Humans have become substantially more obese over time in western civilization, particularly in the US. This increase to obesity occurs more rapidly than seems reasonable on the basis of selective breeding in humans, and is also not advantageous to humans in the absence of famine.

One explanation may be a change in diet, for example a food additive that functions directly as GLP-1 antagonist could cause one to be more hungry. (Semaglutide, a GLP-1 like drug, functions as a weight loss drug.)

That said, food additives are closely scrutinized, and it seems difficult to conclude that less healthy additives are used today than 50 years ago, to an extreme enough extent that it explains the gradual increase of obesity.

Another potential mechanism which could be fast enough, and does not rely on an additive explanation, is a form of selective pressure on gut microbes. The simplest source of this pressure would be a historically novel economic change, that cheap calories are widely available. This includes sugars and fats in the form of junk foods, but also includes healthier calories such as fruits, nuts, and starchy vegetables.

The availability of cheap, calorie-dense food implies that a gut microbe with the effect "makes the host very hungry" will have the effect "exposure to food" more consistently. It will then have a higher population in the gut, which must expand in volume to accommodate food and food waste. The population of competitor microbes (i.e. "free riders" which do not have this impact) will rise correspondingly, however extinction risk of a lineage with this quality could be lower due to a larger habitat, and it can diversify more to counter threats.

A larger population of a given strain may additionally confer greater potential to spread to other humans via fecal matter, since there is more of it in total. Hygiene has reduced potential to spread, but does to equivalently for all strains. Per unit fecal matter in a sewage system, more common strains will originate from more obese individuals at a higher rate per host.

While this is a fundamentally pathogenic evolution, it notably does not take the form of infection (as generally understood), because the obesity-causing pathogen does not invade other tissues. Apart from triggering excessive caloric consumption, it does not differ from ordinary symbiotes. Thus, the immune system does not respond to it as it would a normally-defined infection.

That said, there are pressures which would be correlated. A microbe strain specialized in this way benefits in more cases (i.e. in more hosts) by consuming food faster than competitors and achieving a higher reproduction rate. It can more typically count upon dense calories than other strains.

Thus, competitor strains (with lineages that include more non-obese hosts) may reproduce faster where non-dense calories are the only source available. Moreover, it is likely to specialize strongly towards economically cheaper calories such as sugars rather than economically expensive calories such as protein.

This may explain how switching to a diet of mostly whey protein will typically cause weight loss, as hunger-causing strains will not consume it as readily vs competitors and may go dormant and trigger a shift in relative population.

A potential approach to reverse-evolve gut microbe populations with regards to this trait is as follows:

• A small device is swallowed, which attaches itself to the gut lining.

• When a high calorie food is consumed, causing caloric density to exceed a threshold, an antibiotic is released.

• The device degrades at a certain rate, being dissolved well after the antibiotic store is exhausted.

• Another device with a different antibiotic (to avoid selecting for specific antibiotic resistance over time) is swallowed.

• Repeat the cycle over several years in many hosts.

This causes microbial populations in proximity to the device to decline temporarily in concert with the high calorie food exposure. Thus, an adaptation that is selected for in the proximity of the device is to prevent high calorie exposure. This can occur by novel mechanism, by loss of the mechanism that causes excessive hunger, or by attacking the strain which has the mechanism.