The Biopsychiatric Model
of "Mental Illness"
A Critical Bibliography
Loren R. Mosher M.D.
Presented below is an annotated bibliography addressing today's
widely held belief system about the causes and treatment of disturbed and
disturbing behavior usually labeled as some form of serious mental illness. As
"schizophrenia" is psychiatry's most vexing and perplexing
"disorder" and viewed as the most serious of the "mental
illnesses" it is the primary focus of this list. It excludes children. It
is not exhaustive, but is representative.
Conclusions: Today's dominant theory of serious "mental
illnesses" posits them to be genetically determined (i.e., inherited),
biochemically mediated (via "chemical imbalances"), life-long
"brain diseases" (with associated specific neuropathologic changes)
whose cause(s) and course is more or less independent of environmental factors is
not supported by existing evidence. A critical review of the scientific
available evidence reveals no clear indication of hereditary factors, no
specific biochemical abnormalities, and no associated causal neurologic lesion(s).
However, a number of environmental factors have been found to be related to
their cause(s) and course (bibliography in preparation). It is also generally
held that the anti-psychotic drugs are the mainstay of treatment and should, in
most cases, be taken for a lifetime. In fact, the data indicate that neuroleptic
drug treatment is not usually necessary (especially in persons newly identified
as psychotic) if a proper interpersonal environment and social context is
provided in alternatives to hospital care. It also appears that has drug
treatment has resulted in less favorable long-term outcomes than was the case
before anti-psychotic drugs were introduced. Furthermore, anti-psychotic drug
treatment is associated with the induction of irreversible brain pathology
(resulting in reduced intellectual and abnormal motor functioning) and shortened
life expectancy. Pre-neuroleptic drug era long-term follow-up studies indicate
that recovery can not only occur, but is to be expected in the majority of
cases. Ergo, so called "chronicity" in "mental
illness" is likely the result of its medicalization, institutionalization
with its social network disruption, marginalization, discrimination and the less
specific social consequences (e.g. poverty) that accompany these processes.
General:
Harding, C. M. and Zahniser, J.M. (1994) Empirical Correction of Seven Myths
about Schizophrenia with Implications for Treatment. Acta Psychiatrica
Scandinavica. 90 (suppl.384): 140-146.
Colin Ross & Alvin Pam. (1995). Pseudo-science in biological psychiatry:
Blaming the body. NY, John Wiley
Van Praag, Herman. (1993). "Make-believes" in psychiatry, or the
perils of progress. Clinical and Experimental Psychiatry Monograph No. 7.
New York: Brunner/Mazel.
Siebert, A. (1999) Brain Disease Hypothesis Disconfirmed by All Evidence. J.
of Ethical Human Sciences and Services. 1(2) 179-199.
Valenstein, E (1998) Blaming the Brain: the truth about drugs and mental
illness. NY, Free Press.
Genetics:
Barondes, S. et al (1999) An Agenda for Psychiatric Genetics. Arch. Gen.
Psych. 56: 549-552. ("genetically influenced psychiatric
disorders have so far been resistant to analysis")
Joseph, J. (1998). The equal environment assumption of the classical twin
method: A critical analysis. Journal of Mind and Behavior, 19,
325-358. (Joseph points out that all twin studies of behavioral
characteristics-like those defining "schizophrenia" are fundamentally
flawed because identical twins have been clearly shown to be raised more
similarly than are non-identical ones. Hence, higher rates of the co-existence
of "schizophrenia" among identical twins can be explained by their
having been raised in more similar environments. Even then their rates run only
about 35%vs.10% for non-identicals)
Joseph, J. (1999). A critique of the Finnish Adoptive Family Study of
Schizophrenia. Journal of Mind and Behavior, 20, 133-154. (Joseph
points out that the adoption study methodology depends on random adoption-that
is the adoption agency does not know the mother's background when placing the
child. The Finnish study, the most elegant and sophisticated of all, suffers
from the fact that the first half of the sample was placed with the knowledge
the mothers had "schizophrenia". The widely quoted Danish adoption
studies are plagued with this and a number of other important methodological
problems making their findings highly questionable.)
