Thursday 28 March 2013

Inflammation, oxidative stress and autism: Saudi style

Saudi Arabia and autism research appearing on this blog? Regular readers know that this can mean only one thing: Laila Al-Ayadhi and special guests - in this case Afaf El-Ansary - and their fairly recent paper* (open-access) on plasma lipid mediators in autism.
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You might already know that I'm a bit of a fan of the Saudi autism research group which also on occasion includes Gehan Mostafa. Their papers have an exquisite range of topics around autism, the most recent being that vitamin D and autoimmunity paper** which I recently blogged about (see here). This is a group on an autism research mission which rivals that of the all-powerful MIND Institute in terms of scope if not participant numbers.

This time around there was a familiar sound to the topic in question: inflammation and autism (yes that old hat), and some interesting observations based on some players in lipid mediation.

A few choice points to make bearing in mind the paper is open-access and goes off in quite a few directions:

  • Impaired lipid metabolism was a focus, based on the measurement of three compounds in plasma which in a round-about kinda way tie into lipids, oxidative stress and inflammation: 8-isoprostane, cysteinyl leukotriene and prostaglandin E2.
  • Actually another old favourite, arachidonic acid (AA), is the starting point for these compounds in a roundabout sort of way.
  • As is usual with this research group, the participant numbers were not exactly all that impressive (autism: n=19, controls: n=20) but at least the autism group were well-defined and seemingly crossing over with some of their other research observations.
  • Results: group analysis of all three compounds showed that they were elevated in the autism group compared with controls; indeed in all compounds,  the means and standard deviation (SDs) showing some clear statistical water between the groups, and some significant correlations between levels of the compounds (the leukotriene - PGE2 correlation reaching 0.926).
  • As is also seemingly a pre-requisite for this research group, ROC analyses were also conducted and under certain circumstances showed 100% sensitivity but rather less in terms of specificity as predictive biomarkers for autism.

What more needs to be said? Well, further evidence that oxidative stress might be part and parcel of some cases of autism as per other research in this area***. Also, some support for further investigations into fatty acid metabolism in autism. And indeed inflammation... need I say much more about this?

Having said all that I'm not as sure that their suggestion about this suite of biomarkers informing the use of omega-3 fatty acids as a strategy to ameliorate inflammatory and oxidative stress in autism is necessarily reflected in the current evidence. Yes omega-6 fatty acids might play some role in autism as per (mouse) studies like that of Jones and colleagues**** but questions remain as to whether omega-3 supplementation really is cutting the mustard bearing in mind the heterogeneity and comorbidity present in autism.

Just before I go and hopefully not too far off-topic, did I mention the paper by McNamara and colleagues***** on fatty acid profiles in cases of schizophrenia?


* El-Ansary A. & Al-Ayadhi L. Lipid mediators in plasma of autism spectrum disorders. Lipids Health Dis. 2012; 11: 160.

** Mostafa GA. & Al-Ayadhi LY. Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: Relation to autoimmunity. J Neuroinflammation. 2011; 9: 201.

*** Ming X. et al. Increased excretion of a lipid peroxidation biomarker in autism. Prostaglandins Leukot Essent Fatty Acids. 2005; 73: 379-384.

**** Jones KL. et al. Maternal diet rich in omega-6 polyunsaturated fatty acids during gestation and lactation produces autistic-like sociability deficits in adult offspring. Behav Brain Res. 2012; 238C :193-199.

***** McNamara RK. et al. Adult medication-free schizophrenic patients exhibit long-chain omega-3 Fatty Acid deficiency: implications for cardiovascular disease risk. Cardiovasc Psychiatry Neurol. 2013: 796462.

---------- El-Ansary A, & Al-Ayadhi L (2012). Lipid mediators in plasma of autism spectrum disorders. Lipids in health and disease, 11 (1) PMID: 23170784


  1. It's interesting that (on the net at least) much of the conversation has switched from advocating use of any and all high ORAC substances to appreciating that ROS are used in signaling and perhaps indiscriminate use of antioxidants might not be a good idea (e.g. vitamins C and E, ALA, omega 3 oils). Maybe NAC, a glutathione precursor, is a better choice (PMID 22342106).

    1. Thanks Stephen.

      I have to say that over the years I too have also become a little weary of just 'popping vitamins' as a route towards good health. The fatty acid story is testament to the fact that not everyone seems to benefit from this particular cup of youth.

      Targeting and supporting what we have (whilst obviously ensuring that we have the RDA for everything - perhaps even from the food we eat rather than supplements!) does seem to be the more efficacious way of doing things. (I tend to like my Brussels sprouts for example)

  2. As one who suffers from HFA that appears to be inflammation-based, I agree with Paul and Stephen. Eating a small apple is more efficacious than quercetin supplements, and eating a piece of fish does more good than gobbling a handful of fish oil pills.

    I must say, at least as far as I am concerned, that while diet does help, it is definitely no panacea.

    1. Thanks for the comment Dunnyveg.

      Yes, nature definitely knew what it was doing.


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