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Causes of schizophrenia
From Wikipedia, the free encyclopedia
The causes of schizophrenia have been the subject of much debate, with various f
actors proposed and discounted or modified. The language of schizophrenia resear
ch under the medical model is scientific. Such studies suggest that genetics, pr
enatal development, early environment, neurobiology and psychological and social
processes are important contributory factors. Current psychiatric research into
the development of the disorder is often based on a neurodevelopmental model (p
roponents of which see schizophrenia as a syndrome.)[1][2] However, schizophreni
a is diagnosed on the basis of symptom profiles. Neural correlates do not provid
e sufficiently useful criteria.[3] "Current research into schizophrenia has rema
ined highly fragmented, much like the clinical presentation of the disease itsel
f".[4] The one thing that researchers can agree on is that schizophrenia is a co
mplicated and variable condition. It is best thought of as a syndrome, a cluster
of symptoms that may or may not have related causes, rather than a single disea
se.
It is possible for schizophrenia to develop at any age, but it mostly happens to
people within the ages of 16 30 (generally males 16 25 and females 25 30) - about 75
percent of people living with the illness develop it at this age. There is a lik
elihood of children developing schizophrenia, though it is quite rare before the
age of 12. Also, new cases are uncommon after age 40. In addition, about 1 perc
ent of the world's population will develop schizophrenia over their lifetime, th
erefore out of all the people born, one in 100 will develop schizophrenia by age
55.[5] There is on average a somewhat earlier onset for men than women, with th
e possible influence of the female hormone estrogen being one hypothesis and soc
iocultural influences another.[6]
Contents [hide]
1
Genetics
1.1
Heritability
1.2
Genetic candidates
1.3
Overlap with other disorders
2
Evolutionary psychology
3
Before birth
3.1
Fetal growth
3.2
Hypoxia
3.3
Other factors
4
Infections and immune system
5
Childhood antecedents
6
Substance use
6.1
Cannabis
6.2
Amphetamines and other stimulants
6.3
Hallucinogens
6.4
Alcohol
6.5
Tobacco use
7
Life experiences
7.1
Social adversity
7.2
Urbanicity
7.3
Close relationships
8
Synergistic effects
9
Other views
10
References
11
External links
Genetics[edit]
Heritability[edit]
Evidence suggests that genetic vulnerability with environmental factors can act

in combination to result in the development of schizophrenia.[7] Although schizo

phrenia is very strongly heritable, there is also some evidence that all cases a
re not caused by heredity. Many people who appear to carry "schizophrenia genes"
may not become schizophrenic.[8] Recent research suggests that genetic vulnerab
ility to schizophrenia is multifactorial, caused by interactions of several gene
s.[9]
Individual twin studies and meta-analyses of twin studies have estimated the her
itability of risk for schizophrenia to be approximately 80% (this refers to the
proportion of variation between individuals in a population that is influenced b
y genetic factors, not the degree of genetic determination of individual risk),
but the heritability estimate varies from 41 to 87%.[10] Concordance rates betwe
en monozygotic twins vary in different studies, approximately 50%; whereas dizyg
otic twins was 17%. Some twin studies[11][12] have found rates as low as 11.0% 13.
8% among monozygotic twins, and 1.8% 4.1% among dizygotic twins, however.
Family studies indicate that the closer a person s genetic relatedness to a person
with schizophrenia, the greater the likelihood of developing the disorder. The
paternal age is a factor in schizophrenia because of the increased likelihood of
mutations in the chromosomes of cells that produce sperms. In contrast, women's
oocytes divide twenty-three times before the time of birth and only once after
that. The chance of a copying error in DNA replication during cell division incr
eases with the number of cell divisions, and an increase in copying errors may c
ause an accumulation of mutations that are responsible for an increased incidenc
e of schizophrenia.[8] The average concordance rates are higher for identical tw
ins than for fraternal twins and evidence also suggests that the prenatal and pe
rinatal environments may also affect concordance rates in identical twins.[13]
Genetic candidates[edit]
Although twin studies and family studies have indicated a large degree of herita
bility for schizophrenia, the exact genetic causes remain unclear. Recently howe
ver, quite some large-scale studies have now begun to unravel the genetic underp
innings for the disease. Important segregation should be made between lower risk
, common variants (identified by candidate studies or genome-wide association st
udies(GWAS)) and high risk, rare variants (which could be caused by de novo muta
tions) and copy-number variations (CNVs).
Candidate gene studies[edit]
An older 2003 review of linkage studies also listed seven genes as likely to inc
rease risk for a later diagnosis of the disorder.[7] Two recent reviews[9][14] s
uggested that the evidence was strongest for two genes known as dysbindin (DTNBP
1) and neuregulin (NRG1), and that a number of other genes (such as COMT, RGS4,
PPP3CC, ZDHHC8, DISC1, and AKT1) showed some early promising results. Knockout s
tudies in Drosophila show that reduced expression of dysbindin reduced glutamate
rgic synaptic transmission, resulting in impaired memory.[15] Variations near th
e gene FXYD6 have also been associated with schizophrenia in the UK[16][17] but
not in Japan.[18] In 2008, rs7341475 SNP of the reelin gene was associated with
an increased risk of schizophrenia in women, but not in men. This female-specifi
c association was replicated in several populations.[19] Still another review fo
und evidence that the protein phosphatase 2B (calcineurin) might be involved in
susceptibility to schizophrenia.[3]
The largest most comprehensive genetic study of its kind, involving tests of sev
eral hundred single nucleotide polymorphisms (SNPs) in nearly 1,900 individuals
with schizophrenia or schizoaffective disorder and 2,000 comparison subjects, re
ported in 2008 that there was no evidence of any significant association between
the disorders and any of 14 previously identified candidate genes (RGS4, DISC1,
DTNBP1, STX7, TAAR6, PPP3CC, NRG1, DRD2, HTR2A, DAOA, AKT1, CHRNA7, COMT, and A
RVCF). The statistical distributions suggested nothing more than chance variatio
n. The authors concluded that the findings make it unlikely that common SNPs in

