Free GMAT Reading Comprehension Practice Question

For decades, the trillions of bacteria that inhabit the mammalian gut were treated as passive lodgers, organisms that simply consumed whatever nutrients their host happened to eat and returned, at most, a few useful byproducts. On this older view, the flow of influence ran in one direction: the host chose its diet, and the bacterial community adjusted to it. The host's appetite was the host's own business, governed by its brain and its hormones, and the resident microbes were spectators to a decision already made.

A newer account reverses part of that arrow. It proposes that some gut bacteria do not merely tolerate the host's food choices but actively bias them, nudging the host to crave the very nutrients on which those bacteria most depend. The proposed mechanism is chemical. As certain bacteria break down particular dietary fibers, they release short-chain fatty acids, small molecules that can enter the host's circulation and reach the brain regions that register fullness. By altering when and how strongly the host feels satisfied, a bacterial population could, in effect, lengthen or shorten the meal that feeds it. In most species examined so far, shifts in the abundance of fiber-fermenting bacteria are accompanied by measurable changes in how much fiber the animal subsequently seeks out.

The evidence is suggestive rather than conclusive, and the better investigators in this area say as much. The correlations are robust, but a correlation between bacterial abundance and host appetite does not by itself establish that the bacteria are driving the appetite rather than responding to it. What the newer account has going for it is a plausible signaling pathway and a consistent direction of effect across several species; what it still lacks is a clean demonstration that interrupting the fatty-acid signal blunts the craving it is supposed to produce. Until such a demonstration arrives, the manipulation hypothesis is best regarded as probably correct but not yet proven.