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Ethical Human Psychology and Psychiatry, Volume 11, Number 2, 2009

120 © 2009 Springer Publishing Company DOI: 10.1891/1559-4343.11.2.120

The Need to Operationally Defi ne “Disease” in Psychiatry

and Psychology

David B. Stein, PhD Virginia State University

Petersburg, VA

Robert Foltz, PsyD Chicago School of Professional Psychology, Department of Clinical Psychology, Chicago

A universally accepted operational defi nition for the term “disease” is not yet established in contemporary psychiatry. In clinical psychology and psychiatry, disease has been used indiscriminately. The term disease has been invoked (even when no systemic etiology or pathology has existed) to describe addictions, a cluster of bizarre symptoms, and to justify crude medically based treatments (e.g., electroshock, lobotomy, involuntary commitment, medication prescription). More recently, sophisticated machines such as CAT scans, PET scans, and MRIs have been used for questionable research conducted to try to identify supposed diseases, to justify the overuse of psychotropic drugs. Economic and industry interests have superseded scientifi c concerns. To establish scientifi c rigor in psychiatry and clinical psychology research, an operational defi nition of disease is proposed.

Keywords: mental disease; mental illness; psychiatric diagnosis; mental disorders; mental syndromes; mental symptoms

Everything should be made as simple as possible, but not more so.

Albert Einstein

H istorically, the disease concept has been used in psychiatry to describe a wide range of phenomena. The inception of the idea that abnormal behavior was caused by malfunctions of the body can be traced to the somatogenis hypothesis proposed by

Hippocrates (460–357 b.c.e .). The fi rst modern disease concept was promoted in the nine- teenth century by the German physician, Griesinger (cited in Davison & Neale, 1994). Griesinger proposed that every mental condition had a specifi c physiological etiology. This was outright conjecture however, with no empirical support. Kraepelin (1899) advanced this early biomedical model with the publication of an extensive diagnostic classifi cation system. Kraepelin used the term syndrome to describe a cluster of symptoms that regularly occurred together. This implicated supposed underlying bodily and physical causes (even though no specifi c physical abnormalities had been clearly identifi ed). Kraepelin (1898)

The Need to Defi ne Disease 121

had previously integrated two different ideas. The fi rst idea was from existing knowledge about syphilis. In 1815, the medical establishment had already designated syphilis as a disease and labeled it general paresis. The second idea was borrowed from Pasteur, who in the 1860s and 1870s had promoted the germ theory of disease. Kraepelin (1898) also described a syndrome with symptoms similar to the late stages of general paresis, which consisted of delusions, bizarre behaviors, and hallucinations. He suggested these symptoms should be labeled dementia praecox, thus attempting to integrate general paresis and the new germ theory. Kraft-Ebing (as cited in Davison & Neale, 1994) later showed that paretic patients injected with syphilitic matter did not subsequently develop syphilis. He concluded (incorrectly) that these patients previously had syphilis. Despite the lack of support for Kraepelin’s disease theory, it was subsequently widely accepted into the twen- tieth century era of psychiatry.

Kraepelin’s diagnostic system dominated psychiatry until 1980. The Diagnostic and Sta- tistical Manual of Mental Disorders (American Psychological Association [APA], 1957), and the DSM–II (APA, 1968) were subsequently developed by physicians, psychiatrists, and other members of the American Psychiatric Association. The DSM and DSM–II were founded on disease-type formulations about psychosocial and mental health disorders. The origins of the DSM can readily be traced directly back to Kraepelin’s diagnostic system and associated beliefs about disease states. The biopsychiatric aspects of the DSM however created many critics, including Szasz (1961), Laing (1969), Glasser (1965), and Bateson, Jackson, Haley, and Weakland (1959). All these critics noted the major absence of empiri- cal support for the disease theories. Actually the absence of conclusive data for either side left the argument unresolved.

A second disease movement can be traced to alcohol and drug abuse–addiction litera- ture. In the 1940s, a group of Yale psychiatrists formed the National Council on Alcohol- ism (NCA) to “convince Americans that alcoholism is a disease and the alcoholic is a sick person who needs help and treatment” (Peele, 1989, p. 45). Again, empirical support was lacking. This was actually more of a public relations campaign under the guise of science and medicine, which seems to have succeeded, since 90% of Americans now believe it (Peele, 1989). Jellinek (1960) had borrowed the disease concept and hypothesized about fi ve types of alcoholic. In this framework, only the gamma alcoholic was actually viewed as the product of a disease process. In problem drinking research however, no study has ever confi rmed the existence of a disease in any of the categories described by Jellinek (as cited in Miller & Heather, 1999). A coincidental disease campaign by the founders of Alcohol- ics Anonymous (AA) only added more spurious credibility (Peele, 1989). The AA only stated, as part of their charter, that alcoholism was a disease. No empirical support was even attempted.

A third disease movement can be traced to the attentional disorders literature. The fi rst person to speculate about children who were inattentive and highly misbehaving as being diseased was made in 1902 as a guess by an English pediatrician, George Still. As a physician he was trained to see everything as medically caused, and his interpretation of these children’s behaviors was consistent with his medical orientation. Unfortunately, even though no supportive evidence existed, the disease theory for ADD/ADHD had its beginnings.

Around 1923 a breakout of an encephalitis epidemic left numerous children with this inattentive and hyperactive behavior pattern. Dr. F. G. Ebaugh concluded that perhaps a virus or the encephalitic virus itself caused infl ammation or damage to the brain of

122 Stein and Foltz

children that resulted in this behavior pattern (1923). Without proof and only as a guess, it further fueled the disease notion.

In 1937, Dr. Charles Bradley noticed that stimulant drugs seemed to subdue the behav- ior of highly active and inattentive children. As stated earlier this became known as the paradoxical effect, because he believed that only in these hyper children do we observe this subduing effect. This theory remained popular until fairly recently when researchers began to discover that stimulant drugs produce this same effect on almost everybody, adults or children.

Baldessarini (1985) calls this reasoning allopathic logic , while Elliot Valenstein (1998) calls this ex juvantibus reasoning, meaning that because a drug produces an effect, then there must be a disease. Both view this type of reasoning as false, misleading, and invalid. Since the same reactions are regularly observed in most children, this idea has pretty much faded away and few currently accept the paradoxical effect theory.

