Serotonin Hypothesis of Autism: Implications for Selective Serotonin Reuptake Inhibitor Use During Pregnancy.

Serotonin Hypothesis of Autism: Implications for Selective Serotonin Reuptake Inhibitor Use during Pregnancy.

Autism Res. 2013 Mar 14;
Harrington RA, Lee LC, Crum RM, Zimmerman AW, Hertz-Picciotto I

Serotonin, a neurotransmitter found throughout the brain and body, has long been of interest in autism. Repeated findings of elevated platelet serotonin levels in approximately one third of children with autism has led some to believe that dysfunctional serotonin signaling may be a causal mechanism for the disorder. Because serotonin is critical to fetal brain development, concerns have arisen regarding prenatal exposure to substances that manipulate serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs). This review examines evidence regarding the serotonin system and autism spectrum disorders (ASD), as well as what the literature has reported thus far on developmental effects of prenatal exposure to SSRIs. Possible mechanisms by which SSRIs could affect the fetus during pregnancy and clinical implications are also discussed. Though the majority of studies conducted in infants and children suggest prenatal exposure to SSRIs does not affect neurodevelopment, interpretation must be tempered given small sample sizes. The only published study that focused on prenatal SSRI exposure and ASD found an increased risk with exposure to SSRIs, especially during the first trimester. Obstacles that will be faced in future research are isolating medication effects from maternal depression and, given the infrequent occurrence of exposure and outcome, obtaining an adequate sample size. Whether serotonin is an etiologic factor in ASD, and what it points to as a marker for subgrouping, remains unclear. Understanding how the development of ASD might be affected by prenatal factors that influence serotonin levels, such as SSRIs, could identify modifiable targets for prevention. Autism Res 2013, ??: ??-??. © 2013 International Society for Autism Research, Wiley Periodicals, Inc. HubMed – depression



Depress Anxiety. 2013 Mar 14;
Berenz EC, Trapp SK, Acierno R, Richardson L, Kilpatrick DG, Tran TL, Trung LT, Tam NT, Tuan T, Buoi LT, Ha TT, Thach TD, Gaboury M, Amstadter AB

BACKGROUND: Predisaster risk factors are related to postdisaster psychopathology even at relatively low levels of disaster exposure. A history of panic attacks (PA) may convey risk for postdisaster psychopathology and has been linked to a wide range of psychiatric disorders in Western and non-Western samples. The present study examined the main and interactive effects of pretyphoon PA and level of typhoon exposure in the onset of posttyphoon posttraumatic stress disorder (PTSD), major depression (MDD), and generalized anxiety disorder (GAD) in a Vietnamese sample of typhoon survivors. METHODS: Typhoon Xangsane interrupted a Vietnamese epidemiological mental health needs assessment, providing a rare opportunity for preand posttyphoon assessments. Hierarchical logistic regression analyses evaluated whether the main and interactive effects of typhoon exposure severity and PA history were significantly related to posttyphoon diagnoses, above and beyond age, health status, pretyphoon psychiatric screening results, and history of potentially traumatic events. RESULTS: PA history moderated the relationship between severity of typhoon exposure and posttyphoon PTSD and MDD, but not GAD. Specifically, greater degree of exposure to the typhoon was significantly related to increased likelihood of postdisaster PTSD and MDD among individuals without a history of PA, above and beyond variance accounted for by pretyphoon psychiatric screening results. Individuals with a history of PA evidenced greater risk for postdisaster PTSD and MDD regardless of severity of typhoon exposure. CONCLUSIONS: Preexisting PA may affect the nature of the relationship between disaster characteristics and prevalence of postdisaster PTSD and MDD within Vietnamese samples. HubMed – depression



Depress Anxiety. 2013 Mar 11;
Ionescu DF, Niciu MJ, Mathews DC, Richards EM, Zarate CA

Anxious depression is a common, distinct clinical subtype of major depressive disorder (MDD). This review summarizes current neurobiological knowledge regarding anxious depression. Peer-reviewed articles, published January 1970 through September 2012, were identified via PUBMED, EMBASE, and Cochrane Library, using the following key words: anxious depression electroencephalography (EEG), anxious depression functional magnetic resonance imaging (fMRI), anxious depression genetics, anxious depression neurobiology, and anxious melancholia neurobiology. Despite a general dearth of neurobiological research, the results suggest that anxious depression-when defined either syndromally or dimensionally-has distinct neurobiological findings that separate it from nonanxious depression. Structural neuroimaging, EEG, genetics, and neuropsychiatric studies revealed differences in subjects with anxious depression compared to other groups. Endocrine differences between individuals with anxious depression and those with nonanxious depression have also been noted, as evidenced by abnormal responses elicited by exogenous stimulation of the system. Despite these findings, heterogeneity in the definition of anxious depression complicates the results. Because exploring the neurobiology of this depressive subtype is important for improving diagnosis, prognosis, and treatment, enrichment strategies to decrease heterogeneity within the field should be employed for future research. HubMed – depression