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Live Discussion Transcript


Posted 8 July 2009

E-mail discussion
Printable version

Live Discussion: The Role of the Social Environment in Psychiatric Research: Outstanding Challenges and Future Directions

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Attendees/Participants

Micki Bresnahan, Columbia University
Brian Chiko, Schizophrenia.com
Natalia del Campo, University of Cambridge
Angela Epshtein, Schizophrenia Research Forum
Paul Fearon, Trinity College of Dublin, Ireland
Carla Gallo, Universidad Peruana Cayetano Heredia
Jan Golembiewski, University of Sydney
James Kirkbride, University of Cambridge
Heather Leutwyler, University of California, San Francisco
Hakon Heimer, Schizophrenia Research Forum
Dana March, Columbia University
Maureen Martin, University of California at Irvine
Huan Ngo, Northwestern University
Sami Omer
Kazuko Sakata, University of Tennessee Health Science Center
Linda Scoriels, University of Cambridge
Jean Paul Selten, Utrecht University
Amresh Shrivastava, University of Western Ontario
Nico Stanculescu, Schizophrenia Research Forum
Wim Veling, Parnassia Psychiatric Institute
Victoria Wilcox, Schizophrenia Research Forum

Note: Transcript has been edited for clarity and accuracy.


Hakon Heimer
In our usual informal spirit, I will just say that Dana March is at Columbia University in the United States, James Kirkbride is at the University of Cambridge in the U.K., and Wim Veling is typing at us from Parnassia Psychiatric Center in The Hague, Netherlands. I thank Dana for bringing us this idea and cajoling James and Vim to join us. I'll now turn the floor over to Dana.

Dana March
Good afternoon. Thanks for joining us and welcome to the SRF live discussion. Our discussion today will focus on three important topic areas in the study of social factors in schizophrenia. We will spend about 20 minutes in each domain, and our hope is to engage you in a lively exchange regarding one of the most stimulating frontiers of research in social psychiatry. First, James Kirkbride will kick off the discussion by addressing intriguing patterns of findings across populations and settings. Second, I will move our exchange into issues of exposure conceptualization and relevant timing over the life course. Finally, Wim Veling will lead us downstream into a discussion of biological mechanisms (e.g., social defeat, gene-environment interactions, and epigenetics).

James Kirkbride
Hello everybody, welcome along—great to see so many people here for the discussion.

I’m going to kick things off with a brief recap of the main epidemiology findings on schizophrenia and other psychoses. This will focus on how these patterns vary (or don’t) between populations and settings. They were mostly covered in the background reading, but I’ll put them in simple numbered form so that we’re all on the same page. Then I’ll ask some questions to kick off the discussion about how we might best proceed in order to reach a better understanding of “social” and environmental risk factors for schizophrenia. Okay, here’s a recap of what the epidemiology tells us:

1. There is variation in the incidence of schizophrenia across the globe. Rates vary between countries, within countries (increasing with urbanicity, including urban birth), and within small areas (even, e.g., within cities—see Faris and Dunham, 1939—and subsequent contemporary followers).

2. No such variation is seen for bipolar disorder.

3. Higher rates of schizophrenia are associated with more marked inequalities in social deprivation—in terms of neighborhood poverty to an extent, but also in terms of social disorganization. Areas with less cohesiveness seem to have higher rates.

4. Rates of all psychotic disorders (schizophrenia and bipolar disorder, e.g.) are increased for immigrants and their offspring (so-called second-generation groups; see SRF related news story and SRF news story).

5. This has been found in the U.K., Netherlands, Sweden, Denmark, and other European countries, and the U.S. (Bresnahan et al., 2007).

6. Raised rates appear highest in immigrants and their offspring when skin color differences between the “background” and “immigrant” populations are greatest—in the U.K., for example, incidence rates are around five to eight times higher in black Caribbean and African immigrants and their offspring than in the white British group, three to four times higher for Asian women (not men), and twice as high for non-British white migrants.

7. The risk of schizophrenia in immigrants and their offspring is not explained by: (a) Selective migration (Selten et al., 2002), (b) higher rates in country of origin, (c) misdiagnosis, or (d) sociodemographic confounds such as age, sex, and ethnicity.

8. Ethnic density phenomenon—the risk of schizophrenia increases in immigrants and their offspring when they live farther away from people of the same ethnic group (i.e., when they are more isolated from their own ethnic group).