In 1947 Strauss and Lehtinen proposed the idea that the cause of these behaviors was some type of minimal brain damage (MBD), but it was so minimal that no one could fi nd it. This notion has also mostly disappeared.

The American Psychiatric Association use of the term hyperkinetic reaction of child- hood was published in the DSM–II in 1968. The term hyperkinesis was considered by many psychologists as misleading because it sounded like or connoted a meaning of a disease (Seligman, 1994). During that time period psychologists were not in favor of such pejorative terminology (i.e., negative or implied disease), and the term was dropped.

As Seligman (1994) stated, in the development of the 1980 version of the DSM–III , there was a strong current of feeling, primarily by psychologists, to move away from both pejorative connotations and from disease concepts that had no support. Researcher Vir- ginia Douglas viewed the behavior problems as resulting from a defi cit in attention. The term attention defi cit disorder (ADD) was settled upon. However, the terms ADD or ADHD are still pejorative and carry a strong connotation of an underlying disease (Stein, 1998).

The connotative meaning of words is important, especially in psychiatry and psychol- ogy. Just by naming something presents the problem of reifi cation, which is to make some- thing concrete or real when it is not. Unfortunately, without realizing it reifi cation may be what is happening in too many minds within the professional community. Many profes- sionals are passionate that certain disorders are real diseases without realizing that their arguments are emotional and lack credible scientifi c support; that is, because it sounds like a disease, and may even look like a disease, it therefore is a disease, is a poor substitute in a healthy scientifi c atmosphere.

During the 1960s and 1970s psychology developed its professional profi le in North America and Europe. In the United States, many doctoral programs were accredited, psy- chologists were licensed to practice, and legislation was passed that entitled psychologists to third party payments. In the 1960s there was an ascent of behavioral analysis. The radical behaviorism of the 1970s was associated with psychologists who were trained extensively in scientifi c rigor and experimental methodologies. There were several challenges to the exist- ing orthodox methods and the ineffectiveness of psychotherapies, especially psychoanalysis (Eysenck, 1952). This critical climate stimulated an interest in more scientifi c approaches to treatment (e.g., behavior therapy and behavior modifi cation). These approaches were committed to data collection and outcome evaluation via empiricism and the scientifi c analysis of human behavior.

The Need to Defi ne Disease 123

This renewed interest in science was overdue in psychiatry, much of which had been established on anecdote and reports of “what I saw in my clinic last week.” Nonscientifi c terms like disease were commonplace, as previously stated, in psychiatric diagnostic systems. Professionals had adopted different positions; generally psychiatrists promoted prodisease views and concepts, whereas many psychologists adopted antidisease perspectives, based on a psychosocial framework. The advent of DSM–III (APA, 1980) helped ensure that disease views were abandoned. Moreover, associated terms like psychosis and neurosis were also removed. Coincidentally, however, at the beginning of the 1980s, many advances in medical technology occurred. The considerable advances in information technology were complemented by medical and health innovations such as computerized axial tomogra- phy (CAT) scans, positron emission tomography (PET) scans, magnetic resonance imaging (MRI), electron microscopes, and computerized spectrograms (SPECT). For biopsychia- trists investing in physical treatments like shock and drugs, access to such technology set the conditions for further hypothesizing about disease-type explanations of psychosocial problems (e.g., depression, thought disorder). Unfortunately, however, the claims made in studies based on these technologies were contaminated by inaccurate machine readings or claims of readings irreproducible by other researchers. These overstated claims included inappropriate and unfounded assertions about supposed disease theories. A statement made by Barkley (1995) reveals how premature and inappropriate these claims are:

Misled by research reports that lab measures have found differences between ADHD and non- ADHD children and by the fact that ADHD is a biologically based disorder, many parents ask for medical tests to confi rm the diagnosis of ADHD. At present, there are no lab tests or measures that are of value in making a diagnosis of ADHD, so blood work, urinalysis, chromosome studies, EEGs, averaged evoked responses, MRIs, and computed tomography (CT scans) should not be used routinely in the evaluation of ADHD children. (p. 122)

The illusory precision of PET and SPECT images prompted some biopsychiatrists to overstate their claims about these methodologies. For example, Zametkin and colleagues (Zametkin, Liebenauenauer, Gitzgerald, & King, 1993; Zametkin, Nordahl, et al., 1993) and Barkley (1995) have made claims about a disease etiology for ADD or ADHD based on PET scan fi ndings. These PET scans however are highly inaccurate (Sedvall, 1997). The scans do not yield suffi cient precision to justify any conclusions about any hypotheti- cal underlying disease, illness, or pathological state.

Introduction of these new medical technologies did improve subsequent observation and measurement of associated chemical changes and physiological variances. Nonethe- less, the apparent face validity of these medical machines and associated technologies when used in psychiatric research has been extremely problematic, with unwarranted images of precision, accuracy, and reliability, marketed and sold to the general public (Mayberg, 1998; Sedvall, 1997). Moreover, revival of the disease concept by biopsychia- trists has also been falsely linked to supposed discoveries in biochemistry and physiology (DeGrandpre, 1999). In addition, investment in research programs such as the human genome project has added more complexity to the mired disease campaign by the recent supposed discoveries of genes for schizophrenia, depression, handedness, hyperactivity, substance misuse, aggression, and gambling. Currently there is an ongoing debate about whether or not such supposed changes in biochemical, physiological, genetic, or metabolic functions constitute a true disease process or not. The committee that reformulated the

124 Stein and Foltz

DSM–IV (APA, 1994) had never defi ned mental disease (p. xxxi). Scientifi c challenges to the disease concept (DeGrandpre, 1999; Stein, 1999) however necessitate and require the establishment of a widely accepted operational defi nition.

WHEN USING THE TERM “DISEASE ”

Accuracy, validity, reliability, and utility of operational defi nitions should be at the foundation of both psychology (Skinner, 1957) and psychiatry (Clare, 1976). The term “disease” sets the occasion for particular physical treatment modalities (i.e., medicines, surgery, hospitalization, electroshock). The legal profession has only partly resolved this dilemma. It is well known that in the United States during the 1970s and 1980s lawsuits helped to reduce hospital populations to 10% of their previous size (Bachrach, 1984). Civil commitments were removed from the responsibilities of psychiatrists. Countercon- trols were established on many psychiatric treatments. In the 1990s however there was a revival of many physical treatments, including more use of drugs (Breggin, 1998) and shock to minor clients (Baldwin & Oxlad, 2000; Baldwin & Jones, 1996) and elderly people (Oxlad & Baldwin, 1996).

