Genetic and environmental influences on psychiatric comorbidity: A systematic review

Abstract

Background The purpose of this review is to systematically appraise the peer-reviewed literature about the genetic and environmental determinants of psychiatric comorbidity, focusing on four of the most prevalent types of psychopathology: anxiety disorders, depression, conduct disorder and substance abuse. Methods We summarize existing empirical research on the relative contribution that genetic, nonshared and shared environmental factors make to the covariance between disorders, and evidence about specific genes and environmental characteristics that are associated with comorbidity. Results 94 articles met the inclusion criteria and were assessed. Genetic factors play a particularly strong role in comorbidity between major depression and generalized anxiety disorder or posttraumatic stress disorder, while the non-shared environments makes an important contribution to comorbidity in affective disorders. Genetic and non-shared environmental factors also make a moderate-to-strong contribution to the relationship between CD and SA. A range of candidate genes, such as 5HTTLPR, MAOA, and DRD1-DRD4, as well as others implicated in the central nervous system, has been implicated in psychiatric comorbidity. Pivotal social factors include childhood adversity/ life events, family and peer social connections, and socioeconomic and academic difficulties. Limitations Methodological concerns include the use of clinical case-control samples, the focus on a restricted set of individual-level environmental risk factors, and restricted follow-up times. Conclusions Given the significant mental health burden associated with comorbid disorders, population-based research on modifiable risk factors for psychiatric comorbidity is vital for the design of effective preventive and clinical interventions.

Meta‐analysis argues for a female‐specific role of MAOA‐uVNTR in panic disorder in four European populations

“…The human gene encoding MAO-A (MAOA) maps to chromosome Xp11.4-p11.23 [Levy et al, 1989] and since long has been suggested to be involved in mental disorders [Haavik et al, 2008;Cerda et al, 2010;Nordquist and Oreland, 2010]. Two functional null mutants go along with respective phenotypes: Norrie's disease, the result of a X-chromosomal deletion including monoamine oxidase A (MAOA), causes mental retardation, autistic behavior, and motor hyperactivity [Halpin et al, 2005;Dickinson et al, 2006], while Brunner's syndrome (which is due to a stop mutation in the MAOA gene) goes along with violent and criminal behavior [Brunner et al, 1993].…”

Understanding Psychiatric Comorbidities and Addictions

“…The most highly cited twin research on comorbidity now is from Kendler and colleagues, who found evidence that drug use disorders seem to have disorder-specific genetic risks, whereas externalizing disorders (e.g., conduct disorder; adult antisocial behavior) are more subject to influences of shared environment. Overall, lifetime comorbidity patterns are judged to arise largely due to background genetic influences (Kendler, Prescott, Myers, and Neale, 2003); Cerdá, Sagdeo, Johnson, and Galea (2010) recently have drawn attention to exceptions. Methodological concerns will be discussed in later sections of the chapter.…”

Changes in Gene Expression Profiles in Adult Rat Brain Structures after Neonatal Action of Dipeptidyl Peptidase-IV Inhibitors

“…Gene expression changes can be moderators of such processes [2, 3]. Comorbidity of depression, anxiety, and increased aggressiveness, which is frequently observed in the clinic [4], give grounds for assuming the existence of common genetic risk factors for the development of these psychopathological manifestations [5, 6]. However, despite significant advances in the study of the genetic basis of anxiety and depression in recent years [7-9], much remains unclear.…”