scholarly journals Assessment of Hair Aluminum, Lead, and Mercury in a Sample of Autistic Egyptian Children: Environmental Risk Factors of Heavy Metals in Autism

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Farida El Baz Mohamed ◽  
Eman Ahmed Zaky ◽  
Adel Bassuoni El-Sayed ◽  
Reham Mohammed Elhossieny ◽  
Sally Soliman Zahra ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heavy Metals ◽  
Environmental Risk ◽  
Children With Autism ◽  
Autism Spectrum ◽  
Environmental Risk Factors ◽  
Toxic Heavy Metals ◽  
Egyptian Children ◽  
The Mean ◽  
Genetic And Environmental Factors

Background and Aims. The etiological factors involved in the etiology of autism remain elusive and controversial, but both genetic and environmental factors have been implicated. The aim of this study was to assess the levels and possible environmental risk factors and sources of exposure to mercury, lead, and aluminum in children with autism spectrum disorder (ASD) as compared to their matched controls.Methods. One hundred ASD children were studied in comparison to 100 controls. All participants were subjected to clinical evaluation and measurement of mercury, lead, and aluminum through hair analysis which reflects past exposure.Results. The mean Levels of mercury, lead, and aluminum in hair of the autistic patients were significantly higher than controls. Mercury, lead, and aluminum levels were positively correlated with maternal fish consumptions, living nearby gasoline stations, and the usage of aluminum pans, respectively.Conclusion. Levels of mercury, lead, and aluminum in the hair of autistic children are higher than controls. Environmental exposure to these toxic heavy metals, at key times in development, may play a causal role in autism.

A Review of epigenetics in psychiatry: focus on environmental risk factors

2020 ◽  
Vol 32 (1) ◽  
pp. 57-64
Author(s):  
Jessica Keverne ◽  
Elisabeth B. Binder
Keyword(s):  
Risk Factors ◽  
Psychiatric Disorders ◽  
Environmental Risk ◽  
Cell Function ◽  
Epigenetic Modifications ◽  
Environmental Risk Factors ◽  
Epigenetic Changes ◽  
Cell Type Specificity ◽  
Environmental Signals ◽  
Genetic And Environmental Factors

Abstract Epigenetic modifications play a key role in development and cell type specificity. These modifications seem to be particularly critical for brain development, where mutations in epigenetic enzymes have been associated with neurodevelopmental disorders as well as with the function of post-mitotic neurons. Epigenetic modifications can be influenced by genetic and environmental factors, both known major risk factors for psychiatric disorders. Epigenetic modifications may thus be an important mediator of the effects of genetic and environmental risk factors on cell function. This review summarizes the different types of epigenetic regulation and then focuses on the mechanisms transducing environmental signals, especially adverse life events that are major risk factors for psychiatric disorders, into lasting epigenetic changes. This is followed by examples of how the environment can induce epigenetic changes that relate to the risk of psychiatric disorders.

scholarly journals Influence of the 5-HTTLPR polymorphism and environmental risk factors in a Brazilian sample of patients with autism spectrum disorders

2009 ◽  
Vol 1267 ◽  
pp. 9-17 ◽  
Author(s):  
Dânae Longo ◽  
Lavínia Schüler-Faccini ◽  
Ana Paula Carneiro Brandalize ◽  
Rudimar dos Santos Riesgo ◽  
Claiton Henrique Dotto Bau
Keyword(s):  
Risk Factors ◽  
Autism Spectrum Disorders ◽  
Environmental Risk ◽  
Autism Spectrum ◽  
Environmental Risk Factors ◽  
Brazilian Sample ◽  
Spectrum Disorders

scholarly journals Translational Outcomes Relevant to Neurodevelopmental Disorders Following Early Life Exposure of Rats to Chlorpyrifos

2020 ◽  
Author(s):  
Elizabeth L Berg ◽  
Tianna M Ching ◽  
Donald A Bruun ◽  
Josef K Rivera ◽  
Milo Careaga ◽  
...  
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Social Communication ◽  
Neurodevelopmental Disorders ◽  
Ex Vivo ◽  
Acetylcholinesterase Activity ◽  
Autism Spectrum ◽  
Environmental Risk Factors ◽  
Female Rat ◽  
Short Period

