Schizophreniacan be defined as a syndrome that is characterised by a collection of signs andsymptoms such as delusions and hallucinations (positive symptoms), lack ofmotivation and social withdrawal (negative symptoms) and alterations inneurocognition (Van Os J., Kapur S.
2009). The diathesis stress model of schizophreniahas become established as a framework for explaining how environmental factors(stressors) interact with pre-existing biological or genetic vulnerabilities inthe aetiology and course of the disorder (Jones, S. R., & Fernyhough, C., 2006). Toevaluate the current evidence for the diathesis stress model of Schizophreniaprevious empirical evidence and studies will be used to examine the etiology ofschizophrenia, the gene environment interaction, and effects of cannabis use. Although the majority (>80%) of individuals who are firstdegree relatives of someone with schizophrenia do not develop schizophrenia,data from more than 40 family studies spanning seven decades of researchconsistently show threat risks to different relatives of affected individualsare in fact significantly greater than the population risk (Gottesman, 1991).
Twin studies have also been vital for establishing an important genetic contributionto the etiology of schizophrenia. The five newest studies since 1995 fromEurope and Japan confirmed earlier findings that yielded proband wiseconcordance rates of 41-65% in monozygotic (MZ) twins and 0-28% in dizygotictwins (DZ) and heritability estimates of 80-85% (Cardno, G., & Gottesman,I., 2000). Adoption studies of schizophrenia have established and confirmed thesignificant role of genetic factors in the etiology of the disorder.
TheCopenhagen sample of the Danish-American adoption studies revealed that chronicschizophrenia was observed more frequently among the biological relatives ofadoptees with schizophrenia (5.6%) than in the biological relatives of controladoptees (0.9%) (Ingraham, J., & Kety, S., 2000). This shows that when an adoptedchild develops schizophrenia the disorder is more common in the personsbiological relatives than adopting relatives (Kalat, J.
, 2015). The use offamily, twin and adoption studies proves that a predisposition forschizophrenia may be inherited. Obstetric complications (OC) have also beenproved to be a strong predictor of psychotic risk. Evidence indicates higherrates of adverse prenatal events across the psychosis spectrum, such asprenatal maternal viral exposure, malnutrition, stress and complications ofpregnancy and delivery (Walder, J., Faraone, V.
, Glatt, J., Tsuang, T., &Seidman, J., 2014). One study carried out examined the rate of OC’s in onepopulation of people identified as at risk for schizophrenia to determine ifthey are more likely to have suffered an obstetrical complication compared tonormal comparison subjects. They found that the rate of OC’s increasedsubstantially in the at-risk samples compared to the normal comparison group(Ballon, S., Dean, A.
, & Cadenhead, S., 2008).Some genotypes are more likely than others to develop a disorderin the event of exposure to certain environmental factors. In a longitudinalstudy carried out by Pekka Tienari and colleagues, a Finnish nationwide sampleof adopted away offspring of mothers with diagnoses of schizophrenia-spectrumdisorders was selected for blind comparison with adopted away offspring ofbiological mothers without schizophrenia-spectrum disorder. Adoptive rearingwas assessed using family rating scales based upon family observations atinitial assessment, after a median interval of 12 years, with follow-up after21 years.
They concluded that a high genetic risk nor dysfunctional familyenvironment alone predicts adoptee illness. The genetic risk and the rearingenvironment have an interactive effect, both in the emergence of illness andprotecting against such an outcome (Tienari, P., Wynne, C., Sorri, A., Lahti,I., Läksy, K., Moring, J., .
.. & Wahlberg, E., 2004). A longitudinal studycarried out by Allan Mirsky and colleagues involved the study of a unique groupof monozygotic female quadruplets, who all developed a schizophrenic disorderby the age of 24. The genetic endowment of the genains is presumed to beidentical, however the phenotypic expression of the disorder was relativelyunique in each of the sisters.