these genes account for a substantial proportion of the genetic risk for schizop
hrenia, although small effects could not be ruled out.[20][21]
The perhaps largest analysis of genetic associations in schizophrenia is with th
e SzGene database at the Schizophrenia Research Forum. One 2008 meta-analysis ex
amined genetic variants in 16 genes and found nominally significant effects.[22]
A 2009 study was able to create mice matching schizophrenic symptoms by the dele
tion of only one gene set, those of the neuregulin post-synaptic receptor. The r
esult showed that although the mice mostly developed normally, on further brain
development, glutamate receptors broke down. This theory supports the glutamate
hypothesis of schizophrenia.[23] Another study in 2009 by Simon Fraser Universit
y researchers identifies a link between autism and schizophrenia: "The SFU group
found that variations in four sets of genes are related to both autism and schi
zophrenia. People normally have two copies of each gene, but in autistics some g
enome locations have only single copies and in schizophrenics extra copies are p
resent at the same locations."[24]
Genome-wide association studies[edit]
To increase sample size for a better powered detection of common variants with s
mall effects, GWAS data is continuing to be clustered in large international con
sortia. The Psychiatric Genetics Consortium (PGC) attempts to aggregate GWAS dat
a on schizophrenia to detect associations of common variants with small effect o
n disease risk.[25]
In 2011, this collaboration identified by meta-analyse of genome-wide associatio
n studies that 129 over 136 single-nucleotide polymorphism (SNP) significantly a
ssociated with schizophrenia were located in major histocompatibility complex re
gion of the genome.[26]
In 2013 this dataset was expanded to identify in total 13 candidate loci for the
disease, now also implicating calcium signalling as an important factor in the
disease.[27]
In 2014 this collaboration expanded to an even larger meta-analysis, the largest
to date, on GWAS data (36,989 cases and 113,075 controls) in Nature, indicating
108 schizophrenia-associated genetic loci, of which 83 have not been previously
described.[28] Together, these candidate genes pointed to an importance of neur
otransmission and immunology as important factors in the disease.
Distinct symptomatic subtypes of schizophrenia groups showed to have a different
pattern of SNP variations, reflecting the heterogeneous nature of the disease.[
29]
A 2016 study implicated the C4 gene in schizophrenia risk. C4 was found to play
a role in synapse pruning, and increased C4 expression leads to reduced dendriti
c spines and a higher schizophrenia risk.[30]
Copy-number variations[edit]
Other research has suggested that a greater than average number of structural va
riations such as rare deletions or duplications of tiny DNA sequences within gen
es (known as copy number variants) are linked to increased risk for schizophreni
a, especially in "sporadic" cases not linked to family history of schizophrenia,
and that the genetic factors and developmental pathways can thus be different i
n different individuals.[31][32] A genome wide survey of 3,391 individuals with
schizophrenia found CNVs in less than 1% of cases. Within them, deletions in reg
ions related to psychosis were observed, as well as deletions on chromosome 15q1
3.3 and 1q21.1.[33]
CNVs occur due to non-allelic homologous recombination mediated by low copy repe

ats (sequentially similar regions). This results in deletions and duplications o

f dosage sensitive genes. It has been speculated that CNVs underlie a significan
t proportion of normal human variation, including differences in cognitive, beha
vioral, and psychological features, and that CNVs in at least three loci can res
ult in increased risk for schizophrenia in a few individuals.[34] Epigenetics ma
y also play a role in schizophrenia, with the expression of Protocadherin 11 X/P
rotocadherin Y playing a possible role in schizophrenia.[35]
A 2008 investigation of 2,977 schizophrenia patients and 33,746 controls from se
ven European populations examined CNVs in neurexins, and found that exon-affecti
ng deletions in the NRXN1 gene conferred risk of schizophrenia.[36]
An updated meta-analysis on CNVs for schizophenia published in 2015 expanded the
number of CNVs indicated in the disease, which was also the first genetic evide
nce for the involvement of GABAergic neurotransmission.[37] This study further s
upported genetic involvement for excitatory neurotransmission.
Overlap with other disorders[edit]
Several studies have suggested that genetic overlap exists between schizophrenia
and other psychiatric disorders. In February 28, 2013 The Lancet published an a
rticle about the possible genetic correlation between autism spectrum disorder,
attention deficit-hyperactivity disorder, bipolar disorder, major depressive dis
order, and schizophrenia. They analyzed genome-wide single-nucleotide polymorphi
sm (SNP) data for the five disorders in 33 332 cases and 27 888 controls of Euro
pean ancestry. This group found four gene areas that all overlapped with the fiv
e disorders, two of which regulate calcium balance in the brain.[38]
Evolutionary psychology[edit]
Main article: Evolution of schizophrenia
Schizophrenia has been considered an evolutionary puzzle due to the combination
of high heritability, relatively high prevalence, and reduced reproductive succe
ss. One explanation could be increased reproductive success by close relatives w
ithout symptoms but this does not seem to be the case. Still, it has been argued
that it is possible that a low amount of schizotypy increasing genes may increa
se reproductive success by increasing such traits such as creativity, verbal abi
lity, and emotional sensitivity.[39]
Another evolutionary explanation is the
at psychosis and autism are contrasting
bles. This is argued to be caused by an
aternal genes in the case of autism and
[40]

"imprinted brain theory" which argues th

disorders on a number of different varia
unbalanced genomic imprinting favoring p
maternal genes in the case of psychosis.

