Schizophrenia: a genetic disorder of the synapse?
BMJ 2005; 330 doi: https://doi.org/10.1136/bmj.330.7484.158 (Published 20 January 2005) Cite this as: BMJ 2005;330:158
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“Understanding the cause and pathogenesis of schizophrenia” has been
persistently ignored in favour of profit-making creativity in wishful
thinking, called biopsychiatry. There has never been any objective science
to uphold the persistent dogma for individual differences in liability,
let alone that there is a predominantly genetic reason for ANY severe
“mental illness,” which includes the difference in behaviour that has been
labeled by biopsychiatry as schizophrenia. Biopsychiatry has therefore
never been of any usefulness, neurobiologically, accept to those who
profit by dissemination of its propaganda. Recognition that a drug can
cause harm by upsetting brain chemistry which shows behaviorally (in the
case of a dopaminergic drug causing a psychotic episode) and then
attesting this to proof of biological cause for a psychosocial
dysfunctionality is not just lousy science, it's medical malpractice. The
“potency of antipsychotic drugs is proportional to their ability” to
cause a human being to become 'stupor us' at best and brain-damaged over
time or to suffer “neurocognitive impairments,” both temporary and
permanent.
Perception is a product of mind (consciousness) a nonphysical
element. We are not the sum of our parts. We are greater than the sum of
our parts. And the greater is consciousness. Bio-psychiatry fails to
obtain proofs, because one cannot address a non-physical element with a
physical world tool-kit i.e. objective, empirical science. The
foundational knowledge of psychiatry will always be theorem and never
fact. We need to evolve to the level of gods ourselves to be able to
encompass the knowledge that is required to create the verifiable science
that can be applied toward discovery of that which has 'no organic
substance'.
Competing interests:
Psychiatric Consumer-Survivor X-Patient Self-Advocate
Competing interests: No competing interests
I think one really has to realize how such a model of genetics is
used to persecute people. What one person calls disruptive destructive
behavior to another is simply necessary dissident behavior. To lable this
behavior a disease becomes the task of a fascist society. Again, there is
no medical basis for mental illness, as yet there is no biological proof
for it's existence, the supposed proof for it's genetic existence is so
questionable that it can not be honored in any reasonable sense. The
studies using twins are hampered by all sorts of methods of manipulating
the data (counting one pair of twins twice for example which would put
each twin in the control as well as the random group of the experiment).
The issue of environmental influence is not really investigated in an
articulate manner, if it is one sees that the environment influences
whether or not a person has acquired emotional pain in their life and it
would be abusive behavior which has caused the need for a person to
retreat into a fantasy world. Also the definition for Schizophrenia was
changed to include all sorts of border line diagnosis in order to obtain
enough correlation to have even the minimal correlation with marker genes
(and this still only points to a possiblity not to any concrete evidence).
This would be something like including anyone who ever stole a cookie from
the kitchen in those who exhibit "criminal behavior."
This then after years of recklessly ambitious studies and mania.
What is the result of all of this?
This genetic model of mental illness despite the lack of any proof that
there is anything biological causing it.
A person with a diagnosis is also targeted for reckless, arbitrary and
random prejudiced behavior. The same way as a person who was black used to
be stereotyped (in the United States at least) or a woman was expected to
adhere to certain limitation in behavior applies to people who are called
mentally ill.
A person labeled as being mentally ill and not on medications (not
allowing their minds to be disabled or numbed) is immediately labeled as
being an unsafe person to have around for example and if their behavior at
all deviates from the norm in a fashion that others find needs correction
they are assaulted with biased input from others, alienated in an attempt
to make them feel that they have something inherently wrong with them and
if they express how they feel from this consequent opression in a way that
goes against the grain of what society at large deems as "productive" or
"healthy" behavior they are incarcerated against their will, forced on
medications which have not been scientifically proven to heal but only to
create chemical imbalances and are subjected to an incredible amount of
dishonest, coercive and devious behavior to keep them from being allowed
to openly express themselves and disqualify it if they at all dare to
express themselves despite how they are bullied and oppressed. In short
(As McCawber, David Copperfield's friend would say) – A person who is
labeled as being mentally ill is put in a place where he is legally
allowed to be the object of prejudism and bullied.
