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What Underlies Psychopharmacology?
Thursday, June 23 2011 @ 09:41 PM CDT
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by Allan M. Leventhal
The 20th century witnessed the development of three quite divergent explanatory systems to account for mental illness, each offering a distinctly different approach to treatment: psychoanalytic theory and treatment by psychoanalysis and its variants; a genetic theory of chemical imbalances of neurotransmitters in the brain, with treatment by prescription of psychiatric drugs; and a behavioral learning theory, offering treatments designed to eliminate the behaviors that characterize the mental disorders. Enough time has now passed to allow for a good reading as to the value of these different systems.
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Sigmund Freud proposed psychoanalytic theory with publication in 1900 of his “Interpretation of Dreams” and, in this country, through a series of lectures he gave at Clark University in 1909.1 Although Freud was trained in physiology and began practice as a neurologist, his theory is predominantly psychological in nature. He theorized the presence of a basic force of psychic energy (libido) driving development, with human personality being shaped during childhood by psychological experiences related to the demands imposed by fixed stages of psychosexual development (oral, anal, phallic). Emotional conflicts during these stages are theorized to be processed through fundamental psychic structures Freud called the id, ego, and superego. Psychoanalytic theory views mental disorder as the outcome of unconsciously determined symbolic efforts that only partially resolve these intrapsychic conflicts, resulting in pathological adjustments to the vicissitudes of psychosexual development.
Psychoanalytic treatment in its classical form makes use of the technique of free association, which requires the patient to say whatever comes to mind. Because of the patient’s distress and the absence of direction by the analyst, not infrequently these thoughts are accompanied by strong emotion (catharsis) directed at the analyst. These emotional reactions are referred to as transference, which is theorized to be a projection onto the analyst of unresolved conflicts involving childhood figures. The analyst makes interpretations of these projections aimed at enabling the patient to gain insight into the unconscious (repressed) conflicting elements in his psyche. Patients reject the interpretations (resistance) and the curative “work” of psychoanalysis entails resolving resistance (emotional re-education).
Known by its iconic couch, psychoanalysis is conducted by means of three or more hourly sessions per week for five years or more with a complex orthodoxy of procedures. Qualifying for certification as an analyst requires completion of a program of study at a psychoanalytic training institute and a training analysis. Admission is largely restricted to psychiatrists.
Over the years other theorists who followed Freud (Jung, Adler, Rank, Sullivan) modified some of its basic tenets and psychoanalytic theory became highly elaborated into a fascinating, intricate accounting for human personality and deviancy, eventually gaining quite general acceptance.
Following World War II there was a blossoming of interest in mental health with greatly increased demand for mental health services. Many psychiatrists, psychologists, and social workers were trained in response to this interest and to meet the demand. Psychiatry embraced psychoanalysis as the preferred method of treatment. PhD programs in Clinical Psychology taught basic concepts of psychoanalytic theory along with instruction in other approaches to psychotherapy that were undergoing development in psychology laboratories and university counseling centers. Principal among these techniques were psychodynamic psychotherapy, non-directive counseling, and behavior therapy. Howcver, for much of the next thirty years, psychoanalytic theory and treatment was generally regarded to be the “gold standard” for the explanation and treatment of mental disorder.
Freud and his followers published a vast literature of case studies elucidating interpretations of their method of treatment. Freud’s writings alone cover 23 volumes. These case studies accumulated over the course of more than fifty years and constituted the “data” invoked to corroborate and expand psychoanalytic concepts.
Eventually, because anecdotal reports lack objectivity, a number of attempts were made to apply scientific rigor to testing psychoanalytic theory. However, the theory is so complex and nuanced that objective tests proved to be impossible; there was always another aspect to the theory that could be cited to explain negative results as a proof of the theory rather than a negation. Psychoanalysts dismissed negative critiques as neurotic resistance and for a long time most of the professional community and the public ignored or dismissed problems with a theory that was untestable by the scientific method.
The first major challenge to psychoanalytic theory and treatment occurred in 1958 in relation to the treatment of phobias. Psychoanalysts believed eliminating mental disorder required exploring unconscious psychological forces underlying behavior. They eschewed efforts directed at “symptoms,” viewing the behaviors that characterize the disorders as being decidedly secondary in importance. Phobias (for example, an excessive fear of heights or confined spaces) were interpreted as merely symbolic representations of an underlying intrapsychic conflict. Elimination of a phobia was deemed to require ferreting out the repressed determinants of the disorder. Few phobic patients got better; the condition was regarded as largely intractable.
