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Researchers Probe Generation Gap in Migrants’ Psychosis Risk

21 November 2008. Ever since Norwegian psychiatrist Örnulv Ödegaard found a heightened risk of schizophrenia in Norwegians who migrated to the United States (Ödegaard, 1932), researchers have been trying to understand why some immigrants seem more prone to develop schizophrenia than natives of their chosen land. To untangle the effects of migration and ethnicity, a research team led by Jeremy Coid of St. Bartholomew’s Hospital in London, England, assessed the incidence of psychosis in first- and second-generation migrant groups in the United Kingdom. As reported in the November Archives of General Psychiatry, their study turned up little evidence of generational differences in any ethnic group, except for black Caribbeans. In that community, the second generation seemed more likely than the first to develop nonaffective psychoses.

Coid’s collaborators included two researchers from the earlier population-based Ætiology and Ethnicity in Schizophrenia and Other Psychoses (ÆSOP) study (Kirkbride et al., 2006). Conducted in England, it had found that the incidence of schizophrenia and other psychoses varied with age, sex, ethnicity, and location. The ÆSOP researchers, led by James Kirkbride of the University of Cambridge, England, saw these variations as evidence that genes and environment together shape psychosis risk. The results strongly countered the notion that schizophrenia rates remain constant no matter where in the world you look.

Consistent with prior research on schizophrenia and migration (for reviews, see Cantor-Graae and Selten, 2005; McGrath et al., 2004), the ÆSOP study found a three times higher risk of psychosis in minority ethnic individuals than in white British subjects after adjusting for age, sex, and location. Whether the increased risk in immigrants extends to, or even grows, in their offspring, remains an open question. Coid and associates wondered whether generational effects would differ by ethnicity, gender, or type of psychosis.

Tracking cases in East London
In the East London First Episode Psychosis Study, Coid and coworkers at St. Bartholomew’s Hospital, with their collaborators at the University of Cambridge, studied an ethnically diverse population that lived in poverty-stricken boroughs of East London. The researchers took extra care to identify everyone from 18 to 64 years old who contacted mental health services during a two-year period about a first episode of likely psychotic illness. Willing subjects who had been diagnosed with a psychotic disorder underwent testing, and two researchers used the available clinical and test-based data to arrive at diagnoses by consensus.

A multiethnic panel of researchers coded ethnicity, based on subjects’ self-reported ethnicity, their place of birth, and their parents’ birthplaces. With 484 patients, the study could examine psychosis risk in six ethnic groups: black Caribbean, black African, Asian (Indian, Pakistani, and Bangladeshi), white British, white other (mostly Irish and European), and other (Chinese, other Asian, and mixed ethnicity).

Using the incidence rate ratio (IRR)—quite simply, one incidence rate divided by another—Coid and colleagues compared the risk in various ethnic groups with that in the reference group of white British who were born in the U.K. They separately analyzed the risk of nonaffective and affective psychoses, while controlling for age and sex. Nonaffective psychoses included schizophrenia, schizophreniform disorder, and schizoaffective disorder; affective psychoses consisted of bipolar, depressive, and other psychotic mood disorders.

Talkin’ ’bout which generation?
Turning first to nonaffective psychoses, the investigators found an elevated incidence in all of the migrant groups except the “other” group. Compared to white British individuals, black Caribbeans, the most at-risk group, showed a fourfold increase (IRR, 4.2; 95 percent CI, 3.0-5.8) and black Africans a threefold increase in risk (IRR, 3.4; 95 percent CI, 2.4-4.7). The Asian and white other groups showed smaller, but significant, increases in risk. Previous studies have likewise found a high rate of psychosis in black Caribbean and black African populations in Europe.

Pursuing hints in the data that generational status might be linked to the risk of nonaffective psychoses, Coid and associates found higher rates in the offspring of black Caribbean immigrants than in black individuals who had migrated from the Caribbean themselves (IRR, 1.6; 95 percent CI, 1.1-2.4; P = .02). They ascribe the generational differences to age: most of the second-generation black Caribbeans were less than 44 years old, whereas the preceding generation, which mainly arrived in the U.K. during the 1950s and 1960s, tended to be over 35. In short, the second generation tended to be in the age range at which psychoses typically emerge. The relatively small overlap between the two cohorts’ ages rendered statistical controls for age “somewhat ineffective,” Kirkbride told SRF via e-mail. In the 35-44 age range, where there was a sufficient population of both first- and second-generation black Caribbean immigrants to obtain precise rates, incidence of psychoses was similar between generations, who were both at equally raised rates compared with the white British.