Okay, these are the main findings.

Paul Fearon
Beautiful summary, James.

Jan Golembiewski
Anyone, is there a known correlation between schizophrenia incidence and a highly stratified society?

Dana March
Jan, there doesn't seem to be a social gradient, if that's what you mean. It seems that social adversity seems to matter most in early life.

James Kirkbride
Jan, that’s a good question. When we see greater social fragmentation, there appear to be great rates of schizophrenia—see Allardyce's work (Allardyce et al., 2005) or some of my own (e.g., Kirkbride et al., 2007). But not so much on socioeconomic lines, though.

James Kirkbride
Perhaps I can suggest a more general point for discussion to kick things off? One thing that strikes me as a good starting point for discussion is this:

We suspect that there is likely to be interaction between genes and environments (Wim Veling will discuss this in more detail later in the session). At present, our biggest, most replicable environmental “risk factors” are urbanicity and migration/ethnicity. Urbanicity and migration/ethnicity can only be markers for increased risk due to other underlying social variables/constructs. How do we, as academic researchers, go about getting past urbanicity and migration to more specific risk factors?

Paul Fearon
James, concentrate on the differences in trying to untangle the underlying causes—for example, why variation in schizophrenia and not bipolar disorder? Why greater rates in Africans and African Caribbeans than Asians, etc.?

James Kirkbride
Paul, I agree. We shall come to that distinction between schizophrenia and bipolar disorder.

Dana March
James, I wonder if it is useful to think about mediators of these effects in terms of two broad classes of the physical (e.g., infections, toxins) and the social (crowding, composition).

Jan Golembiewski
James and all, there are conditions when a social group in one country receives little social status, but the same group—with similar social behaviors—receives high status in another. Take Indians, for example. In Australia and most of Africa, they are highly respected; in Europe, they aren’t. In the U.S., even less.

Dana March
Jan, this is true for black Caribbeans. They have higher social status in the U.S. than in the U.K.

James Kirkbride
Jan, I'm not sure if this is true across the whole of Europe. There have been some issues to do with this in the U.K., but Indian groups are fairly well integrated and respected in the U.K. relative to other groups. The more general point is interesting, though. Relativity seems to hold the key to much social research; context mediates individual risk.

Wim Veling
Dana, about social aspects, Jan may be right that social hierarchy is important.

Jan Golembiewski
Misplacement creates conditions of taboo. Mary Douglas (Douglas, 1966. Purity and Danger. New York: Routledge) posits a general rule that applies equally to inanimate objects as to social dynamics. Bolognaise is clean, acceptable, and welcome in its proper place—that is, on a dinner plate on top of spaghetti—but is not okay on the floor or on my tie. Curiously, misplacement is an intrinsic condition of second-generation immigrants.

Dana March
Wim, Jan, agreed. Social hierarchy may be important, but why? Because of discrimination? How might primate models be useful here?

Wim Veling
All, we know the hypothesis of Jean Paul Selten about social defeat (Selten and Cantor-Graae, 2007; Selten and Cantor-Graae, 2005) which tries to integrate findings on urbanicity and migration.

James Kirkbride
Dana, is there much robust evidence for physical factors (toxins, etc.) at present? We seem to have moved toward a more social hypothesis in recent years.

Dana March
James, I think it may vary across groups and settings. The physical aspects have received far less attention, because data (exposure in utero might be really important) are hard to come by.

James Kirkbride
Dana, I agree. I would suspect that the "physical" aspects of environment would have their greatest effects close to birth (prenatally or in the first few years of life). This, of course, makes them very difficult to study.

Micki Bresnahan
James, maybe it would be useful to discuss what we know about timing.

James Kirkbride
Micki, we will come to timing later in the second half of the debate.

Wim Veling
Dana, there is some preliminary evidence (Pedersen, 2004) that air pollution may be related to schizophrenia incidence.

Dana March
Wim, yes, that's another super difficult exposure to measure. But agreed—intriguing findings.

Paul Fearon
Wim, although pollution and other environmental exposures may be plausible candidates for the increased urban incidence, what physical exposure could account for the markedly raised migrant rates in urban settings?

Jan Golembiewski
Wim, I find the social complexity and lack of integration theory more plausible than air pollution, but I know the pollution theory was explored by David Halpern (Halpern, 1995. Mental Health and the Built Environment. London U.K.: Taylor and Francis).

