problems that may place children at relatively greater risk of aggression. To date, there are no studies reported that examine the correlation between prenatal exposure to marijuana and behaviors identified as antecedents to later aggressive behavior.
Heroin: Studies consistently link prenatal heroin exposure to a relatively low incidence of brain damage (6 percent) that includes microcephaly and cerebral palsy.57 As with the other drugs, decreased head circumference, increased prematurity, and decreased birth weight are associated with parental heroin addiction. Like the cocaine-exposed babies, infants born to a mother addicted to heroin go through withdrawal and there is an increased risk of infant death. It is interesting to note that children born to heroin-addicted fathers (7.9 percent) showed higher rates of neurological impairment than children born to heroin-addicted mothers (6 percent).58 It is uncertain whether this is due to a genetic effect or to environmental neglect.
A study of eighty-three Israeli children born to heroin-addicted mothers showed that the environment after birth exerts a strong influence on developmental outcomes. Twenty percent of the heroin-exposed children who were adopted at a young age had attentional problems at ages five and six compared to 75 percent of children raised by a biological parent or parents. The conclusion of this 1995 study was that when one or both parents are addicted, severe environmental deprivation is the key factor influencing children’s performance, rather than the earlier biological vulnerabilities, which appear to diminish in a nurturing home.59
The long-term studies on the impact of prenatal exposure to heroin suggest that by adolescence heroin-exposed children show more behavioral and conduct problems, including impulsivity, criminal activity, early substance abuse, antisocial behavior, and school dropout. Here again, it is not clear how much these problems stem from prenatal heroin exposure and how much they stem from the cumulative effect of the discord and dysfunction that is typical of substance-abusing households.60 There also appears to be a relatively high correlation between attention-deficit/hyperactivity disorder and later opiate use. As is true of cocaine users, ADHD is often seen in heroin addicts.
Prescribed Legal Drugs (also see postscript on page 87): Legal drugs are another category of toxins that bear watching for adverse effects on fetal development. Thalidomide, DES, and Bendectin are examples of prescription drugs once widely prescribed and thought safe that, in fact, proved drastically harmful to fetal development, though none of these was linked either directly or indirectly to damage to the central nervous system or to the variables associated with later violent behavior. As the sensitive processes under way in the embryonic brain are only recently coming to light and their functions still are being discovered, the best policy for pregnant women is “when in doubt, don’t.”
As we become more conscious of the sensitivity of the baby during and immediately following birth, the routine administration of drugs during labor and delivery, once unquestioned, is being examined in relationship to later behavioral outcomes. Several studies indicate that the use of obstetrical anesthesia during delivery may cause subtle alterations in the formation of neurons, synapses, and neural transmitters that are undetectable at birth. One seven-year study of more than three thousand babies showed long-lasting effects of anesthesia on behavior and motor development. These babies were more likely to be slow to sit, stand, and walk. By age seven they lagged in language skills; their capacities for memory and judgment were also affected.61 Dr. Bertel Jacobson, a Swedish researcher, found a connection between adult addiction to opium and the use of opiates, barbiturates, and nitrous oxide at birth.62
Malnutrition: While teratogens such as alcohol and tobacco may cross the placenta to disrupt development in the fetal brain, the absence of essential nutrients during pregnancy may generate similar repercussions. Sensitivity to malnutrition is particularly profound during the period of most rapid brain growth, which occurs from the third prenatal trimester through the second year after birth. The brain is one of the most metabolically active organs, utilizing 20 percent of the body’s total oxygen in a resting state. A steady supply of glucose is essential for brain cells to grow and to communicate with one another. In addition, diet, especially amino acids, appears to play a role in the synthesis and balance of neurotransmitters, which are implicated in neurological and psychiatric disorders. Iron is of particular importance to brain development. Iron deficiency in utero or during the first twenty-four months after birth may cause permanent damage to the brain. Anemia (iron shortage) is associated with short attention spans, impaired memory, and disruptive behavior in preschoolers.63 Low levels of iron also have been linked to lower scores on learning and school achievement tests.64
Protein deficiencies can lead to shortages of tryptophan or tyrosine, amino acids essential to production of serotonin and dopamine, which are linked to reactive behavior. A shortage in either of these neurotransmitters may cause already aggressive children to perceive hostile intentions where none exist. When presented with an ambiguous situation, tryptophan- and tyrosine-deprived boys will read it as threatening and are more inclined to behave impulsively.65
Similar to the effects of alcohol and other drugs, malnutrition during gestation may result in a series of cognitive, social, and behavioral deficits with long-term consequences. Due to obvious ethical considerations, most of our information on malnutrition comes from animal studies or studies of naturally occurring conditions for children in underdeveloped countries. These studies provide information with serious implications. The impact of malnutrition on cognitive skills appears to be less invasive than the impact on social and emotional behaviors. Animals malnourished prenatally may perform essential tasks as quickly and as well as normal animals. But they are less able to learn nonessential skills that demand flexible or adaptive responses, or to perform as well under stress. They show little interest in new environments, are shy or aggressive with cage mates, and tend to withdraw from social situations. And animals malnourished both before and after birth are unpredictable, apprehensive, and aggressive as adults. They do not engage in normal play and are often aggressive toward humans and other animals.66 Studies on humans have shown that children born small for their gestational age later showed lower IQs than normal children. Early and continuing malnutrition combined with extreme deprivation may lead to mental retardation.67