A South African psychiatrist challenged this assumption head on. Making use of research on fear conditioning and extinction that had been carried out on rats and cats in psychology laboratories, Joseph Wolpe devised a treatment technique that focused directly on eliminating the phobic fears.2 Wolpe stated that phobias should be construed simply as deviant behaviors that had been learned according to the same principles as other behaviors and could be eliminated like other learned behaviors if addressed directly. He designed a treatment technique (systematic desensitization) that was based on behavioral extinction procedures regularly used in research on animals to weaken a conditioned response. Psychoanalysts were horrified and warned that focusing on the phobia itself rather than the underlying intrapsychic cause would deprive the patient of his defenses and precipitate a psychosis. A heated controversy erupted in the medical and psychology journals that lasted several years until outcome research disclosed that Wolpe’s method was effective with 90% of patients. Wolpe’s success stimulated considerable research in psychology laboratories and clinics aimed at other disorders and led to what became known as behavior therapy.
By the 1970s, quite a number of more open and flexible psychotherapies had been devised, principally by psychologists. Predominant among these talk therapies was psychodynamic psychotherapy which retained some core psychoanalytic ideas but replaced the couch and free association with a format of two facing chairs and a more interactive conversation that paid more attention to the present than to childhood experiences. Other approaches were based on different theoretical viewpoints (for example, non-directive counseling and behavior therapy) and made use of alternative techniques (for example, active listening and exposure). The success of these more open, flexible, and evidence-based approaches to treatment led to serious questioning of the relative effectiveness and costliness of psychoanalysis. Many patients who had been in psychoanalysis several times a week for several years seemed to have little to show for it. (Woody Allen later offered himself in his movie roles as a prime example of continued unhappiness and haplessness despite years of analysis). Talk therapies practiced by psychologists and social workers who were making use of less intensive treatments, at lower cost, were achieving results at least as good as psychiatrists were achieving with psychoanalysis, in far less time. Moreover, psychologists (that is, Clinical Psychologists with PhDs) were by this time licensed to practice psychotherapy and the treatment costs were partially reimbursed by health insurance, mirroring a financial coverage that had previously been the exclusive province of psychiatry.
The Chemical Imbalance Theory
Psychiatry, which had boomed as a professional choice after WW II, began having considerable difficulty recruiting medical students to the field as psychiatric practices waned in the face of unsatisfactory results with psychoanalytic treatment and stiff competition from other professions. Medical students viewed specializing in psychiatry as a poor way to make a living.3 This crisis, which threatened the continued existence of psychiatry, produced a revolution in the field. In the early 1980s biologically oriented psychiatrists, despite being a small minority, persuaded their psychiatric colleagues to replace the field’s reliance on psychoanalytic (psychological) explanations for mental disorder with a theory based on neurotransmitters in the brain (a biological explanation) as the true cause. Overcoming stiff resistance from the analysts, they argued successfully that survival of the specialty of psychiatry required psychiatrists to practice like “real doctors” by treating their patients with medicine, not talk.
The change entailed explaining mental disorders as being due to genetic defects causing neurotransmitter imbalances in the brain. Four neurotransmitters were cited as being the cause of psychopathology: norepinephrine, dopamine, serotonin, and GABA. A wide array of mental disorders, such as schizophrenia, depression, anxiety, obsessive-compulsive disorder, as well as alcoholism, eating disorders, sleep difficulties, and shyness now were described as resulting from such chemical imbalances. Each disorder was attributed to a chemical imbalance correctable by prescription of drugs targeting particular neurotransmitters.
Psychiatrists, a good number of whom had been allowed to skip a medical internship because of their choice of psychiatry, abandoned their psychoanalytically-oriented practices and began espousing a neurochemical, genetic basis for their patients’ problems and treating their patients with drugs. Psychiatrists in charge of the NIMH reorganized the institute around this basic change in orientation, including eliminating the Psychotherapy Branch, which had supported research on psychotherapy. And a new Diagnostic and Statistical Manual of Mental Disorders (DSM-III) was published in line with this biological explanation for mental illness.
In testimonial to how successful this revolution has been, prescription of psychiatric drugs is now the “gold standard” for treating mental illness; psychiatry has regained its attraction to medical students as a specialty; psychiatric residencies concentrate on teaching brain neurochemistry and provide little training in psychotherapy; other medical practitioners have fully bought into this change, with an estimated 40% of the prescriptions for psychiatric drugs being written by non-psychiatric physicians; and psychiatric drugs now are among the biggest blockbusters in pharmaceutical industry sales, indicative of how the public has been led to embrace this theory and treatment.