May I add that Rüdin, the man who founded psychiatric genetics, at
age 29 formulated his program for a future "racially pure utopia." During
Hitler's era in Germany Rüdin served on a panel with Heinrich Himmel who
was chairman of the Task Force of Hereditary Experts. This task force
drafted the German sterilization law of 1933 and 7 years later 80,000
German mental patients were murdered under the Nazi Euthanasia program.
The first twin study regarding schizophrenia and genetics was performed by
one of Rüdin's top associates.
Competing interests:
I'm not paranoid about mental illness
Competing interests: No competing interests
While accepting that there are both genetic and environmental
elements in all human disorders, those with a major genetic component are
usually uncommon because natural selection keeps them this way. So while I
agree with Profs. Owen, O'Donovan and Harrison (*) that the synapse is the
most likely place for mental disorders like schizophrenia to originate (
and it is very encouraging to hear of more interest at this level),
nevertheless if schizophrenia is still to be regarded as a common
condition - reputedly affecting 1% of the adult population world wide-
then neuron damage affecting the servicing of the synapses is unlikely to
be produced entirely by genetic conditions. Unless , of course, as well as
being unable to regenerate after damage, it is another special feature of
nerve cells in the brain that in about 1% of individuals a significant
proportion of neurons are genetically programmed to fail in early adult
life.
But there are other possible explanations , and to me the one that
seems most convincing is that as well as
in-built programmes prescribing that at a certain level of information
load, or age of component cell, the neuron unit will cease to perform
effectively, some external environmental agents (eg. micro-organisms,
toxic substances or nutritional faults) have damaged the neuron units,
most likely in childhood when rapid growth and development are taking
place.
However in all these situations the first task should be to identify
the main biochemical factors underlying the failure of the neutrons to
service the synapses, and this may not be so difficult as identifying the
multitude of genes that are likely to be involved.Then it may be possible
to help more normal function to return to the neuron units by introducing
modified transmitters to the
central nervous system, or perhaps eventually even by introducing stem
cells directly into the brain.
* Owen M.J., O'Donovan M.C., Harrison P.J. BMJ 2005 330 158/9 22
January
Competing interests:
None declared
Competing interests: No competing interests
The list of discrepencies in judgement here are so numerous that it
makes one dizzy.
To begin with schizophrenia has no biological basis, there is not
proof that there is anything biologically wrong with the people who are
called schizophrenic. What is apparent is that the behavior of a
"schizophrenic" is not understand by many people and that they are placed
in conditions where their inherent freedoms are taken away from them and
they become victims of human rights abuses (for example they are forced on
medications which have only been proven to create chemical imbalances
rather than that they address them). To go around searching for a genetic
"defect" in cases where there is no clear disease but rather a social
judgement is perhaps a disease in itself. This disease then would be
called prejudism or obssessive compulsive paranoia.
If one would find this supposed gene that is involved with
schizophrenia then, with an open mind, one could just as easily claim that
it is a sign of exceptional sensitivity rather than that of a disease. A
sensitive person is not as easily going to fall sway to societal
programming. Further more many of the greatest artists, who have inspired
the multitudes to search for beauty in life and thus find mental well
being have been diagnosed by the current psychiatric community as having
mental illnesses. That the psychiatric community has resorted to
diagnosing dead artists who actually arguably as artists have done more
for mental well being then their discipline is certainly strange if not an
outright attempt to create prejudism against artists. This then is the
genetic material they are looking for. To my view point, it points to a
whole different thing. I would rather have that gene than not have it, if
it exists. In fact, if it exists, I might have it! With me it is an honor
to have such a gene!....... and no you're not going to make me terrified
of it.
Also to say that there is definitive proof that schizophrenia is
genetic but they don't know which gene to begin with is not an honest
statement.