Separate analyses for men and women revealed significant elevations only in Asian women. Notably, the first generation showed a nearly fourfold risk increase in rates of nonaffective psychoses relative to native British white women (IRR, 3.6; 95 percent CI, 2.1-6.4).

As for affective psychoses, the study again found a four times higher risk in black Caribbeans (IRR, 4.0; 95 percent CI, 2.4-6.9) and a three times higher risk in black Africans (IRR, 2.7; 95 percent CI, 1.5-4.9) than in the white British group. In addition, the white other group showed twice the risk of the reference group (IRR, 2.3; 95 percent CI, 1.3-4.0). Contrary to nonaffective psychoses, however, the Asians showed no reliable increase in the relative risk of affective psychoses, nor did generation status and ethnicity interact in any of the groups. Coid and associates point to the cohesiveness of the Asian immigrant community as a factor that may bolster them against discrimination and other tribulations that might otherwise make them vulnerable, though sex differences may remain.

A raft of possible explanations
The researchers view their findings as support for environmental explanations for the increased risk of psychotic illness in migrant groups (see SRF live discussion). Being the new kid on the block can be hard enough; moving to a different culture in a new land might bring out a predisposition to psychosis, according to the stress-vulnerability model. Furthermore, some researchers argue that the prolonged experience of “social defeat,” a consequence of second-class or outsider status, might increase schizophrenia risk via the mesolimbic dopamine system (see Selten and Cantor-Graae, 2007). “That the excess risk of psychoses for Asian immigrants in our sample appeared to be restricted to women provides anecdotal support for the social defeat hypothesis given the additional pressure of marginal status faced by some women in Indian, Pakistani, and Bangladeshi communities,” Coid and colleagues write.

Family structure might also play a role. In their homeland, Caribbeans tend to receive support from an extended family, but the high percentage of black Caribbean families headed by single parents in the U.K. suggests that migration frays these ties. Children who remain separated from a parent for a long time seem to be more susceptible to psychosis.

As for other possible explanations, Coid and colleagues doubt that either social class or cannabis use can account for their findings. They had previously shown that individual differences in social class cannot account for ethnic differences in psychosis rates in this sample, and European studies suggest that the black Caribbean population uses cannabis no more than the general population does.

The East London study did not explicitly test any of these explanations, so the investigators can only connect the dots between their findings and those that came before. Another generation of studies will have to discover whether the conclusions extend to other peoples moving to and from other places, particularly developing nations.—Victoria L. Wilcox.

Reference:
Coid, JW, Kirkbride JB, Barker D, Cowden F, Stamps R, Yang M, Jones PB. Raised incidence rates of all psychoses among migrant groups. Findings from the East London First Episode Psychosis Study. Arch Gen Psychiatry. 2008 Nov;65(11):1250-1258. Abstract

Comments on News and Primary Papers
Comment by:  Elizabeth Cantor-Graae
Submitted 21 November 2008
Posted 21 November 2008

Tracking down the agent(s) responsible for the elusive “migrant” effect in schizophrenia bears similarities with the clever plot twists in a well-crafted crime novel. The new study by Jeremy Coid and coworkers makes substantial headway toward narrowing down the list of suspects, with the spotlight increasingly focused on ethnicity. The current venture has a number of outstanding strengths: large sample size, robust denominator data, and stringent methods of case ascertainment, including leakage analysis. The choice of venue of East London, an area characterized by socioeconomic deprivation, is a strategic advantage, in that the effect of ethnicity can be teased out from socioeconomic disadvantage. The findings indicate that ethnicity had a stronger effect on risk magnitude than did generational status (i.e., place of birth). Black Caribbeans were the only ethnic group where generational status “mattered,” an effect that the authors attribute to differences in the age structures of the underlying populations at risk.