Before birth[edit]
It is well established that obstetric complications or events are associated wit
h an increased chance of the child later developing schizophrenia, although over
all they constitute a non-specific risk factor with a relatively small effect. O
bstetric complications occur in approximately 25 to 30% of the general populatio
n and the vast majority do not develop schizophrenia, and likewise the majority
of individuals with schizophrenia have not had a detectable obstetric event. Nev
ertheless, the increased average risk is well-replicated, and such events may mo
derate the effects of genetic or other environmental risk factors. The specific
complications or events most linked to schizophrenia, and the mechanisms of thei
r effects, are still under examination.[41]
One epidemiological finding is that people diagnosed with schizophrenia are more
likely to have been born in winter or spring[42] (at least in the northern hemi
sphere). However, the effect is not large. Explanations have included a greater
prevalence of viral infections at that time, or a greater likelihood of vitamin
D deficiency. A similar effect (increased likelihood of being born in winter and

spring) has also been found with other, healthy populations, such as chess play
ers.[43]
Women who were pregnant during the Dutch famine of 1944, where many people were
close to starvation (experiencing malnutrition) had a higher chance of having a
child who would later develop schizophrenia.[44] Studies of Finnish mothers who
were pregnant when they found out that their husbands had been killed during the
Winter War of 1939 1940 have shown that their children were significantly more li
kely to develop schizophrenia when compared with mothers who found out about the
ir husbands' death after pregnancy, suggesting that maternal stress may have an
effect.[45]
Fetal growth[edit]
Lower than average birth weight has been one of the most consistent findings, in
dicating slowed fetal growth possibly mediated by genetic effects. In the first
and only prospective study of the low birthweight, schizophrenia, and enlargemen
t of brain ventricles suggestive of cerebral atrophy, Leigh Silverton and collea
gues found that low birthweight (measured prospectively with regard to psychopat
hology) was associated with enlarged ventricles on CT-Scans in a sample at risk
for schizophrenia over 30 years later. These signs suggestive of cerebral atroph
y were associated with schizophrenia symptoms.[46] In a follow up study, Silvert
on et al. noted an interaction between genetic risk for schizophrenia and low bi
rthweight. The risk of enlarged ventricles on brain scan (associated with schizo
phrenia symptoms and biologically suggestive of Emil Kraepelin's dementia praeco
x type of schizophrenia ) was greatly increased if the subjects had both a highe
r genetic load for schizophrenia and lower birthweight. The investigators sugges
ted that in utero insults may specifically stress those with a schizophrenia dia
thesis suggesting to the authors a diathesis stress etiological model for a cert
ain type of schizophrenia (that Kraepelin identified) with early abnormalities s
uggesting brain atrophy.[47]
Some investigators have noted, however, that any factor adversely affecting the
fetus will affect growth rate, however, so believe that this association has may
not be particularly informative regarding causation.[41] In addition, the major
ity of birth cohort studies have failed to find a link between schizophrenia and
low birth weight or other signs of growth retardation.[48] It should be noted,
however, that the majority of studies do not measure the interaction of genetic
risk and birthweight as was done in the Silverton et al. studies.
Hypoxia[edit]
It has been hypothesized since the 1970s that brain hypoxia (low oxygen levels)
before, at or immediately after birth may be a risk factor for the development o
f schizophrenia.[49][50]
Hypoxia is now being demonstrated as relevant to schizophrenia in animal models,
molecular biology and epidemiology studies. One study in Molecular Psychiatry w
as able to differentiate 90% of schizophrenics from controls based on hypoxia an
d metabolism.[51] Hypoxia has been recently described as one of the most importa
nt of the external factors that influence susceptibility, although studies have
been mainly epidemiological. Such studies place a high degree of importance on h
ypoxic influence, but because of familial pattern of the illness in some familie
s, propose a genetic factor also; stopping short of concluding hypoxia to be the
sole cause.[52] Fetal hypoxia, in the presence of certain unidentified genes, h
as been correlated with reduced volume of the hippocampus, which is in turn corr
elated with schizophrenia.[53]
Although most studies have interpreted hypoxia as causing some form of neuronal
dysfunction or even subtle damage, it has been suggested that the physiological
hypoxia that prevails in normal embryonic and fetal development, or pathological
hypoxia or ischemia, may exert an effect by regulating or dysregulating genes i

nvolved in neurodevelopment. A literature review

didate genes for susceptibility to schizophrenia
a regulation or vascular expression" even though
imated to be involved in hypoxia/ischemia or the

judged that over 50% of the can

met criteria for "ischemia hypoxi
only 3.5% of all genes were est
vasculature.[54]