Mirsky and colleagues concluded that thedifferences in the severity of the disorder was due to environmental factorsthat include differing amounts and loci of brain injury at birth, differentialexpectations 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 protectiveagainst the development of a schizophrenic disorder for those who aregenetically 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 reportedthat use of cannabis increases the risk of schizophrenia-like disorder (DiForti, 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 doubledthe risk of schizophrenia in the ensuing 15 years. In addition, they found thatmen who had smoked cannabis on at least 50 occasions were 6 times more likelyto later receive a diagnosis of schizophrenia (Murray, R., Morrison, P.,Henquet, C.
, & Di Forti, M., 2007). A recent study investigated therelation between cannabis use and psychotic symptoms in individuals with aboveaverage predisposition for psychosis who first used cannabis duringadolescence.
Results found that cannabis use at baseline increased thecumulative 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 cannabisat baseline was associated with a 24% increased risk for psychotic symptoms atfollow-up, whereas in non-predisposed individuals who used cannabis the riskwas increased by only 6% (Murray, R.
M., Morrison, P. D., Henquet, C., & DiForti, M., 2007). Caspi and colleagues reasoned that certain individuals werepsychosis-prone due to a genetic basis. Results from a longitudinal studycarried out by Caspi et al provided evidence that a functional polymorphism inthe catechol-O-methyltransferase (COMT) gene interacted with adolescent-onsetcannabis 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 releasedinto synapses, and disturbances in the dopaminergic functions are implicated inthe pathogenesis of schizophrenia (Kapur 2003; Moore et al 1999). The forementioned studies provide evidence that support the diathesis stress model ofschizophrenia.
The diathesis stress model continues to serve as a basis for muchcontemporary theorizing about the origins of schizophrenia (Walker, E., &Diforio, D., 1997). The studies explored in this essay offer substantiveevidence that schizophrenia is a stress sensitive disorder at both biologicaland environmental levels. Theorists assume a biological vulnerability toschizophrenia that is present at birth (Walker, E.
, Kestler, L., Bollini, A.,& Hochman, K.
, 2004). Family, twin and adoption studies carried out byGottesman, Cardno, Ingraham and Kety suggest that there is an underlyinginherited genetic vulnerability to developing schizophrenia. The second sourceof vulnerability are obstetrical complications. Environmental factorsemphasized in this study that increase the risk of developing schizophreniainclude dysfunctional family environments and cannabis use. Other factors mayinclude growing up in an urbanized environment or immigrant ethnic groups (VanOs J., Kapur S.
2009). The diathesis stress model emphasizes genetic vulnerability andhow environmental risk interacts with this vulnerability i.e.
gene-environmentinteraction. Current literature indicates that the diathesis stress modeldominates theories involving the etiology of schizophrenia. Many questionsremain unanswered and further studies must be conducted to enhance the findingson this disorder. Understanding the development of schizophrenia will greatlyprogress advancements of treatment and medication on this inconclusive mentaldisorder. References: London, D. C. P.
(2009). Jim van Os, ShitijKapur. Lancet, 374, 635-45.
Jones, S. R., & Fernyhough, C. (2006). Anew look at the neural diathesis–stress model of schizophrenia: the primacy ofsocial-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 21stcentury.
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 Mxand 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 FamilyHigh 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 PartA, 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 developingschizophrenia. 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.
TheBritish 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-yearfollowup 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 ofpsychosis?.
Psychiatry research, 186(1), 28-33. Di Forti, M., Marconi, A., Carra, E.,Fraietta, S.
, Trotta, A., Bonomo, M., ..
. & Stilo, S. A. (2015). Proportionof patients in south London with first-episode psychosis attributable to use ofhigh 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. NatureReviews Neuroscience, 8(11), 885-895. Caspi, A.
, Moffitt, T. E., Cannon, M., McClay,J., Murray, R.
, Harrington, H., … & Poulton, R. (2005). Moderation of theeffect of adolescent-onset cannabis use on adult psychosis by a functionalpolymorphism in the catechol-O-methyltransferase gene: longitudinal evidence ofa 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). Prospectivecohort study of cannabis use, predisposition for psychosis, and psychoticsymptoms 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.