How best to interpret these results, and where do they lead us?
Coid and colleagues argue that the cumulative effect of the various “pressures” operating on migrants might be roughly similar across generations, with some exceptions. In this case, the exceptions are all the more interesting, and likely to be the most informative. The fact that second-generation black Caribbeans had markedly higher rates of psychoses than black Caribbeans born in the Caribbean suggests differential pressures operating on these two groups. Although these pressures have yet to be identified (more detective work needed!), some mechanisms suggest themselves. The generation of black Caribbeans that emigrated to the U.K. during the 1950s and 1960s were more readily incorporated into the labor market than today’s generation (second-generation immigrants). Although their jobs might have primarily been in the service or unskilled sectors, the ability to get a “foot” into society and earn a living could have represented substantial gains for this generation in terms of positive self-esteem and protection against feelings of negative self-worth and/or outsider status. In contrast, the second generation of African-Caribbean immigrants seems to have more difficulty securing a place within U.K. society. Their difficulties may be compounded by unstable home environments. Ethnic groups with strong familial ties, such as Asians or the example of the Turks in The Netherlands (Selten et al., 2001), appear better able to buffer the negative effects of discrimination and marginalization. Thus, the extent to which families are able to provide stable home environments seems to be a crucial modifier of minority group “stress,” and we may very well see a resurgent interest in the near future in studies focusing on the schizophrenogenic family.

It may be noted that Coid and coworkers’ results are well in line with the social defeat hypothesis (Cantor-Graae and Selten, 2005; Selten and Cantor-Graae, 2005; Selten et al., 2007), which suggests that a key contributor to the migrant psychosis phenomenon is long-term chronic exposure to social defeat, possibly resulting in dopamine disturbances in the brain. While discrimination may play a key role in the experience of social defeat, the mechanisms that enhance vulnerability to psychosis in any specific minority group are probably complex. Certainly there is a need for confirmatory studies from settings where waves of migration span several generations, for example, countries such as France and Spain, in order to re-test Coid and colleagues’ findings. However, results from Israel, a country with a long history of heterogeneous migration, confirm the notion that “outsider” status may vary from group to group (Weiser et al., 2008) and across generations (Corcoran et al., 2008) and that this may in turn determine that group’s risk for schizophrenia. In other words, context may well prove to be “everything.” Thus, investigations that can shed further light on the elements that make up the contextual environment are likely to be especially fruitful.

The broader implications of Coid and coworkers’ important new migrant study are several. We need to once and for all accept the notion that schizophrenia is not uniformly distributed among groups, and to intensify research efforts that may further elucidate the nature of the underlying exposure variable(s). Although it may take considerable effort to track down the “culprit,” the good news is that social factors lend themselves to preventative interventions. There may well be a glimpse of light at the end of the tunnel.

References:

Selten JP, Veen N, Feller W, Blom JD, Schols D, Camoenië W, Oolders J, van der Velden M, Hoek HW, Rivero VM, van der Graaf Y, Kahn R. Incidence of psychotic disorders in immigrant groups to The Netherlands. Br J Psychiatry. 2001 Apr 1;178():367-72. Abstract

Cantor-Graae E, Selten JP. Schizophrenia and migration: a meta-analysis and review. Am J Psychiatry. 2005 Jan 1;162(1):12-24. Abstract

Selten JP, Cantor-Graae E. Social defeat: risk factor for schizophrenia? Br J Psychiatry. 2005 Aug 1;187():101-2. Abstract

Selten JP, Cantor-Graae E, Kahn RS. Migration and schizophrenia. Curr Opin Psychiatry. 2007 Mar 1;20(2):111-5. Abstract

Weiser M, Werbeloff N, Vishna T, Yoffe R, Lubin G, Shmushkevitch M, Davidson M. Elaboration on immigration and risk for schizophrenia. Psychol Med. 2008 Aug 1;38(8):1113-9. Abstract

Corcoran C, Perrin M, Harlap S, Deutsch L, Fennig S, Manor O, Nahon D, Kimhy D, Malaspina D, Susser E. Incidence of Schizophrenia Among Second-Generation Immigrants in the Jerusalem Perinatal Cohort. Schizophr Bull. 2008 Jul 22; Abstract

View all comments by Elizabeth Cantor-Graae

Comments on Related News


Related News: Urban Schizophrenia Risk: A Family Affair?

Comment by:  Patricia Estani
Submitted 13 June 2006
Posted 13 June 2006
  I recommend the Primary Papers

Related News: Urban Schizophrenia Risk: A Family Affair?

Comment by:  Ella Matthews
Submitted 16 June 2006
Posted 5 July 2006

Questions on the different rates of occurrence of the schizophrenia spectrum of brain disorders between northern (developed) and southern underdeveloped countries, between urban and rural, as well as the birth order within the family of those suffering from schizophrenia are important ones.

However, when thinking about family exposure to environmental factors, I think that there is much to learn from social science. Say that a 1970s family moved from the country to the city just at the time when the birth control pill had been developed and began to be widely available in urban industrialized areas: Estrogen levels on the early formulations of the "pill" were too high, causing women to search for other legal birth control methods which they could tolerate more easily. About the only other things that doctors could offer women back then were the highly touted IUDs.

