Perinatal factors in psychosis

2020 ◽  
pp. 399-405
Author(s):  
Mary Clarke ◽  
Mary Cannon
Keyword(s):  
Risk Factor ◽  
Psychotic Disorder ◽  
Environmental Risk ◽  
Strong Evidence ◽  
Mechanisms Of Action ◽  
Developmental Trajectory ◽  
Obstetric Complications ◽  
Environmental Risk Factor ◽  
Molecular Studies ◽  
The Relationship

Obstetric complications are one of the most intensively studied categories of environmental risk factor for psychosis. There is a strong evidence of an association between obstetric complications and the later development of psychotic disorder, but there exists a large amount of heterogeneity in findings for individual complications. There are several potential mechanisms of action that may mediate the relationship between obstetric complications and psychosis. There is also evidence that obstetric complications may represent one “hit” on the developmental trajectory to psychosis. Obstetric complications may play an important role in elucidating the etiology of psychosis by pointing the way to molecular studies.

Obstetric complications in patients with schizophrenia and their unaffected siblings

2005 ◽  
Vol 20 (1) ◽  
pp. 28-34 ◽  
Author(s):  
M. Walshe ◽  
C. McDonald ◽  
M. Taylor ◽  
J. Zhao ◽  
P. Sham ◽  
...  
Keyword(s):  
Risk Factor ◽  
Family History ◽  
Genetic Susceptibility ◽  
Environmental Risk ◽  
Obstetric Complications ◽  
Control Group ◽  
Environmental Risk Factor ◽  
Schizophrenic Patients ◽  
History Of ◽  
Elevated Rate

AbstractObjectiveWe sought to explore whether obstetric complications (OCs) are more likely to occur in the presence of familial/genetic susceptibility for schizophrenia or whether they themselves represent an independent environmental risk factor for schizophrenia.MethodsThe presence of OCs was assessed through maternal interview on 216 subjects, comprising 36 patients with schizophrenia from multiply affected families, 38 of their unaffected siblings, 31 schizophrenic patients with no family history of psychosis, 51 of their unaffected siblings and 60 normal comparison subjects. We examined the familiality of OCs and whether OCs were commoner in the patient and sibling groups than in the control group.ResultsOCs tended to cluster within families, especially in multiply affected families. Patients with schizophrenia, especially those from multiply affected families, had a significantly higher rate of OCs compared to normal comparison subjects, but there was no evidence for an elevated rate of OCs in unaffected siblings.ConclusionOur data provides little evidence for a link between OCs and genetic susceptibility to schizophrenia. If high rates of OCs are related to schizophrenia genes, this relationship is weak and will only be detected by very large sample sizes.

scholarly journals Association between stressful life events and psychotic experiences in adolescence: Evidence for gene–environment correlations

2016 ◽  
Vol 208 (6) ◽  
pp. 532-538 ◽  
Author(s):  
Sania Shakoor ◽  
Helena M. S. Zavos ◽  
Claire M. A. Haworth ◽  
Phillip McGuire ◽  
Alastair G. Cardno ◽  
...  
Keyword(s):  
Risk Factor ◽  
Life Events ◽  
Environmental Risk ◽  
Structural Equation ◽  
Stressful Life Events ◽  
Model Fitting ◽  
Stressful Life ◽  
Environmental Risk Factor ◽  
Psychotic Experiences ◽  
The Relationship

BackgroundStressful life events (SLEs) are associated with psychotic experiences. SLEs might act as an environmental risk factor, but may also share a genetic propensity with psychotic experiences.AimsTo estimate the extent to which genetic and environmental factors influence the relationship between SLEs and psychotic experiences.MethodSelf- and parent reports from a community-based twin sample (4830 16-year-old pairs) were analysed using structural equation model fitting.ResultsSLEs correlated with positive psychotic experiences (r = 0.12–0.14, all P<0.001). Modest heritability was shown for psychotic experiences (25–57%) and dependent SLEs (32%). Genetic influences explained the majority of the modest covariation between dependent SLEs and paranoia and cognitive disorganisation (bivariate heritabilities 74–86%). The relationship between SLEs and hallucinations and grandiosity was explained by both genetic and common environmental effects.ConclusionsFurther to dependent SLEs being an environmental risk factor, individuals may have an underlying genetic propensity increasing their risk of dependent SLEs and positive psychotic experiences.