A longitudinal study found that obstetric complications involving hypoxia were o

ne factor associated with neurodevelopmental impairments in childhood and with t
he later development of schizophreniform disorders.[55] Fetal hypoxia has been f
ound to predict unusual movements at age 4 (but not age 7) among children who go
on to develop schizophrenia, suggesting that its effects are specific to the st
age of neurodevelopment.[56] A Japanese case study of monozygotic twins discorda
nt for schizophrenia (one has the diagnosis while the other does not) draws atte
ntion to their different weights at birth and concludes hypoxia may be the diffe
rentiating factor.[57]
The unusual functional laterality in speech production (e.g. right hemisphere au
ditory processing) found in some individuals with schizophrenia could be due to
aberrant neural networks established as a compensation for left temporal lobe da
mage induced by pre- or perinatal hypoxia.[58] Prenatal and perinatal hypoxia ap
pears to be important as one factor in the neurodevelopmental model, with the im
portant implication that some forms of schizophrenia may thus be preventable.[59
]
Research on rodents seeking to understand the possible role of prenatal hypoxia
in disorders such as schizophrenia has indicated that it can lead to a range of
sensorimotor and learning/memory abnormalities. Impairments in motor function an
d coordination, evident on challenging tasks when the hypoxia was severe enough
to cause brain damage, were long-lasting and described as a "hallmark of prenata
l hypoxia".[60][61]
Several animal studies have indicated that fetal hypoxia can affect many of the
same neural substrates implicated in schizophrenia, depending on the severity an
d duration of the hypoxic event as well as the period of gestation, and in human
s moderate or severe (but not mild) fetal hypoxia has been linked to a series of
motor, language and cognitive deficits in children, regardless of genetic liabi
lity to schizophrenia.[62] One paper restated that cerebellum neurological disor
ders were frequently found in schizophrenics and speculated hypoxia may cause th
e subsequent cognitive dysmetria[63]
Whereas most studies find only a modest effect of hypoxia in schizophrenia, a lo
ngitudinal study using a combination of indicators to detect possible fetal hypo
xia, such as early equivalents of Neurological Soft Signs or obstetric complicat
ions, reported that the risk of schizophrenia and other nonaffective psychoses w
as "strikingly elevated" (5.75% versus 0.39%). Although objective estimates of h
ypoxia did not account for all schizophrenic cases; the study revealed increasin
g odds of schizophrenia according to graded increase in severity of hypoxia.[64]
Other factors[edit]
There is an emerging literature on a wide range of prenatal risk factors, such a
s prenatal stress, intrauterine (in the womb) malnutrition, and prenatal infecti
on. Increased paternal age has been linked to schizophrenia, possibly due to "ch
romosomal aberrations and mutations of the aging germline."[65] Maternal-fetal r
hesus or genotype incompatibility has also been linked, via increasing the risk
of an adverse prenatal environment. Also, in mothers with schizophrenia, an incr
eased risk has been identified via a complex interaction between maternal genoty
pe, maternal behavior, prenatal environment and possibly medication and socioeco
nomic factors.[41] References for many of these environmental risk factors have
been collected in an online database.[66]
There may be an association between celiac disease (gluten intolerance) and schi

zophrenia in a small proportion of patients, though large randomized controlled

trials and epidemiological studies will be needed before such an association can
be confirmed. Withdrawal of gluten from the diet is an inexpensive measure whic
h may improve the symptoms in a small (=3%) number of schizophrenic patients.[67
]
In addition, there is some evidence that exposure to toxins such as lead can als
o increase the risk of later development of schizophrenia spectrum disorders.[68
]
A meta-analysis found that high neuroticism increases the risk of psychosis and
schizophrenia.[69]
Infections and immune system[edit]
Numerous viral infections, in utero or in childhood, have been associated with a
n increased risk of later developing schizophrenia.[70] Schizophrenia is somewha
t more common in those born in winter to early spring, when infections are more
common.[71]
Influenza has long been studied as a possible factor. A 1988 study found that in
dividuals who were exposed to the Asian flu as second trimester fetuses were at
increased risk of eventually developing schizophrenia.[72] This result was corro
borated by a later British study of the same pandemic,[73] but not by a 1994 stu
dy of the pandemic in Croatia.[74] A Japanese study also found no support for a
link between schizophrenia and birth after an influenza epidemic.[75]
Polio, measles, varicella-zoster, rubella, herpes simplex virus type 2, maternal
genital infections, Borna disease virus, and more recently Toxoplasma gondii[76
] have been correlated with the later development of schizophrenia.[77] Psychiat
rists E. Fuller Torrey and R.H. Yolken have hypothesized that the latter, a comm
on parasite in humans, contributes to some, if not many, cases of schizophrenia.
[78]
In a meta-analysis of several studies, they found moderately higher levels of To
xoplasma antibodies in those with schizophrenia[79][80] and possibly higher rate
s of prenatal or early postnatal exposure to Toxoplasma gondii, but not acute in
fection. However, in another study of postmortem brain tissue, the authors have
reported equivocal or negative results, including no evidence of herpes virus or
T. gondii involvement in schizophrenia.[81]
There is some evidence for the role of autoimmunity in the development of some c
ases of schizophrenia. A statistical correlation has been reported with various
autoimmune diseases[82] and direct studies have linked dysfunctional immune stat
us to some of the clinical features of schizophrenia.[83][84]
This is known as the pathogenic theory of schizophrenia or germ theory of schizo
phrenia. It is a pathogenic theory of disease in which it is thought that a prox
imal cause of certain cases of schizophrenia is the interaction of the developin
g fetus with pathogens such as viruses, or with antibodies from the mother creat
ed in response to these pathogens (in particular, Interleukin 8).[85] Substantia
l research suggests that exposure to certain illnesses (e.g., influenza) in the
mother of the neonate (especially at the end of the second trimester) causes def
ects in neural development which may emerge as a predisposition to schizophrenia
around the time of puberty, as the brain grows and develops.[86]
Recent findings support the hypothesis that schizophrenia is associated with alt
erations of the tryptophane-kynurenine metabolic pathway due to activation of sp
ecific sections of the immune system.[87][88]
The relevance of some auto-antibodies that act against the NMDAR and VGKC is bei

