Monday, November 10, 2008

The Meaning of Psychological Abnormality

By: Jerome Kagan Ph.D.,

As reports of childhood behavioral problems increase, Dr. Jerome Kagan raises concern about the reliability of these diagnoses. The rapid rise may stem from children’s experiences and pressures on parents and physicians, he argues.

Widespread diagnoses of childhood disorders trouble scientists such as Dr. Jerome Kagan, who argues here that social conditions, not biology, are often to blame. Kagan elucidates possible reasons for the increase, citing, among other explanations, pressures on parents to raise flawless children. He concludes by proposing ways to avoid misdiagnoses in the future.

The recent increase in the number of children diagnosed with autism, bipolar illness, or attention-deficit/hyperactivity disorder (ADHD), widely reported in the media, has created worry both among the public and among health officials. It is important, therefore, to ask whether this troubling trend reflects a true rise in mental illness or is the result of changes in the definition of childhood psychiatric disorders. The latter explanation is likely because the concept of psychopathology is ambiguous, and physicians have considerable latitude when they classify a child as mentally ill. Because a diagnosis of ADHD, bipolar disorder, or autism allows parents to obtain special educational and therapeutic resources that would not be forthcoming if the child is called mentally retarded, incorrigible, or uninterested in academic progress, doctors are motivated to please the distraught parents who want to help their child.

Psychiatrists diagnose a mental disorder when a set of behaviors or emotions is infrequent (usually possessed by less than 10 percent of the population); when the child or family is distressed by the symptoms; or when the symptoms interfere with the child’s adaptation to his or her society. Often distress and poor adaptation occur together. But because both the frequency of a symptom and its adaptive qualities change with history and across cultures, the prevalence of many mental illnesses also changes. For example, most children living in the American colonies during the 17th century were not required to maintain attention on an intellectual task for five or six hours a day—and there was no concept of ADHD. Social phobia also was less common because youths knew almost everyone in their village or small town. Although a Puritan child who resisted most parental requests would be classified as deviant and in need of help, psychiatrists today would not have classified a 6-year-old who resisted most parental requests as having oppositional disorder if neither the parents nor the child was concerned with the latter’s autonomous behavior and the child performed relatively well in school.

Changing Social Challenges

Each historical era within a society poses special adaptive challenges for its members, and traits that would be regarded as maladaptive and possible signs of a disorder in one era might be more adaptive in another. For example, adolescents who wore sexually provocative clothing and rejected the existence of God would have been both rare and a source of parental worry in 17th-century Massachusetts, but today these traits would not be regarded as signs of pathology.

In addition to changing definitions of pathology, three other factors are contributing to the apparent epidemic of childhood psychopathology in economically developed societies.

First, the contemporary American economy requires every child to complete high school with adequate language and mathematical skills, and preferably go on to receive a college degree, in order to obtain a job with some financial security. These were not requirements in the 18th century; Benjamin Franklin did not have the advantage of a high school education. The pragmatic requirement for academic accomplishment generates worry in parents who are concerned about their child’s future. Hence, they become anxious if they believe their preschool child shows signs of future academic difficulty.

Second, the availability of technologies that detect serious biological problems in the unborn child enables parents to make the legal choice of aborting these embryos. Because many do so, the proportion of severely abnormal children today is smaller than it was a century ago. Hence, a child with an obvious abnormality, such as Down syndrome, has become more conspicuous, leaving parents more vulnerable to a blend of anxiety, shame, and guilt if they sire a child with observable symptoms that are stigmatizing. It is not surprising, therefore, that many parents, especially those not considering abortion, are eager to take advantage of diagnostic techniques that might reveal a potential problem; if there is one, therapeutic interventions might then be implemented early in development.

 The American ethic of egalitarianism, which obligates each individual to award dignity and respect to all citizens independent of their values or practices, is a third factor contributing to the increase in diagnoses with a genetic cause. This moral imperative makes it more difficult to blame parental neglect or ineffective socialization practices as contributors to aggressive behavior or poor academic performance and easy to award power to genes for which no one is responsible. Such an attitude frees parents of excessive guilt for the undesired symptoms and protects them from community criticism. The availability of technologies that assess genomes, along with the media’s advocacy of biological determinism, has persuaded many Americans that genes must be exceedingly potent, even though no scientist has found any particular gene, or cluster of genes, that is a consistent correlate of poor attention skills, hyperactivity, aggressive behavior, academic failure, chronic disobedience, or excessive shyness, independent of the child’s social class, ethnicity, cultural background, gender, and history of experiences.1

The Diversity among Current Diagnostic Categories

 Most diagnoses of child pathology are based primarily on symptoms, usually described by a parent, rather than on a combination of these symptoms, the child’s behavior on a set of psychological tests, and physiological markers that might represent a foundation of the illness. Although most psychiatric disorders are currently defined as if each were one illness, most have multiple origins in a unique profile of genes and personal history. However, a majority of American psychiatrists place greater emphasis on the genetic roots than on the experiential evidence. This bias has the serious disadvantage of predisposing psychiatrists and pediatricians to prescribe drugs as the only therapy, even though non-drug therapies that take experiences into account often reduce the severity of symptoms.