Joseph, J. (1999). The genetic theory of schizophrenia: A critical overview. Ethical
Human Sciences and Services, 1, 119-145. (Conclusion: there is no
evidence of a specific or important genetic component in "mental
illness")
Neuropathology:
Chua, S. E. and McKenna, P.J. (1995) Schizophrenia-a Brain Disease? A critical
review of structural and functional cerebral abnormality in the disorder. Brit.
Jour. Psych., 166: 563-582. (no consistent specific structural or
functional abnormalities found).
Zakzanis, K. et al (2000) Searching the Schizophrenic Brain for Temporal Lobe
Deficits: a systematic review and meta-analysis. Psychol. Med., 30:
491-504. (No specific findings).
Brain Damage Associated with Neuroleptic Drug Treatment:
Ballesteros J, Gonzales-Pinto A, & Bulbena A. Tardive dyskinesia associated
with higher mortality in psychiatric patients: results of a meta-analysis of
seven independent studies. J Clin Psychopharmacology, 20:2,
188-194, 2000.
E Christensen. "Neuropathological investigations of 28 brains from patients
with dyskinesia." Acta Psychiatrica Scandinavica, 46,14-23,
1970. (TD patients have structural abnormalities in the basal ganglia, enlarged
ventricles, and sulcal markings.)
OO Famuyiva. Tardive dyskinesia and dementia. British Journal of Psychiatry,
135, 500-504, 1979. (TD associated with cognitive impairment.)
JT Wegner. Cognitive impairment in tardive dyskinesia. Psychiatry Research,
16, 331-337. 1985. (TD associated with cognitive impairment.)
James Wade. Tardive Dyskinesia and Cognitive Impairment. Biological
Psychiatry, 22, 393-395, 1987. (Association between TD and cognitive
impairment. "The relationship appears to be linear: individuals with severe
forms of the disorder are most impaired cognitively.")
JL Waddington. Cognitive dysfunction, negative symptoms, and tardive dyskinesia
in schizophrenia. Archives of General Psychiatry, 44, 907-912,
1987. (TD associated with cognitive impairment and worsening of negative
symptoms.)
Waddington J et al, Mortality in schizophrenia: Antipsychotic polypharmacy and
absence of adjunctive anticholinergics over the course of a 10-year prospective
study, Br J Psych, 1998, 173; 325-329. (This study found that a
reason that schizophrenics have a shorter life expectancy was neuroleptic drug
treatment)
JB Wade. Cognitive changes associated with tardive dyskinesia. Neuropsychiatry,
Neuropsychology, and Behavioral Neurology. 1, 217-227. 1989. (TD
associated with cognitive impairment. The researchers conclude: "TD may
represent both a motor and dementing disorder.")
R. Yassa. Functional impairment in tardive dyskinesia: medical and psychosocial
dimensions. Acta Psychiatr Scand 80, 64-67. 1989. (TD associated
with gait, speech difficulties, and psychosocial impairment.)
Michael S. Myslobodsky. Central Determinants of Attention and Mood Disorder in
Tardive Dyskinesia (Tardive Dysmentia.). Brain and Cognition, 23,
88-101. 1993. (TD patients lose the motor part of their "road map of
consciousness." TD may represent "larval dementia.")
Herbert Spohn. The effect of attention/information processing impairment of
tardive dyskinesia and neuroleptics in chronic schizoprhenics." Brain
and Cognition 23, 28-39, 1993. (TD exacerbates cognitive impairment.)
Jacinthe Baribeau. Tardive dyskinesia and associated cognitive disorders: a
convergent neuropsycological and neurophysiological approach. Brain and
Cognition 23, 40-55, 1993. (TD associated with cognitive
dysfunction.)
John Waddington. Cognitive dysfunction in schizophrenia: organic vulnerability
factor or state marker for tardive dyskinesia? Brain and Cognition 23,
56-70, 1993. (He reviews 22 studies from 1979 to 1991 that concluded that
patients with TD were cognitively impaired on a variety of measures, which
include learning, memory, cognitive function, intellectual function, visual
retention, orientation, etc.)
James Wade. Factors related to the severity of tardive dyskinesia. Brain and
Cognition 23, 71-80, 1993. (A review of research shows that
"biochemical and neuropathological changes associated with TD indicates
that similar alterations are associated with Hungtington's disease and or
Parkinson's." In their own research, "cortical dysfunction,
characterized by impairment in nonverbal function, is associated with TD
severity.")