ng studied.[89][90] Current estimates suggest that between 1.5 [91] - 6.5[90]% o

f patients have these antibodies in their blood. Preliminary results have shown
that these patients can be treated with immunotherapy such as IVIG or Plasma exc
hange and steroids, on top of anti-psychotic medication, which can lead to a red
uction in symptoms.[92]
Childhood antecedents[edit]
In general, the antecedents of schizophrenia are subtle and those who will go on
to develop schizophrenia do not form a readily identifiable subgroup - which wo
uld lead to identification of a specific cause. Average group differences from t
he norm may be in the direction of superior as well as inferior performance. Ove
rall, birth cohort studies have indicated subtle nonspecific behavioral features
, some evidence for psychotic-like experiences (particularly hallucinations), an
d various cognitive antecedents. There have been some inconsistencies in the par
ticular domains of functioning identified and whether they continue through chil
dhood and whether they are specific to schizophrenia.[48]
A prospective study found average differences across a range of developmental do
mains, including reaching milestones of motor development at a later age, having
more speech problems, lower educational test results, solitary play preferences
at ages four and six, and being more socially anxious at age 13. Lower ratings
of the mother's skills and understanding of the child at age 4 were also related
.[93]
Some of the early developmental differences were identified in the first year of
life in a study in Finland, although generally related to psychotic disorders r
ather than schizophrenia in particular.[94] The early subtle motor signs persist
ed to some extent, showing a small link to later school performance in adolescen
ce.[95] An earlier Finnish study found that childhood performance of 400 individ
uals diagnosed with schizophrenia was significantly worse than controls on subje
cts involving motor co-ordination (sports and handcrafts) between ages 7 and 9,
but there were no differences on academic subjects (contrary to some other IQ fi
ndings).[96] (Patients in this age group with these symptoms were significantly
less likely to progress to high school, despite academic ability.[97])
Symptoms of schizophrenia often appear soon after puberty, when the brain is und
ergoing significant maturational changes. Some investigators believe that the di
sease process of schizophrenia begins prenatally, lies dormant until puberty, an
d then causes a period of neural degeneration that causes the symptoms to emerge
.[8] However, reanalysis of the data from the later Finnish study, on older chil
dren (14 to 16) in a changed school system, using narrower diagnostic criteria a
nd with less cases but more controls, did not support a significant difference o
n sports and handicraft performance.[98] However, another study found that unusu
al motor coordination scores at 7 years of age were associated in adulthood with
both those with schizophrenia and their unaffected siblings, while unusual move
ments at ages 4 and 7 predicted adult schizophrenia but not unaffected sibling s
tatus.[56]
A birth cohort study in New Zealand found that children who went on to develop s
chizophreniform disorder had, as well as emotional problems and interpersonal di
fficulties linked to all adult psychiatric outcomes measured, significant impair
ments in neuromotor, receptive language, and cognitive development.[55] A retros
pective study found that adults with schizophrenia had performed better than ave
rage in artistic subjects at ages 12 and 15, and in linguistic and religious sub
jects at age 12, but worse than average in gymnastics at age 15.[99]
Some small studies on offspring of individuals with schizophrenia have identifie
d various neurobehavioral deficits,[100] a poorer family environment and disrupt
ive school behaviour,[101] poor peer engagement, immaturity or unpopularity[102]
or poorer social competence and increasing schizophrenic symptomology emerging

during adolescence.[103]
A minority "deficit syndrome" subtype of schizophrenia is proposed to be more ma
rked by early poor adjustment and behavioral problems, as compared to non-defici
t subtypes.[104]
There is evidence that childhood experiences of abuse or trauma are risk factors
for a diagnosis of schizophrenia later in life.[105] Some researchers reported
that hallucinations and other symptoms considered characteristic of schizophreni
a and psychosis were at least as strongly related to neglect and childhood abuse
as many other mental health problems.[106] The researchers concluded that there
is a need for staff training in asking patients about abuse, and a need to offe
r appropriate psychosocial treatments to those who have been neglected and abuse
d as children.[106]
Substance use[edit]
The relationship between schizophrenia and drug use is complex, meaning that a c
lear causal connection between drug use and schizophrenia has been difficult to
tease apart. Some substances can induce psychosis. The use of various drugs make
s a diagnosis of schizophrenia more complicated. A person cannot be diagnosed wi
thout symptoms persisting after drug use have ended.[107] There is strong eviden
ce that using certain drugs can trigger either the onset or relapse of schizophr
enia in some people. It may also be the case, however, that people with schizoph
renia use drugs to overcome negative feelings associated with both the commonly
prescribed antipsychotic medication and the condition itself, where negative emo
tion, paranoia and anhedonia are all considered to be core features.
The rate of substance use is known to be particularly high in this group. In a r
ecent study, 60% of people with schizophrenia were found to use substances and 3
7% would be diagnosable with a substance use disorder.[108]
Cannabis[edit]
Main article: Cannabis and schizophrenia
There is some evidence that cannabis use can contribute to schizophrenia. Some s
tudies[clarification needed] suggest that cannabis is neither a sufficient nor n
ecessary factor in developing schizophrenia, but that cannabis may significantly
increase the risk of developing schizophrenia and may be, among other things,[w
hich?] a significant causal[clarification needed] factor. Nevertheless, some pre
vious research in this area has been criticised as it has often not been clear w
hether cannabis use is a cause or effect of schizophrenia. To address this issue
, a recent review of prospective cohort studies has suggested that cannabis[clar
ification needed] statistically doubles the risk of developing schizophrenia on
the individual level, and may, if a causal relationship is assumed, be responsib
le for up to 8% of cases in the population.[clarification needed][3][8][31][41][
48][55][56][65][68][77][109][110][111][112][113][114][115][116]
Cannabis misuse by young people is suspected of causing schizophrenia in later l
ife by interfering with and distorting neurodevelopment particularly of the pref
rontal cortex region of the brain.[110] An older longitudinal study, published i
n 1987, suggested a sixfold increase of schizophrenia risks for high consumers o
f cannabis (use on more than fifty occasions) in Sweden.[31][117]
Cannabis use is also suspected to contribute to the hyperdopaminergic state that
is characteristic of schizophrenia.[8][118] Compounds found in cannabis, such a
s THC, have been shown to increase the activity of dopamine pathways in the brai
n,[119] suggesting that cannabis may exacerbate symptoms of psychosis in schizop
hrenics.
Despite increases in cannabis consumption in the 1960s and 1970s in western soci
ety, rates of psychotic disorders such as schizophrenia remained relatively stab

