In their editorial defending the ‘schizophrenia’ concept, apparently
sparked by a press conference at which one of us participated, Professors
Lieberman and First recycle some enduring myths about psychiatric
diagnoses.
Here are some of the myths. Lieberman and First assert that, “Many
studies have shown that these diagnostic criteria [for ‘schizophrenia’]
can be applied reliably and accurately”. However, the accuracy of a
diagnosis can only be determined if there is an absolute benchmark to
compare it against. Moreover, agreement between different operational
definitions of schizophrenia is poor (in the UK 700 study the number of
‘schizophrenia’ patients varied between 268 and 387 according to whether
RDC, DSM-III-R or ICD-10 definitions were used [1]); and clinicians using
the same criteria show poor agreement if they use different methods of
interviewing patients [2]. Lieberman and First say, “Schizophrenia is not
caused by disturbed psychological development or bad parenting” but there
is compelling evidence that being unwanted at birth [3] , early separation
from parents [4], sexual abuse [5-7] and other kinds of adverse family
relationships [8] all increase the risk of psychosis in adult life. Nor
is it true that, “abnormalities in brain structure and function seen on
neuroimaging and electrophysiological tests” establish the reality of
‘schizophrenia’ as a biological disorder, as diverse neurobiological
findings have been reported in ‘schizophrenia’ patients, as many brain
abnormalities are not specific to the diagnosis [9], and as animal and
human studies have shown that adverse early experience can lead to
profound changes in brain structure and function of the kind seen in
patients [10, 11]. The claim that “the evidence that vulnerability to
schizophrenia is at least partly genetic is indisputable” is undermined
when it is noted that methodological biases in the behavioural genetics
literature have led to over-estimation of the heritability of the
diagnosis [12], that no genes of major effect for ‘schizophrenia’ have
ever been discovered, and that those genes of minor effect that have been
identified also confer vulnerability to other diagnoses [13]. Finally,
Lieberman and First’s implication that a diagnosis of 'schizophrenia' is
useful in guiding treatment makes no sense when it is realised that
relapse is better predicted by psychosocial than psychopathological
variables [14] and that responses to psychiatric medications are not
predicted by diagnosis [15]. Indeed, it is often forgotten that the
therapeutic effect of the antipsychotics was first demonstrated on manic
patients [16].
In the seventeenth century, the Roman Catholic Church asserted that
the Earth was the centre of the Universe but this did not make it so. The
assertion by members of the medical-pharmaceutical establishment that
'schizophrenia' is a useful concept does not make it so either. The
results of continuing with the old assumptions about mental illness are
plain for all to see. After 100 years of research on ‘schizophrenia’,
researchers have not provided us with a single biological marker of
diagnostic value. The promotion of biological models of psychosis, far
from reducing the stigma experienced by patients, has increased it [17].
The outcomes for psychotic patients have not improved [18, 19] and the
number of people suffering from enduring psychiatric disability has
increased [20]. Patients in third-world countries do better than those in
the industrialised world who avail themselves of modern psychiatric
services [21]. Meanwhile, new and expensive antipsychotic drugs are
marketed as better than the old ones although they are no better in
reality [22, 23]; their main beneficiaries seem to be drug company share-
holders.
Psychosis should be seen on a continuum with normal experience, and
biological findings should be integrated with observations from psychology
and the social sciences [24]. Care should be offered on the basis of
patients’ needs and strengths rather than diagnosis. What is needed is no
less than a revolution in our scientific approach to understanding severe
mental illness, paralleled by a humane revolution in the way we try and
help some of the most vulnerable and disadvantaged members of our society.
1. van Os, J., et al., A comparison of the utility of dimensional and
categorical representations of psychosis. Psychological Medicine, 1999.
29: p. 595-606.
2. McGorry, P.D., et al., Spurious precision: Procedural validity of
diagnostic assessment in psychotic disorders. American Journal of
Psychiatry, 1995. 152: p. 220-223.
3. Myhrman, A., et al., Unwantedness of preganancy and schizophrenia in
the child. British Journal of Psychiatry, 1996. 169: p. 637-640.