The studies which have been sited to prove the statement are full of
untenable theoretical assumptions (e.g., that identical and fraternal
twins grow up in identical environments) and have very serious
methodological problems (e.g., expanding the diagnosis of schizophrenia to
include conditions no one thinks are schizophrenia). Any results that
would remain after accounting for these manipulations can be fully
explained on non-genetic grounds.
To advertise a false statement in order to look for a supposed flaw
which might just as well point out an exceptional person as a diseased one
is.........
it is insane
Competing interests:
I am a human being not an object for paranoia
Competing interests: No competing interests
Dr John Howard says I have misunderstood his theory that
DHEAndrostenedione deficiency in early foetal development is involved in
causing schizophrenia. In my previous response I referred to Hamadi et
al’s finding that even mild zinc deficiency caused significant decrease in
testicular androgens including androstenedione. Severe zinc deficiency
caused the greatest decrease.1,2
Zinc is the commonest deficiency before conception, during foetal
development, in children and in adults of all ages. Zinc deficiency in
early foetal life reduces the production of foetal steroid hormones but
also, in animals and humans in my experience of dyslexic individuals,
causes a reduced ability to cope with stress and a predisposition for zinc
deficiency throughout life.
If I am not wrong, as Dr Nehrlich kindly writes, it is because I have
had the advantage of measuring mineral levels in my patients for 35 years,
including hundreds of preconception couples, who usually have histories of
unexplained infertility and recurrent miscarriages. In London, clinicians
are especially fortunate in being able to employ the tests available at
www.biolab.co.uk. Dr John McLaren Howard’s sweat mineral test measures
zinc and other essential minerals to an accuracy of parts per billion.
Functional tests for B vitamins show that vitamin B 6, pyridoxine, is most
commonly deficient. Red blood cell essential fatty acid profiles find that
delta-desaturase enzyme blocks commonly cause deficiencies in EFA
pathways. Enzyme blocks result from zinc, magnesium, vitamin C,
pyridoxine, niacin, folate and magnesium deficiencies, and excessively
high or low copper levels, and alcohol consumption. The late professor
David Horrobin wrote, “Attempts at treatment (of schizophrenia) without
attention to nutritional status are doomed to failure or, at the very best
suboptimal performance”.3
Ananda Prasad has difficulty understanding why zinc repletion has not
become a key therapeutic tool in establishment medicine and has been
ignored for 40 years. A major stumbling block has been the diagnosis of
copper stores deficiency. Women taking hormones usually have abnormally
high levels of copper in their sweat, hair and serum but copper stores
become depleted. A red functional blood cell superoxide dismutase test is
the best indicator of depleted copper stores, but may also be due to
manganese deficiency. Zinc needs to be repleted with enough copper to
maintain copper stores but not enough to block EFA pathways by excess
copper intake. Ideally such tests should be part of routine medical
assessments and not relegated, as supplementation with minerals and
vitamins was described on the BBC news this morning, to alternative or
complimentary medicine.
1 Grant ECG Schizophrenics need zinc and not DHEA or testosterone
supplements. bmj.com, 1 Feb 2005
2 Hamdi SA, Nassif OI, Ardawi MS. Effect of marginal or severe
dietary zinc deficiency on testicular development and functions of the
rat. Arch Androl. 1997; 38(3):243-53.
3 Horrobin DF. A possible biochemical basis for alcoholism and for
schizoid reactions during alcohol withdrawal. In Biological Aspects of
Schizophrenia and Addiction. Ed G Hemmings. 1982 John Wiley & Sons
Ltd. Chichester
4 Grant ECCG. Preventing schizophrenia
http://bmj.com/cgi/eletters/329/7474/1058#84958, 11 Nov 2004
“Preventing schizophrenia” seems to need repeating.
Editor – I remain puzzled why it is so easy to find published
evidence of the importance of the effects of essential nutrient
deficiencies or excesses in toxic metals in nearly all mental and systemic
illnesses and why such evidence is being still being ignored by
clinicians.1
Are zinc (Zn) supplements too cheap compared with drugs? Is the problem
lack of generally available laboratories carrying out the most relevant
tests?
Nechifor et al consider plasma Cu(2+)/erythrocyte Mg(2+) and plasma
Cu(2+)/Zn(2+) ratio two important biological markers of the acute paranoid
schizophrenia. 2 There is no good reason for these tests not being
available.