Sami Omer
Hello everybody. What strikes me is that social deprivation has usually been linked to urbanicity. If deprivation per se had a role, one would expect much higher rates in developing countries.

Jan Golembiewski
Sami, developing countries often (usually) have tight-knit and highly supportive social structures; developed countries don't. In Nigeria, there is no granny dumping; it is a Western phenomenon. The same might be true for those suffering the stress of onset schizophrenia.

Wim Veling
Sami, that also relates to developing countries, because most people share the deprivation.

James Kirkbride
Sami, it's an interesting point. What seems to be true here is that there are possibly different directions to such findings at different levels. For example, take treatment. Treatment with antipsychotics is generally accepted to improve the positive symptoms of psychosis (based on Western medicine), yet there is evidence that course and outcome are better in the developing countries—so what appears to operate in one direction at the individual level may operate in a different direction at the national level.

James Kirkbride
Sami, but I also believe that socioeconomic deprivation per se is probably not a "risk factor" for psychosis. It is probably something more on the lines of relative deprivation or factors correlated with this. The ethnic density effect is one such example. Perhaps there is also a relative deprivation effect?

Sami Omer
Indeed, one would also expect rates of schizophrenia to drop by a significant level with improvement in socioeconomic conditions, similarly to rheumatic heart disease.

Jan Golembiewski
James, one of the ideas I have attempted to study is the variance of texture as visual stimulus, in varying milieu. In some places, white textureless surfaces are normal; in others, they are abnormal. These textures give depleted sensory functions something to process.

Dana March
Okay all, so I would like to start the thread regarding exposure conceptualization and timing of exposure.

We were headed in that direction. With urbanicity, the relevant timing of exposure seems to be at birth (proxy for in utero exposures?), with the effect diminishing markedly after age 15.

Wim Veling
Dana, the same for cannabis: It also has the largest effect when people use it before they are 15. We are working on analyzing age at migration; it might be that those immigrants who migrate at a younger age have higher risk.

Dana March
With the most recent findings on ethnic density (Boydell et al., 2001; Kirkbride et al., 2008; Veling et al., 2008), the exposure was measured at first contact. Is it possible that ethnic density is protective earlier in life, around the transition to adulthood, etc.?

Without systematic data across the life course, it is difficult to know. To understand the relevant timing of exposure would help us eventually to target interventions.

Victoria Wilcox
Dana, speaking of the life course, would it be useful to look at the second peak in incidence in women that occurs later in life and how that might relate to environmental factors?

Dana March
Victoria, that's a really interesting suggestion. Age of onset may be critical in unraveling some of these patterns.

James Kirkbride
Dana, timing around adolescence might be important. This is often a time when we are exploring social contacts, developing peer relationships, and so forth, so perhaps ethnic density at this time has strong effects. I am not sure how it would relate closer to birth.

Dana March
James, that's my hunch as well. I wonder, however, if it might be helpful in buffering the moms from discrimination when they are pregnant, thus bearing on a stress cascade that would otherwise be harmful. We can set up competing hypotheses to figure it out.

Micki Bresnahan
James, adolescence may be the time when the developmental deviation begins to become apparent, even if it was there before.

James Kirkbride
Micki, yes, that's a good point. You are suggesting that these factors have been present from a much earlier period but only become manifest at the time of adolescence? Dana/Wim, this raises the timing issue more generally. Is it likely that the critical timing points for exposure to social factors are around the periods of critical development, both biologically speaking and socially speaking?

Dana March
I agree that we need studies aimed at critical and sensitive periods in social development.

Paul Fearon
James et al., I agree. But I think it’s important to conceptualize this as multiple critical periods (which, socially, might differ between cultural groups).

James Kirkbride
Paul, this is a good point. There is considerable difference by cultural group in terms of the structure of family environments, and such differences may have more pronounced effects in some groups than others on later risk of psychosis—particularly, for example, if the family unit is more fragmented, and there is less familial support around. This is difficult to measure, though, and would require longitudinal data. Does AESOP (Aetiology and Ethnicity of Schizophrenia and Other Psychoses) have much familial data?

Paul Fearon
James, I agree. I was also thinking in terms of age. Regarding family data, they’re limited. Jane Boydell is looking at relatives in the follow-up.