le over time.[120][121][122]
Amphetamines and other stimulants[edit]
Main article: Stimulant psychosis
As amphetamines trigger the release of dopamine and excessive dopamine function
is believed to be responsible for many symptoms of schizophrenia (known as the d
opamine hypothesis of schizophrenia), amphetamines may worsen schizophrenia symp
toms.[123] Methamphetamine, a potent neurotoxic amphetamine derivative, induces
psychosis in a substantial minority of regular users which resembles paranoid sc
hizophrenia. For most people, this psychosis fades away within a month of abstin
ence but for a minority the psychosis can become chronic. Individuals who develo
p a long lasting psychosis, despite abstinence from methamphetamine, more common
ly have a family history of schizophrenia.[124]
Concerns have been raised that long-term therapy with stimulants for ADHD might
cause paranoia, schizophrenia and behavioral sensitization.[125] Family history
of mental illness does not predict the incidence of stimulant toxicosis in ADHD
children. High rates of childhood stimulant use have been noted in patients with
a diagnosis of schizophrenia and bipolar disorder independent of ADHD. Individu
als with a diagnosis of bipolar or schizophrenia who were prescribed stimulants
during childhood typically have a significantly earlier onset of the psychotic d
isorder and suffer a more severe clinical course of psychotic disorder. It has b
een suggested that this small subgroup of children who develop schizophrenia due
to stimulant use during childhood have a genetic vulnerability to developing ps
ychosis.[126] In addition, amphetamines are known to cause a stimulant psychosis
in otherwise healthy individuals that superficially resembles schizophrenia, an
d may be misdiagnosed as such by some healthcare professionals.
Hallucinogens[edit]
See also: LSD and schizophrenia
Drugs such as ketamine, PCP, and LSD have been used to mimic schizophrenia for r
esearch purposes. Using LSD and other psychedelics as a model has now fallen out
of favor with the scientific research community, as the differences between the
drug induced states and the typical presentation of schizophrenia have become c
lear. The dissociatives ketamine and PCP, however, are still considered to produ
ce states that are remarkably similar, and are considered to be even better mode
ls than stimulants since they produce both positive and negative symptoms.
Alcohol[edit]
Approximately three percent of people who are alcohol dependent experience psych
osis during acute intoxication or withdrawal. The mechanism of alcohol-related p
sychosis is due to distortions to neuronal membranes, gene expression, as well a
s thiamin deficiency. There is evidence that alcohol abuse via a kindling mechan
ism can occasionally cause the development of a chronic substance induced psycho
tic disorder, i.e. schizophrenia.[127]
Tobacco use[edit]
Further information: Schizophrenia and smoking
People with schizophrenia tend to smoke significantly more tobacco than the gene
ral population. The rates are exceptionally high amongst institutionalized patie
nts and homeless people. In a UK census from 1993, 74% of people with schizophre
nia living in institutions were found to be smokers.[128][129] A 1999 study that
covered all people with schizophrenia in Nithsdale, Scotland found a 58% preval
ence rate of cigarette smoking, to compare with 28% in the general population.[1
11] An older study found that as much as 88% of outpatients with schizophrenia w
ere smokers.[112]
Despite the higher prevalence of tobacco smoking, people diagnosed with schizoph
renia have a much lower than average chance of developing and dying from lung ca
ncer. While the reason for this is unknown, it may be because of a genetic resis

tance to the cancer, a side effect of drugs being taken, or a statistical effect
of increased likelihood of dying from causes other than lung cancer.[130]
A 2003 study of over 50,000 Swedish conscripts found that there was a small but
significant protective effect of smoking cigarettes on the risk of developing sc
hizophrenia later in life.[131] While the authors of the study stressed that the
risks of smoking far outweigh these minor benefits, this study provides further
evidence for the 'self-medication' theory of smoking in schizophrenia and may g
ive clues as to how schizophrenia might develop at the molecular level. Furtherm
ore, many people with schizophrenia have smoked tobacco products long before the
y are diagnosed with the illness, and a cohort study of Israeli conscripts found
that healthy adolescent smokers were more likely to develop schizophrenia in th
e future than their nonsmoking peers.[132]
It is of interest that cigarette smoking affects liver function such that the an
tipsychotic drugs used to treat schizophrenia are broken down in the blood strea
m more quickly. This means that smokers with schizophrenia need slightly higher
doses of antipsychotic drugs in order for them to be effective than do their non
-smoking counterparts.[citation needed]
The increased rate of smoking in schizophrenia may be due to a desire to self-me
dicate with nicotine. One possible reason is that smoking produces a short term
effect to improve alertness and cognitive functioning in persons who suffer this
illness.[113] It has been postulated that the mechanism of this effect is that
people with schizophrenia have a disturbance of nicotinic receptor functioning w
hich is temporarily abated by tobacco use.[113] However, some researchers have q
uestioned whether self-medication is really the best explanation for the associa
tion.[133]
A study from 1989[134] and a 2004 case study[135] show that when haloperidol is
administered, nicotine limits the extent to which the antipsychotic increases th
e sensitivity of the dopamine 2 receptor. Dependent on the dopamine system, symp
toms of Tardive Dyskinesia are not found in the nicotine administered patients d
espite a roughly 70% increase in dopamine receptor activity, but the controls ha
ve more than 90% and do develop symptoms. A 1997 study showed that akathisia was
significantly reduced upon administration of nicotine when the akathisia was in
duced by antipsychotics.[136] This gives credence to the idea tobacco could be u
sed to self-medicate by limiting effects of the illness, the medication, or both
.
Life experiences[edit]
Social adversity[edit]
The chance of developing schizophrenia has been found to increase with the numbe
r of adverse social factors (e.g. indicators of socioeconomic disadvantage or so
cial exclusion) present in childhood.[137][138] Stressful life events generally
precede the onset of schizophrenia.[139] A personal or recent family history of
migration is a considerable risk factor for schizophrenia, which has been linked
to psychosocial adversity, social defeat from being an outsider, racial discrim
ination, family dysfunction, unemployment, and poor housing conditions.[114][140
] Unemployment and early separation from parents are some important factors whic
h are responsible for the higher rates of schizophrenia among British African Ca
ribbean populations, in comparison to native African Caribbean populations. This
is an example which shows that social disadvantage plays an equally major hand
in the onset of schizophrenia as genetics.[141]
Childhood experiences of abuse or trauma are risk factors for a diagnosis of sch
izophrenia later in life.[142][143][144][145] Recent large-scale general populat
ion studies indicate the relationship is a causal one, with an increasing risk w
ith additional experiences of maltreatment,[146] although a critical review sugg
ests conceptual and methodological issues require further research.[147] There i