In the 1970s we found that Charing Cross Hospital migraine patients,
many of whom also had mood disturbances, with the highest serum
copper/zinc (Cu/Zn) ratios also had the most reactions to foods and
chemicals.3 When I visited patients in the hospitals psychiatric wards,
who also had migraine, I could hardly see for cigarette smoke. The recent
legislation in Scotland to ban indoor smoking seems to acknowledge the
desperate need of some of the mentally ill to smoke by excluding mental
hospital wards from the ban.
Do psychiatrists still not see smoking as a cause of mental illness?
Increased cadmium (Cd) and lead and reduced Zn levels have been reported
in patients with mental illnesses, and criminals had lower mean plasma Zn
values but higher serum Cu values than non-criminal subjects. 4,5
Johnson’s excellent 2001 Hypothesis explains the importance of Zn for
brain development and maintenance.6 Zn binds to p53, preventing it from
binding to supercoiled DNA and ensuring that p53 cause the expression of
several paramount genes, such as the one that encodes for the type I
receptors to pituitary adenine cylase-activator peptide (PACAP), which
directs embryonic development of the brain cortex, adrenal glands, etc.;
it is required for the production of CuZnSOD and Zn-thionein, which are
essential to prevent oxidative damage; it is required for many proteins,
some of them with Zn fingers, many of them essential enzymes for growth
and homeostasis. As the synthesis of serotonin involves Zn enzymes and
since serotonin is necessary for melatonin synthesis, a Zn deficiency may
result in low levels of both hormones. Zn levels tend to be low when there
is excess Cu and Cd. Moreover, high estrogen levels tend to cause
increased absorption of Cu and Cd, and smoking and eating food
contaminated with Cd result in high levels of the latter. Also , ethanol
ingestion increases the elimination of Zn and Mg (which acts as a cofactor
for CuZnSOD).Therefore, the developing fetus of a pregnant women who is
low in Zn and high in Cu may experience major difficulties in the early
development of the brain, which may later manifest themselves as
schizophrenia, autism or epilepsy. Similarly, a person who gradually
accumulates Cu, (this can be detected by testing genetic SOD variants)
will tend to experience a gradual depletion of Zn, with a corresponding
increase in oxidative damage, eventually leading to Parkinson's disease.
Herron et al found serum copper levels were significantly higher in
schizophrenic patients (mean 117.4 microg/dl; S.D. 23.4) than in healthy
controls (105.6+/-27.9). Those patients on treatment with depot
neuroleptics had higher copper levels. 7
Chronic haloperidol treatment for both 45 and 90 days significantly
decreased manganese-superoxide dismutase (MnSOD), copper-zinc superoxide
dismutase (CuZnSOD) and catalase activity with parallel marked increase in
hydroxyalkenals, a marker of lipid peroxidation in rat brain.8
Brown reviewed the emerging evidence that schizophrenia may in some
cases be a neurodevelopmental disorder, resulting in part from the effects
of prenatal exposures and concluded that there is sufficient evidence to
warrant further studies of prenatal nutritional deficits as risk factors
for schizophrenia.9 Foresight, The Association for the Promotion for
Preconceptual Care, has been attempting to replete nutritional
deficiencies and lowering toxic metal levels in preconception couples
since the 1970s but no large scale financial back up has been forthcoming
for this fundamentally important work.10
The Schizophrenia Association of Great Britain is concerned that
practitioners often do not understand the illnesses they treat and
ridicule nutritional treatment for mental illnesses.11
1 Turner TH. Long term outcome of treating schizophrenia
Antipsychotics probably help—but we badly need more long term studies.BMJ
2004;329:1058-1059 (6 November), doi:10.1136/bmj.329.7474.1058
2 Nechifor M, Vaideanu C, Palamaru I, Borza C, Mindreci I. The
influence of some antipsychotics on erythrocyte magnesium and plasma
magnesium, calcium, copper and zinc in patients with paranoid
schizophrenia. J Am Coll Nutr. 2004 ;23:549S-551S.