Emmanuelle Pourcher. Organic brain dysfunction and cognitive deficits in young
schizophrenic patients with tardive dyskinesia. Brain and Cognition 23,
81-87, 1993. (This is a study of patients under 40. They find that TD is
associated with cerebral dysfunction, which in turn is associated with exposure
to neuroleptic drugs.)
Thomas Gualtieri. The problem of tardive akathisia. Brain and Cognition 23,
102-109, 1993. (He states that tardive akathisia may be thought of as a disease
of the basal ganglia, much like Parkinson's, Huntington's and Wilson's. MRI
studies have demonstrated basal ganglia lesions in TD patients, especially in
the caudate nucleus. Basal ganglia diseases all cause behavioral instability and
intellectual impairment (even psychosis and dementia)).
Miranda Chakos. Increase in Caudate Nuclei Volumes of First-Episode
Schizophrenic Patients Taking Antipsychotic Drugs. Am Jour Psych 151,
1430-1435. 1994. (Neuroleptics increase caudate volumes 5.7% during first 18
months of treatment in first-episode schizophrenic patients. Higher dosage is
associated with larger increase in caudate volumes.)
J.S. Paulsen. Neuropsychological impairment in tardive dyskinesia. Neurospsychology
8, 227-241. 1994. (Review of 31 studies that compared cognitive function
in schizophrenics with and without TD. In 24 studies, TD patients were found to
do worse. The more severe the TD, the greater the impairment in cognitive
function. They conclude that "TD involves an alteration of brain function
that affects both motor and cognitive control.")
P. Sachdev. Negative symptoms, cognitive dysfunction, tardive akathisia and
tardive dyskinesia." Acta Psychiatr Scand. 93, 451-459. 1996.
(Both tardive akathisia and tardive dyskinesia are associated with more
cognitive deficits and negative symptoms. This association is stronger with TA
than with TD. The implication is that movement disorders seen in TA and TD are
"but one feature of complex syndromes that include motor and cognitive
features. A comparison must be made with other movement disorders, such as
Parkinson's disease and Huntington's disease, in which neuropsychological
deficits, and indeed subcortical dementia are known to occur.")
John Waddington. Cognitive dysfunction in chronic schizophrenia followed
prospectively over 10 years and its longitudinal relationship to the emergence
of tardive dyskinesia. Psychological Medicine, 26, 681-688. 1996.
(Progressive deterioration in cognitive function is seen even late in chronic
phase of schizophrenic illness. Deterioration derives primarily from emergence
of TD. They find that marked deterioration in cognitive function occurs at same
time as emergence of movement disorder.)
Rupert McShane. Do Neuroleptic Drugs Hasten Cognitive Decline in Dementia?
Prospective Study with Necropsy Follow Up. British Medical Journal, 314,
266-270. 1997. (The decline in cognitive function in dementia patients who take
neuroleptics is twice the decline in patients who did not take he drugs.)
Raquel Gur,et. Al. Subcortical MRI Volumes in Neuroleptic-Naïve and Treated
Patients with Schizophrenia. American Journal of Psychiatry, 155,
1711-1717. 1998. (Drugs cause hypertrophy of the caudate, putamen, and thalamus,
which is thought to be "structural adaptation to receptor blockade."
The drug-induced hypertrophy is also "mildly associated with greater
severity of both negative and positive symptoms.")
Raquel Gur, et. Al. A follow-up of magnetic resonance imaging study of
schizophrenia. Archives of General Psychiatry, 55, 145-151, 1998.
(Use of neuroleptics is associated with volume reduction (or atrophy) of frontal
lobes and temporal lobes. As the brain atrophies in this way, here is said to
improvement in delusions and thought disorder (the brain-damaging principle at
work). A greater rate of reduction in volume is associated with higher dose. At
the same time, reduction in volume is associated with decline in some
neurobehavioral functions.)
Al Madsen. Neuroleptics in progressive structural brain abnormalities in
psychiatric illness. The Lancet, 352, 784-785. Sept. 5, 1998. (Neuroleptic
use is associated with atrophy of cerebral cortex. The estimated risk of atrophy
increases by 6.4% for each additional 10 grams of neuroleptic drug.)
