SCHIZOPHRENIA - THERE IS HOPE AND SCHIZOPHRENIA CAN BE CURED. IT IS A BIOCHE

[Guest guest]

Go to: http://www.mosher-soteria.com

 

You'll find your answers there ;-). Lynn

---------=

----

 

Loren R. Mosher M.D.

A Critical Bibliography:

The Biopsychiatric Model of " Mental Illness "

 

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

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)

 

------

 

 

 

 

Gettingwell, Morton Bodanis <mortonmb@c...> wrote:

> I had been looking for sites which address schizophrenia - and

possible

> cures - other than via conventional drugs. In anticipation of

there

> being others who may be interested, I recommend this site.

> Morton

>

>

http://www.4optimallife.com/Alternative-Medicines-Cures-For-Sc

hizophrenia-Mental-Illness.html

>

>

>