3 Grant ECG. Allergies, smoking and the contraceptive pill. In
Biological Aspects of Schizophrenia and Addiction.1982.Ed Hemmings G, John
Wiley & Sons, Chichester pp 263-72
4 Stanley PC, Wakwe VC Toxic trace metals in the mentally ill
patients. Niger Postgrad Med J. 2002; 9:199-204.
5 Tokdemir M, Polat SA, Acik Y, et al. Blood zinc and copper
concentrations in criminal and noncriminal schizophrenic men. Arch Androl.
2003;49:365-8.
6 Johnson S Micronutrient accumulation and depletion in
schizophrenia, epilepsy, autism and Parkinson's disease? Med Hypotheses.
2001; 56: 641-5.
7 Herran A, Garcia-Unzueta MT, Fernandez-Gonzalez MD, et al. Higher
levels of serum copper in schizophrenic patients treated with depot
neuroleptics. Psychiatry Res. 2000 Apr 24; 94: 51-8.
8 Parikh V, Khan MM, Mahadik SP. Differential effects of
antipsychotics on expression of antioxidant enzymes and membrane lipid
peroxidation in rat brain. J Psychiatr Res. 2003; 37: 43-51.
9 Brown AS, Susser ES, Butler PD, et al. Neurobiological plausibility
of prenatal nutritional deprivation as a risk factor for schizophrenia.
10 Grant ECG. Nutritional supplements to prevent pregnancy
complications.
http://bmj.com/cgi/eletters/329/7458/152#67502, 16 Jul 2004
11 Hemmings G. Summer 2004 Newsletter, The Schizophrenia Association
of Great Britain. 2004: 38; 2-12.
Competing interests:
None declared
Competing interests: No competing interests
Almost as many theories about the cause of Schizophrenia exist as
remedies for pimples.
I am not impressed with the DHEA hypothesis as it seems very far fetched
and akin to the old saying that Jews have high levels of hear disease
because they eat a lot of onions.
It was in the 1950's when Abram Hoffer MD, PhD, introduced the
Adrenochrome theory, and to this day, nothing has been able to refute it.
Adrenochrome is a hallucinogenic that originates in the person's
adrenalin and Hoffer's treatment of Schizophrenia aims to disrupt this
"error in metabolism" through the application of the principles of
Orthomolecular Medicine.
O.M. attempts to restore a balance in the body of nutrients, as opposed
to the use of substances foreign to the body.
Almost 50 years of nutritional therapy with nutrients such as Niacin
(or Niacinamide)have shown that successful management of the illness can
be accomplished by this route and there are many examples of recovered
schizophrenics in responsible positions throughout the world that would be
zombies on the conventional treatment.
Dr. Grant is correct (I haven't seen her being wrong as yet) in
pointing to zinc as was originally brought to everyone's attention by the
late Dr. Carl Pfeiffer. Unfortunately, only few listened.
Horrobin added another missing link to the understanding and
treatment of S. through his expertise in essential fatty acids.
Orthomolecular treatment of schizophrenia is not as simple as
applying a handful of supplements to the problem, in a "one-size-fits-all"
manner, as individual differences need to be considered.
Personally I have found that the need for extra zinc can often be
determined by observation: Look for stretchmarks on the skin. And if zinc
is found to be indicated, the question to ask is the one about dream
recall, which of course, leads one to B 6.
It hasn't been very long that the establishment put the blame for the
very existence of the illness squarely on the shoulders of the mothers
(perhaps that's where shoulder pads for women originated). The history of
psychiatry has been rather dull, if not to say shameful and, to this day,
conventional treatment of mental illness is a disgrace.
The jury may still be out on all the causes of why the body expresses
its genetic peculiarities in this way but looking for hormonal treatment
or other far-fetched cures will be no more effective than current
conventional treatment.
About 15 % of diagnosed schizophrenics recover, return to work, pay
taxes, (one of Hoffer's criterions of having recovered) under conventional
treatment.