What is the evidence for the chemical imbalance theory? The theory arose from observations by researchers in the 1950s of the side effects of several drugs being tested for other purposes. Miltown (meprobamate), the first drug marketed to treat anxiety, was discovered during research aimed at finding an effective agent against gram-negative microorganisms. Marsilid (iproniazid), the first drug offered as an antidepressant, was discovered during research on V-2 rocket fuel. Lithium, the drug still used to treat bipolar disorder, was discovered because of its industrial usefulness in metallurgy and ceramics. Researchers noticed that some of these compounds appeared to induce a sedative effect and others an energizing effect when people were exposed to them. Psychiatric researchers (many of whom were supported by the drug companies) began studying these compounds and when it was discovered that these drugs had an influence on neurotransmitters in the brain they speculated that an imbalance in neurotransmitters is the cause of mental illness. This was the prime basis psychiatry invoked in making the transformation from a psychological to a biological explanation for mental disorder.
Such backward reasoning, however, is not good science and subsequent research results bear this out. Contrary to the ads frequently seen on TV, studies have shown these claims to be without scientific merit. As Valenstein has pointed out the fact that aspirin helps to relieve headaches does not mean there is an aspirin deficiency in the brain. We now know there are not four neurotransmitters, there are hundreds, interacting with billions of neurons and trillions of synapses in complex and largely unknown ways. After more than fifty years of research, no single neurotransmitter or combination of neurotransmitters (serotonin, norepinehphrine, dopamine, acetylcholine) has been shown to be the cause of anxiety, depression, or schizophrenia.4
Depression, today’s prime psychiatric diagnosis, provides a ready example of the failure of the theory to be validated. Although antidepressant drugs are prescribed to boost serotonin, most depressed patients do not have low levels of serotonin or norepinephrine and some have very high levels; patients with no history of depression have been found to have low levels of serotonin and norepinephrine; studies have shown that reducing the levels of these neurotransmitters (with cocaine, for example) doesn’t cause depression, nor does increasing these neurotransmitters reduce depression. Reviewers of the scientific literature have reported not being able to find a single peer-reviewed study that supports the serotonin chemical imbalance theory for any mental disorder.5
The Physicians’ Desk Reference (PDR) is the main resource doctors use for information on drug actions and safety. Examination of the PDR discloses that regardless of which psychiatric drug is being reviewed, the evidence for a neurochemical explanation for effectiveness is described as “suggestive.” This characterization has about as much substance as red traffic lights in Naples, which drivers and the local police regard as “suggestions.” In science, when observations are suggestive one is at the level of hypothesis generation, not at a conclusion.
Thus, research results show that the chemical imbalance theories, just as was the case with psychoanalytic theories, are hypotheses, not verified statements of actions or outcomes – hypotheses that have failed when tested scientifically.
What about the claim of a genetic basis for these disorders? The prime contributors to our understanding of genetics are Darwin’s theory of natural selection and Mendel’s discovery of “units” (now called “genes”) passed on from one generation to the next. Darwin’s theory holds that the differences between species occurred as a result of taking different evolutionary paths from similar ancestries. Mendel’s research on pea plants established how these evolutionary paths are controlled by genetic factors passed on to the next generation. Dawkins, in The Selfish Gene, succinctly ties these principles together in his description of plants and animals as fundamentally survival machines, programmed to preserve the DNA in those genes that ensure having descendants. Results from the Human Genome Project, which deciphered the human genetic code, are providing a basis for comprehension of how and how much various genes affect health and disease.
Genes determine such physical features as gender and eye color, genes make a significant contribution to height and weight, and they have an important bearing on traits, such as introversion/extraversion. However, many human characteristics and traits are now well known to have a basis both in genetics and life experiences. Research related to the Human Genome Project indicates that many effects of genes are not rigidly expressed. Researchers were surprised to find that how and when genes are activated are importantly affected by the environment (epigenetics). And environmental factors appear to be predominant in many behaviors of interest. Kendler has studied genetic and environmental factors in mental disorder for many years. On the basis of his review of twin studies and the Human Genome Project, he reports that the strength of association between genes and psychiatric disorders is weak and non-specific and that environmental factors are more significant than genes as determinants of mental disorder.6
Nevertheless, with the advent of the biological revolution in psychiatry, whereas previously traits were regarded as normal variations in individual differences influenced by social learning, many traits (shyness and boisterousness in children, for example) now are presented as genetically determined illnesses, which qualify for drug treatment. In other instances, diagnoses are justified in the absence of meeting the previously required criteria for these diagnoses (depression and bipolar disorder, for example), by referring to them as “sub-threshold” incipient illnesses, warranting drug treatment. Notwithstanding an enormous growth in such diagnoses, there are no scientific grounds for these claims.