Abstract Background: Neurodevelopmental disorders (NDDs), including intellectual disability, attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), are pervasive, lifelong disorders for which pharmacological interventions are not readily available. Substantial increases in the prevalence of NDDs over a relatively short period cannot be attributed solely to genetic factors and/or improved diagnostic criteria. There is now a consensus that multiple genetic loci combined with exposure(s) to environmental risk factors during critical periods of neurodevelopment influence NDD susceptibility and symptom severity. Organophosphorus (OP) pesticides have been identified as potential environmental risk factors. Epidemiological studies suggest children exposed prenatally to the OP pesticide chlorpyrifos (CPF) have significant mental and motor delays and strong positive associations for the development of a clinical diagnosis of developmental delay, ADHD, or ASD. Methods: We tested the hypothesis that developmental CPF exposure impairs behavior relevant to NDD phenotypes, i.e., deficits in social communication and repetitive, restricted behavior. Male and female rat pups were exposed to CPF at 0.1, 1.0, or 3.0 mg/kg (s.c.) from postnatal days 1-4. Results: These CPF doses did not significantly inhibit acetylcholinesterase activity in the blood or brain but significantly impaired pup ultrasonic vocalizations (USV) in both sexes. Social communication in juveniles via positive affiliative 50-kHz USV playback was absent in females exposed to CPF at 0.3 mg/kg and 1.0 mg/kg. In contrast, this CPF exposure paradigm had no significant effect on gross locomotor abilities or contextual and cued fear memory. Ex vivo magnetic resonance imaging largely found no differences between the CPF rats and the corresponding vehicle controls; however there were some interesting trends in females at a dosage of 0.3 mg/kg. Conclusions: This work characterizes a rat model of developmental CPF exposure that exhibits adverse behavioral phenotypes resulting from perinatal exposures at levels that did not significantly inhibit acetylcholinesterase activity in brain or blood. These data suggest that current regulations regarding safe levels of CPF need to be reconsidered.

scholarly journals Translational Outcomes Relevant to Neurodevelopmental Disorders Following Early Life Exposure of Rats to Chlorpyrifos

2020 ◽  
Author(s):  
Elizabeth L Berg ◽  
Tianna M Ching ◽  
Donald A Bruun ◽  
Josef K Rivera ◽  
Milo Careaga ◽  
...  
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Social Communication ◽  
Neurodevelopmental Disorders ◽  
Acetylcholinesterase Activity ◽  
Autism Spectrum ◽  
Environmental Risk Factors ◽  
Female Rat ◽  
Male And Female ◽  
Short Period

Abstract Background: Neurodevelopmental disorders (NDDs), including intellectual disability, attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), are pervasive, lifelong disorders for which pharmacological interventions are not readily available. Substantial increases in the prevalence of NDDs over a relatively short period cannot be attributed solely to genetic factors and/or improved diagnostic criteria. There is now a consensus that multiple genetic loci combined with exposure(s) to environmental risk factors during critical periods of neurodevelopment influence NDD susceptibility and symptom severity. Organophosphorus (OP) pesticides have been identified as potential environmental risk factors. Epidemiological studies suggest children exposed prenatally to the OP pesticide chlorpyrifos (CPF) have significant mental and motor delays and strong positive associations for the development of a clinical diagnosis of developmental delay, ADHD, or ASD. Methods: The hypothesis that developmental CPF exposure impairs behavior relevant to NDD phenotypes, i.e., deficits in social communication and repetitive, restricted behavior, is now currently being explored by us and others. To add knowledge in this research area, we exposed male and female rat pups to CPF at 0.1, 1.0, or 3.0 mg/kg (s.c.) from postnatal days 1-4. Results: These CPF doses did not significantly inhibit acetylcholinesterase activity in the blood or brain but significantly impaired pup ultrasonic vocalizations (USV) in both sexes. Social communication in juveniles via positive affiliative 50-kHz USV playback was absent in females exposed to CPF at 0.3 mg/kg and 1.0 mg/kg. Ex vivo magnetic resonance imaging revealed many neuroanatomical phenotypes in male and female juvenile rats; however, only the females exposed to the 0.3 mg/kg dose passed our strict correction for multiple comparisons. In contrast, this CPF exposure paradigm had no significant effect on gross locomotor abilities or contextual and cued fear memory. Conclusions: This work characterizes a rat model of developmental CPF exposure that exhibits adverse behavioral and widespread anatomical phenotypes resulting from perinatal exposures at levels that did not significantly inhibit acetylcholinesterase activity in brain or blood. These data suggest that current regulations regarding safe levels of CPF need to be reconsidered. Keywords: Animal models, behavior, autism, neurodevelopment, toxicology, pesticides, chlorpyrifos, imaging, social, rat

Bulimia nervosa and major depression: a study of common genetic and environmental factors

1992 ◽  
Vol 22 (3) ◽  
pp. 617-622 ◽  
Author(s):  
Ellen E. Walters ◽  
Michael C. Neale ◽  
Lindon J. Eaves ◽  
Andrew C. Heath ◽  
Ronald C. Kessler ◽  
...  
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Environmental Factors ◽  
Family Environment ◽  
Environmental Risk ◽  
Population Based ◽  
Environmental Risk Factors ◽  
Future Research ◽  
Clinical Diagnoses ◽  
Genetic And Environmental Factors

SynopsisA genetic analysis of the co-occurrence of bulimia and major depression (MD) was performed on 1033 female twin pairs obtained from a population based register. Personal interviews were conducted and clinical diagnoses made according to DSM-III-R criteria.Additive genes, but not family environment, are found to play an important aetiological role in both bulimia and MD. The genetic liabilities of the two disorders are correlated 0·456. While unique environmental factors account for around half of the variation in liability to both bulimia and MD, these risk factors appear to be unrelated, i.e., each disorder has its own set of unique environmental risk factors. Thus, the genetic liability of bulimia and MD is neither highly specific nor entirely nonspecific. There is some genetic correlation between the two disorders as well as some genetic and environmental risk factors unique to each disorder. Limitations and directions for future research are discussed.

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