Most researchers agree that it is difficult to separate the purely biological impact of malnutrition from other environmental influences. For the last twenty years, malnutrition has been seen as inseparable from its environmental context, where a host of conditions such as poverty, illness, and competition for resources are typically intertwined in their impact. The ongoing interactive nature of these variables is poignantly illustrated in a 1979 study by Dr. Barry Lester that examines the relationship between newborn nutritional status and the responsiveness of parents to their child’s cry. As is typical, the “small-for-date” babies studied generally showed poor organization of their physical responses. They were easily startled, had tremors, and showed abnormal skin color changes compared with babies who were adequately nourished. Their cries, which were acoustically evaluated by the researchers, were higher, of shorter duration, and had longer gaps between them. Instead of engendering loving and protective feelings from parents, these cries often caused parents to feel irritated or alarmed and anxious. In responding to their babies, the parents were often upset and agitated rather than calm and soothing. Malnutrition inhibited the babies’ development of the skills that typically elicit sympathetic emotional responses from caregivers, responses that are particularly essential to future gains by malnourished babies.68
While the cognitive performances of malnourished children are clearly compromised, particularly in impoverished environments, a greater threat for these babies is in the area of emotional and social behaviors. Malnourished babies appear to have difficulty attending to directions, persisting in a difficult task, and screening out irrelevant details. Attentiveness in general is compromised, as are persistence, curiosity, interest in exploration, and demonstration of initiative. They become more agitated, especially under stress. These qualities persist over time and take their toll in cognitive tasks as the children move into adolescence. Even when nutritional problems are remediated after the first two years, malnourished children may have temperamental characteristics such as hyperalertness and distractibility. The caregiver reacts negatively to those characteristics, and the child’s learning then suffers.69 A growing body of evidence suggests that the damage done by prenatal malnutrition is greatly exacerbated in deprived social environments.
The behaviors of prenatally malnourished children bear a similarity to those of children who are alcohol or drug affected. It appears that either toxins or the absence of essential nutrients at this crucial time causes children to be distracted and inattentive and reduces their ability to relate to other people. It is also likely that neglectful emotional environments commonly contribute to these similarities in the lives of both malnourished and drug-affected children. For many children, this may pave a path to later antisocial behavior. Because there is a high correlation between poverty and malnutrition, this information, though mostly from animal subjects, has important policy implications, especially when we realize that more than a quarter of American children under four now live below the poverty level. Americans have long been familiar with the extreme cases of malnourished children in faraway places like Somalia, India, and Rwanda. We read the statistics or see footage of American Red Cross rescue efforts elsewhere in the world and fail to recognize that in any month in the United States we have more children malnourished than the total number of children in Angola, Haiti, Zimbabwe, El Salvador, or Cambodia.70
Genetic Influences: It is important in any discussion of the term “genetics” to understand that great confusion often results from the imprecise way in which this term is used. Many people assume that genetic means an unalterable condition or trait that is inherited from parents or ancestors. In fact, it means only that the trait or condition in question came through the genes and is part of the biological makeup of the organism. Genes do carry hereditary information, but this can be at least partially altered by environmental factors in the womb. For example, ADHD is considered a genetic condition, but it is not clear whether it comes through the genes because it is inherited from a biological relative or because of damage to the baby’s genes (e.g., from prenatal exposure to alcohol or cocaine). A child’s genes may be shaped by either nature (inherited factors) or nurture (the chemical or hormonal environment during gestation).
In his book The Psychopathology of Crime, which attempts to redefine violent crime as a form of mental illness, Dr. Adrian Raine summarizes the role of heritability in criminal behavior by reviewing all known studies in this area.71 Much of the data is from studies of twins reared apart or of children adopted from or by criminal parents. Studies originating from several different countries seem to conclude that there is no heritability for either juvenile delinquency or violent crime. Interestingly, 14 out of 15 of these studies point to heritability for petty property crimes.
There does appear to be some evidence that people with certain biological vulnerabilities born into high-risk environments are more likely to act in violent ways. For example, scientists hypothesize that people who are born with relatively “low arousal” or nervous systems that are slow to reach a point of emotional excitement are more able to face risky situations with minimal stress. A child with such qualities might in one environment develop into a race car driver or a stockbroker, and in another turn to robbing convenience stores. Research on this variable, known as serotonin (5HT) system function, has linked this low-arousal pattern with aggressive disorders and suicide in humans and with aggressive and self-injuring behavior in animals.72 Emotional problems, particularly major depression, is linked to the serotonin-norepinephrine systems as well as to imbalances of other brain chemicals such as dopamines.73 These factors, while environmentally influenced, are also partially genetically controlled and may be heritable.74 Alcohol and other toxins may cause the mutation of the genes that control the production or set points (established levels) of these neurotransmitters.75
A controversial but respected figure in the study of the potential role of genetics is Dr. Sarnoff Mednick at the University of Southern California. Dr. Mednick’s work focuses on schizophrenia, which he believes is caused by prenatal exposure to the flu virus during the second trimester of pregnancy. He also believes that this environmentally induced genetic alteration produces an increased risk of violent behavior in subsequent generations. In a study of forty-seven children of schizophrenic mothers, Dr. Mednick found that 55 percent of the children developed a serious psychiatric disorder that included violent behavior. Of the forty-seven, five became schizophrenic, eleven are in prison for violent offenses, and nine have been diagnosed as sociopaths. Dr. Mednick attributes these outcomes to a combination of altered genetics and environmental neglect due to the mothers’ mental illness.