A prime question to be answered is how helpful are psychiatric drugs? While these drugs are being prescribed on the basis of unsatisfactory neurochemical and genetic explanations, their effectiveness can be judged independent of the theories. Research results show that despite widespread acceptance of psychiatric drug treatment by the medical profession and the general public, outcome studies have failed to find psychiatric drugs to be effective.
Because depression is today’s most prevalent psychiatric diagnosis the value of antidepressants has been studied extensively. Measures of effectiveness of antidepressants have been taken at two points in time: after three months of treatment (short-term effectiveness) and after twelve months of treatment (long term effectiveness). In double blind studies, about 25% – 30% of patients report benefit from antidepressants after taking the drugs for three months, the same percentage regularly found in double blind studies for patients treated with a placebo, raising serious doubts about what is being contributed by the active ingredients in antidepressant drugs.7 An estimate of long-term outcome is best provided by the NIMH’s recently published STAR*D study (2006). This study was of 4,041 patients being treated at various centers in this country who were diagnosed as moderately to severely depressed. At a cost of 35 million dollars, it is by far the largest depression study ever conducted and was led by psychiatrists who are firm advocates of drug treatment.
The STAR*D study aimed at a thorough examination and refinement of current psychiatric guidelines for treating moderate to severe depression which call for long-term continued use of antidepressants to achieve remission of the disorder and to prevent relapse. The researchers expected results to endorse and more fully clarify how the guidelines should be exercised. However, in contradiction to the guidelines, results showed that after a year’s time all but 108 of the 4,041 patients had either dropped out of treatment or relapsed.8 This represents 3% of those originally enrolled in the study (7% of those who made it into continuing care), a shockingly poor showing for long-term antidepressant drug treatment.
Short-term results for STAR*D were in the same range found in other studies using placebo and are in good agreement with the first NIMH depression treatment study (the Collaborative Treatment of Depression study published in 1989), which found no difference in effectiveness between the drug and placebo conditions, short-term or long-term. Moreover, STAR*D’s results failed to support the latest chemical imbalance theory (a heterogeneity theory that different patients require different antidepressants) because a wide range of antidepressant drugs with divergent neurochemical actions were equivalent in their ineffectiveness.
Simply put, the current guidelines calling for treatment of depression by antidepressants failed to be supported. Antidepressants are placebos short-term and practically no good at all, long-term.
Reviews of published research against the FDA data base have documented a significant pro-drug bias in psychiatric publications that has promoted a mistaken belief in the effectiveness of antidepressant drugs. Meta-analyses have documented how studies showing negative results for antidepressants were not published or were published as if the results were positive by changing the criterion measures after the data were collected. This form of researcher bias is now so prevalent in reports of drug studies it has acquired a name in science, “HARKing” (hypothesizing after the results are known). Bias in articles published in medical journals gives doctors a very misleading impression of drug effectiveness. Marcia Angell, the former editor of the New England Journal of Medicine, has written of an alarmingly corrupt alliance that has developed between doctors and the drug companies, such that “it is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative guidelines.” She states “the most florid example” of the problem is found in psychiatric research.9 The editors of two other prominent medical journals have raised the same kind of alarm. Richard Horton, editor of the Lancet, wrote, “Journals have devolved into information laundering operations for the pharmaceutical industry.” Richard Smith, former editor of the British Medical Journal, also has written of how the pharmaceutical industry is corrupting doctors and patient advocacy organizations and recounted his own experience as an editor, “Journal editors are becoming increasingly aware of how they are being manipulated… but I must confess that it took me almost a quarter of a century editing for the BMJ to wake up to what was happening.” He lists eight ploys the drug companies have used to get the results they want from clinical trials.10 Since we depend on publications in the medical journals for development of our understanding of disorders and their treatments, the charges by these distinguished editors are very serious and deserve far more attention than they have received.
Acceptance of Drugs
These findings are, of course, quite inconsistent with the claims made for the effectiveness of antidepressant drugs and with the enormous increase in their prescription. Antidepressants not only are now the most highly prescribed psychiatric drugs, they are among the most highly prescribed drugs of any kind. How is it that millions of people have been persuaded to spend billions of dollars on antidepressants? How do we explain this acceptance in the face of such poor effectiveness?
Several factors clearly are involved (and, of course, this is hardly the first time large numbers of people have been led down some garden path). Most importantly there is the attractiveness attached to being able to solve one’s problems simply by taking a pill. Few among us resist complying when doctors offer to prescribe a pill as the answer to our problem.
