Fatty acid metabolism in neurodevelopmental disorder: a new perspective on associations between attention-deficit/hyperactivity disorder, dyslexia, dyspraxia and the autistic spectrum

[Guest guest]

http://www.jneuroinflammation.com/content/pdf/1742-2094-7-20.pdf

Full 30 pg article can be found at the link above. Abstract and the conclusions

are pasted below. Worth a read for all those interested to understand how

environmental triggers affect our genes and these in turn affect our ability to

process nutrients and how food intolerances and autoimmune disorders as well as

neurological problems are all connected for some patients with developmental

problems. Like I always say--the neuroscience and microbiology research is

there--it is clinical practice that needs a few decades to catch up.

How much time do our neurologically damaged children have?

Regular Article

Fatty acid metabolism in neurodevelopmental disorder: a new perspective

on associations between attention-deficit/hyperactivity disorder,

dyslexia, dyspraxia and the autistic spectrum

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A. J. b, a, f1 and M. A. Rossca University Laboratory of Physiology,

Oxford, UK

b MRI Unit, MRC Clinical

Sciences Centre, Imperial College School of Medicine, London, UK

c Highland Psychiatric Research Foundation, UK Received 12 June 2000; accepted

14 June 2000. ; Available online 12 March 2002.

Abstract

There is increasing evidence that

abnormalities of fatty acid and membrane phospholipid metabolism play a

part in a wide range of neurodevelopmental and psychiatric disorders.

This proposal is discussed here in relation to

attention-deficit/hyperactivity disorder (ADHD), dyslexia, developmental

coordination disorder (dyspraxia) and the autistic spectrum. These are

among the most common neurodevelopmental disorders of childhood, with

significant implications for society as well as for those directly

affected. However, controversy still surrounds both the identification

and management of these conditions, and while their aetiology is

recognized as being complex and multifactorial, little progress has yet

been made in elucidating predisposing factors at the biological level.

An overview is provided here of the contents of this Special Issue, which

contains a selection of reports from a unique multidisciplinary workshop

involving both researchers and clinicians. Its purpose was to explore

the possibility that ADHD, dyslexia, dyspraxia and autism fall within a

phospholipid spectrum of disorders. This proposal could explain the high degree

of co-morbidity between these conditions, their aggregation

within families and relation to other psychiatric disorders, and a range of

associated features that are already well known at a clinical level. The

existing evidence for fatty acid abnormalities in these disorders

is summarized, and new approaches are outlined that have the potential

to improve both the identification and the management of these and

related neurodevelopmental and psychiatric conditions.

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Also, there are a series of epidemiological studies conducted in the USA that

have found

significant associations between environmental sources of mercury exposure and

ASDs [51]. In

addition, patients with severe ASD have evidence of significantly increased

urinary porphyrins

consistent with mercury intoxication [52-55]. Mercury toxicity may also affect

critical

methylation pathways in vulnerable cells [56].

ASD are a group of pervasive developmental disorders that include autistic

disorder, Asperger’s

disorder, and atypical autism - also known as pervasive developmental

disorder-not otherwise

specified (PDD-NOS). These are neurodevelopmental disorders diagnosed in early

childhood

[57]. They are characterized by various degrees of dysfunctional communication

and social

skills, repetitive and stereotypic behaviors, as well as attention, cognitive,

learning and sensory

defects [57, 58]. ASD cases have increased more than 10-fold during the last

decade to a

prevalence of 1/100 children [44, 57, 59]. However, there is no known distinct

pathogenesis,

there are no biomarkers, and there is no effective treatment [60].

ASD may result from a combination of genetic/biochemical susceptibility and

epigenetic

exposure to environmental factors, including reduced ability to excrete mercury

and/or exposure

to mercury at critical developmental periods [2, 56]. A number of papers have

suggested that

ASD may be associated with immune dysfunction [61], while a recent review made

the case that

ASD may be a neuroimmune disorder involving mast cell activation [34

Conclusions

The results of the present study support the biological plausibility of how

mercury could

contribute to ASD pathogenesis by inducing VEGF and IL-6 release from mast

cells, and as a

result disrupt the BBB and thus permit brain inflammation. Further studies

should investigate the

effect of mercury and thimerosal alone or together with allergic and non-immune

triggers.