Schizophrenia relatives than adopting relatives (Kalat, J.,

Schizophrenia
can be defined as a syndrome that is characterised by a collection of signs and
symptoms such as delusions and hallucinations (positive symptoms), lack of
motivation and social withdrawal (negative symptoms) and alterations in
neurocognition (Van Os J., Kapur S. 2009). The diathesis stress model of schizophrenia
has become established as a framework for explaining how environmental factors
(stressors) interact with pre-existing biological or genetic vulnerabilities in
the aetiology and course of the disorder (Jones, S. R., & Fernyhough, C., 2006). To
evaluate the current evidence for the diathesis stress model of Schizophrenia
previous empirical evidence and studies will be used to examine the etiology of
schizophrenia, the gene environment interaction, and effects of cannabis use.

Although the majority (>80%) of individuals who are first
degree relatives of someone with schizophrenia do not develop schizophrenia,
data from more than 40 family studies spanning seven decades of research
consistently show threat risks to different relatives of affected individuals
are in fact significantly greater than the population risk (Gottesman, 1991).
Twin studies have also been vital for establishing an important genetic contribution
to the etiology of schizophrenia. The five newest studies since 1995 from
Europe and Japan confirmed earlier findings that yielded proband wise
concordance rates of 41-65% in monozygotic (MZ) twins and 0-28% in dizygotic
twins (DZ) and heritability estimates of 80-85% (Cardno, G., & Gottesman,
I., 2000). Adoption studies of schizophrenia have established and confirmed the
significant role of genetic factors in the etiology of the disorder. The
Copenhagen sample of the Danish-American adoption studies revealed that chronic
schizophrenia was observed more frequently among the biological relatives of
adoptees with schizophrenia (5.6%) than in the biological relatives of control
adoptees (0.9%) (Ingraham, J., & Kety, S., 2000). This shows that when an adopted
child develops schizophrenia the disorder is more common in the persons
biological relatives than adopting relatives (Kalat, J., 2015). The use of
family, twin and adoption studies proves that a predisposition for
schizophrenia may be inherited. Obstetric complications (OC) have also been
proved to be a strong predictor of psychotic risk. Evidence indicates higher
rates of adverse prenatal events across the psychosis spectrum, such as
prenatal maternal viral exposure, malnutrition, stress and complications of
pregnancy and delivery (Walder, J., Faraone, V., Glatt, J., Tsuang, T., &
Seidman, J., 2014). One study carried out examined the rate of OC’s in one
population of people identified as at risk for schizophrenia to determine if
they are more likely to have suffered an obstetrical complication compared to
normal comparison subjects. They found that the rate of OC’s increased
substantially in the at-risk samples compared to the normal comparison group
(Ballon, S., Dean, A., & Cadenhead, S., 2008).

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Some genotypes are more likely than others to develop a disorder
in the event of exposure to certain environmental factors. In a longitudinal
study carried out by Pekka Tienari and colleagues, a Finnish nationwide sample
of adopted away offspring of mothers with diagnoses of schizophrenia-spectrum
disorders was selected for blind comparison with adopted away offspring of
biological mothers without schizophrenia-spectrum disorder. Adoptive rearing
was assessed using family rating scales based upon family observations at
initial assessment, after a median interval of 12 years, with follow-up after
21 years. They concluded that a high genetic risk nor dysfunctional family
environment alone predicts adoptee illness. The genetic risk and the rearing
environment have an interactive effect, both in the emergence of illness and
protecting against such an outcome (Tienari, P., Wynne, C., Sorri, A., Lahti,
I., Läksy, K., Moring, J., … & Wahlberg, E., 2004). A longitudinal study
carried out by Allan Mirsky and colleagues involved the study of a unique group
of monozygotic female quadruplets, who all developed a schizophrenic disorder
by the age of 24. The genetic endowment of the genains is presumed to be
identical, however the phenotypic expression of the disorder was relatively
unique in each of the sisters. Mirsky and colleagues concluded that the
differences in the severity of the disorder was due to environmental factors
that include differing amounts and loci of brain injury at birth, differential
expectations of and treatment by parents and the operation of chance factors (Mirsky,
A., Bieliauskas, L., French, L., Van Kammen, D., Jönsson, E., & Sedvall, G.,
2000). Studies have shown that a positive family environment may be protective
against the development of a schizophrenic disorder for those who are
genetically susceptible (González-Pinto, A., de Azúa, S., Ibáñez, B.,
Otero-Cuesta, S., Castro-Fornieles, J., Graell-Berna, M., … & Baeza, I.,
2011). These studies support the diathesis stress model.