Jan Golembiewski
James, the data exist, naturally as we look from country to country. Surely, it isn't latitude and longitude that create variability.

James Kirkbride
Jan, sorry, I don't understand. I think we can make more use of data available across different settings. Presumably, there is an underlying latent construct that we are trying to measure across these settings even if the specific "exposures" we are attempting to measure are different.

Jan Golembiewski
James, in Australia, the media-projected perception that schizophrenics are evil killers is listed as the number one stigma for sufferers. It occurs late, but it may well have a place in the vicious circle. Dana, we should buffer everyone from discrimination!

Dana March
Jan, agreed. The issue is that discrimination assumes many forms, which is a nice segue into conceptualization of exposure. It's a multilevel concept. At the area level, we deal with both structural and interpersonal discrimination.

Micki Bresnahan
There is a loose use of "social." We have "social" exposures, individual "social" development, and socially structured exposures that may or may not be social. Dana, are you convinced that social development is only shaped by social interaction/factors?

Jan Golembiewski
Micki, I doubt it. Social acceptance is a very complex thing that relates to every aspect of life including eye color.

Dana March
Micki, I think it's also heavily materially influenced (which is a social factor in many senses). I have a broad conception of what social factors are. Perhaps we need better construct refinement and common terms to reshape our research agenda.

Micki Bresnahan
Yes, this is what I am suggesting.

Dana March
Micki, could you be more specific?

Micki Bresnahan
External social factors (that are inherently social in nature) should be different from external factors that are socially structured (e.g., the difference between discrimination and poor housing).

Internal development—developing social skills—that should be shaped by both internal capacities and faculties as well as external exposures (family, peer, society).

Amresh Shrivastava
What really are the constituents of “social factors”? It’s an ill-defined concept that encompasses everything non-biological.

Dana March
Amresh, this is the problem!

Amresh Shrivastava
Yes, but it can certainly be looked at differently. I call all non-biological factors “ecological” and think these factors may have collective influence.

James Kirkbride
Amresh, agreed. We need to be thinking more carefully about "social" exposures and specifying at which level they occur and when (with a priori reasoning) over the life course they may be relevant.

Dana March
Amresh, Micki, I think it would be productive to have a working group to come to some consensus to set our research agenda in terms of priorities.

Amresh Shrivastava
I think the real name would be “environmental factors”—that means factors like developmental, family, cultural, etc. Yes, we need to think about it clearly.

Wim Veling
Amresh, James, we have plenty of ideas of social exposures (fragmentation, exclusion, family structures, etc.). We only need to explain properly what we mean.

Micki Bresnahan
If you think of social development qua autism, the necessity of making these distinctions becomes clear.

Dana March
Micki, yes! Also, another related question: Do "social factors" also bear on the distribution of psychotic symptoms, and at what age do they appear? I’m thinking of Kristen Laurens' recent paper (Laurens et al., 2008).

Amresh Shrivastava
Like childhood abuse, humiliation, violence, deprivation, etc., affects neurotransmitters? Don’t you think it needs clear quantification and measurement to make a statement?

James Kirkbride
Wim, presumably, see comment above to Jan, they are tapping into one or more common underlying latent traits—stress response to adverse life events/environments at critical periods.

Micki Bresnahan
If the consequence of early exposures (of any external variety) is on the development of social skills in the individual....

Amresh Shrivastava
How then do we explain that many who suffer similar stressful conditions do not develop psychopathology?

Hakon Heimer
Amresh, I think we can chalk it up to differential genetic make-up plus all environmental exposures up to that point.

Jan Golembiewski
Amresh, could it not be something as simple as thought patterns? And how people as individuals cope or rather break down when exposed to stress?

Dana March
James, Wim, I think we are headed toward talk of mechanisms—but how can we get there when we have such crude exposure measurements? One way to move forward is to take the study of the upstream social pathways as seriously as the biological pathways. And Micki, we meet somewhere in between with individuals and groups.

Wim Veling
All, we should study different environmental aspects at different points in the lifetime. During pregnancy: factors related to brain development; during childhood and adolescence: social development, cannabis, etc. Then we can include both biological and social factors, because we know better which aspect we are studying.

James Kirkbride
Micki, it is possible that there are early life insults, which set you off on a life-course trajectory, which increases the probability of further negative events—possibly leading to processes such as sensitization. In other words, early life insults may lead to a self-perpetuating cascade of ever increasing deleterious environments, thus culmulating in increased risk of psychosis?