Moreover, some people who are simply unhappy are being diagnosed as ill – and prescribed a pill – when they are experiencing a normal, time-limited reaction to life’s trials and tribulations. There is good reason to conjecture that many of the satisfied customers of antidepressant drug treatment have been misdiagnosed as depressed instead of being recognized as sad. Sadness is a normal, time-limited response to loss. Losses in life are common and sadness induced by loss can range from mild to severe (as in grief). Because sadness is a temporary reaction any treatment can look good. Patients not treated at all would likely fare as well. Patients who make occasional or regular use of antidepressants following experiences of loss in their lives may be mistakenly attributing their improvement to their medications. And, since losses are experienced throughout life, sadness can be expected to recur.
Well-intentioned doctors, who have been influenced by the biased scientific literature and slanted handouts given to them by drug company representatives, are believers in the drugs. They readily prescribe antidepressants (often in response to patients’ citing drug ads on TV), and encourage their patients to take these meds when there is a new sign of sadness to another loss.
The placebo effect is an important contributor to belief in antidepressants. Fear and sadness are forms of pain and it is well known that pain is highly susceptible to placebos. Kirsch has reviewed the data for the clinical trials conducted by the drug companies that were submitted to the FDA for approval of the antidepressants. His statistical analyses indicate that many of the drug trials were non-significant and when significance was found the predominant factor accounting for antidepressant effectiveness was a placebo effect.11 Placebo effects occur when a doctor is accepting, reassuring, and confidant in the treatment being offered, inspiring hope. The side effects of these drugs play an important role in the placebo effect. Patients undergoing drug treatment interpret side effects as meaning the drug is taking action, which significantly increases the placebo effect. In recent years, placebo effects have been strengthened by direct to consumer advertising on television of prescription drugs, which beginning in 1998 was allowed in the U.S. (New Zealand is the only other country to permit this). These TV ads promote unwarranted positive belief in antidepressant drugs by exaggerating their effectiveness.
But the hopeful expectations at the heart of placebo effects often are short-lived. This is because the behaviors that are contributing to and maintaining depression go unchanged by drug treatment. For most patients who are truly depressed, the realities of the patient’s life eventually conflict with the positive expectations connected with the placebo effect. The drugs also cause aversive side effects, which leads most patients to dislike taking them. Absence of improvement in the patient’s life situation and the presence of negative side effects cause people to lose faith in the drugs.
In some instances, belief in the value of these drugs also is due to misunderstanding the withdrawal effects associated with ending drug use. Negative physiological reactions induced by withdrawal often are misinterpreted by the patient and by the doctor as a recurrence of depression, an error that serves to keep the patient on the drugs – a mistake that is expensive and has negative consequences.
The regimen of drug treatment also is a significant contributor not only to the use of these drugs, but to the disorder by promoting dysfunctional behavior. Patients are told they have a malfunction in their brain that needs to be corrected chemically by ingesting a pill, which the doctor will prescribe and monitor. They are told they will need to wait for the pill to kick in, the dosage will likely need to be adjusted by the doctor to get it right, and the drug may need to be replaced by a different pill before the right one is found. Passivity is encouraged at each step in the process. Patients are led to expect their depression will disappear without they themselves having to do anything about it. Since passivity is a hallmark of depression, this is a process that promotes the very condition that needs to be remedied. Moreover, explaining the problem as a brain defect serves to exacerbate the problem by inducing a seriously negative self-definition – an explanation, which we have seen, lacks a scientific basis.
Each of these psychological reactions contributes to initial acceptance of prescriptions written for these drugs and for some patients continues to operate longer term. However, as results of the STAR*D study and other studies have shown, much more often than not patients eventually become dissatisfied and discontinue taking these prescriptions.
How has the transformation of psychiatry affected diagnoses of mental illness?
In 1985, epidemiological studies found the lifetime incidence of diagnoses of depression for males to be 3-5% and for females, 6-9%; in 1994, the rates were estimated as 15% for males and 24% for females; in 2005 it was reported that the combined lifetime prevalence of diagnoses of depression by age 75 was 60%. Since we know that genetic changes take many thousands of years, these figures make no sense as reflective of genetics. They also make no sense in terms of environmental influences since cultural changes of this kind and magnitude very rarely occur so quickly. This pathologizing of normality also has been given a name, “disease mongering,” which is defined as the practice of expanding the definition of illness to increase markets for those who sell or offer treatments.
