Body: | Anti-psychotic drugs cause brain damage.
Reading list: Chemical imbalances are bogus and mythical by Loren R. Mosher
M.D.
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The Biopsychiatric Model
of "Mental Illness"
"A Critical Bibliography" by Loren R. Mosher M.D.
"Conclusion: the brain abnormalities attributed causal significance in mental illness are most likely the result of neuroleptic drug treatment." (Loren R. Mosher M.D.)
See also: Psychiatrist Loren Mosher resigns from the American Psychiatric
Association (APA) because of bogus scientific claims related to chemical
imbalances and corrupt support of the drug companies to perpetuate this
myth.
Dr Mosher writes:
"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." (Loren R. Mosher M.D.)
Dr Mosher's 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." (Loren R. Mosher M.D.)
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Brain Damage Associated with Neuroleptic Drug Treatment:
(tranquilizers used to treat psychotic conditions when a calming effect is desired)
"Conclusion: the brain abnormalities attributed causal significance in mental illness are most likely the result of neuroleptic drug treatment." (Loren R. Mosher M.D.)
Reading list: Anti-psychotic drugs cause brain damage:
"Conclusion: the brain abnormalities attributed causal significance in
mental illness are most likely the result of neuroleptic drug treatment."
(Loren R. Mosher M.D.)
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.)
By Dr. Loren R. Mosher
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