Prospective epidemiological studies have consistently reported
that use of cannabis increases the risk of schizophrenia-like disorder (Di
Forti, M., Marconi, A., Carra, E., Fraietta, S., Trotta, A., Bonomo, M., …
& Stilo, S., 2015). A study examining 50,000 young Swedish male conscripts,
found that men who had smoked cannabis by the age of conscription had doubled
the risk of schizophrenia in the ensuing 15 years. In addition, they found that
men who had smoked cannabis on at least 50 occasions were 6 times more likely
to later receive a diagnosis of schizophrenia (Murray, R., Morrison, P.,
Henquet, C., & Di Forti, M., 2007). A recent study investigated the
relation between cannabis use and psychotic symptoms in individuals with above
average predisposition for psychosis who first used cannabis during
adolescence. Results found that cannabis use at baseline increased the
cumulative incidence of psychotic symptoms at follow up four years later (Henquet,
C., Krabbendam, L., Spauwen, J., Kaplan, C., Lieb, R., Wittchen, H. U., &
Van Os, J., 2004). However, among psychosis-prone individuals, use of cannabis
at baseline was associated with a 24% increased risk for psychotic symptoms at
follow-up, whereas in non-predisposed individuals who used cannabis the risk
was increased by only 6% (Murray, R. M., Morrison, P. D., Henquet, C., & Di
Forti, M., 2007). Caspi and colleagues reasoned that certain individuals were
psychosis-prone due to a genetic basis. Results from a longitudinal study
carried out by Caspi et al provided evidence that a functional polymorphism in
the catechol-O-methyltransferase (COMT) gene interacted with adolescent-onset
cannabis use to predict the emergence of adult psychosis (Caspi, A., Moffitt,
T., Cannon, M., McClay, J., Murray, R., Harrington, H., … & Poulton, R., 2005).
Catechol-O-methyltransferase is involved in the metabolism of dopamine released
into synapses, and disturbances in the dopaminergic functions are implicated in
the pathogenesis of schizophrenia (Kapur 2003; Moore et al 1999). The fore
mentioned studies provide evidence that support the diathesis stress model of
schizophrenia.

The diathesis stress model continues to serve as a basis for much
contemporary theorizing about the origins of schizophrenia (Walker, E., &
Diforio, D., 1997). The studies explored in this essay offer substantive
evidence that schizophrenia is a stress sensitive disorder at both biological
and environmental levels. Theorists assume a biological vulnerability to
schizophrenia that is present at birth (Walker, E., Kestler, L., Bollini, A.,
& Hochman, K., 2004). Family, twin and adoption studies carried out by
Gottesman, Cardno, Ingraham and Kety suggest that there is an underlying
inherited genetic vulnerability to developing schizophrenia. The second source
of vulnerability are obstetrical complications. Environmental factors
emphasized in this study that increase the risk of developing schizophrenia
include dysfunctional family environments and cannabis use. Other factors may
include growing up in an urbanized environment or immigrant ethnic groups (Van
Os J., Kapur S. 2009).  The diathesis stress model emphasizes genetic vulnerability and
how environmental risk interacts with this vulnerability i.e. gene-environment
interaction. Current literature indicates that the diathesis stress model
dominates theories involving the etiology of schizophrenia. Many questions
remain unanswered and further studies must be conducted to enhance the findings
on this disorder. Understanding the development of schizophrenia will greatly
progress advancements of treatment and medication on this inconclusive mental
disorder.