Say also that a woman tried the birth control pill but, because her taking of the pill was spotty, she became pregnant with her first child. After delivering their first children, many 1970s women then turned to IUDs, which did not cause bloating or the other nasty physical side effects of the pill. What IUDs did have was a hidden wicking string. Those strings were ladders for infection moving into the uterus. So when thinking of environmental factors at the level of the family, one has to ask broad-spectrum socioeconomic questions about what families were actually up against in the 1970s.

Birth control methods could also add insight into why schizophrenia was identified in the late 1800s, a time when women were moving into paid labor outside the home. It had been common knowledge since ancient times that any foreign object inserted into the uterus (IUD) would interfere with pregnancy. Working women had to limit the number of children they had. There was information-sharing among female coworkers.

Think about the implications of IUD use in Catholic countries such as Ireland, which has a high rate of schizophrenia. Catholic mothers of schizophrenics would be loath to discuss birth control methods used prior to or during the birth of a child born with schizophrenia. Moreover, during the Dalkon Shield scandal and IUD birth defect lawsuits of the 1970s and 1980s, the schizophrenias did not get any coverage because children born with these disorders hadn't reached the age of onset yet.

I am a parent of a second-born adult daughter suffering from schizophrenia. Families, especially mothers, do not want to go back to the days when it was said that bad mothering caused schizophrenia. Yet, we who carried these children to term have to ask ourselves what was different going into and throughout these pregnancies?

Skilled researchers need to formulate and ask probing questions about what the mother was exposed to prior to and during these pregnancies.

View all comments by Ella Matthews

Related News: Research Roundup —The Tapestry of Environmental Influences in Psychosis

Comment by:  John McGrath, SRF Advisor
Submitted 5 November 2010
Posted 5 November 2010

The large study from Nuevo and colleagues is very thought provoking. There was substantial between-site variation in response to various psychosis-screening items. Assuming that endorsement of these items is a mix of: 1) "true" psychotic-like experiences, 2) "true" responses that are understandable from the perspective of local cultures and beliefs, and 3) innocent misinterpretations of the questions, why is there such marked variation? For example, why do 46 percent of respondents from Nepal endorse at least one psychotic-like experience and a third report auditory hallucinations?

It seems self-evident that populations with strong religious and/or cultural beliefs related to psychotic-like experiences might endorse psychosis-screening items more readily (type 2 in the above list). But could it be feasible that these same populations might also “kindle” psychotic experiences in vulnerable people? This notion is pure speculation, but we should remain mindful that dopaminergic pathways related to psychosis are vulnerable to the process of endogenous sensitization (Laruelle, 2000).

What does it mean to be a member of a cultural group that is more “prone” to psychotic-like experiences? Tanya Luhrmann, an anthropologist based at Stanford University, has examined individuals attending evangelical churches who “hear” the voice of God during prayer (Luhrmann et al., 2010). The vignettes suggest that some individuals reported more “hearing the voice of God” after improving their prayer skills. Practice makes perfect, but could it also kindle pathways related to schizophrenia?

Regardless of the underlying mechanisms, understanding variations in these symptoms is a fascinating topic worthy of more multidisciplinary research.

References:

Laruelle M. The role of endogenous sensitization in the pathophysiology of schizophrenia: implications from recent brain imaging studies. Brain Res Brain Res Rev. 2000;31(2-3):371-84. Abstract

Luhrmann TM, Nusbaum H, Thisted R. The absorption hypothesis: learning to hear God in evangelical Christianity. American Anthropologist. 2010;112 (1):66-78.

View all comments by John McGrath

Related News: Research Roundup —The Tapestry of Environmental Influences in Psychosis

Comment by:  Tanya Luhrmann
Submitted 12 November 2010
Posted 12 November 2010

It seems to me that there may be two different patterns that show up in these large epidemiological studies: the psychotic continuum and phenomena associated with absorption. Absorption is basically a capacity for/interest in being caught up in your imagination. It is associated with hypnotizability and dissociation, but not identical to them (Tellegen and Atkinson, 1974).

In my own work on evangelical Christianity, I identify a pattern in which people report hallucination-like phenomena that are rare, brief, and not distressing (as opposed to the pattern associated with psychotic disorder, in which the hallucinations are often frequent, extended, and distressing). Those who report hearing God’s voice audibly or seeing the wing of an angel are also more likely to score highly on the Tellegen absorption scale (Luhrmann et al., 2010). This relationship between unusual experiences and absorption also shows up in a significant relationship between absorption and the Posey-Loesch hearing voices scale when these scales are given to undergraduates. Among undergraduates, the rates for hallucination-like phenomena are also consistently far higher than the Nuevo paper reports, perhaps because neither the absorption scale nor the Posey-Loesch scale seems to probe for pathology (Luhrmann, forthcoming).

