Pole position in autism research

Many research groups are at work in the autism research arena. I have blogged about a few of them over the past few months, and in some cases readily admit to being a bit of fan of some of their ideas and produce. One group has kinda crept up on my autism research radar with no or only little media publicity for their research findings, some of which actually might be quite important.

The group in question is a team based at the Technical University of Lodz in Poland (hence the 'Poles') and the author who keeps cropping up is Dr Joanna Kaluzna-Czaplinska (apologies for the lack of Latin characters in her name). I posted an entry about some research from this group recently and their interesting findings related to the big 'H' - homocysteine - which seems to also potentially tie into quite a few other areas.

A recent paper from this Polish group also piqued my interest; this one* looking at what happened to urinary levels of various dicarboxylic acids in children with autism in response to a supplementation regime which included magnesium and vitamins B6 (pyridoxine) and B2 (riboflavin). I should perhaps back up a little and explain what exactly dicarboxylic acids are and which ones were examined in this study. Dicarboxylic acids are organic acids which, chemically, have two carboxyl functional groups (hence the di-).

The paper describes results based on the application of gas chromatography mass spectrometry (GC-MS) to analyse for several dicarboxylic acids in urine including succinic, adipic and suberic acids. Some of these dicarboxylic acids are involved in things like the Krebs cycle among other things.

Anyhow, the results suggested that the supplementation protocol (listed in the paper) seemed to have had quite an effect on the quantities of the dicarboxylic acids measured; adjusting of course for our old friend urinary creatinine. This is not really startling news considering that elevated urinary levels of compounds such as succinic acid for example, might (might!) indicate a deficiency of vitamin B2 [or coenzyme Q10] among other things.

Some caution needs to be attached to these findings as they stand. There were only 30 participants included for study and no control group used. Having said that the main thrust of the paper seems to be about what happened to detected compound levels in children with autism following supplementation, so maybe I should not be so critical at this stage.

There are perhaps a few ways that this collected data can be interpreted. Elevated levels of such organic acids as markers of some kind of disorder of metabolism is perhaps one way. Another is the possibility that a proportion of people with an autism spectrum condition might actually be deficient in various vitamins and minerals and what is being seen are the knock-on effects of that. I stand back at this point preferring not to speculate which option might be most applicable, bearing in mind that metabolic disorders involving such parameters might show 'overlap' with some of the characteristics seen in autism.

* Kaluzna-Czaplinska J. et al. B vitamin supplementation reduces excretion or urinary dicarboxylic acids in autistic children. Nutrition Research. August 2011.