Micki Bresnahan
That is what I am thinking.

Dana March
James, an excellent point. What are the trajectories and turning points?

James Kirkbride
Dana, turning points? Not sure. What about familial and neighborhood-level social support/cohesion as a potential buffer for some individuals against these environments? I also agree with you that we struggle from a theoretical base to define our constructs, which limits our ability to measure them.

Wim Veling
James, exactly. Sensitization of the dopamine system is a useful paradigm.

James Kirkbride
Wim, yes, dopamine sensitization is a candidate mechanism, but there are also others.

Amresh Shrivastava
Yes, but these need to be well established. How do we find out biological correlates of social brain insults?

Wim Veling
All, we are already talking about a mix of genes, environment, biological factors. However, there are some complicated issues:

1. There are no consistent findings of genes related to schizophrenia.

2. But we know that 80 percent of schizophrenia "is determined" by genes—this includes GxE (gene-environment) interactions. 3. To advance research, we need to think of a priori specified hypotheses, studying well-specified genes in relation to functions, for example, stress-related genes, or genes involved in dopamine metabolism.

Micki Bresnahan
Wim, I believe that this figure is considered inflated.

Amresh Shrivastava
Yes, it is—very much.

Dana March
Wim, and what about epigenetics?

James Kirkbride
Micki, Wim, me, too—particularly to start with as it includes GxE. It must contain an element of E.

Amresh Shrivastava
Is social cohesion a buffer against psychosis, then?

James Kirkbride
Amresh, it is surely a possibility. Neighborhoods with less social disorganization show lower rates of schizophrenia.

Dana March
James, in other words, are some people on the path to psychosis, and are prevented from reaching that point, or vice versa; something sets them off course developmentally? I think the old distinction of predisposing/precipitating is useful here.

Jan Golembiewski
Amresh, from what I understand all the components that make up the aetiology of schizophrenia are found in normal controls. Even voices are heard by 10-15 percent of normal people. It is how this escalates that seems to be problematic—and these “patterns” are likely set up in early life.

Amresh Shrivastava
Do we have any data on gene expression under social stress? Is there a common pathway for all social stress which affects brain biology?

Micki Bresnahan
It may be that studying a metabolic pathway would be more useful. That allows for multiple genes to influence the same outcome.

Dana March
Wim, do you feel like we are moving down the functional road, as opposed to "finding the gene for schizophrenia"?

Wim Veling
Dana, yes, we should focus more on function, not on the Holy Grail of the cause of schizophrenia.

Paul Fearon
Wim, I agree. I'd go as far as to say that with so many different potential exposures, we may never find the “cause” of schizophrenia!

Victoria Wilcox
Amresh, do we even know that social stress is the kind of stress that matters for schizophrenia? Could it be physical stress (e.g., malnutrition, lack of health care) that's responsible for variations in schizophrenia incidence across time, place, and group?

Amresh Shrivastava
Is that neurohormone mediated?

James Kirkbride
Dana, yes, agreed; the distinction between precipitating and predisposing is key. There are developmental trajectories (though subtle) (see Jones et al., 1993; Jones et al., 1994), but presumably, I agree; there must exist "turning points," which could steer you toward or away from schizophrenia—such as the decision to start smoking pot.

Amresh Shrivastava
Maybe yes, you are right. The data are always overstretched in this context.

Wim Veling
Amresh, there are examples from animal research that relate social stress to changes in dopamine system as in schizophrenia patients.

Amresh Shrivastava
I suggest we have an e-mail group to continue our discussion. Bye for now.

Dana March
Wim, whew! How do we join forces productively with geneticists? The E is usually e in GxE investigations. Paul, Wim, we could take a note from Geoffrey Rose here and the folks who study social inequalities as well: The causes of cases are not necessarily the causes of rates.

James Kirkbride
Dana, I think there are increasing numbers of groups of G researchers taking E more seriously. The failure of large main effects of G has helped in this regard. I agree with Wim that we need very careful thought as to putative GxE—i.e., what is theoretically grounded rather than just launching ourselves in.

