A genomic point-of-view on environmental factors influencing the human brain methylome

LaSalle, Janine M.

doi:10.4161/epi.6.7.16353

Cited by 77 publications

(62 citation statements)

References 102 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The recent surge in frequency may be partly attributed to increased awareness/ diagnosis; however, intrinsic and extrinsic factors (including environmental chemicals, diet alterations, metabolic status, and microbiota changes) cannot be excluded (Rizzo et al, 1997;Bello, 2007;Newschaffer et al, 2007;Deth et al, 2008;Rogers, 2008;Leeming and Lucock, 2009;Currenti, 2010;Landrigan, 2010;Beard et al, 2011;LaSalle, 2011;Chaste and Leboyer, 2012;Krakowiak et al, 2012;Jones et al, 2013;Lyall et al, 2013;Gore et al, 2014;Sullivan et al, 2014). While extensive heterogeneity exists in ASD patients, this class of disorders is typified by a range of symptoms including decreased verbal communication and social skills, outright withdrawal, insistence on sameness in the daily routine, engagement in repetitive behaviors, and heightened response to external stimuli.…”

Section: Introductionmentioning

confidence: 99%

Microbiome Disturbances and Autism Spectrum Disorders

2015

View full text Add to dashboard Cite

Autism spectrum disorders (ASDs) are considered a heterogenous set of neurobehavioral diseases, with the rates of diagnosis dramatically increasing in the past few decades. As genetics alone does not explain the underlying cause in many cases, attention has turned to environmental factors as potential etiological agents. Gastrointestinal disorders are a common comorbidity in ASD patients. It was thus hypothesized that a gut-brain link may account for some autistic cases. With the characterization of the human microbiome, this concept has been expanded to include the microbiota-gut-brain axis. There are mounting reports in animal models and human epidemiologic studies linking disruptive alterations in the gut microbiota or dysbiosis and ASD symptomology. In this review, we will explore the current evidence that gut dysbiosis in animal models and ASD patients correlates with disease risk and severity. The studies to date have surveyed how gut microbiome changes may affect these neurobehavioral disorders. However, we harbor other microbiomes in the body that might impact brain function. We will consider microbial colonies residing in the oral cavity, vagina, and the most recently discovered one in the placenta. Based on the premise that gut microbiota alterations may be causative agents in ASD, several therapeutic options have been tested, such as diet modulations, prebiotics, probiotics, synbiotics, postbiotics, antibiotics, fecal transplantation, and activated charcoal. The potential benefits of these therapies will be considered. Finally, the possible mechanisms by which changes in the gut bacterial communities may result in ASD and related neurobehavioral disorders will be examined.

show abstract

Section: Introductionmentioning

confidence: 99%

Microbiome Disturbances and Autism Spectrum Disorders

2015

View full text Add to dashboard Cite

show abstract

“…Advances are being made in understanding the genetic basis of many mental health problems, and the role of gene-environment interactions and epigenetic factors in these disorders (61)(62)(63) . The neurotrophic hypothesis suggests that stress reduces the activity of neurotrophins such as BDNF, resulting in decreased hippocampal function and ultimately depression.…”

Section: Nutrition Genes and Mental Disordersmentioning

confidence: 99%

Recent advances in nutrition, genes and brain health

Dauncey

2012

Proc. Nutr. Soc.

117

View full text Add to dashboard Cite

Molecular mechanisms underlying brain structure and function are affected by nutrition throughout the life cycle, with profound implications for health and disease. Responses to nutrition are in turn influenced by individual differences in multiple target genes. Recent advances in genomics and epigenomics are increasing understanding of mechanisms by which nutrition and genes interact. This review starts with a short account of current knowledge on nutrition-gene interactions, focusing on the significance of epigenetics to nutritional regulation of gene expression, and the roles of SNP and copy number variants (CNV) in determining individual responses to nutrition. A critical assessment is then provided of recent advances in nutrition-gene interactions, and especially energy status, in three related areas: (i) mental health and well-being, (ii) mental disorders and schizophrenia, (iii) neurological (neurodevelopmental and neurodegenerative) disorders and Alzheimer's disease. Optimal energy status, including physical activity, has a positive role in mental health. By contrast, sub-optimal energy status, including undernutrition and overnutrition, is implicated in many disorders of mental health and neurology. These actions are mediated by changes in energy metabolism and multiple signalling molecules, e.g. brain-derived neurotrophic factor (BDNF). They often involve epigenetic mechanisms, including DNA methylation and histone modifications. Recent advances show that many brain disorders result from a sophisticated network of interactions between numerous environmental and genetic factors. Personal, social and economic costs of sub-optimal brain health are immense. Future advances in understanding the complex interactions between nutrition, genes and the brain should help to reduce these costs and enhance quality of life.

show abstract

“…In utero, DNA methylation alters expression of multiple proteins through epigenetics [42] and as a result DNA hypomethylation can lead to an epigenetic reprogramming of the fetal brain to adjust to sulfur deficiency [13,14,43]. It has also been demonstrated that parents of children with ASD have the same impairment in sulfur metabolism observed in ASD [44].…”

Section: Asd Sulfur Metabolism Glutathione and Ammoniamentioning

confidence: 99%

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Seneff¹,

Lauritzen

Davidson³

et al. 2013

Entropy

View full text Add to dashboard Cite

This paper makes two claims: (1) autism can be characterized as a chronic lowgrade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether. OPEN ACCESSEntropy 2013, 15 373

show abstract

A genomic point-of-view on environmental factors influencing the human brain methylome

Cited by 77 publications

References 102 publications

Microbiome Disturbances and Autism Spectrum Disorders

Microbiome Disturbances and Autism Spectrum Disorders

Recent advances in nutrition, genes and brain health

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Contact Info

Product

Resources

About