In the 2000s use of the disease concept has been associated with purposes of cor- porate and personal gain. Political agendas, special interest groups (e.g., Alcoholics Anonymous, Narcotics Anonymous) global economic industries (e.g., pharmaceuticals) all threaten to further erode scientifi c standards. The term “disease” has been manipu- lated, marketed, and retailed to the public as a product base for pharmaceutical drug sales (Breggin, 1998). The incorporation of the disease concept into the professional territories of clinical psychology and psychiatry has been a useful platform to launch pharmaceutical products for supposed pathophysiological states such as depression and schizophrenia. Unfortunately however the scientifi c evidence for these conditions as ill- nesses or diseases does not exist. Since 1990, overwhelming volumes of poorly designed and fl awed studies have been published that claimed to have found the disease causing attention defi cit disorder (ADD) and attention defi cit hyperactivity disorder (ADHD), depression, and schizophrenia. These studies, however, have been a camoufl age of junk science (DeGrandpre, 1999; Schlesinger, 1998) many of which are unethical (Stein, 1998; see Tables 1, 2, and 3) and none of which has been accepted as valid. For example the following statement was made in the summation about ADHD at the NIH Consen- sus Conference, 1998:

At this time, we do not have a diagnostic test for ADHD (biochemical, physiological, anatomi- cal, genetic, etc.). Therefore, the validity of the disorder continues to be a problem. (p. 3)

The same may be said for depression, schizophrenia, obsessive-compulsive disorder, and so forth. Many may wholeheartedly believe that some of these disorders are diseases, but belief should not overzealously replace the validity of real scientifi c fi ndings, which at present, do not exist. As will be discussed later, if such fi ndings were to be made, several potential contaminations must be cleared up to make the claim of disease. These clarifi ca- tions will later be made clear in the development of a defi nition of disease in psychiatry and psychology.

The Need to Defi ne Disease 125

TABLE 1. Representative Studies of Brain and Nervous System Dysfunction in ADD/ADHD

Area of the Brain or Chemical Imbalance Implicated Author/Date of Study

1. Brain stem Lahat et al. (1995)

2. Caudate nucleus Castellanos et al. (1994)

3. Corpus callosum Giedd et al. (1994)

4. Dopamine Levy (1991)

5. Folic acid Greenblatt, Huffman, & Reiss (1994)

6. Frontal lobe Heilman, Voeller, & Nadeau (1991)

7. Brain metabolism Zametkin, Libenauenauer, et al. (1993)

8. Prefrontal cortex Amen, Paldi, & Thisted (1993)

9. Serum lipid Arnold, Kleykamp, Votolato, & Gibson (1994)

10. Serotonin Halperin et al. (1997)

TABLE 2. Representative Studies of Brain and Nervous System Dysfunction in Depression

Area of the Brain or Chemical Imbalance Implicated Author/Date of Study

1. Serotonin Goodwin & Jamison (1990)

2. Dopamine Depue & Iacono (1989)

3. Dopamine agonists Silverstone (1985)

4. Norepinephine Samson, Mirin, Hauser, Fenton, Schidkraut (1992)

5. Dexamethasone Gibbons (1964)

6. Catecholamines Schildkraut (1965)

7. Cortisol Christensen, Hadzi-Pavloc, Andrews, Mattrick (1988)

8. Melatonin Shafi i & Shafi i (1998)

What Underlies Premature Disease Claims

Pharmaceutical companies have fi nanced large research grants to generate fi ndings that promote disease discoveries as well as the positive qualities of their drug products. Pharma- ceutical products have both positive and negative effects. The ingestion of drugs (especially by minors) however is a serious activity. Formal drug prescription should be predicated on rigorous scientifi c analysis of risks and benefi ts (i.e., monitoring of side effects, collection of follow-up data). Scientifi c, not economic, interests should underpin prescription drug use. As many modern drugs are marketed, targeted, and directed toward children and teen- agers, this is especially salient (Baldwin & Anderson, 2000; Stein, 1999). The money trail unfortunately has unduly infl uenced researchers doing so-called scientifi c investigation. Negative results or fi ndings by drug company researchers are ignored, suppressed, and are never submitted to the pharmaceutical-sponsored psychiatric journals (Valenstein, 1998;

126 Stein and Foltz

TABLE 3. Representative Studies of Brain and Nervous System Dysfunction in Schizophrenia

Area of the Brain or Chemical Imbalance Implicated Author/Date of Study

1. Dopamine Carlsson (1995)

2. Serotonin Meltzer (1992)

3. Enlarged ventricles Cannon and Marco (1994)

4. Smaller frontal lobe Gur & Pearlson (1993)

5. Smaller cortical gray matter Buchanan et al. (1998)

6. Reduced blood fl ow Zemishlany et al. (1996)

7. Viral infections before birth Torrey (1988)

8. Defi cient activity in the dorsolateral prefrontal cortex (DLPFC)

Berman & Weinburger (1990)

9. Lack of migration of nicotinamide-adenine dinucleotide phosphate-diaphorase (NADPH-d)

Akbarian et al. (1993)

Jackson, 2005). Hundreds of fl awed research articles about disease fi ndings and studies only espousing the positive qualities of drugs have been published in psychiatric journals funded mostly by drug companies. The sheer volume of these papers that promote disease and the virtues of pharmacotherapy contribute directly to the promotion and sale of drug products (Baldwin & Anderson, 2000; Breggin, 1998; DeGrandpre, 1999; Stein, 1999; Valenstein, 1998). Has volume replaced quality and integrity?

THE IMPACT OF THE DISEASE CONCEPT ON SCIENCE

At the interface of psychiatry and clinical psychology, several related concepts intersect. There are two major components to the disease concept. First, there have been several previous (unsuccessful) attempts to defi ne disease. Second, there is also a low-level, poor- quality research campaign to fi nd magic bullets that supposedly cause and explain these psychiatric conditions. In the fi eld of problem drinking, for example, the search for a biochemical marker, specifi c gene, or metabolic trigger has remained elusive for more than 50 years. As yet, no conclusive scientifi c evidence for a biochemical trigger has been estab- lished (Miller & Heather, 1999). The same is true for other behavioral disorders. Especially during the 1990s, bioeconomic interests prevailed, with the generally fruitless search for the supposed underlying pathological conditions of thought disorder (aka schizophrenia), bipolar disorders, drug and alcohol problems, and ADD/ADHD research.

