Abnormal fatty acids in Canadian children with autism

Jory, Joan

doi:10.1016/j.nut.2015.10.019

Cited by 48 publications

(39 citation statements)

References 43 publications

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“…Other micronutrient deficiencies have been reported in autism, including magnesium, zinc, selenium, and vitamins A, D, E, and B complex . Brain deficiency of essential PUFAs, especially DHA, also deserves consideration, as noted above , and one review observed that “the majority of studies on attention‐deficit/hyperactivity disorder (ADHD) and autism found a significant decrease in DHA levels” . Whether brain deficiency of carnitine or PUFA might relate to the etiology of ADHD is beyond the scope of this discussion, but we note that ADHD also affects far more males than females.…”

Section: Non‐mendelian Non‐dysmorphic (Nomend) Autism and The Brainmentioning

confidence: 83%

Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis

Beaudet

2017

BioEssays

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Could 10–20% of autism be prevented? We hypothesize that nonsyndromic or “essential” autism involves extreme male bias in infants who are genetically normal, but they develop deficiency of carnitine and perhaps other nutrients in the brain causing autism that may be amenable to early reversal and prevention. That brain carnitine deficiency might cause autism is suggested by reports of severe carnitine deficiency in autism and by evidence that TMLHE deficiency – a defect in carnitine biosynthesis – is a risk factor for autism. A gene on the X chromosome (SLC6A14) likely escapes random X-inactivation (a mixed epigenetic and genetic regulation) and could limit carnitine transport across the blood-brain barrier in boys compared to girls. A mixed, common gene variant-environment hypothesis is proposed with diet, minor illnesses, microbiome, and drugs as possible risk modifiers. The hypothesis can be tested using animal models and by a trial of carnitine supplementation in siblings of probands. Perhaps the lack of any Recommended Dietary Allowance for carnitine in infants should be reviewed.

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Section: Non‐mendelian Non‐dysmorphic (Nomend) Autism and The Brainmentioning

confidence: 83%

Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis

Beaudet

2017

BioEssays

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“…Total n-3 PUFAs in the plasma of autistic children are decreased without any changes in the n-6 PUFAs family [147, 148]. A positive association between anti-myelin basic protein (MBP) antibodies and low levels of the main n-3 PUFA found in the brain (docosahexaenoic acid, DHA) has been reported in autistic children [149].…”

Section: Risk Factors For Neuroinflammation and Autismmentioning

confidence: 99%

Neuroinflammation in Autism: Plausible Role of Maternal Inflammation, Dietary Omega 3, and Microbiota

et al. 2016

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Several genetic causes of autism spectrum disorder (ASD) have been identified. However, more recent work has highlighted that certain environmental exposures early in life may also account for some cases of autism. Environmental insults during pregnancy, such as infection or malnutrition, seem to dramatically impact brain development. Maternal viral or bacterial infections have been characterized as disruptors of brain shaping, even if their underlying mechanisms are not yet fully understood. Poor nutritional diversity, as well as nutrient deficiency, is strongly associated with neurodevelopmental disorders in children. For instance, imbalanced levels of essential fatty acids, and especially polyunsaturated fatty acids (PUFAs), are observed in patients with ASD and other neurodevelopmental disorders (e.g., attention deficit hyperactivity disorder (ADHD) and schizophrenia). Interestingly, PUFAs, and specifically n-3 PUFAs, are powerful immunomodulators that exert anti-inflammatory properties. These prenatal dietary and immunologic factors not only impact the fetal brain, but also affect the microbiota. Recent work suggests that the microbiota could be the missing link between environmental insults in prenatal life and future neurodevelopmental disorders. As both nutrition and inflammation can massively affect the microbiota, we discuss here how understanding the crosstalk between these three actors could provide a promising framework to better elucidate ASD etiology.

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“…We have previously reviewed the genetic and environmental risk factors that cause defects in the signalling of the COX‐PGE 2 pathway and lead to neurodevelopmental disorders such as ASD (Tamiji & Crawford, ; Wong et al ., , ). For example, various studies reported lower levels of arachidonic acid, abnormal levels and activity of PLA2, and increased levels of COX‐2 and PGE 2 in blood plasma of individuals with ASD (Bell et al ., , ; El‐Ansary et al ., ; Tostes et al ., ; Brigandi et al ., ; El‐Ansary et al ., ; Jory, ). These changes were correlated with abnormalities in sensory behaviours of ASD (El‐Ansary et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Microarray analysis of gene expression in the cyclooxygenase knockout mice – a connection to autism spectrum disorder

Rai-Bhogal

Ahmad

et al. 2017

Eur J of Neuroscience

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The cellular and molecular events that take place during brain development play an important role in governing function of the mature brain. Lipid-signalling molecules such as prostaglandin E (PGE ) play an important role in healthy brain development. Abnormalities along the COX-PGE signalling pathway due to genetic or environmental causes have been linked to autism spectrum disorder (ASD). This study aims to evaluate the effect of altered COX-PGE signalling on development and function of the prenatal brain using male mice lacking cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2 ) as potential model systems of ASD. Microarray analysis was used to determine global changes in gene expression during embryonic days 16 (E16) and 19 (E19). Gene Ontology: Biological Process (GO:BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were implemented to identify affected developmental genes and cellular processes. We found that in both knockouts the brain at E16 had nearly twice as many differentially expressed genes, and affected biological pathways containing various ASD-associated genes important in neuronal function. Interestingly, using GeneMANIA and Cytoscape we also show that the ASD-risk genes identified in both COX-1 and COX-2 models belong to protein-interaction networks important for brain development despite of different cellular localization of these enzymes. Lastly, we identified eight genes that belong to the Wnt signalling pathways exclusively in the COX-2 mice at E16. The level of PKA-phosphorylated β-catenin (S552), a major activator of the Wnt pathway, was increased in this model, suggesting crosstalk between the COX-2-PGE and Wnt pathways during early brain development. Overall, these results provide further molecular insight into the contribution of the COX-PGE pathways to ASD and demonstrate that COX-1 and COX-2 animals might be suitable new model systems for studying the disorders.

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Abnormal fatty acids in Canadian children with autism

Cited by 48 publications

References 43 publications

Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis

Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis

Neuroinflammation in Autism: Plausible Role of Maternal Inflammation, Dietary Omega 3, and Microbiota

Microarray analysis of gene expression in the cyclooxygenase knockout mice – a connection to autism spectrum disorder

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