 

 

 

 

 

References:

London, D. C. P. (2009). Jim van Os, Shitij
Kapur. Lancet, 374, 635-45.

 

Jones, S. R., & Fernyhough, C. (2006). A
new look at the neural diathesis–stress model of schizophrenia: the primacy of
social-evaluative and uncontrollable situations. Schizophrenia Bulletin,
33(5), 1171-1177.

 

Moldin, S. O., & Gottesman, I. I. (1997).
Genes, experience, and chance in schizophrenia—Positioning for the 21st
century. Schizophrenia Bulletin, 23(4), 547-561.

 

Cardno, A. G., & Gottesman, I. I. (2000).
Twin studies of schizophrenia: from bow?and?arrow concordances to star wars Mx
and functional genomics. American Journal of Medical Genetics Part A, 97(1),
12-17.

 

Walder, D. J., Faraone, S. V., Glatt, S. J.,
Tsuang, M. T., & Seidman, L. J. (2014). Genetic liability, prenatal health,
stress and family environment: risk factors in the Harvard Adolescent Family
High Risk for Schizophrenia Study. Schizophrenia research, 157(1),
142-148.

 

Ingraham, L. J., & Kety, S. S. (2000).
Adoption studies of schizophrenia. American Journal of Medical Genetics Part
A, 97(1), 18-22.

 

Kalat, J. W. (2015). Biological Psychology.
11th edition. Cengage Learning.

 

Ballon, J. S., Dean, K. A., & Cadenhead,
K. S. (2008). Obstetrical complications in people at risk for developing
schizophrenia. Schizophrenia research, 98(1), 307-311.

 

Tienari, P., Wynne, L. C., Sorri, A., Lahti,
I., Läksy, K., Moring, J., … & Wahlberg, K. E. (2004).
Genotype-environment interaction in schizophrenia-spectrum disorder. The
British Journal of Psychiatry, 184(3), 216-222.

 

Mirsky, A. F., Bieliauskas, L. A., French, L.
M., Van Kammen, D. P., Jönsson, E., & Sedvall, G. (2000). A 39-year
followup of the Genain quadruplets. Schizophrenia bulletin, 26(3),
699-708.

 

González-Pinto, A., de Azúa, S. R., Ibáñez,
B., Otero-Cuesta, S., Castro-Fornieles, J., Graell-Berna, M., … & Baeza,
I. (2011). Can positive family factors be protective against the development of
psychosis?. Psychiatry research, 186(1), 28-33.

 

Di Forti, M., Marconi, A., Carra, E.,
Fraietta, S., Trotta, A., Bonomo, M., … & Stilo, S. A. (2015). Proportion
of patients in south London with first-episode psychosis attributable to use of
high potency cannabis: a case-control study. The Lancet Psychiatry, 2(3),
233-238.

 

Murray, R. M., Morrison, P. D., Henquet, C.,
& Di Forti, M. (2007). Cannabis, the mind and society: the hash realities. Nature
Reviews Neuroscience, 8(11), 885-895.

 

Caspi, A., Moffitt, T. E., Cannon, M., McClay,
J., Murray, R., Harrington, H., … & Poulton, R. (2005). Moderation of the
effect of adolescent-onset cannabis use on adult psychosis by a functional
polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of
a gene X environment interaction. Biological psychiatry, 57(10),
1117-1127.

 

Henquet, C., Krabbendam, L., Spauwen, J.,
Kaplan, C., Lieb, R., Wittchen, H. U., & Van Os, J. (2004). Prospective
cohort study of cannabis use, predisposition for psychosis, and psychotic
symptoms in young people. Bmj, 330(7481), 11.

 

Walker, E. F., & Diforio, D. (1997).
Schizophrenia: a neural diathesis-stress model. Psychological review, 104(4),
667.

 

Walker, E., Kestler, L., Bollini, A., &
Hochman, K. M. (2004). Schizophrenia: etiology and course. Annu. Rev.
Psychol., 55, 401-430.