Multiple Defi nitions

A literature search for a defi nition of so-called mental disease has yielded multiple defi - nitions (see Table 4). None of these conditions however fulfi ll the scientifi c conditions of clarity and precision required for an empirically anchored, operational defi nition for psychiatric disease.

The Need to Defi ne Disease 127

TABLE 4. Attempts at Operationally Defi ning Disease in Psychology and Psychiatry

1. Peele (1989) Disease might be defi ned as an abnormality of bodily form or function that causes an adverse or unfavorable effect. (pp. 5–7)

2. Kaplan, H. I. and Sandock, B. J. (1995) The social construction, or illness, involves a series of intersecting or nested explanatory models for the diseases, held or promulgated variously by the patient, the family, the physician, other health-care personnel, and the larger culture as represented, for example, by religious authority or the law. (pp. 351–352)

3. Lavin, M. (1985) Disease is at once a biological event, a generation-specifi c repertoire of verbal constructs refl ecting medicine’s intellectual and institutional history, an aspect of a potential legitimization for public policy, a potentially defi ning element of social role, a sanction for cultural norms, and a structuring element in doctor–patient interactions. (pp. 535–543)

4. Rosenberg, K. E. (1989) Many words have been used to refer to conditions whose defi nitions to date have been generally unsatisfactory; among them are abnormality, affl iction, condition, defect, deviation, disability, disfi gurement, disorder, disturbance, dysfunction, impediment, illness, injury, lesion, reaction, variant, and wound. In medical anthropology, disease refers to whatever biological reality underlies the disorder in question; illness refers to the social construction of the disease (e.g., the explanatory model that is favored by the culture). (pp. 1–15)

5. Damjanov, I. (1995) The psychological and social aspects of disease are as important as their biological basis. As a result, a person does not have to be physically ill to feel sick. (pp. 167–168)

Magic Bullets

Tables 1, 2, and 3 list samples from many studies whose authors have claimed to have found the magical medically based etiology, or magic bullets, of ADD and ADHD, depression, and schizophrenia. Examination of these studies however has revealed a sideshow of inadequate research. No study has yet received overall recognition within the scientifi c community, because every study has been seriously fl awed. In many studies, participants were taking psy- chotropic medications, either during the study or in the preceding years (Breggin, 1998). These psychotropic drugs can typically produce identical effects improperly attributed to a supposed disease state. They can cause the chemical and physiological changes that are touted as disease etiologies. Often the discussion section in these studies has marginalized the signifi cance of such drug contaminations and confounds.

Pharmaceutical companies have developed an almost unlimited power to fund psychi- atric research that produces outcomes consistent with their own drug product marketing needs. Researchers in universities frequently have collapsed their ethical principles to secure and win large drug research grants. Universities generally do not discriminate about the source of funding and their administrators may perceive such large grants as presti- gious. Researchers who accept this money may be seduced into making untrue statements about their work (e.g., methylphenidate is not addictive) to appease powerful pharmaceu- tical company sponsors. In general medical research, drugs control (or do not control) an identifi able disease entity. Only in psychiatric research however, vagueness and confusion often obscures conceptual clarity. Although behavioral control can be achieved with psy- chiatric drugs, this is not de facto evidence for the presence of a disease state (Baldessarini,

128 Stein and Foltz

1985; Valenstein, 1998). It has already been established that the sedative, tranquilizing effects properties of antipsychotic drugs (Julien, 1998) are the characteristics most valued by psychiatrists and family members. There is however no clear scientifi c evidence that specifi c receptor site action infl uences neurotransmitter levels to directly modify abnormal individual thought patterns. Rather, it can also be interpreted that the celebrated effects of antipsychotic (more properly called antibehavioral ) medications (Julien, 1998) may be based on their ability to exert restraint and to establish akinesis.

Scientists should protect the general public by adhering to excellent standards. When scientifi c standards are compromised, the general public can suffer severe and sometimes irreversible consequences (e.g., when a dangerous drug such as Thalidomide is licensed). The nature of human service provision and honest science means that corruption is eventually exposed, although this may take time. Tobacco industry-type investigations are now being applied to psychiatry, psychology, and pharmaceutical companies, to deter- mine confl icts of interest and insider trading. As self-regulation by psychiatrists within psychiatry seems impossible, stronger countercontrols clearly are required from indepen- dent, external monitoring agencies.

LACK OF REPLICABILITY ADDS ANOTHER CONTAMINATION

This fl awed research based on volumes of weak nonscientifi c reports has unduly infl uenced the uncritical psychiatric community. The issue of the nonreplicability of the huge volume of disease claiming research was discussed earlier. The general public and professional community has been duped about the nonexistent disease validity of concepts such as hyperactivity, depression, obsessive-compulsive disorder, and schizophrenia. The external monitoring of journals, university research, and professional organizations should be more rigorous to prevent the hijacking of science to achieve other goals.

DNA RESEARCH IS ALSO BEING COMPROMISED

The substitution of volume at the expense of quality has also occurred in the DNA fi eld. In Table 3 many different genes supposedly cause ADHD. The identifi cation of multiple genes to explain behavior wholly undermines the scientifi c enterprise. Genetic research has proved an ideal arena for unethical researchers to identify disease states in both psy- chiatry and clinical psychology. In the ADD and ADHD fi elds, for example, diagnosis has increased at a yearly rate of 400%–500% (Stein, 1999). Genetic disease however does not increase at such rates. Only a major environmental event (e.g., a massive radiation leak) could account for such an increase. In the absence of such an event, only politics and eco- nomic interests can explain this explosion of ADHD diagnosis (Stein, 1999).

THE STRESS–DIATHESIS ISSUE

The stress–diathesis model (Zubin & Spring, 1979) presents still another problem. In this model it is assumed that there exists a genetic predisposition to develop a disorder in the

The Need to Defi ne Disease 129

presence of suffi cient stress levels. This model is now being expanded to include many types of disorders and lends to the reifi cation of these disorders into diseases. No proof of diathe- sis exists, and yet it seems to have taken on a life of its own because it seems to be appearing in more and more abnormal psychology textbooks. There is no available evidence for the existence of any DNA, or gene, or chromosome that produces a state of diathesis. There is no evidence of an anatomical, chemical, or physiological thing called diathesis. It is a name, a hypothesis that is taking on an unfounded and unsubstantiated reality.