4. Morgan, C., et al., Parental separation, loss and psychosis in
different ethnic groups: A case-control study. Psychological Medicine,
2006.
5. Bebbington, P., et al., Psychosis, victimisation and childhood
disadvantage: Evidence from the second British National Survey of
Psychiatric Morbidity. British Journal of Psychiatry, 2004. 185: p. 220-
226.
6. Janssen, I., et al., Childhood abuse as a risk factor for psychotic
experiences. Acta Psychiatrica Scandinavica, 2004. 109: p. 38-45.
7. Read, J., et al., Sexual and physical abuse during childhood and
adulthood as predictors of hallucinations, delusions and thought disorder.
Psychology and Psychotherapy: Theory, Research and Practice, 2003. 76: p.
1-22.
8. Wahlberg, K.E., et al., Thought disorder index of Finnish adoptees and
communication deviance of their adoptive parents. Psychological Medicine,
2000. 30: p. 127-136.
9. Geuze, E., E. Vermetten, and J.D. Bremner, MR-based in vivo hippocampal
volumetrics: 2. Findings in neuropsychiatric disorders. Molecular
Psychiatry, 2005. 10: p. 160-184.
10. Read, J., et al., The contribution of early traumatic events to
schizophrenia in some patients: A traumagenic neurodevelopmental model.
Psychiatry: Interpersonal and Biological Processes, 2001. 64: p. 319-345.
11. Selten, J.-P. and E. Cantor-Graae, Social defeat: Risk factor for
psychosis? British Journal of Psychiatry, 2005. 187: p. 101-102.
12. Joseph, J., The gene illusion: Genetic research in psychology and
psychiatry under the microscope. 2003, Ross-on-Wye: PCCS Books.
13. Craddock, N. and M.J. Owen, The beginning of the end of the
Kraepelinian dichotomy. British Journal of Psychiatry, 2005. 186: p. 364-
366.
14. Canive, J.M., et al., Family environment predictors of outcome in
Spaniard schizophrenic patients: A nine-month follow-up study. Acta
Psychiatrica Scandinavica, 1995. 92: p. 371-377.
15. Johnstone, E.C., et al., The Northwick Park 'functional' psychosis
study: Diagnosis and treatment response. Lancet, 1988. ii: p. 119-125.
16. Swazey, J.P., Chlorpromazine in psychiatry: A study of therapeutic
innovation. 1974, Cambridge, Mass: MIT Press.
17. Read, J., et al., Prejudice and schizophrenia: A review of the 'mental
illness is an illness like any other' approach. Acta Psychiatrica
Scandinavica, 2006. 114: p. 303-318.
18. Healy, D., et al., Service utilization in 1896 and 1996: Morbidity and
mortality data from North Wales. History of Psychiatry, 2005. 16: p. 27-
41.
19. Healy, D., et al., Lifetime suicide rates in treated schizophrenia:
1875-1924 and 1994-1998 cohorts compared. British Journal of Psychiatry,
2006. 188: p. 223-228.
20. Whitaker, R., Anatomy of an epidemic: Psychiatric drugs and the
astonishing rise of mental illness in America. Ethical Human Psychology
and Psychiatry, 2005. 7: p. 23-35.
21. Sartorius, N., et al., Course of schizophrenia in different countries:
Some results of a WHO comparative 5-year follow-up study, in Search for
the causes of schizophrenia, H. Hafner, W.G. Gattaz, and W. Janzarik,
Editors. 1987, Springer: Berlin. p. 909-928.
22. Jones, P.B., et al., Randomized controlled trial of the effect on
quality of life of second- vs first-generation antipsychotic drugs in
schizophrenia. Archives of General Psychiatry, 2006. 63: p. 1079-1087.
23. Lieberman, J.A., et al., Effectiveness of antipsychotic drugs in
patients with chronic schizophrenia. New England Journal of Medicine,
2005. 353: p. 1209-1223.
