I had to do some digging, but it appears that the sensitivity of the test was 92% (i.e. it accurately identified people with ASD 92% of the time) and the specificity was 84% (i.e. it correctly identified people without ASD 84% of the time).
Apply this to a real-world scenario: ASD occurs about 1 in 100 children. If you screen 100 children with this test, it will find 16 with ASD. But only one has ASD. The test will identify the one child correctly 92% of the time. Unlikely to be good enough as is to have much clinical utility.
You also have to wonder how the experimental design impacts these numbers. For example, how much of the ASD group's metabolome was impacted by ASD meds? I'd also be curious to know more about the severity of ASD in the children in the study.
Since the press article was pretty light on details, here is the [link to the research article](https://molecularautism.biomedcentral.com/articles/10.1186/s13229-017-0183-3
) if anyone is interested.
Clinical chemistry tests for autism spectrum disorder (ASD) are currently unavailable. The aim of this study was to explore the diagnostic utility of proteotoxic biomarkers in plasma and urine, plasma protein glycation, oxidation, and nitration adducts, and related glycated, oxidized, and nitrated amino acids (free adducts), for the clinical diagnosis of ASD.
Thirty-eight children with ASD (29 male, 9 female; age 7.6 ± 2.0 years) and 31 age-matched healthy controls (23 males, 8 females; 8.6 ± 2.0 years) were recruited for this study. Plasma protein glycation, oxidation, and nitration adducts and amino acid metabolome in plasma and urine were determined by stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry. Machine learning methods were then employed to explore and optimize combinations of analyte data for ASD diagnosis.
We found that children with ASD had increased advanced glycation endproducts (AGEs), Nε-carboxymethyl-lysine (CML) and Nω-carboxymethylarginine (CMA), and increased oxidation damage marker, dityrosine (DT), in plasma protein, with respect to healthy controls. We also found that children with ASD had increased CMA free adduct in plasma ultrafiltrate and increased urinary excretion of oxidation free adducts, alpha-aminoadipic semialdehyde and glutamic semialdehyde. From study of renal handling of amino acids, we found that children with ASD had decreased renal clearance of arginine and CMA with respect to healthy controls. Algorithms to discriminate between ASD and healthy controls gave strong diagnostic performance with features: plasma protein AGEs—CML, CMA—and 3-deoxyglucosone-derived hydroimidazolone, and oxidative damage marker, DT. The sensitivity, specificity, and receiver operating characteristic area-under-the-curve were 92%, 84%, and 0.94, respectively.
Changes in plasma AGEs were likely indicative of dysfunctional metabolism of dicarbonyl metabolite precursors of AGEs, glyoxal and 3-deoxyglucosone. DT is formed enzymatically by dual oxidase (DUOX); selective increase of DT as an oxidative damage marker implicates increased DUOX activity in ASD possibly linked to impaired gut mucosal immunity. Decreased renal clearance of arginine and CMA in ASD is indicative of increased arginine transporter activity which may be a surrogate marker of disturbance of neuronal availability of amino acids. Data driven combination of these biomarkers perturbed by proteotoxic stress, plasma protein AGEs and DT, gave diagnostic algorithms of high sensitivity and specificity for ASD.
Posted elsewhere, so here's what I have already said:
[Here is a somewhat (!) more technical explanation](https://warwick.ac.uk/newsandevents/pressreleases/blood_and_urine/
). Tthe researchers are aware, paediatric medicine has been looking at reactive oxygen species damage for decades - [review here](http://www.ingentaconnect.com/content/ben/cmc/2007/00000014/00000003/art00007
). Amongst the relevant molecules is indeed dityrosine. The researchers say:
> [Other workers] found a link between ASD and damage to proteins in blood plasma by oxidation and glycation – processes where reactive oxygen species (ROS) and sugar molecules spontaneously modify proteins.
What seems to be happening is that the body both relies upon oxygen and is damaged by it, and by molecules formed from it. Children who have poor control systems to manage this conflict suffer neural damage. This shows up as, amongst other things, autism spectrum disorder. (ROS are also implicated in neuro-degeneration in older people.)
What this means, unhappily, is that whilst the relationship may give a pointer to at least some sources of ASD, there is unlikely to be a cure - the damage having been done when the symptoms appear. Children with high levels of ROS and markers of them can, perhaps, be put on an anti-oxidant regime, although what that would look like in practice and how successful it would be is unclear.
That link to AGEs is interesting...
They tend to pop up in some degenerative diseases such as Alzheimer's too.
And interestingly (well for me, I'm doing a PhD on it now), they are present at a relatively high level (compared to their presence in other foods) in infant formula.
There might be a link there. Then again, might not. But worth investigating.