TRIGGERS: SAME DISORDER—DIFFERENT CAUSES

The disease business has involved a quest to discover and name the biological triggers that cause each of the disorders (i.e., conditions categorized in DSM—IV ). A trigger is that which initiates or causes a behavioral disorder to occur. This quest involves the traditional deterministic search for the discovery of cause–effect relationships. The establishment of such a relationship implies that prediction and control (i.e., treatment) is possible. The quest for disease states is to fi nd a reductionistic trigger. This requires a shift in the level of explanation of causation, from the molar (environmental) level, to the molecular (biologi- cal) level. Even if the cause of the cause–effect relationship is molecular or biological, then control or treatment does not necessarily have to be biological (i.e., medical). For example, behavioral interventions can be highly effective to modify action repertoires with biologi- cal conditions such as Down’s syndrome and autism (Kazdin, 1994; Lovaas, 1987).

There is much literature about the supposed causes of many of these disorders. Dif- ferent authors have viewed causes, or triggers, at different physical levels. Some authors have argued for molar or environmental causes. These include Seligman’s (1975) theory of learned helplessness underlying depression. Others have argued solely for molecular or biological causes. These authors include Schildkraut’s (1965) theory of catecholamine imbalance that supposedly causes depression. Arguments about biological or environmen- tal causes often have become quite impassioned. There is abundant evidence that disorders can be triggered or caused by events at different physical levels.

Depression (i.e., affect disorder) for example can be triggered by events at several differ- ent levels. Research studies have been presented that support the hypothesis for different triggers or causes of depression. Types of triggers (from molar to molecular) include:

1. Environmental depression 2. Cognitive or behavioral depression 3. Systemic depression (i.e., biological, disease, organic illness).

Viable Research for Each of the Triggers

1. Environmental depression: There are two time periods for environmental depression. a. Immediate stressors b. Early life stressors

The primary working model for the DSM–III was based on stressors or environmental causes (Seligman, 1994). Beck’s (1967) contention was that severe and immediate envi- ronmental stressors (e.g., loss) could trigger depression. Most people have experienced

130 Stein and Foltz

depression triggered by a loss. Such events are an inevitable, painful part of life. However, early life environmental stressors may also trigger depression. Lewinsohn and Rosenbaum (1987) demonstrated that an ongoing negative family environment could contribute to depression. This depression is produced by a high frequency of punishment, or by a low frequency of positive reinforcement (love) that can trigger a lifetime of recurring depres- sive episodes. Thus, both immediate loss and early life stressors can be environmental triggers for depression.

2. Cognitive or behavioral depression: Seligman (1975), Beck (1967), Ellis (1961), and many others have demonstrated that ongoing cognitive or behavioral patterns could trigger recurrent depressive episodes. They have also demonstrated that by altering behaviors and restructuring cognitions, the frequency, duration, and severity of depressive episodes can be reduced. The development of maladaptive, cognitive, or behavioral patterns can be attributed to environ- mental problems (e.g., early life stressor events). If faulty cognitive or behavioral patterns have been established, they can trigger recurrent depressive episodes.

3. Systemic depression: Research at this level has become muddied and unclear. Depue and Spoont (1986) have argued that depression can be triggered systemically. To confi rm or refute this hypothesis, research methods will need to be improved, using: (a) improved technology, (b) improved integrity in research, and (c) elimination of arguments with the development of a solid, operational defi nition of the term disease. The argument about a variety of triggers for depression can also be made for other psychosocial problems (e.g., hyperarousal disorders, schizophrenia, attentional disorders, alcohol problems, and addictive disorders). All three types of triggers are potentially valid explanations. However, an operational defi nition of disease is required for the third trigger to be valid (i.e., systemic disease) in the psychiatric nosology.

Identifi cation of correct triggers for these disorders will require more sophisticated levels of analysis, diagnosis, and treatments for psychiatric and psychological conditions. The training and detection skills of practitioners should be improved. Practitioner analytic skills to detect triggers should be more sophisticated. Correct identifi cation of a trigger helps a more appropriate choice between treatments. If the trigger is a stressor (e.g., a loss triggering depression) the therapy could be focused on the stressor. If the trigger is cogni- tive or behavioral, therapy should focus on rational restructuring. If the trigger is systemic (i.e., where a biochemical imbalance has been clearly and accurately identifi ed), a phar- macologic treatment may be indicated. Nonetheless even when systemic etiology exists, behavioral and cognitive treatments may still be preferred.

RECIPROCITY BETWEEN TRIGGERS

Neuropeptides can be stored as memory or may migrate to receptor sites to trigger cellular activity. This activity occurs in the central nervous system (CNS) and throughout all cells creating global bodily responses. Such responses translate into a range of cellular activity (e.g., mobilizing the immune system, excitation of neurotransmitters, initiating behavioral responses). Brasfi eld (1999) noted that either repeated experiences, repetitive cognitions, or repeated use of psychotropic drugs can reorganize the molecular confi guration of recep- tor sites. This can alter the type of neuropeptides that adhere to the CNS or body cells. There are interesting implications for treatment, as the use of a drug is the least healthy form of intervention (Breggin, 1991; Jackson, 2005).

The Need to Defi ne Disease 131

Any of the triggering mechanisms can initiate this global bodily response pattern (i.e., there is reciprocity interaction between triggers). Any trigger can start events, but a systemic trigger requires special consideration. Disease theorists (incorrectly) believe that systemic triggers initiate all behavioral occurrences. This claim is false, although sometimes there may be a causal sequence from cellular to behavioral levels. The poor quality of existing research is hampering the search for systemic causality, or trigger, and this research is hampered even further by the absence of a precise defi nition of disease. The interpretation of most systemic causality studies is therefore virtually meaningless. Hence an operational defi nition of the term disease is required.

