Increased excretion of a lipid peroxidation biomarker in autism

Ming, Xue; Stein, T. P.; Brimacombe, Michael; Johnson, William G.; Lambert, George H.; Wagner, George C.

doi:10.1016/j.plefa.2005.06.002

Cited by 222 publications

(137 citation statements)

References 35 publications

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“…6 However, whether and how the effects of GDM and PGDM differ is still debatable. Although the 2 studies differentiating PGDM and GDM in the meta-analysis both reported larger odds ratios (ORs) for PGDM than GDM, 15,16 Xiang et al 17 found that only GDM diagnosed before 26 weeks, but not GDM diagnosed 7…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities

Li¹,

Fallin²,

Riley³

et al. 2016

Pediatrics

247

200

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show abstract

Section: Discussionmentioning

confidence: 99%

“…5 Emerging evidence links maternal prenatal diabetes with the risk of ASD in children. 6 Research on the connection between maternal obesity and the risk of ASD has produced inconsistent results. [7][8][9][10] Although obesity and diabetes are highly comorbid, 11 rarely have studies attempted to disentangle their independent and combined effects on ASD.…”

mentioning

confidence: 99%

The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities

Li¹,

Fallin²,

Riley³

et al. 2016

Pediatrics

247

200

View full text Add to dashboard Cite

show abstract

“…A growing literature has been published that cites evidence for oxidative disturbances in autism, including genetic polymorphisms affecting oxidative metabolic pathways (James et al, 2006), reduced antioxidant capacity (Chauhan et al, 2004;James et al, 2004James et al, , 2006, antioxidant enzyme changes (Sogut et al, 2003;Yorbik et al, 2002;Zoroglu et al, 2004) and enhanced oxidative stress biomarkers (Chauhan et al, 2004;James et al, 2004;Ming et al, 2005;Sogut et al, 2003;Yao et al, 2006b;Zoroglu et al, 2004). Impaired oxidative status has also been reported for ADHD, and a randomized, controlled trial of Pycnogenol, a pine bark extract with potent antioxidant properties, in children diagnosed with ADHD (n=61) has found symptomatic and biochemical improvements (Chovanova et al, 2006;Dvorakova et al, 2006;Trebaticka et al, 2006).…”

Section: Other Conditionsmentioning

confidence: 99%

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

879

569

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Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Previews, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

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“…One of the more destructive free radicals is peroxynitrite, which is generated through a combination of superoxide and NO, both of which are generated in excess with excitotoxicity. Significant elevations in measures of oxidative stress and LPP in autistic children were demonstrated [135,136].…”

Section: The Role Of Mercurymentioning

confidence: 98%

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

Blaylock

Strunecká

2009

CMC

125

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Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.

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Increased excretion of a lipid peroxidation biomarker in autism

Cited by 222 publications

References 35 publications

The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities

The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

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