s some evidence that adversities may lead to cognitive biases and altered dopami
ne neurotransmission, a process that has been termed "sensitization".[148] Child
hood trauma, and bereavement or separation in families, have been found to be ri
sk factors for schizophrenia and psychosis.[149]
Specific social experiences have been linked to specific psychological mechanism
s and psychotic experiences in schizophrenia. In addition, structural neuroimagi
ng studies of victims of sexual abuse and other traumas have sometimes reported
findings similar to those sometimes found in psychotic patients, such as thinnin
g of the corpus callosum, loss of volume in the anterior cingulate cortex, and r
educed hippocampal volume.[150]
Urbanicity[edit]
A particularly stable and replicable finding has been the association between li
ving in an urban environment and the development of schizophrenia, even after fa
ctors such as drug use, ethnic group and size of social group have been controll
ed for.[151] A recent study of 4.4 million men and women in Sweden found a 68% 77%
increased risk of diagnosed psychosis for people living in the most urbanized e
nvironments, a significant proportion of which is likely to be described as schi
zophrenia.[152]
The effect does not appear to be due to a higher incidence of obstetric complica
tions in urban environments.[153] The risk increases with the number of years an
d degree of urban living in childhood and adolescence, suggesting that constant,
cumulative, or repeated exposures during upbringing occurring more frequently i
n urbanized areas are responsible for the association.[154]
Various possible explanations for the effect have been judged unlikely based on
the nature of the findings, including infectious causes or a generic stress effe
ct. It is thought to interact with genetic dispositions and, since there appears
to be nonrandom variation even across different neighborhoods, and an independe
nt association with social isolation, it has been proposed that the degree of "s
ocial capital" (e.g. degree of mutual trust, bonding and safety in neighborhoods
) can exert a developmental impact on children growing up in these environments.
[155]
Close relationships[edit]
Evidence is consistent that negative attitudes from others increase the risk of
schizophrenia relapse, in particular critical comments, hostility, authoritarian
, and intrusive or controlling attitudes (termed 'high expressed emotion' by res
earchers).[156] Although family members and significant others are not held resp
onsible for schizophrenia - the attitudes, behaviors and interactions of all par
ties are addressed - unsupportive dysfunctional relationships may also contribut
e to an increased risk of developing schizophrenia.[115][157] The risk of develo
ping schizophrenia can also be increased by an individual developing a very low
sense of self, in which one's boundaries become confused with that of the mother
and/ or father. Firm psychological boundaries should be established between one
's self and one's identity and one's parents. Pushing the role of parents into t
he background and developing a healthy sense of self can be a method for recover
y.[158] Social support systems are very important for schizophrenics and the peo
ple with whom they are in relationships.[159] Recovery from schizophrenia is pos
sible when one develops a healthy self and establishes firm psychological bounda
ries with each of their parents.[158]
Synergistic effects[edit]
Experiments on mice have provided evidence that several stressors can act togeth
er to increase the risk of schizophrenia. In particular, the combination of a ma
ternal infection during pregnancy followed by heightened stress at the onset of
sexual maturity markedly increases the probability that a mouse develops symptom
s of schizophrenia, whereas the occurrence of one of these factors without the o

ther does not.[160]