THE NEED FOR AN OPERATIONAL DEFINITION OF DISEASE IN PSYCHIATRY AND CLINICAL PSYCHOLOGY

In contrast to psychiatry, clear defi nitions of disease entities have anchored most patho- logical conditions in mainstream medicine. Clinical research has focused on the pres- ence of identifi able germ organisms, observable trauma, or systemic cellular damage. In medicine, a disease is believed to exist when there is identifi able and observable physical (i.e., cellular/organic damage) and etiology (i.e., pathological process[es]). In psychiatry and clinical psychology, however, different standards have been applied. There has been a lack of conceptual clarity about what is observed and measured in psychiatry and in clinical psychology. This has promoted incorrect statements about nonexistent processes and false declarations about so-called diseases or illnesses in the absence of any real evi- dence. So-called personality theories, psychological testing, and theories about psycho- logical abnormality have been littered with claims based on nebulous, dubious, obscure, and often fatuous postulations about human behavior. In the 1950s Eysenck had revealed how therapies based on such theories (e.g., psychoanalysis or humanism) did not work. Many clients treated with psychoanalytic methods and humanistic interventions failed to improve and some people deteriorated.

As previously stated, in the 1990s, scientifi c standards and principles in psychiatry and clinical psychology were abused to make false claims about diseases and illnesses. These claims were made in the absence of valid and reliable data. Moreover, operational defi ni- tions of disease and illness have not been developed and have paved the way for poor qual- ity research. To reduce the problems and abuses inherent in psychiatric disease research, an operational defi nition is now required.

THE CRITERIA FOR DEFINING DISEASE IN PSYCHIATRY–PSYCHOLOGY

Attempts to defi ne disease have been made at different physical levels, none of which have to date been satisfactory.

Levels

Attempts to defi ne disease in psychiatry and clinical psychology have been made at three different levels:

132 Stein and Foltz

1. Molar: Patterns of behaviors and cognitions 2. Molecular: Etiology, or presence of cellular, chemical, genetic, pathologic, metabolic, or

physiological abnormalities 3. Genetic: DNA identifi ers, and histories of disorders in family and twin studies.

To operationally defi ne the term disease, the themes and consequences involved in each of these levels should be resolved.

1. Molar: DSM–IV listed the presence or absence of abnormal patterns of diagnostic symp- toms, or symptom clusters, at the molar level. Diagnosis is based on recorded behaviors or cognitions (based on observable self-reports). By general consent in the psychiat- ric community these conditions in the DSM–IV are accepted as abnormal. Attempts to define what is considered abnormal and unacceptable versus normal and acceptable however have produced considerable controversy. Therefore, the DSM is a manual of consensus within psychiatry and psychology about what has been agreed as abnormal behavior.

Nonetheless, inclusion of a disorder, syndrome, or cluster of behaviors or cognitions in the DSM–IV does not confi rm a disease state or pathology. The recent controversy (Selig- man, 1994) has been focused on which of the DSM–IV diagnoses are real diseases rather than socially constructed labels. Moreover the most recent informal discussions about what should be included in the proposed forthcoming DSM–V have featured debates about whether road rage and smoking behavior should be included in the revised manual. Such biopsychiatric excesses have fueled speculation that hidden pharmaceutical com- pany agendas seek to identify and label up to 50% of U.S. citizens with a psychiatric diagnosis in the 2000s.

This debate about disease states cannot however be resolved at the molar level. For thousands of years, there has been debate about which molar processes can be legiti- mately considered a disease. The defi nition of disease at this level is frequently a matter of nothing more than opinion, rather than established fact. Even the oddest patterns of behaviors and cognitions (e.g., autism and schizophrenia) cannot be operationally defi ned and classifi ed as diseases at this level. Disputation about disease for conditions listed in the DSM–IV cannot be resolved at the molar level. People do show the most bizarre behaviors without being diseased, sick, or even ill. Dollard and Miller (1950) identifi ed numerous disordered acts as stupid behaviors. Some people will show very bizarre behaviors to benefi t from immediate reinforcement (i.e., social gratifi cation or escape from interpersonal discomfort). There have been many attempts to operationalize the defi nition of disease at the molar level. Trying to resolve the defi nition at this level cannot be achieved. By restricting the debate to this level, the defi nition of psychiatric disease will never be achieved. To behave abnormally does not indicate the presence of a disease state.

2. Molecular: The controversy about disease should be settled at this level. The proliferation of new medical technologies is at the core of the current disease controversy. The identifi cation and discovery of systemic pathology is a necessary but not suffi cient condition for an opera- tional defi nition of disease. For the term disease to be applied, several preconditions should have been established.

The Need to Defi ne Disease 133

POTENTIAL CONTAMINATIONS

If anatomical, physiological, or chemical anomalies are found, it may be that they did not trigger, or cause, the disorder, but were instead the result of potential con- taminants that must be ruled out before making claims of systemic disease. These include:

1. External events causing systemic changes: Systemic pathology should be clearly established to precede and cause, i.e. to trigger, a pattern of abnormal behavior. The mere detection of a pathological process is insuffi cient to establish the presence of a disease or biologi- cally based psychiatric condition. Systemic pathology can be a resultant, which means that pathology can be produced by external events (Brasfi eld, 1999; Breggin, 1998; DeGrandpre, 1999; Stein, 1999). These external events may include early childhood stressors (e.g., a dys- functional family). Alternatively, they may include severe current stressors (e.g., repeated setbacks, losses, and failures). Early life or even recent stressors can change body functions (Brasfi eld, 1999; Breggin, 1998). The person may react to these molar life problems, with possibly depression, hyperarousal, or even schizophrenia. Simultaneously, subtle bodily changes occur. Detection of these co-occurring bodily changes does not however support the proposition that they cause the psychological problems of depression, hyperarousal, or schizophrenia. Thus, detection of a systemic pathological process is insuffi cient by itself to establish the presence of a psychiatric disease state. a. Resultant diseases: Many diagnoses in the DSM–IV qualify as resultant diseases. In these

examples, there is clear evidence of cellular or other structural damage resulting from the environment or the behaviors inherent in the psychological disorder. An example of this disorder type is Wernicke-Korsakoff syndrome. This syndrome is a resultant disease pathology but not a psychiatric disease. The excessive alcohol intake that produces the massive irreversible cellular damage does not qualify as a psychiatric disease. Instead, alcohol problems and problem drinking can be argued to be a potentially reversible behavioral disorder (Baldwin, 1990, 1991; Heather & Robertson, 1983; Peele, 1989). Again, systemic disease has not been proven to cause the abuse of substances. Rather, there is an association between events.