G. Tsai. Markers of glutamergic neurotransmission and oxidative stress
associated with tardive dyskinesia. American Journal of Psychiatry, 155,
1207-1213. 1998. (This study suggests that neuroleptics cause neuronal damage as
a result of oxidative stress, and that this is the degenerative process that
produces TD.)
Conclusion: the brain abnormalities attributed causal significance in mental
illness are most likely the result of neuroleptic drug treatment.
Long Term Follow-up Studies:
Bleuler, M. (1968). A 23 Year Follow-up Study of 208 Schizophrenics. In
Rosenthal and Kety (eds.) The Transmission of Schizophrenia. Oxford:
Pergamen Press.
Ciompi, L. (1980) Catamnestic Long Term Study of the Life Course and Aging of
Schizophrenics. Schiz. Bull. 6, 606-618.(30 year follow-up).
Harding, C. et. Al. (1987). The Vermont Longitudinal Study of Persons with
Severe Mental Illness. (32 year follow-up). Am. J. Psychiatry, 144,
718-726. (A remarkable study because in contrast to the European ones-Ciompi and
Bleuler- who studied consecutively admitted cohorts- Harding et.al. studied a
group of so-called "chronic back-ward" patients discharged with an
individualized rehabilitation program to the community.)
Hegarty, J.D.et. al. (1994) One Hundred Years of Schizophrenia: a meta-analysis
of the outcome literature. Am. J. Psychiatry 151: 1409-1416.
(Poorer outcomes in last third of the 20th century and best in the middle
third.)
Cross-Cultural Studies:
Jablensky, A.; Sartorius, N.; Ernberg, G.; Anker, M.; Korten, A.; Cooper,
J.E.; Day, R.; and Bertelsen, A. (1992) Schizophrenia: Manifestations,
incidence, and course in different cultures. A World Health Organization
ten-country study. Psychological Medicine, Monograph Supplement 20:97 pp.
Lin, K.M., and Kleinman, A.M. (1988) Psychopathology and clinical course of
schizophrenia: A cross-cultural perspective. Schizophrenia Bulletin, 14(4):
555-567.
Leff, J.; Sartorius, N.; Jablensky, A.; and Korton, A. (1992) The international
pilot study of schizophrenia: Five-year follow-up findings. Psychological
Medicine, 22(1): 131-145.
Murphy, H.B. and Raman, A. C. (1971) The Chronicity of Schizophrenia in
Indigenous Tropical People: Results of a 12-year Follow-up. Brit. Jour. Psych.
118: 489-497.
Warner, R. (1994) Recovery from schizophrenia: Psychiatry and political
economy. (2nd Edition) London: Routledge and Kegan Paul.
World Health Organization, (1979) Schizophrenia: An international follow-up
study. New York: John Wiley & Sons.
(all these studies find relatively benign long term outcomes -- 50 to 75% full
and social recoveries -- before neuroleptics or when they were little used.
Also, striking cross-cultural differences in outcome were found favoring
"developing" countries -- best explained by little or no neuroleptic
drug use in those countries.)
Alternatives to Psychiatric Hospitalization:
Braun, P.B., Kochansky, G., Shapiro, R., Greenberg. S., Gudeman, J.E., Johnson,
S., & Shore, M.F. (1981) Overview: Deinstitutionalization of psychiatric
patients: A critical review of outcome studies. American Journal of
Psychiatry, 138, 736-749.
Kiesler, C.A. (1982a) Mental hospitals and alternative care:
Noninstitutionalization as potential public policy for mental patients. American
Psychologist, 37, 349-360.
Kiesler, C.A. (1982b) Public and professional myths about mental
hospitalization: An empirical reassessment of policy-related beliefs. American
Psychologist, 37, 1323-1339.
Mosher LR. (1999) Soteria and other alternatives to acute hospitalization: A
personal and professional review. Jour. Nerv. Ment. Dis. 187:
142-149.
Mosher LR, Burti L (1994) Community mental health: A practical guide.
N.Y.: W.W. Norton.
Straw, R.B. (1982) Meta-analysis of deinstitutionalization. (Doctoral
dissertation). University Microfilms, Ann Arbor, MI: Northwestern University.
Warner, R. (Ed.) (1995) Alternatives to the mental hospital for acute
psychiatric treatment. Wash. DC: American Psychiatric Press.