This treatment also causes some significant side effects such as tardive
dyskinesia and weight gain, it almost always results in the temporary
replacement of the psychosis of schizophrenia by a (n iatrogenic) new
condition, a tranquillizer psychosis.
Untreated, about 15 % (in Western society, more in primitive regions)
of schizophrenics recover. They will not have a tranquillizer psychosis.
The recovery rate under Orthomolecular Medicine is considerably
higher, although for more details those interested in obtaining the very
best, most promising remedies for their patients are encouraged to contact
Dr. Hoffer.
Competing interests:
None declared
Competing interests: No competing interests
My hypothesis is that low DHEA in utero, later in life reduced by the
actions of cortisol and testosterone, is involved in causing
schizophrenia. I think you missed my point.
You need to demonstrate that zinc deficiency is common in
schizophrenia and reduces DHEA production.
Competing interests:
None declared
Competing interests: No competing interests
Schizophrenics need zinc and not dehydroandrostenedione (DHEA) or
testosterone supplements. John Howard might stop advocating DHEA
supplementation as a universal panacea if he took the trouble to confirm
that zinc deficiency is the commonest cause of low levels of steroid
hormones in schizophrenia and other diseases. 1-4
It has been known although zinc deficiency that zinc deficiency
inhibits spermatogenesis since Ananda Prasad’s seminal paper on the
findings in Iranian dwarfs.5 Professor Prasad writes that global health
organisations have ignored the importance and implications of zinc
deficiency for 40 years.6 More than 300 catalytically active zinc
metalloproteins and more than 2000 zinc dependent transcription factors
involved in gene expression of various proteins have been recognised.
Hamdi and colleagues found that marginal zinc-deficient diet (MZD)
rats exhibited significant decreases in serum levels of testosterone
(62.6%, p < .001) and progesterone (18.2%, p < .05) with no changes
in that of FSH or LH. 7
Severe zinc-deficient diet(SZD rats showed marked decreases in serum
levels of testosterone (17.8-fold, p < .001) and progesterone (28.8%, p
< .001), whereas FSH showed an increase (34.4%, p < .05) as compared
with respective controls.
In vitro acute stimulation by hCG on testicular tissue preparation
obtained from MZD rats resulted in much less androgen production (sum of
androstenedione, testosterone, and androstanediol) (72.4%, p < .001) as
compared with controls. Testicular androgen contents (sum of
androstenedione, testosterone, and androstanediol) decreased significantly
in MZD and SZD) rats, with the latter showing the greatest decrease.
SZD rats were asospermic, whereas MZD rats exhibited marked decrease in
sperm counts (by 22.9%, p < .05) as compared with respective controls.
These results reflected a direct action of zinc deficiency on
testicular steroidogenesis and strongly supported the idea that
hypogonadism of zinc deficiency results mainly from changes in testicular
steroidogenesis or indirectly from Leydig cell failure.
Ai and colleagues found that in zinc-deficient rats, testosterone
supplements inhibit endogenous synthesis of testosterone and cause further
atrophy of testes.8
Gunnarsson and colleagues write that the well-known antisteroidogenic
effect of cadmium contamination from tobacco smoking may be due to a
strong induction of testicular prostaglandin F(2 alpha) production . Zinc
pre-treatment abolished not only the cadmium-induced rise in this
prostaglandin but also prevented also the accompanying testosterone
reduction. 9
I have been advising stopping smoking and repleting zinc and other
essential nutrients deficiencies in men with low counts of poor quality
sperm for decades as part of highly effective preconception care
programmes.
1 Goyal RO, Sagar R, Ammini AC, Khurana ML, Alias AG. Negative
Correlation between Negative Symptoms of Schizophrenia and Testosterone
Levels. Ann N Y Acad Sci. 2004; 1032: 291-4.
2 Grant ECG. Mineral deficiencies lower testosterone levels in
diseases and contribute to sexual dysfunction.
http://bmj.com/cgi/eletters/330/7484/192#93873, 23 Jan 2005
3 Pfeiffer CC. A study of zinc deficiency and copper excess in the
schizophrenis. 1972 Int Rev Neurobiol Suppl.1.