scholarly journals Chronic Lead Exposure Causes Theta and Gamma Hypersynchrony in the Hippocampus and Disrupts Sensorimotor Gating

2020 ◽  
Author(s):  
Nathan W. Schultheiss ◽  
Jennifer L. McGlothan ◽  
Tomás R. Guilarte ◽  
Timothy A. Allen
Keyword(s):  
Risk Factor ◽  
Environmental Risk ◽  
Field Potential ◽  
Startle Reflex ◽  
Developmental Trajectory ◽  
Acoustic Startle Reflex ◽  
Female Rats ◽  
Network Activity ◽  
Environmental Risk Factor ◽  
The Impact

ABSTRACTChronic lead (Pb2+) exposure from childhood contributes to an array of cognitive and behavioral dysfunctions including impaired attention and intellectual ability, learning and memory deficits, and delinquency. It is also an environmental risk factor for adult psychopathologies, most notably schizophrenia. Pb2+ is a potent N-methyl-D-aspartate receptor (NMDAR) antagonist and exposure during early life elicits a cascade of cellular neurotoxic effects that alter the developmental trajectory leading to a loss of parvalbumin-expressing interneurons in hippocampus and altered synaptic transmission. Little is known, however, about the impact of chronic Pb2+ exposure on hippocampal network dynamics which serve as a link between cellular-molecular effects and cognitive-behavioral consequences of Pb2+ neurotoxicity. Here, we tested the effects of chronic Pb2+ exposure on local field potential activity (LFP) in the hippocampus of freely-behaving rats. We demonstrate that Pb2+ exposure causes striking hypersynchrony in both the theta- and gamma-frequency bands, in addition to more modest changes in delta. Next, we tested the effect of Pb2+ exposure on prepulse inhibition of the acoustic startle reflex (PPI) in male and female rats at different developmental timepoints. We found that adult males (PN50 and 120), but neither females nor juvenile males, showed reduced PPI that could not be attributed to changes in the startle reflex. This pattern recapitulates sex- and age-dependencies of PPI disruption in schizophrenic patients. Overall, these results are consistent with the hypothesis that Pb2+ is an environmental risk factor for psychopathology in adulthood, especially those symptoms related to cognitive and sensory-motor gating processes that depend on rhythmic coordination of network activity in the hippocampus.

scholarly journals AB0925-PARE A NARRATIVE REVIEW ASSESSING THE ROLE OF DIETARY SALT AS AN ENVIRONMENTAL RISK FACTOR FOR THE ONSET AND SEVERITY OF RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1484.1-1484
Author(s):  
S. Ahmed ◽  
E. Nikiphorou ◽  
J. Bayliss
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factor ◽  
Autoimmune Disease ◽  
Environmental Risk ◽  
Narrative Review ◽  
Environmental Risk Factor ◽  
T Helper ◽  
Dietary Salt ◽  
Salt Consumption

Background:The role of dietary salt consumption in the etiopathogenesis of Rheumatoid Arthritis (RA), and autoimmune disease in general, has received renewed interest. This has been fueled by the increased prevalence of autoimmune disease worldwide correlating with western diets and heightened consumption of salt rich foods and also studies at the cellular level demonstrating induction of IL 17 producing T helper cells (Th17) by dietary salt.Objectives:To conduct a narrative review of observational studies and clinical trials on the role of dietary salt as an environmental risk factor for the onset and development of RA.Methods:A comprehensive search was done of the literature from 2010 to 2021, using the search terms dietary salt and RA; the native interfaces EBSCO and Ovid were used. Databases searched included Pubmed, Embase, EMCare, Medline and CINAHL using a Population, Exposure and Outcome framework; the MESH terms RA, risk factors, nutrition and salt were used. Data was extracted by an independent reviewer.Results:Out of the 72 studies initially identified, 50 were included in this review. Studies in murine models have demonstrated that high concentrations of sodium chloride promote the differentiation of T helper lymphocytes, via the serum- and glucocorticoid- inducible kinase 1 (SGK1) mediator towards the proinflammatory Th17 driven immune response. Six studies were carried out in human subjects. Study design ranged from cross sectional observational to nested case control studies. Sodium intake amongst participants characterized as having high intake, or being placed in the higher quartiles, ranged from 4.5-5grams per day. 5 out of 6 studies demonstrated that increased dietary salt consumption is associated with earlier onset RA. One study suggested an association between high salt intake and erosive disease at diagnosis and the development of anti-citrullinated protein antibodies (ACPA), although evidence was weak and from a single study only. Another study found that increased consumption of salt was only associated with risk of RA in smokers, highlighting the need to explore confounding variables further.Conclusion:This narrative review of the literature provides some evidence that supports a role of excess dietary salt consumption as a risk factor for the onset and severity of RA.Disclosure of Interests:None declared