DSM-III, published in 1980 as one of the building blocks in the biological transformation of psychiatry, has been central to inflation of diagnoses of mental illness. Previous editions of the DSM had been found to be embarrassingly unreliable, failing to meet the most elementary requirements for a sound diagnostic system. Beginning with its publication in 1980, DSM-III was heralded as correcting the problem, but this claim is in full consonance with the false claims made for the chemical imbalance theories. No studies have demonstrated DSM-III or DSM-IV’s reliability to be improved.12, 13 Moreover, because the number of diagnoses in these newer editions has more than tripled, room for error was expanded. Since reliability sets the ceiling for validity, there is considerable reason to view psychiatric diagnoses as having dubious validity.
As noted above, diagnoses of depression also have been profoundly affected by a change instituted with publication of DSM-III when sadness was conflated with depression. Prior to that time sadness was regarded as a normal response to loss. Experiences of loss are a salient aspect to ordinary life, which often includes losses of important relationships, status, limitations imposed by one’s own ill health and that of loved ones, financial losses, etc. A great deal of empirical evidence verifies a connection between losses in life and feeling sad.
Sadness, like fear, signals distress. Our capacity to experience these negative emotions is of genetic origin, but this does not mean fear and sadness are abnormal states. They qualify as normal because they are time limited functional reactions to threats to survival. The connection between fear and the flight/fight response was selected genetically as an integrated survival mechanism. Similarly, the connection between loss and sadness reveals the importance to survival of establishing and maintaining social relationships and holding onto valued conditions and objects. Because fear and sadness accompany behaviors that are disruptions of other behaviors necessary for survival, of necessity these states ordinarily operate only temporarily. When the stressors to survival that elicited fear disappear the organism returns to normal behaviors that sustain life. Likewise, with respect to sadness, with time the losses that elicited sadness are replaced by accommodation or compensation, enabling the individual to return to normal activities. Since fear and sadness serve a purpose as temporary survival mechanisms, they do not ordinarily represent illnesses.
Fear becomes abnormal when it continues to govern actions in the absence of objective danger. Fear then functions to maintain recurring dysfunctional behaviors. Phobias are a readily recognizable example of this abnormality. Sadness also becomes abnormal, i.e., is properly diagnosed as depression, when the behaviors necessary to replace what has been lost are blocked.14 When this happens sadness is transformed into depression because, as is the case with fear, the individual comes to function in such a way as to maintain recurring dysfunctional behaviors. Contrary to current practice, diagnoses of depression should be reserved for patients who meet this standard. There is abundant evidence that normal states of sadness are today being diagnosed as illnesses, with many people who are not ill being prescribed antidepressant drugs.
What evidence do we have bearing on the safety of these drugs? There are significant reasons to believe psychiatric drug treatment often is iatrogenic. The first wave of drugs associated with the biological revolution in psychiatry were the anti-anxiety (anxiolytic) drugs. These were the benzodiazepines (xanax, valium, librium) and they proved to be dangerous. They are highly addictive, with estimates of 10 million valium addicts in this country. Many automobile accidents were found to be associated with the anxiolytic drugs and the interaction of these drugs with alcohol can be life threatening. Recognition of the serious adverse effects of the anti-anxiety drugs led to Congressional hearings, provoking much negative publicity and stronger restrictions on their prescription.
Unfavorable publicity about anti-anxiety drugs and curtailment in their prescription served to usher in, instead, greatly increased diagnoses of depression and prescription of antidepressants. With plenty of allegedly safe and effective antidepressant drugs on hand, depression soon replaced anxiety as the prime psychiatric diagnosis. However, there is considerable evidence that the harmful effects of psychiatric drugs are not restricted to the benzodiazepines.15 Harmful effects of antidepressants and antipsychotic drugs may be less immediately apparent, but they are substantial. Whitaker points out that since the introduction of these drugs the disability rates for mental disorder have multiplied six times what they were in 1955. With respect to schizophrenia, before the arrival of thorazine, 65% of patients were able to live independently in the community five years after initial hospitalization; today only 5% of medicated patients end up “recovered” and able to work over the long term. In 1955 about 50,000 patients were hospitalized for affective disorders (depression and bipolar disorder); today, 1.4 million adults receive a federal payment because they are disabled by an affective disorder. Since the SSRIs began being prescribed to children twenty years ago, the disability rates for children have increased thirty five times. Prescription of antidepressants, anti-psychotics, and anti-seizure drugs to military personnel parallels an increase in suicides.16 There is evidence of significant under-reporting of increased suicidality associated with antidepressants17 and of a significant association between antidepressants and acts of violence toward others.18 Whitaker sums up the great increase in disability rates that has accompanied the psychiatric drug era, taken together with the explosion in prescription of psychiatric drugs written for children, as indicating the likelihood of an impending catastrophe of widespread iatrogenic illnesses.15
In summary, we now have better than thirty years of experience available to us to examine the effectiveness of psychoanalysis and another thirty plus years available to examine the effectiveness of psychopharmacological treatment for mental disorder. And for each of these treatments we have at least as many years testing the theories on which these approaches rest. Both of these theories and both of these treatments have failed to be substantiated when exposed to scientific scrutiny – and drug treatment has raised serious concerns about safety. Failure to validate these two systems should not be surprising since neither of these systems grew out of replicated empirical research, as characterized the development of our understanding and treatment of physical illness.