24. Bentall, R. P. Madness explained: Psychosis and human nature.
2003. London: Penguin Press
Competing interests:
None declared
Competing interests:
No competing interests
07 February 2007
Richard P Bentall
Professor of Experimental Clinical Psychology
Peter Kinderman, Carmelo Vázquez
University of Manchester, Oxford Road, Manchester M13 9PL
Rapid Response:
The schizophrenia myth
In their editorial defending the ‘schizophrenia’ concept, apparently
sparked by a press conference at which one of us participated, Professors
Lieberman and First recycle some enduring myths about psychiatric
diagnoses.
Here are some of the myths. Lieberman and First assert that, “Many
studies have shown that these diagnostic criteria [for ‘schizophrenia’]
can be applied reliably and accurately”. However, the accuracy of a
diagnosis can only be determined if there is an absolute benchmark to
compare it against. Moreover, agreement between different operational
definitions of schizophrenia is poor (in the UK 700 study the number of
‘schizophrenia’ patients varied between 268 and 387 according to whether
RDC, DSM-III-R or ICD-10 definitions were used [1]); and clinicians using
the same criteria show poor agreement if they use different methods of
interviewing patients [2]. Lieberman and First say, “Schizophrenia is not
caused by disturbed psychological development or bad parenting” but there
is compelling evidence that being unwanted at birth [3] , early separation
from parents [4], sexual abuse [5-7] and other kinds of adverse family
relationships [8] all increase the risk of psychosis in adult life. Nor
is it true that, “abnormalities in brain structure and function seen on
neuroimaging and electrophysiological tests” establish the reality of
‘schizophrenia’ as a biological disorder, as diverse neurobiological
findings have been reported in ‘schizophrenia’ patients, as many brain
abnormalities are not specific to the diagnosis [9], and as animal and
human studies have shown that adverse early experience can lead to
profound changes in brain structure and function of the kind seen in
patients [10, 11]. The claim that “the evidence that vulnerability to
schizophrenia is at least partly genetic is indisputable” is undermined
when it is noted that methodological biases in the behavioural genetics
literature have led to over-estimation of the heritability of the
diagnosis [12], that no genes of major effect for ‘schizophrenia’ have
ever been discovered, and that those genes of minor effect that have been
identified also confer vulnerability to other diagnoses [13]. Finally,
Lieberman and First’s implication that a diagnosis of 'schizophrenia' is
useful in guiding treatment makes no sense when it is realised that
relapse is better predicted by psychosocial than psychopathological
variables [14] and that responses to psychiatric medications are not
predicted by diagnosis [15]. Indeed, it is often forgotten that the
therapeutic effect of the antipsychotics was first demonstrated on manic
patients [16].
In the seventeenth century, the Roman Catholic Church asserted that
the Earth was the centre of the Universe but this did not make it so. The
assertion by members of the medical-pharmaceutical establishment that
'schizophrenia' is a useful concept does not make it so either. The
results of continuing with the old assumptions about mental illness are
plain for all to see. After 100 years of research on ‘schizophrenia’,
researchers have not provided us with a single biological marker of
diagnostic value. The promotion of biological models of psychosis, far
from reducing the stigma experienced by patients, has increased it [17].
The outcomes for psychotic patients have not improved [18, 19] and the
number of people suffering from enduring psychiatric disability has
increased [20]. Patients in third-world countries do better than those in
the industrialised world who avail themselves of modern psychiatric
services [21]. Meanwhile, new and expensive antipsychotic drugs are
marketed as better than the old ones although they are no better in
reality [22, 23]; their main beneficiaries seem to be drug company share-
holders.
Psychosis should be seen on a continuum with normal experience, and
biological findings should be integrated with observations from psychology
and the social sciences [24]. Care should be offered on the basis of
patients’ needs and strengths rather than diagnosis. What is needed is no
less than a revolution in our scientific approach to understanding severe
mental illness, paralleled by a humane revolution in the way we try and
help some of the most vulnerable and disadvantaged members of our society.
1. van Os, J., et al., A comparison of the utility of dimensional and
categorical representations of psychosis. Psychological Medicine, 1999.
29: p. 595-606.
2. McGorry, P.D., et al., Spurious precision: Procedural validity of
diagnostic assessment in psychotic disorders. American Journal of
Psychiatry, 1995. 152: p. 220-223.
3. Myhrman, A., et al., Unwantedness of preganancy and schizophrenia in
the child. British Journal of Psychiatry, 1996. 169: p. 637-640.