4 Prasad AS. Clinical spectrum of human zinc deficiency. In: Prasad
AS, ed. Biochemistry of zinc. New York: Plenum Press, 1993:219-258.
5 Prasad AS, Halsted JA, Nadimi M. Syndrome of iron deficiency
anemia, hepatosplenomegaly, hypogonadism, dwarfism and geophagia. Am J Med
1961; 31: 532-546.
6 Prasad AS. Zinc deficiency. Has been known of for 40 years but
ignored by global health organisations BMJ 2003;326:409-410 ( 22 February
)
7 Hamdi SA, Nassif OI, Ardawi MS. Effect of marginal or severe
dietary zinc deficiency on testicular development and functions of the
rat. Arch Androl. 1997; 38(3):243-53.
8 Ai H, Chen J, He S. The effects of zinc deficiency and
testosterone supplement on testosterone synthesis and skeletal muscle of
rats. Wei Sheng Yan Jiu. 1997;26 (3):211-5.
9 Gunnarsson D, Svensson M, Selstam G, Nordberg G.
Pronounced induction of testicular PGF(2 alpha) and suppression of
testosterone by cadmium-prevention by zinc. Toxicology. 2004 Jul
15;200(1):49-58.
Competing interests:
None declared
Competing interests: No competing interests
I just found this on "PubMed;" it provides support of my hypotheses.
Ann N Y Acad Sci. 2004 Dec;1032:291-4.
Negative Correlation between Negative Symptoms of Schizophrenia and
Testosterone Levels.
Goyal RO, Sagar R, Ammini AC, Khurana ML, Alias AG.
Chester Mental Health Center, Chester Rd., Chester, IL 62233-003.
aliasag@yahoo.com.
We conducted a pilot study in 10 adult male schizophrenics, 5 with
predominantly positive symptoms (group I) and 5 with predominantly
negative symptoms (group II), and 10 healthy matched controls. No
significant differences in serum levels of testosterone (T),
dehydroepiandrosterone sulfate (DHEAS), estradiol, and cortisol were found
between patients as a whole and controls, using radioimmunoassay. However,
serum T and DHEAS levels were lower (P <0.05) in group II patients than
in group I. Body hair and aggression scores also were lower (P <0.05)
in group II. In a much larger sample, Shirayama and colleagues also showed
that "moderate negative symptoms, but not low negative symptoms"
correlated negatively with T (P <0.05), but positively with ACTH (P
<0.05) and cortisol (P <0.01) levels in plasma. Neuroactive
steroids, such as DHEAS, and other sex hormones, including their synthetic
derivatives, may have an adjunctive role in reversing or slowing the
progression of negative symptoms. Indeed, "DHEA augmentation" improved
"negative (P <0.01), depressive (P <0.05), and anxiety (P <0.01)
symptoms."
Competing interests:
None declared
Competing interests: No competing interests
Re: Schizophrenia:A genetic disorder of the synapse?
Frank N. Garratt states that, “(w)hile accepting that there are both
genetic and environmental elements in all human disorders...”
This statement encompasses two falsehoods.
1) It turns an objective science on its ear by alluding to it as though
its' empirical science was no different than tarot card readings.
2) It suggests (in context) that human behaviour is a medical disorder
when it is different from the accepted cultural norms.
3) In combination (a) tarot card readings and (b) behavioural differences
as medical disease, we have the basis for the corruptive influence of
psychiatric thought-processing impacting against medical science while
promoting oppressive social policies, which invariably leads to great
profits for a few and perpetration of great harms to the many.
Some of these harms you mentioned, such as “external environmental
agents (eg. micro-organisms, toxic substances or nutritional faults)
(which) have damaged the neuron unit.” To this I would add diverse
oppressive public policies and community (re)traumatizations. Your final
statement, that “the first task should be to identify the main
biochemical factors underlying the failure of the neurons to service the
synapses ... Then it may be possible to help more normal function ...” is
to deny your own statement.
Sir: You grasped the truth of it. Now you need to accept the truth of
it!
Competing interests:
Psychiatric Consumer-Survivor X-Patient Self-Advocate
Competing interests: No competing interests