Schizophrenia
can be defined as a syndrome that is characterised by a collection of signs and
symptoms such as delusions and hallucinations (positive symptoms), lack of
motivation and social withdrawal (negative symptoms) and alterations in
neurocognition (Van Os J., Kapur S. 2009). The diathesis stress model of schizophrenia
has become established as a framework for explaining how environmental factors
(stressors) interact with pre-existing biological or genetic vulnerabilities in
the aetiology and course of the disorder (Jones, S. R., & Fernyhough, C., 2006). To
evaluate the current evidence for the diathesis stress model of Schizophrenia
previous empirical evidence and studies will be used to examine the etiology of
schizophrenia, the gene environment interaction, and effects of cannabis use.

Although the majority (>80%) of individuals who are first
degree relatives of someone with schizophrenia do not develop schizophrenia,
data from more than 40 family studies spanning seven decades of research
consistently show threat risks to different relatives of affected individuals
are in fact significantly greater than the population risk (Gottesman, 1991).
Twin studies have also been vital for establishing an important genetic contribution
to the etiology of schizophrenia. The five newest studies since 1995 from
Europe and Japan confirmed earlier findings that yielded proband wise
concordance rates of 41-65% in monozygotic (MZ) twins and 0-28% in dizygotic
twins (DZ) and heritability estimates of 80-85% (Cardno, G., & Gottesman,
I., 2000). Adoption studies of schizophrenia have established and confirmed the
significant role of genetic factors in the etiology of the disorder. The
Copenhagen sample of the Danish-American adoption studies revealed that chronic
schizophrenia was observed more frequently among the biological relatives of
adoptees with schizophrenia (5.6%) than in the biological relatives of control
adoptees (0.9%) (Ingraham, J., & Kety, S., 2000). This shows that when an adopted
child develops schizophrenia the disorder is more common in the persons
biological relatives than adopting relatives (Kalat, J., 2015). The use of
family, twin and adoption studies proves that a predisposition for
schizophrenia may be inherited. Obstetric complications (OC) have also been
proved to be a strong predictor of psychotic risk. Evidence indicates higher
rates of adverse prenatal events across the psychosis spectrum, such as
prenatal maternal viral exposure, malnutrition, stress and complications of
pregnancy and delivery (Walder, J., Faraone, V., Glatt, J., Tsuang, T., &
Seidman, J., 2014). One study carried out examined the rate of OC’s in one
population of people identified as at risk for schizophrenia to determine if
they are more likely to have suffered an obstetrical complication compared to
normal comparison subjects. They found that the rate of OC’s increased
substantially in the at-risk samples compared to the normal comparison group
(Ballon, S., Dean, A., & Cadenhead, S., 2008).

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For You For Only $13.90/page!


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Some genotypes are more likely than others to develop a disorder
in the event of exposure to certain environmental factors. In a longitudinal
study carried out by Pekka Tienari and colleagues, a Finnish nationwide sample
of adopted away offspring of mothers with diagnoses of schizophrenia-spectrum
disorders was selected for blind comparison with adopted away offspring of
biological mothers without schizophrenia-spectrum disorder. Adoptive rearing
was assessed using family rating scales based upon family observations at
initial assessment, after a median interval of 12 years, with follow-up after
21 years. They concluded that a high genetic risk nor dysfunctional family
environment alone predicts adoptee illness. The genetic risk and the rearing
environment have an interactive effect, both in the emergence of illness and
protecting against such an outcome (Tienari, P., Wynne, C., Sorri, A., Lahti,
I., Läksy, K., Moring, J., … & Wahlberg, E., 2004). A longitudinal study
carried out by Allan Mirsky and colleagues involved the study of a unique group
of monozygotic female quadruplets, who all developed a schizophrenic disorder
by the age of 24. The genetic endowment of the genains is presumed to be
identical, however the phenotypic expression of the disorder was relatively
unique in each of the sisters. Mirsky and colleagues concluded that the
differences in the severity of the disorder was due to environmental factors
that include differing amounts and loci of brain injury at birth, differential
expectations of and treatment by parents and the operation of chance factors (Mirsky,
A., Bieliauskas, L., French, L., Van Kammen, D., Jönsson, E., & Sedvall, G.,
2000). Studies have shown that a positive family environment may be protective
against the development of a schizophrenic disorder for those who are
genetically susceptible (González-Pinto, A., de Azúa, S., Ibáñez, B.,
Otero-Cuesta, S., Castro-Fornieles, J., Graell-Berna, M., … & Baeza, I.,
2011). These studies support the diathesis stress model.