(Conclusions: every study shows alternatives to be as, or more effective, than
hospital treatment and less costly.)
Psychosocial Treatment with minimal or no drug use:
Alanen, Y.O.; Ugelstad, E.; Armelius, B.A.; Lehtinen, K.; Rosenbaum, B.; and
Sjostrom, R., Eds. (1994) Early treatment for schizophrenic patients:
Scandinavian psychotherapeutic approaches. Oslo, Norway: Scandinavian
University Press.
Alanen, Y.O.; Lehtinen, V.; Lehtinen, K.; Aaltonen, J.; and Rakkolainen, V.
(2000) The Finnish model for early treatment of schizophrenia and related
psychoses. In: Martindale, B., Bateman, A., Crowe, M., and Margison, F., Eds. Psychosis:
Psychological approaches and their effectiveness. London: Gaskell. (The
centerpiece of their approach is rapid in-home family and social network
intervention to avoid hospitalization and medicalization.)
Ciompi, L., Duwalder, H.-P., Maier, C., Aebi, E., Trutsch, K., Kupper, Z., &
Rutishauser, C. (1992). The pilot project "Soteria Berne": Clinical
experiences and results. British Journal of Psychiatry, 161(suppl. 18),
145-153. (A replication of Mosher and co-workers Soteria Project in California.
Similar results-about 2/3rds of newly diagnosed psychotics recovered without
neuroleptic drug treatment)
Lehtinen, V. et. al. (2000). Two-Year Follow-up of First Episode Psychosis
Treated According to an Integrated Model: Is immediate neuroleptisation always
needed? European Psychiatry, 15(5): 312-320. (44% of the randomly
assigned subjects received no neuroleptic drug treatment-vs. 6% of the controls-
over the two-year period and their outcomes were comparable or better than those
treated with drugs.)
Matthews SM, Roper MT, Mosher LR, and Menn AZ. (1979) A non-neuroleptic
treatment for schizophrenia: Analysis of the two-year post-discharge risk of
relapse. Schiz. Bull. 5: 322-333. (Soteria treated patients-as compared
with hospital treated- had a significantly lower rehospitalizaton rate over two
years despite few being neuroleptic maintained. First cohort analysis)
Mosher, L.R. & Bola, J.R. (2000) The Soteria Project: Twenty-five Years of
Swimming Upriver. Complexity and Change, 9: 68-74. (Soteria patients-43%-
who received no neuroleptics over the two year follow-up period did
substantially better than those who did. As a group the Soteria treated patients
had better outcomes than a control group that received "usual"
hospital and drug treatment. The subgroup of "poor prognosis" subjects
treated at Soteria had better outcomes than the Soteria group as a whole. First
combined cohort analysis)
Mosher LR & Menn A Z (1978) Community residential treatment for
schizophrenia: Two-year follow-up. Hosp Comm Psych 29: 715-723. (Better
psychosocial outcomes for Soteria treated 1st and 2nd episode patients compared
with control subject receiving "usual" treatment. First cohort.)
Mosher LR, Vallone R, and Menn AZ .(1995) The treatment of acute psychosis
without neuroleptics: Six-week psychopathology outcome data from the Soteria
project. Int. J. Soc. Psych. 41: 157-173. (2nd cohort: as was true of the
1st cohort, at six weeks the Soteria group had improved as much without meds as
the hospital group-all of whom received neuroleptics.)
Tuori, T. et al (1998) The Finnish National Schizophrenia Project 1981-1987: 10
year evaluation of its results. Acta. Psychiatrica Scandinavica 97:
10-18. (In the presence of comprehensive "need adapted"psychosocial
treatment, drugs are unneccesary for the most part and may, in fact, prevent
recovery.)
Soteria Associates
Loren R. Mosher M.D., Director
2616 Angell Ave.
San Diego, CA 92122
Phone: 858-550-0312
Fax: 858-558-0854
Email: MosherSchreiber@compuserve.com
Website: moshersoteria.com
This bibliography was compiled in large part from ones collected by: Volkmar
Aderhold, David Cohen, Jay Joseph, Vera Sharav, Doug Smith, Ron Unger and Robert
Whitaker. I owe them my heartfelt thanks. LRM (2-20-01)
