While we know that hormones and genetics play a big role in the physiology of hunger, there are around a trillion other reasons that are getting more credit for their contributions these days – and those are the bacteria in our intestines! A recent review article published in The New England Journal of Medicine provides a fascinating update on the physiology of hunger, including how our gut bacteria may influence how much we eat.
The gut bacteria (aka microbiota) is an ecosystem of bacteria that have many functions, including protection from infection with other bacteria, immune system programming, energy metabolism, and providing us with energy through the release of enzymes and metabolites. These bacteria are hypothesized to influence our hunger by:
- Hormonal effects. In people with obesity, a ‘leaky gut’ (increased gut permeability) can allow gut bacteria components to enter fat tissue and decrease leptin signaling (one of our fullness hormones).
- Fermentation of prebiotics from gut bacteria, like inulin and oligofructose , may inhibit hunger by increasing our production of GLP1 and PYY (fullness hormones) and decreasing ghrelin (hunger hormone) production.
- Postbiotics (metabolites of bacteria), including some short-chain fatty acids may stimulate hunger, while others may suppress hunger.
- Certain proteins produced by gut bacteria (called peptidomimetics) mimic our own hunger and fullness hormones, and may thus impact hunger as well.
While we don’t yet have any microbiome-targeted treatments that result in significant weight loss, there is a lot of research being done in this area. And there’s no doubt that this discussion reminds us that hunger is not about willpower – it’s deeply influenced by biological processes, including even the tiny bacteria living in our gut.
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