Jan Golembiewski
Paul, Dr. Humphrey Osmond (Osmond, 1966. Some Psychiatric Aspects of Design. In LB Holland [Ed.], Who Designs America? Garden City, NY: Anchor, pp. 281-318) and ET Hall (Hall, 1975. Mental health research and out of awareness cultural systems. In L Nader and TW Maretzki [Eds.], Cultural Illness and Health. Washington, DC: American Anthropological Association, pp. 97-103) both claimed that schizophrenia was always associated with a retardation of perceptual ability.

Hakon Heimer
James, any way (plans?) to look at genetic variation in genes that code for HPA (hypothalamic-pituitary-adrenal) axis proteins in the AESOP population?

James Kirkbride
Hakon, maybe this is a question better targeted at Paul; he is involved in the AESOP follow-up. I don't know the answer, I'm afraid!

Wim Veling
Paul, no, but we should use the genetic knowledge we have to go further. For instance, on stress sensitivity and COMT gene differences, Jim van Os's group has found some interesting things (Simons et al., 2009; van Winkel et al., 2008; Stefanis et al., 2007). Or expression of pro-inflammatory genes, influenced by infectious agents or stress, etc.

James Kirkbride
Wim, do we believe in COMT? It is on shaky ground among most geneticists (though acknowledged, an absence of main effects should not preclude interactions).

Dana March
James, Wim, I'm not a COMT believer, but I could be converted with evidence.

Wim Veling
James, COMT is an example; if that is out of date, we should study BDNF or whatever more convincing candidate.

Dana March
Lauren Ellman at Columbia is doing really interesting work with cortisol and stress during pregnancy in our schizophrenia cohort in the U.S.

Wim Veling
All, my main point is that there are several interesting biological pathways, of which we know part of the biological chain. We should relate that to our environmental knowledge. Geneticists cannot do that.

Paul Fearon
Jan, we are collecting DNA in the AESOP sample. Robin Murray and others are more up to speed regarding what plans they have for it. I know that Carmine Pariatne has an interest in the pituitary and found increased pituitary volume in the AESOP sample.

Hakon Heimer
Paul, Dana, I wondered if genetic variation in the Afro-Caribbean population might show up.

Paul Fearon
Hakon, in what sense?

James Kirkbride
Hakon, Paul, an interesting, tantalizing finding which needs careful (very careful) handling, but it’s important to address genetic variation by ancestry.

Dana March
James, tricky!

James Kirkbride
Dana, agreed.

Dana March
James, how would you see such research proceeding?

James Kirkbride
Dana, with care! We have these "threads" of clues, and we should follow them—as is Wim's point more generally; take the genetic clues and think theoretically about which would hold up to interaction with environmental stimuli. Dana, a more fully fledged answer: I am not sure. But we do know that the val/val genotype has a higher prevalence in black Caribbean populations than others. I think some brave funders and researchers are, at some point, going to have to dispassionately address such issues. We are dealing with an incredibly complex set of disorders with complex aetiology, an aetiology that doesn't stop when it meets political sensitivity.

Paul Fearon
James, I agree absolutely.

Dana March
James, but potentially—then onto manic psychosis—we could impact policy in a very positive way, if we learn our lessons from history well.

James Kirkbride
Dana, yes. I need to think about this more than time here allows. Paul, thanks. Sorry we didn't get a chance to come back to this: I wonder whether the findings that schizophrenia is associated with urbanicity may be partially confounded by parental cognitive ability. We know cognition differs between schizophrenia and bipolar disorder. Since it is a heritable trait, perhaps this explains drift to poorer areas for schizophrenia but not bipolar disorder.

Dana March
James, you raise a good point about urbanicity and parental cognitive function.

Paul Fearon
James, maybe. It’s certainly plausible. I can’t help but feel (or maybe I just want to feel) that it’s something more fundamental.

James Kirkbride
Paul, how do you mean more fundamental? Do you mean there is a causative role of the social environment? Despite my parental cognitive function hypothesis, I think there is room for both social drift and cause—mutually reinforcing processes?

Dana March
James, Mark Weiser (Weiser et al., 2007) has looked at diminished cognitive function and urbanicity, though not in the parents.

Jan Golembiewski
Veling, James, do these genes have any other more observable expressions other than increased chance at schizophrenia, such as color blindness or short-sightedness?

Wim Veling
Jan, yes, we know that they are involved in regulation of different brain processes.

Hakon Heimer
Paul, unexpected population difference in common gene SNPs (single-nucleotide polymorphisms) of Afro-Caribbeans or Africans in genes that code for possible mediators of "environmental" stress? Or is that too naive an experimental question? All, we're about five minutes from the official end (though the room is open, and we encourage loitering). Any final statements?