scholarly journals Brain Structure Correlates of Urban Upbringing, an Environmental Risk Factor for Schizophrenia

2014 ◽  
Vol 41 (1) ◽  
pp. 115-122 ◽  
Author(s):  
L. Haddad ◽  
A. Schafer ◽  
F. Streit ◽  
F. Lederbogen ◽  
O. Grimm ◽  
...  
Keyword(s):  
Risk Factor ◽  
Environmental Risk ◽  
Brain Structure ◽  
Environmental Risk Factor

scholarly journals Spatial scale effects in environmental risk-factor modelling for diseases

2013 ◽  
Vol 7 (2) ◽  
pp. 169 ◽  
Author(s):  
Ram K. Raghavan ◽  
Karen M. Brenner ◽  
John A. Jr. Harrington ◽  
James J. Higgins ◽  
Kenneth R. Harkin
Keyword(s):  
Risk Factor ◽  
Spatial Scale ◽  
Environmental Risk ◽  
Scale Effects ◽  
Environmental Risk Factor

scholarly journals Multi-omics analysis reveals the influence of genetic and environmental risk factors on developing gut microbiota in infants at risk of celiac disease

Microbiome ◽  
2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Maureen M. Leonard ◽  
◽  
Hiren Karathia ◽  
Meritxell Pujolassos ◽  
Jacopo Troisi ◽  
...  
Keyword(s):  
Risk Factors ◽  
At Risk ◽  
Risk Factor ◽  
Celiac Disease ◽  
Cesarean Section ◽  
Gut Microbiota ◽  
Environmental Risk ◽  
Environmental Risk Factors ◽  
Environmental Risk Factor ◽  
Cesarean Section Delivery

Abstract Background Celiac disease (CD) is an autoimmune digestive disorder that occurs in genetically susceptible individuals in response to ingesting gluten, a protein found in wheat, rye, and barley. Research shows that genetic predisposition and exposure to gluten are necessary but not sufficient to trigger the development of CD. This suggests that exposure to other environmental stimuli early in life, e.g., cesarean section delivery and exposure to antibiotics or formula feeding, may also play a key role in CD pathogenesis through yet unknown mechanisms. Here, we use multi-omics analysis to investigate how genetic and early environmental risk factors alter the development of the gut microbiota in infants at risk of CD. Results Toward this end, we selected 31 infants from a large-scale prospective birth cohort study of infants with a first-degree relative with CD. We then performed rigorous multivariate association, cross-sectional, and longitudinal analyses using metagenomic and metabolomic data collected at birth, 3 months and 6 months of age to explore the impact of genetic predisposition and environmental risk factors on the gut microbiota composition, function, and metabolome prior to the introduction of trigger (gluten). These analyses revealed several microbial species, functional pathways, and metabolites that are associated with each genetic and environmental risk factor or that are differentially abundant between environmentally exposed and non-exposed infants or between time points. Among our significant findings, we found that cesarean section delivery is associated with a decreased abundance of Bacteroides vulgatus and Bacteroides dorei and of folate biosynthesis pathway and with an increased abundance of hydroxyphenylacetic acid, alterations that are implicated in immune system dysfunction and inflammatory conditions. Additionally, longitudinal analysis revealed that, in infants not exposed to any environmental risk factor, the abundances of Bacteroides uniformis and of metabolite 3-3-hydroxyphenylproprionic acid increase over time, while those for lipoic acid and methane metabolism pathways decrease, patterns that are linked to beneficial immunomodulatory and anti-inflammatory effects. Conclusions Overall, our study provides unprecedented insights into major taxonomic and functional shifts in the developing gut microbiota of infants at risk of CD linking genetic and environmental risk factors to detrimental immunomodulatory and inflammatory effects.

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