The third model to offer an explanation for mental illness and propose a treatment is learning theory and behavior therapy. A fundamental strength to the behavioral system is that the theory and the therapy evolved empirically. In this regard the behavioral model parallels development of the germ theory in medicine and the discovery of effective treatments originating in the germ theory. Just as basic research in anatomy and physiology led to an understanding of the mechanisms responsible for many physical illnesses and how to treat them, basic research on the process of learning has produced a coherent description of the mechanisms governing mental disorder and this understanding has guided the design of therapeutic interventions.
Establishment of psychology as a science usually is traced to Wilhelm Wundt, who set up the first psychology laboratory in Leipzig in 1879 (to study consciousness), but perhaps a better point of origin is found in the work of John B. Watson. In 1912 Watson set up a psychology laboratory at the University of Chicago to study the relationship between the behavior of animals and variables he manipulated experimentally.
Psychology is defined as the science of behavior in context, a science that examines what an organism does that is observable, how these behaviors are related to environmental conditions, and how these behaviors are modifiable. Fundamentally, this approach entails studying learning and “unlearning” (extinction).
Two forms of learning have been identified: classical (or respondent) conditioning, which pertains mainly to involuntary muscular reactions and secretions, and instrumental (or operant) conditioning, which applies to voluntary activities. Classical conditioning, the simplest form of learning, was first demonstrated experimentally by Pavlov in the late 1920s when he showed how new stimuli could be conditioned.19 In this form of learning a stimulus-response connection that is built-in genetically comes to be elicited by a previously neutral stimulus as a result of experience. A second form of learning, instrumental (or operant) conditioning, occurs entirely because of the animal’s interactions with the environment. Instrumental conditioning depends upon the environmental effects on an organism after a response occurs. Successful responses are selected by their consequences (reinforcement). These consequences are labeled positive or negative depending upon whether their occurrence reinforces behavior when they appear or when they disappear. Fundamental in Nature is selection on the basis of consequences. Evolution selects the fittest to survive (selection occurs because with time the less fit meet their demise). Similarly, instrumental conditioning, the primary determinant of human learning, selects those behaviors that are reinforced by their consequences (selection occurs because with time non-reinforced behaviors drop out).
From an infant’s earliest days learning takes place continuously. A considerable amount of research has explored learning in lower animals and humans, studying the effects of positive and negative reinforcement by means of cumulative records of various schedules of reinforcement, shaping of responses, discrimination and generalization, chaining of responses, language acquisition and expression, imitation, habituation, and extinction. Over the course of almost a hundred years’ time a vast body of basic and applied research has accumulated concerning the process of learning. Unlike psychoanalytic case histories and the alleged basis for the chemical imbalance theories, behavioral research meets scientific standards. Behavioral studies have yielded results that agree with predictions derived from research on learning and are replicated. These studies show that a broad range of human behavior is attributable to learning, including behaviors we regard as deviant. On the basis of this research, Skinner stated that an adequate explanation for behavior depends only on description of organism/environment interactions, specifying the setting for the behavior, the behavior itself, and the reinforcing consequences of the behavior.20
Learning theory views the behaviors that characterize mental illness as acquired by the same principles as other behaviors. This is not to say that genetic influences are deemed to be irrelevant. An important genetic factor that has been found to govern learning is that learning occurs on the basis of the immediate effects of reinforcement, not the long-term consequences. In fact, many deviant behaviors are acquired because of this feature to how we are wired. Some deviant behaviors characterizing mental illness are construed as learned on this basis as a function of positive reinforcement (obesity, alcoholism, drug addiction) and others because of negative reinforcement (phobias, obsessive-compulsive states, social anxiety, depression). Learning in these two ways occurs because of behaviors that have immediate reinforcing effects despite eventually inducing serious disorders. This effect probably is attributable to an ancient survival mechanism that applies poorly to the more secure conditions of modern society.