More than 90 percent of childhood diagnoses are based only on the parents’ descriptions of the child without the addition of psychological testing and biological measures, which would provide a more accurate basis for diagnosis. For example, some children diagnosed with ADHD have difficulty maintaining prolonged attention to others’ speech but attend well when playing soccer on the playground and are neither hyperactive nor excessively restless. Other children are restless in the classroom but have no problem paying attention. Only a small proportion display both symptoms. Nonetheless, many pediatricians classify all three types of children as having ADHD and prescribe the drug Ritalin because, as I noted, parents can request special educational advantages for children with this diagnosis and the physician would like to satisfy the parents.

Equally serious, if not more so, is the dramatic rise (more than 40 percent in the past decade) in diagnoses of bipolar disorder in young children, based on parental complaints of chronic levels of extreme disobedience, impulsive bursts of aggression, and an inability to control emotion. These symptoms can in part be the product of permissive socialization practices by parents who are reluctant to induce anxiety or guilt in children placed in surrogate care because both parents are working. Most children classified as bipolar do not display the cycles of manic excitement and depression that define this disease in adults. Thus it is a diagnostic error to call children who cannot regulate their moods “bipolar” simply because they seem to have a single feature in common with the adult disorder: uncontrolled behavior. I do not believe that psychiatrists have detected a new childhood disorder; they have used a new term for a serious rise in poor regulation of emotion that is probably a result of experiential rather than genetic factors.

One reason the diagnosis of bipolar disorder in young children has become popular is that the adult form has a genetic component. Hence, physicians would like to assume that the child’s symptoms are also the product of genes, rather than a combination of a temperamental bias that interferes with effective regulation of behavior and family practices. Hence, drugs are the preferred therapy, rather than suggestions to parents as to how they might behave in order to alter their child’s behavior.

Diagnoses of autism are also on the rise. The symptoms that lead to this diagnosis are serious impairment of cognitive functions, especially language, compromised social skills, inappropriate emotion, and stereotyped motor acts, such as pulling at the hair, rocking, and head banging. These features, alone or in combination, can be the product of a large, but still unknown, number of distinct biological conditions, including altered genes or chromosomes, maternal illness during pregnancy, early postnatal infections, or rare immune reactions in the young infant.2 When I was a graduate student in the 1950s, most of these children were assigned the amorphous label “brain damaged.” The word “damaged” has stigmatic connotations that are missing from the category “autistic.”

Parents of autistic children have persuaded the federal government and private foundations to increase funding for research that in theory will find the cause of what is actually a number of different conditions; the habit of diagnosing a child as belonging to an “autistic spectrum” implies, incorrectly, a single cause for a condition that varies in severity. This is not a wise strategy, and applying it to other disorders sounds absurd. No physician would place a child with a headache in a category called “headache spectrum” because scientists know many of the reasons why a child might have a headache—a brain tumor, concussion, infection, high blood pressure, among others. Similarly, oncologists do not use the concept “cancer spectrum” because they have learned that, for example, leukemia, tumors of the colon, and breast cancer are caused by different genes and life experiences. The odds of finding the gene that is a risk factor for one form of breast cancer would be very low if investigators lumped all patients with any form of cancer into one category called the “cancer spectrum.”

Because we do not know the host of biological conditions that can cause the symptoms that define autism, the concept of an autistic spectrum survives and is interfering with research attempts to find the many separate causes of these traits. The habit of pooling into one group all the children given the diagnosis of autistic spectrum makes it difficult to discover a particular etiology that affects a small proportion with some of the unique symptoms that define this family of illnesses.

New Strategies

The adoption of two practices will have benevolent consequences. First, every child who appears to have a psychiatric illness should have psychological tests administered to determine, with greater specificity, the exact pattern of cognitive and emotional impairments, as well as appropriate assessments of brain and bodily function. An example: Among children who are excessively shy and timid, those who also display greater neuronal arousal in the frontal lobe of the right hemisphere, rather than the left, along with greater activation of a cluster of neurons in the brain stem that respond to sound are most likely to remain shy and timid through adolescence.3 These two distinct biological features can be measured using an electroencephalogram, which detects changes in brain activity via painless electrodes placed on the scalp. This additional evidence would allow investigators and clinicians to parse the currently heterogeneous category of social anxiety disorder into those who do and those who do not possess the two biological features. The therapeutic recommendations should be different for these two forms of social anxiety.

Second, scientists and clinicians should not equate the presence of an abnormal gene with the existence of a disease. We don't make such a jump in other circumstances. For example, most adults with Helicobacter pylori in the stomach do not have ulcers; most with staphylococci bacteria on their skin do not develop an infection. I suspect that at least half of the children currently diagnosed with ADHD and who take Ritalin in order to increase dopamine activity in the brain do not have a genetic compromise in dopamine function. A careful examination of the child and the home environment might reveal why a particular child is having difficulty paying attention in school.