Another researcher, Dr. David Lykken, formerly of the University of Minnesota’s Twin and Family Research Center, found that the traits of aggressiveness and impulsivity correlate as strongly in twins who have been raised apart as in twins who have been raised together.76 But like the research on malnutrition, the research on genetics leads to the conclusion that none of these factors in isolation causes negative outcomes. Rather, it is the interaction of biological variables with environmental variables that results in prosocial or antisocial outcomes. The linchpin in this relationship is consistently the baby’s developing brain. While such genetic vulnerabilities may not be preventable, their presence can be ameliorated with nurturing care from the first years of life.
Minor Physical Anomalies: Eric Smith’s strange ears are a classic example of minor physical anomalies (MPAs)—external physical signs that correlate highly with central nervous system damage during gestation. A growing body of research links MPAs with aggression, attentional problems, and hyperactivity. Researchers specializing in hyperactivity suspect that the same prenatal insults that cause MPAs inflict minor damage to the central nervous system, often resulting in a predisposition toward impulsive behavior. This impulsivity, particularly in combination with negative familial or environmental factors, may lead to antisocial behavior later in life.77
A longitudinal study of 129 twelve-year-old boys with minor physical anomalies found that they had significantly higher rates of arrest through the age of twenty-one than normal boys matched for other variables. This relationship was statistically related to violent crime and was also strongly linked to recidivistic violent arrests.78 While the number of studies linking minor physical anomalies with violence is not large enough to be conclusive, the existing evidence warrants further inquiry and may provide us with an overt physical signal that neurological assessments are warranted when unusual physical features are detected at birth. Focused health and educational interventions on Eric and his family from the beginning of his life could have made a great difference for Eric and for his little victim, Derrick.
POSTSCRIPT
The rate of smoking in the United States hit an all-time low in 2012: Only 1 out of 5 Americans smokes, according to Gallup, which has been tracking this issue since 1944. The downward trend began in the 1970s in a long, slow decline, dropping from 22 percent in 2011 to 20 percent in 2012. Smoking rates have dropped particularly sharply in young adults ages eighteen to twenty-nine as well as among college nongraduates and those living in the East and West: from 34 percent in 2001–2005 to 25 percent in 2011–2012.79
However, this millennium has seen a rising problem in the abuse of prescription drugs, particularly the common prescriptions for opiates, sleeping medications, muscle relaxants, and antianxiety agents (e.g., Valium and Xanax). Each of these, particularly the pain medications, can alter a parent’s availability, attachment, and attunement with a child. While these agents are not recognized as contributing to fetal abnormalities, one can’t help but be concerned about the relationship between the growing use of such substances and the increase in brain-based learning problems and developmental challenges—each of which is currently escalating in our nation. And even when the use of such substances has not altered a fetal brain during gestation, if it is affecting the mother after birth, the likely result is alteration to her capacity to provide a constructive attachment relationship—the developing child’s best insurance against mental as well as physical illness.
Abuse of prescription drugs, especially prescription painkillers, is an insidious and rapidly escalating form of addiction. According to CDC data, prescriptions for painkillers rose 400 percent between 2004 and 2008, and the CDC has deemed the addiction to these substances an epidemic. Since they are legal to have with a prescription and can readily be found in medicine cabinets across the nation, they often seem more innocent and legitimate and can easily be obtained from friends or family—with or without medical authority. In 2010, 2 million people reported that they had begun to use prescription drugs for nonmedical purposes during the previous year.
The CDC reports that 100 people die from drug overdoses every day in the United States, a rate that has more than tripled since 1990. Much of the increase in mortality from overdose is attributed to prescription drugs. This unprecedented rise in overdose deaths parallels a 300 percent increase since 1999 in the use of strong painkillers. In 2010, 12 million people reported using prescription painkillers without a prescription for the physical and emotional effects. In 2009, misuse or abuse of prescription painkillers resulted in more than 475,000 emergency room visits, a number that nearly doubled in just five years.
Most at risk are individuals who:
• obtain multiple prescriptions for controlled substances from various doctors and/or dentists unaware of the duplication, known as “doctor shopping”;
• take high daily dosages of prescription painkillers and those who misuse multiple abuse-prone drugs;
• have low incomes and/or live in rural areas;
• suffer mental illness and/or have a history of substance abuse;
• are on Medicaid (they are twice as likely to be prescribed painkillers and six times more likely to die of an overdose than those not on Medicaid).80