I am not the only one to have found a significant association between unusual sensory experiences and absorption. Aleman and Laroi (2008) report that a handful of other researchers have also found significant correlations between hallucination scales and the absorption scale. As a result of this work, I think that there may be different pathways to hallucination-like phenomena—some pathological, others less so.

Yet, I also wonder whether there is indeed something like “priming” psychosis, as John suggested. This would arise if there were some looseness in the relationship between psychosis and dissociation, which there appears to be. At least that's the way I interpret some of the phenomena that Romme and Escher (1993) report. If there is some kind of loose relationship, it would suggest that someone could have an absorption/dissociation response to trauma that would look psychotic; it might also suggest that an intensely absorbing negative imaginative experience (being pursued by demons, e.g.) might contribute to a vulnerable person exhibiting more psychotic-like symptoms.

How would we begin to pull this apart?

References:

Aleman A, Laroi F. Hallucinations: The science of idiosyncratic perception. Washington, DC: American Psychological Association, 2008.

Luhrmann TM. When God speaks back. New York: Knopf, forthcoming.

Luhrmann TM, Nusbaum H, Thisted R. The absorption hypothesis: learning to hear God in evangelical Christianity. American Anthropologist. 2010;112 (1):66-78.

Romme M, Escher S. Accepting voices. London: Mind, 1993.

Tellegen A, Atkinson G. Openness to absorbing and self-altering experiences (“absorption”): a trait related to hypnotic susceptibility. J Abnorm Psychol. 1974;83(3):268-77. Abstract

View all comments by Tanya Luhrmann

Related News: Research Roundup —The Tapestry of Environmental Influences in Psychosis

Comment by:  Mary Cannon
Submitted 15 November 2010
Posted 15 November 2010

This beautifully written piece serves to excite interest in the fascinating epidemiology of schizophrenia. In our search for the “missing heritability” of schizophrenia, we don’t have to look too far for clues. There are many contained in this piece. It just requires some Sherlock Holmes-type deductive reasoning to put them all together now!

The realization that psychotic symptoms (or psychotic-like experiences) can be used as a proxy for schizophrenia risk has opened up new vistas for exploration (Kelleher and Cannon, 2010). For instance, the paper by Nuevo and colleagues will provide a fertile ground for testing ecological hypotheses on the etiology of schizophrenia—such as examining cross-national vitamin D levels (McGrath et al.) or fish oil consumption. Geneticists have yet to appreciate the potential value of studying such symptoms. Ian Kelleher, Jack Jenner, and I have argued in a recent editorial that the non-clinical psychosis phenotype provides us with a population in which to test hypotheses about the evolutionary benefit of psychosis genes (Kelleher et al., 2010; see also Nesse, 2004). This non-clinical psychosis phenotype gives rise to the possibility of moving beyond just-so stories into the realm of testable hypotheses.

References:

Kelleher I, Cannon M. Psychotic-like experiences in the general population: characterizing a high-risk group for psychosis. Psychol Med. 2010 May 19:1-6. Abstract

Kelleher I, Jenner JA, Cannon M. Psychotic symptoms in the general population - an evolutionary perspective. Br J Psychiatry. 2010 Sep;197(3):167-9.

Nesse RM. Cliff-edged fitness functions and the persistence of schizophrenia. Behav Brain Sci. 2004;27:862-3.

View all comments by Mary Cannon

Related News: Research Roundup —The Tapestry of Environmental Influences in Psychosis

Comment by:  Jean-Paul Selten
Submitted 17 November 2010
Posted 17 November 2010
  I recommend the Primary Papers

With interest, I read Victoria Wilcox's summary of some thought-provoking papers published this year. It seems that schizophrenia, like cancer, has many different causes. I would like to point out that three of the studies (Zammit et al., 2010; Wicks et al., 2010; Schofield et al., 2010) support the idea that social defeat and/or social exclusion increase risk. The paper by Zammit et al. showed this in an elegant way: being different from the mainstream, no matter on what account, increased the subject's risk. The next step is to show that social exclusion has an impact on an individual's dopamine function. My group is examining this in young adults with an acquired hearing impairment, using SPECT.

