My comment to The Scientist site (4/5/13):
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?