Considerable research has demonstrated how powerfully these learning processes control behavior in ordinary life. The neurologist Oliver Sacks has written of how profoundly the human brain has evolved to support learning even under other than ordinary circumstances. He has described our brain’s remarkable plasticity for new learning when there has been loss of vision or hearing by substituting information from other sensory systems. Human beings have a powerful genetic legacy of being wired for learning even when key senses are seriously injured.
Behavior therapy was spawned by research studying how to change (eliminate, replace) learned behaviors. Wolpe’s treatment of phobias (now practiced as in vivo desensitization) developed out of this context, as have other therapies for other mental disorders. Foa’s treatment21 for obsessive-compulsive disorder (exposure) comes from this line of laboratory research, as do treatments devised by Barlow22 for social anxiety (cognitive behavior therapy), Linehan’s treatment23 for borderline personality disorder (dialectical behavior therapy), and behavioral treatments for depression (behavioral activation).14 Cognitive behavior therapy, a frequent element in behavior therapy, is based on the assumption that irrational ideas about oneself, others, and the future contribute to mental disorder by creating a sense of helplessness and hopelessness, which in turn, negatively affect behavior. The goal of this form of behavior therapy is to replace dysfunctional beliefs and expectations with more adaptive ideas, thereby promoting positive behavioral change.
The learning model, unlike the disease model, does not assume an underlying deviant physical cause for mental disorder. The chemical imbalance theories discussed earlier presume (a priori) the same disease model for mental illness as has been established (empirically) for physical illness. While the disease model fits the data very well for physical illnesses, the value of the disease model for mental illness is open to question. Research studying the process of learning indicates a very different model for mental disorder may make better sense.
Learning theory is based on a theoretical model which asserts that behavior is a function of individual/environmental contingencies, not on an underlying biological or psychological abnormality. This is not a denial of the fact that we are physical creatures who depend upon biological functions to sustain life. It is simply a statement that describing the functional relationships between an individual and his environment will account for behavior, including the preponderance of behaviors that characterize mental disorder.
An important point to be made is that a behavioral approach works well without the requirement of our being able to accurately identify the physical substrate in the individual that at a physiological level supports learned behavior. Given the complexity of the brain, it is no wonder that we are still so ignorant of the brain’s functioning. It also would not be surprising if we never arrive at the level of biological knowledge necessary to predict a specific behavior at a specific time or to affect the nervous system so directly and precisely in the moment as to control behavior to our wishes. Fortunately, although we know there is a biological substrate of neurological memory functions and mechanics underlying the performance of a learned response, producing the desired outcome is not contingent upon knowledge of such physical processes.
Appealing to physical or psychological processes inside the individual may have distracted us from the more productive route of examining the observable contingencies available for objective study and management. Behavioral research indicates understanding the learning paradigm is sufficient to account for the behavior and to specify a remedy. Since the deviant behavior has been acquired according to well-understood individual/environmental interactions and can be extinguished through behavioral change programs devised in therapy, there is considerable evidence indicating we are in the position of being able to treat most mental disorder absent an understanding of the brain’s enormous complexity.
Possible exceptions to this conceptualization are schizophrenia, autism, and mania. These are very serious and relatively uncommon conditions. The jury is still out on this issue, but accounting for them may require including underlying physical factors as contributors along with learning. Arriving at an answer to this question is complicated by the unreliability of psychiatric diagnosis and the over assignment of psychiatric diagnoses described earlier. What qualifies as schizophrenia is poorly understood and the threshold for making the diagnosis has been lowered to a point that the diagnosis is now quite compromised. Much the same can be said for bipolar disorder, formerly known as manic-depressive disorder, in that mania, the primary defining feature to this condition, often no longer is required to make this diagnosis. Diagnostic errors undoubtedly have hampered our understanding of these disorders.
Nevertheless, it may be that a small percentage of patients diagnosed as mentally ill are suffering from disorders that are properly considered illnesses as the term is used for physical ills. Even if true, this may not be a persuasive argument for drug treatment. Studies indicate social treatments for schizophrenia are safer and more effective in preventing relapse than drug treatments.15 Current psychiatric guidelines for depression, which call for long term use of antidepressants, and the greatly expanded prescription of antipsychotic drugs, has led to a significant increase in rates of disability attributable to long term use of these powerful drugs. The greatly increased number of mentally ill being reported in epidemiological surveys undoubtedly includes mainly patients who have been assigned a diagnosis inappropriately, but there is reason to believe the number of patients being rendered more prone to relapse by their prescriptions is growing considerably.
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