4. Morgan, C., et al., Parental separation, loss and psychosis in
different ethnic groups: A case-control study. Psychological Medicine,
2006.
5. Bebbington, P., et al., Psychosis, victimisation and childhood
disadvantage: Evidence from the second British National Survey of
Psychiatric Morbidity. British Journal of Psychiatry, 2004. 185: p. 220-
226.
6. Janssen, I., et al., Childhood abuse as a risk factor for psychotic
experiences. Acta Psychiatrica Scandinavica, 2004. 109: p. 38-45.
7. Read, J., et al., Sexual and physical abuse during childhood and
adulthood as predictors of hallucinations, delusions and thought disorder.
Psychology and Psychotherapy: Theory, Research and Practice, 2003. 76: p.
1-22.
8. Wahlberg, K.E., et al., Thought disorder index of Finnish adoptees and
communication deviance of their adoptive parents. Psychological Medicine,
2000. 30: p. 127-136.
9. Geuze, E., E. Vermetten, and J.D. Bremner, MR-based in vivo hippocampal
volumetrics: 2. Findings in neuropsychiatric disorders. Molecular
Psychiatry, 2005. 10: p. 160-184.
10. Read, J., et al., The contribution of early traumatic events to
schizophrenia in some patients: A traumagenic neurodevelopmental model.
Psychiatry: Interpersonal and Biological Processes, 2001. 64: p. 319-345.
11. Selten, J.-P. and E. Cantor-Graae, Social defeat: Risk factor for
psychosis? British Journal of Psychiatry, 2005. 187: p. 101-102.
12. Joseph, J., The gene illusion: Genetic research in psychology and
psychiatry under the microscope. 2003, Ross-on-Wye: PCCS Books.
13. Craddock, N. and M.J. Owen, The beginning of the end of the
Kraepelinian dichotomy. British Journal of Psychiatry, 2005. 186: p. 364-
366.
14. Canive, J.M., et al., Family environment predictors of outcome in
Spaniard schizophrenic patients: A nine-month follow-up study. Acta
Psychiatrica Scandinavica, 1995. 92: p. 371-377.
15. Johnstone, E.C., et al., The Northwick Park 'functional' psychosis
study: Diagnosis and treatment response. Lancet, 1988. ii: p. 119-125.
16. Swazey, J.P., Chlorpromazine in psychiatry: A study of therapeutic
innovation. 1974, Cambridge, Mass: MIT Press.
17. Read, J., et al., Prejudice and schizophrenia: A review of the 'mental
illness is an illness like any other' approach. Acta Psychiatrica
Scandinavica, 2006. 114: p. 303-318.
18. Healy, D., et al., Service utilization in 1896 and 1996: Morbidity and
mortality data from North Wales. History of Psychiatry, 2005. 16: p. 27-
41.
19. Healy, D., et al., Lifetime suicide rates in treated schizophrenia:
1875-1924 and 1994-1998 cohorts compared. British Journal of Psychiatry,
2006. 188: p. 223-228.
20. Whitaker, R., Anatomy of an epidemic: Psychiatric drugs and the
astonishing rise of mental illness in America. Ethical Human Psychology
and Psychiatry, 2005. 7: p. 23-35.
21. Sartorius, N., et al., Course of schizophrenia in different countries:
Some results of a WHO comparative 5-year follow-up study, in Search for
the causes of schizophrenia, H. Hafner, W.G. Gattaz, and W. Janzarik,
Editors. 1987, Springer: Berlin. p. 909-928.
22. Jones, P.B., et al., Randomized controlled trial of the effect on
quality of life of second- vs first-generation antipsychotic drugs in
schizophrenia. Archives of General Psychiatry, 2006. 63: p. 1079-1087.
23. Lieberman, J.A., et al., Effectiveness of antipsychotic drugs in
patients with chronic schizophrenia. New England Journal of Medicine,
2005. 353: p. 1209-1223.
24. Bentall, R. P. Madness explained: Psychosis and human nature.
2003. London: Penguin Press
Competing interests:
None declared
Competing interests: No competing interests