Prospective epidemiological studies have consistently reported
that use of cannabis increases the risk of schizophrenia-like disorder (Di
Forti, M., Marconi, A., Carra, E., Fraietta, S., Trotta, A., Bonomo, M., …
& Stilo, S., 2015). A study examining 50,000 young Swedish male conscripts,
found that men who had smoked cannabis by the age of conscription had doubled
the risk of schizophrenia in the ensuing 15 years. In addition, they found that
men who had smoked cannabis on at least 50 occasions were 6 times more likely
to later receive a diagnosis of schizophrenia (Murray, R., Morrison, P.,
Henquet, C., & Di Forti, M., 2007). A recent study investigated the
relation between cannabis use and psychotic symptoms in individuals with above
average predisposition for psychosis who first used cannabis during
adolescence. Results found that cannabis use at baseline increased the
cumulative incidence of psychotic symptoms at follow up four years later (Henquet,
C., Krabbendam, L., Spauwen, J., Kaplan, C., Lieb, R., Wittchen, H. U., &
Van Os, J., 2004). However, among psychosis-prone individuals, use of cannabis
at baseline was associated with a 24% increased risk for psychotic symptoms at
follow-up, whereas in non-predisposed individuals who used cannabis the risk
was increased by only 6% (Murray, R. M., Morrison, P. D., Henquet, C., & Di
Forti, M., 2007). Caspi and colleagues reasoned that certain individuals were
psychosis-prone due to a genetic basis. Results from a longitudinal study
carried out by Caspi et al provided evidence that a functional polymorphism in
the catechol-O-methyltransferase (COMT) gene interacted with adolescent-onset
cannabis use to predict the emergence of adult psychosis (Caspi, A., Moffitt,
T., Cannon, M., McClay, J., Murray, R., Harrington, H., … & Poulton, R., 2005).
Catechol-O-methyltransferase is involved in the metabolism of dopamine released
into synapses, and disturbances in the dopaminergic functions are implicated in
the pathogenesis of schizophrenia (Kapur 2003; Moore et al 1999). The fore
mentioned studies provide evidence that support the diathesis stress model of
schizophrenia.

The diathesis stress model continues to serve as a basis for much
contemporary theorizing about the origins of schizophrenia (Walker, E., &
Diforio, D., 1997). The studies explored in this essay offer substantive
evidence that schizophrenia is a stress sensitive disorder at both biological
and environmental levels. Theorists assume a biological vulnerability to
schizophrenia that is present at birth (Walker, E., Kestler, L., Bollini, A.,
& Hochman, K., 2004). Family, twin and adoption studies carried out by
Gottesman, Cardno, Ingraham and Kety suggest that there is an underlying
inherited genetic vulnerability to developing schizophrenia. The second source
of vulnerability are obstetrical complications. Environmental factors
emphasized in this study that increase the risk of developing schizophrenia
include dysfunctional family environments and cannabis use. Other factors may
include growing up in an urbanized environment or immigrant ethnic groups (Van
Os J., Kapur S. 2009).  The diathesis stress model emphasizes genetic vulnerability and
how environmental risk interacts with this vulnerability i.e. gene-environment
interaction. Current literature indicates that the diathesis stress model
dominates theories involving the etiology of schizophrenia. Many questions
remain unanswered and further studies must be conducted to enhance the findings
on this disorder. Understanding the development of schizophrenia will greatly
progress advancements of treatment and medication on this inconclusive mental
disorder.

