Psychiatry's failed paradigm
The solution to mental illness has seemed to lie in application of drugs. If a serious psychiatric disorder arises, the reasoning goes, it must be centered in the brain - and, the reasoning further assumes, the most successful treatment is a biological one. Or is it? In his book, "Doctoring the Mind: Is Our Current Treatment of Mental Illness Really Any Good?" Richard P. Bentall challenges psychiatry's presumption that drugs are best for tackling mental illnesses. Bentall, a professor of clinical psychology at the University of Bangor in Wales, argues for treatment that focuses on the patient as much as on the brain in a setting that stresses a strong relationship between patient and doctor.
GUEST BLOGGER: Richard P. Bentall
Recent decades have seen dramatic improvements in the survival rates of patients suffering from heart diseases and cancer. But the same cannot be said of psychiatric disorders.
So far as we can tell, outcomes for patients suffering from the most severe forms of psychiatric disorders -- the psychoses -- have hardly changed since the Victorian period. Poor countries without well-resourced psychiatric services seem to do about as well or even better than the developed world. There is therefore little evidence that modern psychiatric services have had a global, positive impact on mental health, but the perception is often different.
The medical historian Edward Shorter has remarked that, "If there is one central intellectual reality at the end of the twentieth century, it is that the biological approach to psychiatry -- treating mental illness as a genetically influenced disorder of the brain chemistry -- has been a smashing success."
In fact, the contrary seems to be the case. Attempts to find a genetic basis for schizophrenia or bipolar disorder have led to the identification of a number of candidate genes, for example COMT, NRG1 and DTNBP1, each announced with enormous fanfare. Similarly, huge attention has been given to the discovery of an allele (variant) of one gene, 5-HTTLPR, which appears to make people liable to depression if they are exposed to negative life events.
But, without exception, later studies have failed to replicate these findings. In one of the largest psychiatric genetic studies ever published, which appeared in the American Journal of Psychiatry last year, no association was found between any candidate gene and schizophrenia. A recent analysis of the evidence on 5-HTTLPR found no evidence that the gene directly causes depression, or that it makes people liable to become depressed if something unpleasant happens. However, the study observed a direct relationship between depression and adversity. As our mothers could have told us, bad experiences make us miserable.
This last "discovery" is consistent with other evidence that life experiences shape even the most severe forms of mental illness. Research has consistently shown that migrants have at least a four times increased risk of psychosis compared to other groups, and the effect is most pronounced if they live in areas in which they are in a minority.
Early separation from parents has also been shown to increase the risk of psychosis, as has growing up in an urban environment and chronic bullying. An association between trauma in early life and psychosis has been well-replicated: one recent study estimated that individuals who had been sexually abused in childhood had a twelve times increased risk of serious mental illness. As one of the researchers who carried out this study told me, "Any geneticist who had found such a strong association would have already booked his steamer ticket to Stockholm."
Psychiatrists often downplay these findings with a variety of argument. I have heard it reasoned that findings of this kind are offensive to families, that patients' genes might cause them to seek out experiences that are abusive, or that environmental effects are weak in comparison to those of genes. (However, one study calculated that the population attributable risk of schizophrenia associated with an inner city childhood is 15 percent -- there would be 15 percent fewer cases if we all grew up in the countryside -- whereas the population attributable risk of having a parent with the diagnosis is only 7 percent.)
Some dismiss patients' accounts of their childhoods as untrustworthy (although, when attempts have been made to corroborate them, they are usually proven accurate). It is also said that environmental effects are non-specific, and that early trauma causes a wide range of problems (neglecting the fact that the same is true of genes -- on the most optimistic estimate NG1 is found in about 15 percent of schizophrenia patients and 7 percent of healthy people but, as there are approximately 100 healthy people for every schizophrenia patient, this means that there are about 70 people with NG1 for every patient). Some simply dismiss the evidence with the cry of, "I don't believe it."
Why does all this matter? First, research efforts to understand the causes of mental illness have become hopelessly unbalanced. Only about 5 percent of studies on schizophrenia focus on patients' subjective experiences and research projects on the biological causes of psychosis outnumber those on environmental factors by at least 5 to 1; funding differences are no doubt greater, as much of the research on psychosocial factors is done on a shoestring.
The same is true of treatment studies; to date about 30 trials of cognitive therapy for psychosis have been published; by comparison, in a three-year period nearly 400 drug trials were published in the five leading U.S. psychiatric journals. Despite these efforts, there is little evidence of important advances in psychiatric drug treatment.
Recent studies of antidepressants suggest that they are barely better than placebo, although drug companies have made the data look otherwise by selectively reporting positive results. The second generation antipsychotics, introduced with great fanfare and to the enormous benefit of drug company shareholders, have also proved a disappointment; there is no evidence that these drugs are better than the old medications they have replaced.
Just as important, the obsession with the genetic origins of mental illness has created a climate in which many clinicians do not understand the significance of adverse experiences in the lives of their patients. An observational study of psychiatrists practicing in London found that, when patients asked questions about the meaning of their experiences, the doctors typically changed the subject.
When journalist Lauren Slater faked psychotic symptoms and sought help from U.S. psychiatric services, she found that she was treated with kindness, but was only once asked a question that went beyond the symptoms she was complaining of (the question was about her religion). Patients in these circumstances, often find that they are regarded as (to quote an actual patient) "an imbecile ... just another dribbler."
If we are to improve outcomes for people with severe mental illness, we need to abandon the idea that all the answers lie in genes and biochemisty. We need to develop a less drug-based, more person-centerd approach, which takes the experiences of patients seriously.
By Steven E. Levingston |
January 4, 2010; 5:30 AM ET
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