In This Issue

A suicide attempt by a depressed woman registered to use medical marijuana for pain highlights the risk of psychiatric complications from the rapidly increasing legal use of marijuana. Nussbaum et al. (p. 778) describe marijuana's relationships to psychotic disorders, depression, impulsivity, and suicidality. Widespread use in the United States began in 2009, when the federal government announced it would not prosecute users of medical marijuana where it has been legalized at the state level. These jurisdictions include the District of Columbia and 14 states, including Colorado, where the suicidal woman lived. Approximately 2% of Colorado's population were registered for medical marijuana in 2010, and physicians there are not required to examine people applying for registration.

Two independent studies focusing on distinct subgroups of patients with major depressive disorder both showed linkage of the disorder to chromosomal region 3p25-26. Breen et al. (p. 840) found the association among 839 families containing pairs of siblings both affected by severe, recurrent major depression. The linkage discovered by Pergadia et al. (p. 848) emerged from sibling pairs with major depression in 95 families of heavy smokers. The identified region contains a glutamate-regulating gene and other genes that are plausible for involvement in depression. The review by Hamilton (p. 783) illustrates the overlap of these linkage results with findings in two earlier genome-wide association studies.

Extended studies tracking outcomes in people infected with Toxoplasma gondii and in a group exposed to herpes simplex virus 1 (HSV1) bolster the evidence for associations of these infections with schizophrenia. In a cohort of 45,609 women in Denmark, Pedersen et al. (p. 814) demonstrated that T. gondii infection increased the risk for subsequent development of schizophrenia spectrum disorders. Prasad et al. (p. 822) documented losses over 1 year in executive functioning and posterior cingulate gyrus volume in HSV1-positive patients with schizophrenia but not in seronegative patients or HSV1-seropositive or -seronegative subjects without schizophrenia. Connections between schizophrenia and environmental factors are especially promising, notes Brown in an editorial (p. 764), because many of these exposures are preventable or treatable.