Some medication-induced movement disorders (e.g., akinesias) are also resultant dis- eases. One example is the Parkinsonism caused by neuroleptic medication (e.g., Breggin, 1991). Such movement disorders include tardive dyskinesia and kinesthesias. An opera- tional defi nition should be applied to separate causative from resultant diseases. To qualify as psychiatric disease (i.e., causative disease) the operational requirement is to establish whether an abnormal pattern of behavior is caused by systemic pathology.

2. Medication caused systemic changes: It is well established that prolonged intake of medi- cations (psychotropic and nonpsychotropic) can produce iatrogenic bodily changes. This is in fact one of the main contaminations in most disease studies. For example, almost every study about ADHD that claims to have discovered the systemic cause of the condi- tion has been contaminated by the ongoing medication of the children. These medications can produce the systemic readings (i.e., elevated arousal levels) attributed as causative of ADHD. Systemic studies should be designed to isolate the medications that can produce pathological processes. Therefore, the biopsychiatric claims that systemic pathology causes the behavioral or cognitive diagnosis have been premature. Professional journals should not accept research articles when the medication histories of participants have not been properly documented, are unclear, or have been dismissed as irrelevant.

3. Environmental caused systemic changes: Prolonged environmental stresses, whether cur- rent or early childhood, can produce systemic changes and should be ruled out before

134 Stein and Foltz

making the assumption that the systemic changes were there fi rst and were responsible for the behavioral problems.

4. Cognitive caused systemic changes: Cognitive patterns can cause systemic changes and must be ruled out before making the assumption that the systemic anomalies produced the behavioral problems.

5. Contaminated studies: The training of psychologists includes experimental research design and applications of sophisticated statistical techniques and methods to reduce the risk of random error and contamination. Yet many studies of systemic diseases or the biological basis of behaviors have been deeply fl awed by weak experimental design, poor methodol- ogy, or inadequate statistical analysis. These studies have been used to bolster the persistent biopsychiatric claims about supposed disease states. There has been too much appeasement amongst psychiatric researchers of pharmaceutical companies for fi nancial gain. The quest to discover disease etiology in psychiatry and clinical psychology has promoted fl agrant irresponsibility and a total disregard of ethics. Examples of poor science have included: (a) insuffi cient information about medication histories, (b) selection of research participants from biased population samples where selected participants have been from lower socio- economic strata (where early environmental stressors can produce systemic changes; i.e., confounds), (c) failure to separate diagnostic disorders within the studies, (e.g., not studying ADD separately from ADHD), and (d) failure to include properly controlled participant groups. With such poor quality research methodologies, a proper discovery of disease enti- ties can never be made. Ironically, the continued use of poor methods selected by disease researchers to search for diseases means they are unlikely to ever be found.

6. Lack of replicability: Premature declarations have been made about diseases and about the supposed biological basis of psychiatric conditions. In science, new fi ndings should be subject to replication, without undue infl uence from external vested interests (e.g., from pharmaceutical companies). Interpretations from these contaminated studies however are meaningless until responsible, independent scientists (who are not funded by the drug companies) have completed successful replications. As indicated earlier, the mod- ern day revivalist of ADD and ADHD disease theories, Barkley (1995), readily admits that these studies cannot be replicated on a clinical level. In fact, close examination of the literature indicates that Barkley has backed off from using the term disease, and instead has been substituting “biologically based disorder” or, more recently “develop- mental disorder” (Barkley, 1995). However, it is proposed that neither the public nor the professional community fully understand the different meanings of the terms and tend to interpret them all as some type of systemic disease.

Replication should be of suffi cient quality that subsequent measurement could be con- ducted at the standard beyond the research level (i.e., in the clinic). When clinical mea- surement is suffi ciently reliable so it can be used as a diagnostic tool, then it may be possible to specify a disease or biological disorder. The term biologically based disorder should not be used as a clever substitute for the term disease. Again, both Swanson (1998) and Barkley (1995) have made claims of fi nding biological bases of ADHD/ADD in their research that even they admit cannot be repeated under everyday clinical conditions.

3. Genetics: In psychiatry and psychology, there has been an ongoing quest for the genetic base of behavior as proof of the existence of a disease. Two types of studies have been included: (a) twin studies and (b) DNA discoveries. a. Twin studies: These studies have been used to attempt to prove a genetic basis in dis-

orders such as schizophrenia, depression, problem drinking, and more recently ADD and ADHD. Twin studies however have not been widely accepted as proof of a disease

The Need to Defi ne Disease 135

entity. The extensive review of twin studies by Joseph (1999, 2003) showed the over- whelming contamination and fl awed methodologies embedded in these reports. All twin studies moreover are correlational; such research proves nothing. Correlational evidence even at best is merely suggestive and cannot support defi nitive claims about causal evidence of diseases.

b. DNA discoveries: Many ADHD studies have been used to make claims about the discov- ery of the genetic basis for abnormal conditions (e.g., schizophrenia, depression, problem drinking, and ADD/ADHD; see Table 5). Close examination of these studies has revealed a slew of fi ndings that have the same problems as the previously mentioned disease studies: they are not replicable, with poor methodologies and (unsubstantiated) premature claims; there is a mass production of numerous unsubstantiated claims of fi nding the gene; and volume has replaced quality. However, in DNA research, any fi ndings associated with an unproven systemic etiology are meaningless (Joseph, 1999, 2003). Again, the lack of an operational defi nition of disease prevents real understanding. DNA fi ndings may be associ- ated with a molar behavior pattern represented as abnormal in the DSM–IV . These fi nd- ings however do not prove the existence of a disease. For a DNA fi nding to be meaningful and valid, it should predict an identifi able systemic disease (i.e., fulfi lling criterion two), which is clearly causative of a behavioral abnormality. It is incorrect to jump from a DNA fi nding to a behavioral abnormality that has not been proven to be a disease.

Again, attempts to convince practitioners in the psychiatric and psychological commu- nity about disease states based on DNA fi ndings may be strongly motivated by economic interests and political agendas. If a disease entity has not been established, scientists can- not claim that a DNA fi nding proves the existence of a disease, or the biological basis of behavior. The conceptual shift from DNA fi ndings to molar (or overt) behavior is implausible. Even if a DNA fi nding has a 100% (1.00) correlational relationship with a behavioral disorder, this fi nding is not evidence of a disease. As noted in criterion one, no such disease can be established at the molar level. Therefore, jumping from DNA to molar is insuffi cient. It is the elements in criterion two (i.e., at the molecular level) that should be satisfi ed as evidence for a real systemic basis for a disease. Then, accurate DNA fi ndings can lend powerful support to the statement of a disease fi nding.

