There’s experts out there who claim that you can think yourself thin. A lot of this is mainly motivational, giving yourself realistic targets and actions you will be able to do. Makes sense – we’ll drive ourselves to do something as long as it isn’t improbable where you are now. I’d like to run a marathon, one of the big ones like the Boston, New York, or Chicago (because I live in the United States), now that I know that with the right shoes, I can run until my lungs go ragged instead of my legs. However, I didn’t know there are qualifying times for those marathons. So there goes that idea. However, a study that just came out in Nature Communications suggests that the brain may have more to do with it than you think (lol, wordplay).
Meet serotonin, the neurotransmitter that people have probably heard of but can’t exactly place what it is. It’s popularly known as a neurochemical that contributes to happiness, but it turns out that most of our serotonin isn’t even located in the brain – it’s mostly in our digestive systems. If there’s enough resources, like food, serotonin kicks up and we feel happy because we have all that we need. I’m sure it’s much more complicated than that, but please remember that 1) we’re trying to be casual here and 2) I’m not a psychologist, so let’s just leave it at that. Feel free to read up on the various binding profiles, though: it’s really amazing how much of our moods depends on serotonin. Why else would it be the target of a large class of antidepressants?
Back to the article: serotonin can make us happy, but how does it get on with burning fat? Serotonin can’t do it alone; it will require certain proteins in the nervous system to be activated and not others, which is pretty much what metabolism is to begin with. What’s important is that the proteins were discovered: UNC-13 and UNC-31. The names aren’t terribly important for this post, but by tooling around with some genetics, one set that promotes UNC-13 and another that promotes UNC-31, the authors found that the UNC-31 sample had more body fat than the UNC-13 sample. The authors also found a genetic sequence, flp-7, that causes the release of peptides that regulate how the intestines stretch and contract (‘motility’), and overexpressing this sequence can reduce body fat storage by making the gut move faster. Makes sense: your intestines are moving faster, so it’s not really storing fat anymore. On the other hand, just how fast do you really want your intestines to move? I’m just saying…
Of course, a massive, MASSIVE caveat regarding this research has to do with the fact that it was not demonstrated on humans. This was demonstrated on Caenorhabditis elegans, which looks like this:
So now I’m sure wondering ‘what’s the point of all this, then?’ The thing is, C. elegans is a model organism for neuron development, thanks to the work of Nobel laureate Sydney Brenner. C. elegans is one of the simplest organisms with a nervous system that could be studied if one is interested in what is happening in the nervous system without necessarily looking at how it’s interacting with other systems or even how it interacts with human psychology. It’s a roundworm, do we really need psychology for this? Of course more studies will need to be done to see if this is how it plays out in human systems (that ought to be a nightmare for institutional review boards), but at least in the biochemical sense, it may actually work. After all, we do have the human genome, now we just have to find the human equivalent of flp-7. It’s got to be somewhere in here…
Featured Article: Palamiuc L, Noble T, Witham E, Ratanpal H, Vaughan M, Srinivasan S. (2017) A tachykinin-like neuroendocrine signalling axis couples central serotonin action and nutrient sensing with peripheral lipid metabolism. Nature Communications 8. doi:10.1038/ncomms14237.
Featured Image: Public Domain (Author: Rebecca Matthews/StillWorksImagery)