These observations suggest that the voice-hearing experiences of people with serious psychotic disorder are shaped by local culture. These differences may have clinical implications.

This study compares 20 subjects, in each of three different settings, with serious psychotic disorder (they meet inclusion criteria for schizophrenia) who hear voices, and compares their voice-hearing experience. We find that while there is much that is similar, there are notable differences in the kinds of voices that people seem to experience. In a California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in our West African sample, they were more likely to describe them as morally good and causally powerful. What we think we may be observing is that people who fall ill with serious psychotic disorder pay selective attention to a constant stream of many different auditory and quasi-auditory events because of different "cultural invitations"-variations in ways of thinking about minds, persons, spirits and so forth. Such a process is consistent with processes described in the cognitive psychology and psychiatric anthropology literature, but not yet described or understood with respect to cultural variations in auditory hallucinations. We call this process "social kindling."

Gene polymorphisms of the 3' untranslated region (3'-UTR) of the dopamine transporter (DAT1), Dopamine receptor exon 3 D4 variable number tandem repeat (DRD4VNTR), nicotinic acetylcholine receptor alpha 4 subunit (CHRNA4) and serotonin transporter promoter (SLC6A4-5HTTLPR) are under consideration as potential risk factors for attention-deficit/hyperactivity disorder (ADHD). A post-hoc attempt was made to investigate the association between the allelic variations of these candidate genes and retrospective parental report of response to methylphenidate in an ADHD-enriched, population-based twin sample. Subjects (N = 243) were selected from the twin sample based on parent report that the child had been treated with methylphenidate for ADHD symptoms. The functional polymorphisms screened were the VNTR located in the 3'-UTR of the dopamine transporter, DRD4 VNTR, CHRNA4 (rs1044396 and rs6090384) and the long (L(A) and L(G)) and short (S) forms of the serotonin transporter promoter region. Logistic regression did not demonstrate a significant association between methylphenidate treatment response and the relevant polymorphisms. The sample size had high power to detect effect sizes similar to those reported in some prior methylphenidate pharmacogenetic studies; however, the categorical (yes/no) measure of parent-reported treatment response may not have been sensitive enough to pick up statistically significant differences in treatment response based on genotype. Further studies including quantitative measures of treatment response are warranted.