Other views[edit]
Schizophrenia is suggested to be a brain disorder rather than a mental illness.
It is labeled as a mental illness because the symptoms align as such and the cau
ses of the disorder are not completely known and understood.[161] Psychiatrists
R. D. Laing, Silvano Arieti, Theodore Lidz and others have argued that the sympt
oms of what is called mental illness are comprehensible reactions to impossible
demands that society and particularly family life places on some sensitive indiv
iduals. Laing, Arieti and Lidz were notable in valuing the content of psychotic
experience as worthy of interpretation, rather than considering it simply as a s
econdary and essentially meaningless marker of underlying psychological or neuro
logical distress. Laing described eleven case studies of people diagnosed with s
chizophrenia and argued that the content of their actions and statements was mea
ningful and logical in the context of their family and life situations.[162]
In 1956, Gregory Bateson and his colleagues Paul Watzlawick, Donald Jackson, and
Jay Haley[163] articulated a theory of schizophrenia, related to Laing's work,
as stemming from double bind situations where a person receives different or con
tradictory messages. Madness was therefore an expression of this distress and sh
ould be valued as a cathartic and transformative experience. In the books Schizo
phrenia and the Family and The Origin and Treatment of Schizophrenic Disorders L
idz and his colleagues explain their belief that parental behaviour can result i
n mental illness in children. Arieti's Interpretation of Schizophrenia won the 1
975 scientific National Book Award in the United States.
The concept of schizophrenia as a result of civilization has been developed furt
her by psychologist Julian Jaynes in his 1976 book The Origin of Consciousness i
n the Breakdown of the Bicameral Mind; he proposed that until the beginning of h
istoric times, schizophrenia or a similar condition was the normal state of huma
n consciousness.[116] This would take the form of a "bicameral mind" where a nor
mal state of low affect, suitable for routine activities, would be interrupted i
n moments of crisis by "mysterious voices" giving instructions, which early peop
le characterized as interventions from the gods. Researchers into shamanism have
speculated that in some cultures schizophrenia or related conditions (such as s
chizotypal personality disorder) may predispose an individual to becoming a sham
an;[164][165] the experience of having access to multiple realities is not uncom
mon in schizophrenia, and is a core experience in many shamanic traditions. Equa
lly, the shaman may have the skill to bring on and direct some of the altered st
ates of consciousness psychiatrists label as illness. Psychohistorians, on the o
ther hand, accept the psychiatric diagnoses. However, unlike the current medical
model of mental disorders they may argue that poor parenting in tribal societie
s causes the shaman's schizoid personalities.[166] Commentators such as Paul Kur
tz and others have endorsed the idea that major religious figures experienced ps
ychosis, heard voices and displayed delusions of grandeur.[167]
Modern clinical psychological research has indicated a number of processes which
may cause or bring on episodes of schizophrenia.
A number of cognitive biases and deficits have been identified. These include at
tribution biases in social situations, difficulty distinguishing inner speech fr
om speech from an external source (source monitoring), difficulty in adjusting s
peech to the needs of the hearer, difficulties in the very earliest stages of pr
ocessing visual information (including reduced latent inhibition), and an attent
ional bias towards threats.
Some of these tendencies have been shown to worsen or appear when under emotiona
l stress or in confusing situations. As with related neurological findings, they
are not shown by all individuals with a diagnosis of schizophrenia, and it is n
ot clear how specific they are to schizophrenia.[168] However, the findings rega

rding cognitive difficulties in schizophrenia are reliable and consistent enough

for some researchers to argue that they are diagnostic.[169]
Impaired capacity to appreciate one's own and others' mental states has been rep
orted to be the single-best predictor of poor social competence in schizophrenia
,[170] and similar cognitive features have been identified in close relatives of
people diagnosed with schizophrenia.[171]
A number of emotional factors have been implicated in schizophrenia, with some m
odels putting them at the core of the disorder. It was thought that the appearan
ce of blunted affect meant that sufferers did not experience strong emotions, bu
t more recent studies indicate there is often a normal or even heightened level
of emotionality, particularly in response to negative events or stressful social
situations.[172] Some theories suggest positive symptoms of schizophrenia can r
esult from or be worsened by negative emotions, including depressed feelings and
low self-esteem[173] and feelings of vulnerability, inferiority or loneliness.[
174] Chronic negative feelings and maladaptive coping skills may explain some of
the association between psychosocial stressors and symptomology.[175] Critical
and controlling behaviour by significant others (high expressed emotion) causes
increased emotional arousal[176] and lowered self-esteem[177] and a subsequent i
ncrease in positive symptoms such as unusual thoughts. Countries or cultures whe
re schizotypal personalities or schizophrenia symptoms are more accepted or valu
ed appear to be associated with reduced onset of, or increased recovery from, sc
hizophrenia.
Related studies suggest that the content of delusional and psychotic beliefs in
schizophrenia can be meaningful and play a causal or mediating role in reflectin
g the life history, or social circumstances of the individual.[178] Holding mino
rity socio-cultural beliefs, for example due to ethnic background, has been link
ed to increased diagnosis of schizophrenia. The way an individual interprets his
or her delusions and hallucinations (e.g. as threatening or as potentially posi
tive) has also been found to influence functioning and recovery.[179]
Some experts think autonomy vs intimacy is a motivation for schizophrenic sympto
ms.[180]
Other lines of work relating to the self in schizophrenia have linked it to psyc
hological dissociation[181] or abnormal states of awareness and identity as unde
rstood from phenomenological, such as in self-disorders, and other perspectives.
[182][183]
Psychiatrist Tim Crow has argued that schizophrenia may be the evolutionary pric
e we pay for a left brain hemisphere specialization for language.[184] Since psy
chosis is associated with greater levels of right brain hemisphere activation an
d a reduction in the usual left brain hemisphere dominance, our language abiliti
es may have evolved at the cost of causing schizophrenia when this system breaks
down.
In alternative medicine, some practitioners believe that there are a vast number
of physical causes of what ends up being diagnosed as schizophrenia.[185] While
some of these explanations may stretch credulity, others (such as heavy metal p
oisoning and nutritional imbalances) have been supported at least somewhat by re
search.[68][186][187] However, it is not entirely clear how many (if any) patien
ts initially diagnosed with schizophrenia these alternative explanations may acc
ount for.
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External links[edit]
Causes of schizophrenia at DMOZ
Schizophrenia at the National Institute of Mental Health

Categories: Abnormal psychologySchizophreniaEtiology

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