Paul Fearon
We didn't get a chance to come to it, but I think James's findings of lack of variation for manic psychosis is fascinating and needs explanation.

Jean Paul Selten
All, I think it would be useful if we remind the scientific community that the heritability index is so misleading. The misinterpretation of this index is the reason why all the money goes to the geneticists. They will not remind the community of this.

Hakon Heimer
All, any ideas for large-scale collaborations that could be initiated/encouraged?

Dana March
Hakon, "Desperately Seeking Cross-national Collaborators!" We should harmonize studies where possible. The NIH (National Institutes of Health) is putting cash into this!

Wim Veling
Hakon, Dana, we need to get consensus about which E and which G to study, to define priorities. Collaboration is desperately needed, indeed!

James Kirkbride
Paul, how do you mean more fundamental? Do you mean there is a causative role of the social environment? Despite my parental cognitive function hypothesis, I think there is room for both social drift and cause—mutually reinforcing processes?

Jan Golembiewski
James, I find the observation that schizophrenia patients are less likely to develop cancer a really curious one. Any word?

James Kirkbride
Jan, variation exists in a variety of disorders by a variety of sociodemographic markers; such is the rich heterogeneity of populations. I can't comment with specific reference to cancer as I don't know the literature well enough.

Kazuko Sakata
Wim and Hakon, Dr. Sklar's group published the population genetic study of BDNF Val/Met over the world (Petryshen et al., 2009). I think this kind of study is necessary for future studies to determine the genetic factor.

Wim Veling
Kazuko, thank you, good example.

Victoria Wilcox
James, is there any reason to believe that Asians might have a gene that buffers against migration/ethnicity effects?

James Kirkbride
Victoria, no, but I am not convinced the rate in Asians is as low as commonly suggested. Excess in Asian women in Coid's East London sample was five times that of white British women. It could be differential social support rather than genetics that makes the difference—there may be many cultural differences between Asian women and men in the U.K. to explain these findings.

Jan Golembiewski
James, Asian women in London often have extreme stress but often lack the social support they had at “home.”

James Kirkbride
Jan, this is one working hypothesis we should test. It is possible that Asian women lose the social support they had in their country of origin and may occupy a more marginal place in the U.K. Jan, they are more first-generation—see our paper (Coid et al., 2008).

Jan Golembiewski
James, it would be very interesting to see if those women are more first-generation or second. They could have married into migration, so to speak, and live with impossible in-laws.

Dana March
All, we do need to think about how people come to be in places in which they are exposed. In much the same way that we're interested in migration, geographic and social mobility are key.

James Kirkbride
Dana, I think it has to be in parents because of the urbanicity at birth and later risk of schizophrenia effects. I have read the Weiser paper, though.

Dana March
James, do you know of any data to test directly?

James Kirkbride
Dana, no, sadly not. I’d like some, though! Do you know of any? It’s possible to do in birth cohorts, I think, but N becomes the issue.

Dana March
All, another important issue to study is the multiple disadvantaged roles occupied by migrants and ethnic minorities.

James Kirkbride
Dana, yes, agreed.

Paul Fearon
Everyone, I’ve got to go. James, yep, I agree there's room for drift and cause. I’m just hoping there's some cause there, too. Cheers, all!

Dana March
Happy St. Pat’s, Paul.

Hakon Heimer
Thanks to everyone for coming.

Angela Epshtein
Thank you and bye.

Micki Bresnahan
Thank you for the lively conversation!

Jan Golembiewski
Thanks, everyone.

Sami Omer
Enjoyed the discussion; thanks all.

James Kirkbride
Micki, thanks! You kept us grounded, to an extent.

Wim Veling
Thanks, everyone!

Dana March
Yes, thanks, everyone, for an interesting exchange!

James Kirkbride
Thanks, all.

Hakon Heimer
Dana, James, Wim, thanks so much for preparing the text and leading us.

Victoria Wilcox
Nice chatting!

Dana March
Thanks Hakon, Nico, for a great resource!

Nico Stanculescu
And thank you, Dana!

James Kirkbride
Yeah, Dana, Wim, Nico, Hakon—thanks, all.

Dana March
Signing off, all. See you soon in the virtual world or otherwise....

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