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To what extent this reflects biology isn’t understood fully. There is a more fundamental issue here: how do we see genetic variation in general leading to phenotypes. Is it linear? Is it pleiotropic? When we analyse the data how do we take this into account? I think we need a more sophisticated analysis, but I’m a psychiatrist and I need a mathematician to help here. Lee: I am just trying to find a positive spin on this! To increase effect size, could you use drug responses as a readout? Flint: Pharmacogenomics.

Raff: I’d like to carry on this discussion but change it a bit to consider candidate gene approaches. If you had some clue about the neurobiological basis of narcissism, for example, you could sequence candidate genes in affected individuals in multiplex families. This approach has been useful in autism. Is the future to try to move the neurobiology to a point where you could sensibly choose such candidate genes? Flint: I’ll be positive about whole gene association studies: they will work. They won’t deliver everything.

Akil: A compromise vision of where we might go is the neuroscience parallel of systems biology that people talk about at the cellular level in other fields. These involve cascades of signalling events. We haven’t said much about the genetics of tuning circuitry. Take the caspase study: what this tells us is that some people have differential stress vulnerability, so it is the genetics of their stress system that is being inherited. But there are many ways that you can fi ne-tune stress responsiveness, neuronally, developmentally and genetically.

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