 

 

 

 

 

References:

London, D. C. P. (2009). Jim van Os, Shitij
Kapur. Lancet, 374, 635-45.

 

Jones, S. R., & Fernyhough, C. (2006). A
new look at the neural diathesis–stress model of schizophrenia: the primacy of
social-evaluative and uncontrollable situations. Schizophrenia Bulletin,
33(5), 1171-1177.

 

Moldin, S. O., & Gottesman, I. I. (1997).
Genes, experience, and chance in schizophrenia—Positioning for the 21st
century. Schizophrenia Bulletin, 23(4), 547-561.

 

Cardno, A. G., & Gottesman, I. I. (2000).
Twin studies of schizophrenia: from bow?and?arrow concordances to star wars Mx
and functional genomics. American Journal of Medical Genetics Part A, 97(1),
12-17.

 

Walder, D. J., Faraone, S. V., Glatt, S. J.,
Tsuang, M. T., & Seidman, L. J. (2014). Genetic liability, prenatal health,
stress and family environment: risk factors in the Harvard Adolescent Family
High Risk for Schizophrenia Study. Schizophrenia research, 157(1),
142-148.

 

Ingraham, L. J., & Kety, S. S. (2000).
Adoption studies of schizophrenia. American Journal of Medical Genetics Part
A, 97(1), 18-22.

 

Kalat, J. W. (2015). Biological Psychology.
11th edition. Cengage Learning.

 

Ballon, J. S., Dean, K. A., & Cadenhead,
K. S. (2008). Obstetrical complications in people at risk for developing
schizophrenia. Schizophrenia research, 98(1), 307-311.

 

Tienari, P., Wynne, L. C., Sorri, A., Lahti,
I., Läksy, K., Moring, J., … & Wahlberg, K. E. (2004).
Genotype-environment interaction in schizophrenia-spectrum disorder. The
British Journal of Psychiatry, 184(3), 216-222.

 

Mirsky, A. F., Bieliauskas, L. A., French, L.
M., Van Kammen, D. P., Jönsson, E., & Sedvall, G. (2000). A 39-year
followup of the Genain quadruplets. Schizophrenia bulletin, 26(3),
699-708.

 

González-Pinto, A., de Azúa, S. R., Ibáñez,
B., Otero-Cuesta, S., Castro-Fornieles, J., Graell-Berna, M., … & Baeza,
I. (2011). Can positive family factors be protective against the development of
psychosis?. Psychiatry research, 186(1), 28-33.

 

Di Forti, M., Marconi, A., Carra, E.,
Fraietta, S., Trotta, A., Bonomo, M., … & Stilo, S. A. (2015). Proportion
of patients in south London with first-episode psychosis attributable to use of
high potency cannabis: a case-control study. The Lancet Psychiatry, 2(3),
233-238.

 

Murray, R. M., Morrison, P. D., Henquet, C.,
& Di Forti, M. (2007). Cannabis, the mind and society: the hash realities. Nature
Reviews Neuroscience, 8(11), 885-895.

 

Caspi, A., Moffitt, T. E., Cannon, M., McClay,
J., Murray, R., Harrington, H., … & Poulton, R. (2005). Moderation of the
effect of adolescent-onset cannabis use on adult psychosis by a functional
polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of
a gene X environment interaction. Biological psychiatry, 57(10),
1117-1127.

 

Henquet, C., Krabbendam, L., Spauwen, J.,
Kaplan, C., Lieb, R., Wittchen, H. U., & Van Os, J. (2004). Prospective
cohort study of cannabis use, predisposition for psychosis, and psychotic
symptoms in young people. Bmj, 330(7481), 11.

 

Walker, E. F., & Diforio, D. (1997).
Schizophrenia: a neural diathesis-stress model. Psychological review, 104(4),
667.

 

Walker, E., Kestler, L., Bollini, A., &
Hochman, K. M. (2004). Schizophrenia: etiology and course. Annu. Rev.
Psychol., 55, 401-430.

x

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