TABLE 5. Gene and Chromosome Theories of ADD/ADHD

Gene Author/Date of Study

Fragile X Samango-Sprouse (1999)

Dopamine transporter Comings et al. (1996)

Dopamine 4-D receptor

Dopamine B—hydroxylase

Dopamine D2 receptor

Serotonin 1A receptor

Tryptophan 2, 3—dioxygenase

Monomine oxygenase A & B

C 4B Odell et al. (1997)

DAT 1 Cook, Stein, & Leventhal (1995)

Monosomy AX Samango-Sprouse (1999)

136 Stein and Foltz

OPERATIONALLY DEFINING THE DISEASE CONCEPT

In order to develop an operational defi nition of disease in psychiatry and psychology the three previously discussed issues must be addressed.

1. Molar level: A molar description of behaviors and cognitions can signify clusters of symp- toms as pathology, abnormality, or as a syndrome. At this level, however, these behavioral or cognitive patterns cannot qualify for the use of the term disease or biologically based disor- der. Inclusion of a symptom pattern in the DSM–IV does not qualify for the use of the term disease. Severity of the behavioral or cognitive pattern (i.e., schizophrenia, autism, major depression) does not qualify for the use of the term disease.

2. Molecular level: The presence of systemic, physiological, or biochemical abnormalities should be present to qualify the condition as a disease, with the establishment of the following neces- sary and suffi cient conditions: a. Causative and not resultant: It should be established that the systemic pathology causes

the molar pattern of behavior. Detection of the systemic pattern should predict onset of the condition, as shown in several well-conducted studies, before any molar symp- toms have appeared. Prediction is a basic aspect of the defi nition of causation in the deterministic philosophy of science and should be fully satisfi ed in this defi nition. Sys- temic patterns resulting from the environment, drug use or medications, and cognitive or behavioral patterns do not qualify a condition for the use of the term disease. If any of these entities precedes the onset of the systemic pattern, then the term disease is inap- propriate.

b. Clear noncontaminated research: Establishment of a systemic causation etiology should be made in the context of well-designed and well-conducted research. The criteria for publishing in refereed psychiatry–psychology journals should be much improved (i.e., more scientifi c rigor). Ethical policies should determine the publishing of scientifi c papers and not pressure from pharmaceutical companies.

c. Replication: The term disease should not be used until well-conducted studies have replicated the causative systemic etiology with an abnormal behavior pattern. Replica- tion studies should be completed independently of pharmaceutical company fi nancial support. The level of replication should be available at the clinical level and detection should be evident so that measures of systemic pathology can be used on routine, out- patient, offi ce, and clinic visits. If such a routine level of clinical identifi cation is not possible at that stage of development of technology, the term disease should not be used. Without clearly well-established causative systemic pathology, the term disease should not be used.

3. Genetic level: Twin and familial studies should not be used to justify the use of the term disease. They are only correlational studies and have many contaminations. DNA fi ndings strongly support a disease concept if they are clearly related to a well-established systemic pathology (outlined in the molecular level, criteria two). If criteria two has not been satisfi ed, then DNA fi ndings are insuffi cient for the use of the term disease.

QUALIFYING DISEASES

Few diagnoses would fulfi ll the requirements for the proposed operational defi nition of disease. With such diagnoses : systemic damage has been clearly established; the damage is clearly causative of the molar behavior patterns; neither medications, environmental

The Need to Defi ne Disease 137

stressors, nor cognitive or behavioral patterns clearly have produced the systemic dam- age; the research has a suffi cient history of uncontaminated inquiry; and there is suffi cient replication of fi ndings. These diseases include:

1. Some forms of mental retardation (e.g., Down’s syndrome, hydrocephalus) 2. Certain forms of dementia (such as Alzheimer’s, Pick’s, and dementia due to other general

medical conditions; i.e., GPI) 3. Amnestic disorders due to general medical conditions 4. Certain forms of sleep disorders, (e.g., sleep apneas) where criterion two has been met 5. Certain forms of communication disorders (e.g., some aphasias) where criterion two has

been met 6. Certain forms of perceptual and sensory disorders (e.g., alexias, proposagnosia) where

criterion two has been met.

Some severe behavioral disorders can be tempting to claim as having causative diseases, current research fi ndings however are presently inadequate to make that judgment. The severities of the behavioral and cognitive abnormalities are insuffi cient to be identifi ed as psychiatric diseases (i.e., clear evidence for criterion two has not been fulfi lled). These dis- orders include schizophrenia, pervasive developmental disorders, and bipolar disorders.

Attentional disorders, learning disorders, and depressive disorders are even less well established. The molar and behavioral patterns of the attentional disorders are subtler and even more disputed. Addictive disorders are also not supported for systemic causation. Historically, use of the term disease for addictions is based on molar behavioral patterns. The term disease has been used metaphorically and politically for addictive behaviors. Even Jellinek’s (1960) gamma alcoholic does not qualify in this scientifi c context. The designation of any of the above disorders as causative diseases will depend on whether future research fi ndings fulfi ll the requirements of the operational defi nition of disease.

PROPOSED REVISION OF DIAGNOSIS BASED ON TRIGGERS OR CAUSES

The discovery of any causative disease will not be a panacea for a specifi c diagnosis. Even with establishment of a true systemic etiology, almost any diagnosis will require further subdiagnosis, according to the trigger. For example, a systemic cause for depression may be discovered. This does not however mean that all depression is a disease. There is still environmental depression, cognitive or behavioral depression and then possibly systemic depression. The same is true for numerous other diagnoses. This will require realignment (or even abandonment) of DSM . A formal scientifi c system will reduce confusion about which diagnosis is (not) considered a disease. With an accurate diagnostic system, direc- tions for intervention will be clearer. Incorrect treatment prescriptions will be reduced with improved treatment matching.

CLOSING COMMENTS

Use of the term disease in psychology and psychiatry sets the conditions for the use of medications. This is crucial when the psychological and physical health of children is

138 Stein and Foltz

involved. Vague use of the term disease and the poor quality of disease research have justi- fi ed the epidemic use of drug treatments. An operational defi nition of disease is required for professional practice complemented by a return to ethical research.

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Correspondence regarding this article should be directed to David B. Stein, PhD, Virginia State University, Petersburg, VA. E-mail: [email protected]