References:

Zammit S, Lewis G, Rasbash J, Dalman C, Gustafsson J-E, Allebeck P. Individuals, schools, and neighborhood: a multilevel longitudinal study of variation in incidence of psychotic disorders. Arch Gen Psychiatry. 2010 Sep;67(9):914-22. Abstract

Wicks S, Hjern A, Dalman C. Social risk or genetic liability for psychosis? A study of children born in Sweden and reared by adoptive parents. Am J Psychiatry. 2010 Oct;167(10):1240-6. Epub 2010 Aug 4. Abstract

Schofield P, Ashworth M, Jones R. Ethnic isolation and psychosis: re-examining the ethnic density effect. Psychol Med. 2010 Sep 22:1-7. Abstract

View all comments by Jean-Paul Selten

Related News: Research Roundup —The Tapestry of Environmental Influences in Psychosis

Comment by:  Chris Carter
Submitted 26 November 2010
Posted 26 November 2010
  I recommend the Primary Papers

I have been collecting diverse references for environmental risk factors in schizophrenia at Schizophrenia Risk Factors. These include many prenatal influences due to maternal infection, usually with some sort of virus, or immune activation with fever. Several animal studies have shown that infection or immune activation in mice can produce schizophrenia-like symptoms in the offspring. Toxoplasmosis has often been cited as a risk factor in adulthood.

Many of the genes implicated in schizophrenia are also involved in the life cycles of these pathogens, and interactions between genes and risk factors can together contribute to endophenotypes; for example, MICB and Herpes simplex infection have single and combined effects on grey matter volume in the prefrontal cortex.

Over 600 genes have been associated with schizophrenia. When these were pumped through a Kegg pathway analysis, the usual suspects (neuregulin, dopamine, and glutamate pathways, among others) figure highly in the list of pathways. Immune-related pathways are also highly represented, as are many pathogen entry pathways, including that for toxoplasmosis, which heads the list. Some of the more exotic pathways, for example, Chaga’s disease, should be considered as generic, as well as specific.

These Kegg-generated data suggest that there are strong relationships between genes and risk factors. Perhaps stratification of GWAS data in relation to infection could take this into account.

References:

Bortolato M, Godar SC. Animal models of virus-induced neurobehavioral sequelae: recent advances, methodological issues, and future prospects. Interdiscip Perspect Infect Dis . 2010 Jan 1 ; 2010():380456. Abstract

Carter CJ. Schizophrenia susceptibility genes directly implicated in the life cycles of pathogens: cytomegalovirus, influenza, herpes simplex, rubella, and Toxoplasma gondii. Schizophr Bull . 2009 Nov 1 ; 35(6):1163-82. Abstract

Fatemi SH, Emamian ES, Kist D, Sidwell RW, Nakajima K, Akhter P, Shier A, Sheikh S, Bailey K. Defective corticogenesis and reduction in Reelin immunoreactivity in cortex and hippocampus of prenatally infected neonatal mice. Mol Psychiatry . 1999 Mar 1 ; 4(2):145-54. Abstract

Fatemi SH, Pearce DA, Brooks AI, Sidwell RW. Prenatal viral infection in mouse causes differential expression of genes in brains of mouse progeny: a potential animal model for schizophrenia and autism. Synapse . 2005 Aug 1 ; 57(2):91-9. Abstractx

Ozawa K, Hashimoto K, Kishimoto T, Shimizu E, Ishikura H, Iyo M. Immune activation during pregnancy in mice leads to dopaminergic hyperfunction and cognitive impairment in the offspring: a neurodevelopmental animal model of schizophrenia. Biol Psychiatry . 2006 Mar 15 ; 59(6):546-54. Abstract

Prasad KM, Bamne MN, Shirts BH, Goradia D, Mannali V, Pancholi KM, Xue B, McClain L, Yolken RH, Keshavan MS, Nimgaonkar VL. Grey matter changes associated with host genetic variation and exposure to Herpes Simplex Virus 1 (HSV1) in first episode schizophrenia. Schizophr Res . 2010 May 1 ; 118(1-3):232-9. Abstract

Yolken RH, Torrey EF. Are some cases of psychosis caused by microbial agents? A review of the evidence. Mol Psychiatry . 2008 May 1 ; 13(5):470-9. Abstract

Zuckerman L, Weiner I. Maternal immune activation leads to behavioral and pharmacological changes in the adult offspring. J Psychiatr Res . 2005 May 1 ; 39(3):311-23. Abstract

View all comments by Chris Carter