“Breathprints” Could Diagnose Disease

Researchers can identify individuals by the unique chemical signatures in their breath, suggesting that exhalations could be used for metabolomic tests.

By Dan Cossins | April 5, 2013

XUE LI / ETH ZURICHEvery individual has a signature composition of metabolites—or compounds produced by chemical reactions in the body—in their exhaled breath, according to a study published this week (April 3) in PLOS ONE. These unique “breathprints” could one day be used in addition to blood or urine tests to reveal biomarkers of disease or test athletes for doping.

Previous work indicated that the presence of infections or even cancer might be detected in breath, but it was not clear whether the metabolic contents of breath varied enough between individuals, and whether each individual’s breathprint remained stable enough over time, to make it a genuine candidate for diagnostic use. To find out, a group of researchers led by Renato Zerobi of the Swiss Federal Institute of Technology in Zurich got 11 volunteers to blow into a mass spectrometer, which almost instantly parsed the exhalation into its chemical components.

Although each person’s breathprint changed slightly from sample to sample over the course of nine days of testing, the researchers observed that every volunteer had a chemical signature that was stable and specific enough to identify them. The findings suggest that like blood and urine samples, breath samples are reflective of the body’s internal chemistry and could therefore be used for metabolomic studies. Indeed, the fact that the method is non-invasive and produces results almost immediately makes it particularly appealing. 

For the moment, however, the researchers still need to work out exactly what the chemical readings of breath can tell us. “We're at the onset of learning about what the compounds are,” Zenobi told BBC News. “Just a small fraction of the peaks that we see are identified at this point, so there's a lot of footwork to be done.”

 (Hat tip to ScienceInsider)

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Avatar of: James V. Kohl

James V. Kohl

Posts: 525

April 5, 2013

Disclaimer / Conflict of Interest: I own the domain Pheromones.com

Sex-dependent production of a mouse “chemosignal” with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline. The result of this synergy is 1) a liver enzyme that oxidizes trimethylamine to 2) an odor that causes 3) species-specific behaviors. Thus, the complex systems biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).  

The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause "fish odor syndrome." The aversive body odor has been attributed to a missense "mutation" (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor. This synergy requires at least two things to simultaneously happen: for example, 1) natural selection for nutrient chemicals and 2) sexual selection for odor production. Sexual selection for nutrient-dependent odor production is not likely to be achieved via one missense "mutation" involved in nutrient acquisition and another missense "mutation" that is involved in odor production because two mutations are not likely to simultaneously occur.

In my model, the adaptive evolution of nutrient-dependent pheromones controls reproduction and non-random species divergence. Is there a reason for use of the term “breathprint” in humans, or does “breathprint” intentionally infer that human pheromones do not exist? Would it not be unusual for chemical signals that control reproduction in species from microbes to man, to not exist in the context of human pheromones?

Dolphin, C. T., Janmohamed, A., Smith, R. L., Shephard, E. A., & Phillips, l. R. (1997). Missense mutation in flavin-containing mono-oxygenase 3 gene, FMO3, underlies fish-odour syndrome. Nat Genet, 17(4), 491-494. http://dx.doi.org/10.1038/ng1297-491

Li, Q., Korzan, Wayne J., Ferrero, David M., Chang, Rui B., Roy, Dheeraj S., Buchi, M., et al. (2013). Synchronous Evolution of an Odor Biosynthesis Pathway and Behavioral Response. Curr Biol, 23(1), 11-20. http://www.ncbi.nlm.nih.gov/pubmed/23177478


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