It is important to appreciate that the majority of children under age 6 with some form of psychopathology will not become seriously disturbed as adults, especially if they are growing up with nurturing, middle-class families, because most children grow toward health.4 My colleagues and I are studying a large sample of children observed first at 4 months and evaluated regularly through early adolescence. Most of the extremely shy, fearful 2-year-olds who were temperamentally vulnerable to anxiety over novel events (about 20 percent of the sample) were well adapted to their school and social settings by the time they were 15 years old. Only about one-third of this group were still socially anxious and unhappy with their personality.3 Scientists who study conduct disorder report that the majority of middle-class children under age 10 who are diagnosed with oppositional or conduct disorder do not become criminals or delinquents.

Critically, the social class in which the child is reared is far more predictive of future psychopathology than is a particular gene or type of behavior displayed at two years of age. Anxiety disorder, depression, criminality, and drug addiction are more frequent among youth and adults who grew up in poorer families with less-educated parents, whether in developed or less-well-developed societies.5 The fact that academic failure, conduct disorder, substance abuse, anxiety disorder, and depression are more strongly associated with the education and income of the family of rearing than with a particular gene implies that scientists have to balance their study of the genetic causes of illness with probes of the environmental contributions and clinicians should consider therapeutic strategies other than drugs. At the moment, public and private agencies allocate more research funds for study of the biological rather than the psychological circumstances that underlie disorders. This imbalance is odd in a society that prides itself on being practical and hostile to abstract philosophical arguments. The American attraction to material causes, and the presumed certainty that they promise, sustain the belief that biological therapeutic interventions will be more effective and easier to implement than sociological or psychological ones. This premise has defeated much of the motivation to alter the life conditions of economically compromised members of our society and to improve the quality of the schools they attend.

Bouts of anxiety, fear, guilt, shame, sadness, depression, anger, and envy are inherent in the human condition because, after age two, humans can anticipate the distant future, possess a moral sense, and wish to regard the self as worthy and good. A few children experience the above disturbing emotional states far more often than their peers do. But the sharp rise in the incidence of bipolar disorder in children is more likely the result of changing social conditions, parental practices, and/or diagnostic criteria than the discovery of a new genetically mediated illness. The current confusion among parents over the best way to raise children and the ethical values to instill, the large gap in family income between the top and bottom quartiles that has developed during the past 25 years, and the need to accommodate to the extraordinary diversity in the values and socialization practices of the many ethnic groups in American society have generated parental interactions with children that have produced profiles that fit the criteria of a mental disorder. Yet, surprisingly, most scientists are searching only for the genetic contribution to these symptoms. This bias is not new; the 19th-century French attributed the presence of large numbers of prostitutes to their degenerate heredity rather than their life of poverty.

I am not claiming that all psychopathology is socially mediated. There are individuals with hallucinations, delusions, panic attacks, manic moods, crippling levels of anxiety, and numbing depression who inherited a biological disposition that rendered them vulnerable to these debilitating symptoms. However, the prevalence of these serious pathologies has remained relatively stable over long periods of time. If there has been a real rise in one or more of the categories of childhood pathology, it is likely that changing social conditions and altered diagnostic criteria are the major reasons for this disturbing phenomenon.


  1. J. Kaufman, B. Z. Yang, H. Douglas-Palumberi, S. Houssyar, D. Lipschitz, J. H. Krystal, and J. Gelertner, “Social Supports and Serotonin Transporter Gene Modulate Depression in Maltreated Children,” Proceedings of the National Academy of Sciences 101 (2004): 17316–17321.
  2. M. Rutter, “Incidence of Autism Spectrum Disorders: Changes over Time and Their Meaning,” Acta Paediatrica 94 (2005): 2–15.
  3. J. Kagan, N. Snidman, V. Kahn, and S. Towsley, “The Preservation of Two Infant Temperaments into Adolescence,” Monographs of the Society for Research in Child Development 72 (2007): 1–93.
  4. T. N. Crawford, P. Cohen, M. B. First, A. E. Skodol, J. G. Johnson, and S. S. Kasen, “Comorbid Axis I and Axis II Disorders in Early Adolescence,” Archives of General Psychiatry 65 (2008): 641–648.
  5. V. Lorant, C. Croux, S. Weich, D. Deliege, J. Mackenbach, and M. Ansseau, “Depression and Socio-economic Risk Factors,” British Journal of Psychiatry 190 (2007): 293–298.

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Scientific Advisory Board
Joseph T. Coyle, M.D., Harvard Medical School
Kay Redfield Jamison, Ph.D., The Johns Hopkins University School of Medicine
Pierre J. Magistretti, M.D., Ph.D., University of Lausanne Medical School and Hospital
Robert Malenka, M.D., Ph.D., Stanford University School of Medicine
Bruce S. McEwen, Ph.D., The Rockefeller University
Donald Price, M.D., The Johns Hopkins University School of Medicine

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