scholarly journals Non-Genetic Factors in Schizophrenia

2019 ◽  
Vol 21 (10) ◽  
Author(s):  
Simona A. Stilo ◽  
Robin M. Murray

Abstract Purpose of Review We review recent developments on risk factors in schizophrenia. Recent Findings The way we think about schizophrenia today is profoundly different from the way this illness was seen in the twentieth century. We now know that the etiology of schizophrenia is multifactorial and reflects an interaction between genetic vulnerability and environmental contributors. Environmental risk factors such as pregnancy and birth complications, childhood trauma, migration, social isolation, urbanicity, and substance abuse, alone and in combination, acting at a number of levels over time, influence the individual’s likelihood to develop the disorder. Summary Environmental risk factors together with the identification of a polygenic risk score for schizophrenia, research on gene–environment interaction and environment–environment interaction have hugely increased our knowledge of the disorder.

2008 ◽  
Vol 11 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Toos C. E. M. van Beijsterveldt ◽  
Dorret I. Boomsma

AbstractA consistent finding from twin studies is that the environment shared by family members does not contribute to the variation in susceptibility to asthma. At the same time, it is known that environmental risk factors that are shared by family members are associated with the liability for asthma. We hypothesize that the absence of a main effect of shared environmental factors in twin studies can be explained by gene–environment interaction, that is, that the effect of an environmental factor shared by family members depends on the genotype of the individual. We explore this hypothesis by modeling the resemblance in asthma liability in twin pairs as a function of various environmental risk factors and test for gene–environment interaction. Asthma data were obtained by parental report for nearly 12,000 5-year-old twin pairs. A series of environmental risk factors was examined: birth cohort, gestational age, time spent in incubator, breastfeeding, maternal educational level, maternal smoking during pregnancy, current smoking of parents, having older siblings, and amount of child care outside home. Results revealed that being a boy, born in the 1990s, premature birth, longer incubator time, and child care outside home increased the risk for asthma. With the exception of premature birth, however, none of these factors modified the genetic effects on asthma. In very premature children shared environmental influences were important. In children born after a gestation of 32 weeks or more only genetic factors were important to explain familial resemblance for asthma.


2011 ◽  
Vol 14 (6) ◽  
pp. 544-552 ◽  
Author(s):  
Venla S. Laitala ◽  
Jacob Hjelmborg ◽  
Markku Koskenvuo ◽  
Ismo Räihä ◽  
Juha O. Rinne ◽  
...  

We analyzed the association between mean height and old age cognition in two Nordic twin cohorts with different childhood living conditions. The cognitive performance of 4720 twin individuals from Denmark (mean age 81.6 years, SD = 4.59) and Finland (mean age 74.4 years, SD = 5.26) was measured using validated cognitive screens. Taller height was associated with better cognitive performance in Finland (β-estimates 0.18 SD/10cm, p value < .001, for men and 0.13 SD, p = .008, for women), but this association was not significant in Denmark (β-estimates 0.0093 SD, p value = .16, for men and 0.0075 SD, p value = .016, for women) when adjusted for age and education/social class. Among Finnish participants higher variability of cognitive performance within shorter height quintiles was observed. Analysis using gene-environment interaction models showed that environmental factors exerted a greater impact on cognitive performance in shorter participants, whereas in taller participants' it was explained mainly by genetic factors. Our results suggest that shorter participants with childhood adversity are more vulnerable to environmental risk factors for cognitive impairment.


2012 ◽  
Vol 200 (6) ◽  
pp. 439-441 ◽  
Author(s):  
Jeremy Holmes

SummaryPsychodynamic psychiatry makes a significant educational, scientific and therapeutic contribution to contemporary psychiatry. Recent developments in gene–environment interaction, neuropsychoanalysis and the accumulating evidence base for psychoanalytic therapies and their implications for practice are reviewed.


BMC Cancer ◽  
2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Trinidad Dierssen-Sotos ◽  
Camilo Palazuelos-Calderón ◽  
José-Juan Jiménez-Moleón ◽  
Nuria Aragonés ◽  
Jone M. Altzibar ◽  
...  

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Viktoria Chubar ◽  
Karla Van Leeuwen ◽  
Patricia Bijttebier ◽  
Evelien Van Assche ◽  
Guy Bosmans ◽  
...  

Abstract Background. Social anxiety symptoms (SAS) are among the most common mental health problems during adolescence, and it has been shown that parenting influences the adolescent’s level of social anxiety. In addition, it is now widely assumed that most mental health problems, including social anxiety, originate from a complex interplay between genes and environment. However, to date, gene–environment (G × E) interactions studies in the field of social anxiety remain limited. In this study, we have examined how 274 genes involved in different neurotransmission pathways interact with five aspects of perceived parenting as environmental exposure (i.e., support, proactive control, psychological control, punitive control, and harsh punitive control) to affect SAS during adolescence. Methods. We have applied an analytical technique that allows studying genetic information at the gene level, by aggregating data from multiple single-nucleotide-polymorphisms within the same gene and by taking into account the linkage disequilibrium structure of the gene. All participants were part of the STRATEGIES cohort of 948 Flemish adolescents (mean age = 13.7), a population-based study on the development of problem behaviors in adolescence. Relevant genes were preselected based on prior findings and neurotransmitter-related functional protein networks. Results. The results suggest that genes involved in glutamate (SLC1A1), glutathione neurotransmission (GSTZ1), and oxidative stress (CALCRL), in association with harsh punitive parenting, may contribute to social anxiety in adolescence. Isolated polymorphisms in these genes have been related to anxiety and related disorders in earlier work.Conclusions: Taken together, these findings provide new insights into possible biological pathways and environmental risk factors involved in the etiology of social anxiety symptoms’ development. Conclusions. Taken together, these findings provide new insights into possible biological pathways and environmental risk factors involved in the etiology of social anxiety symptoms’ development.


Sign in / Sign up

Export Citation Format

Share Document