brain in mah belly
I have been doing some light leisure reading – “Gut feelings: the emerging biology of gut-brain communication” by Mayer, E.A. (2011). [Full pdf is here for your viewing pleasure].
This shit is pretty cool.
Excuse me, while I geek out for a bit.
You’ve all heard of gut feelings. Perhaps, you’ve even acted on them. You know – a certain person gives you the wrong vibe. You get a funny feeling, while walking down a particular street, so you decide to take a different path.
Perhaps, you’ve experienced loss of appetite when upset. [What’s that like?]
BRAIN TALKS TO THE GUT, GUT TALKS TO THE BRAIN
More and more research evidence is pointing to the fact that the brain and the gut are connected in even more meaningful way than we initially thought.
The middle of 19th century brought the discovery of ENS – enteric nervous system, now considered to be the third branch of the autonomic nervous system. It is so complex, it has been referred to as the “second brain”.
Developmentally, ENS can be viewed as a peripheral extension of the limbic system into the gut.
Lymbic system? Oh, the cluster of structures responsible for EMOTION? It’s connected to the… GUT? You don’t say. 🙂
Curiously, the signalling between the brain and the gut is bi-directional. Not only the brain talks to the gut and impacts what happens in the gut, but the gut also talks to the brain, and impacts what happens in the brain.
Top-down signalling involves modulating of the gastrointestinal functions by stress and emotions (both experienced in the brain/spinal cord, aka central nervous system). Brain experiences emotions, and in turn, has an effect on your GI function. You know that time someone breaks up with you and you literally feel sick to your stomach?
In bottom-up signalling the output from the viscera could create or regulate a particular emotional experience. In other words, your gut can create an emotion.
MY GUT TELLS ME I AM SCARED
The latter hypothesis is not new. You may recall learning about theories of emotion in your introductory psychology class (possibly taught by me!) – James-Lange, Lazarus and Cannon-Bard all proposed different mechanisms of action when explaining the experience of emotion.
The James-Lange theory explained formation of emotion via the bodily cues. For example, an external stimulus like speaking in public elicits the bodily responses such as “butterflies in the stomach”, which brain then perceives as fear or anxiety.
Public speaking —> butterflies in the stomach—> fear.
Ta-da! Emotion has been created in the gut. 🙂
“Despite the continuous stream of interoceptive signals from the gut to the brain, only a small fraction of this information is consciously perceived, usually that which requires a conscious behavioral response (for example, ingestive behaviors and defecation).”
There is a poop joke there somewhere. Possibly on conscious vs. unconscious defecation. Anyone?
Ok, now same thing but in human language: Gut talks to the brain ALL THE TIME, yet we only perceive a tiny fraction of that communication. Most of the stuff we actually get is the stuff that requires us to act – gut says “we need to eat”, or gut says “we need to poop”.
IF YOU ARE OBESE, ONE CUPCAKE IS NOT ENOUGH
A fantastic example of gut to brain communication is the observation that food consumption inhibits pain-related behaviours in the rat. In other words, eating acts as a pain killer, potentially teaching the organism the shortcuts “when I eat, it hurts less” and “when it hurts, eating helps”.
Does that sound familiar?
Emotional eating. For. The. Win.
The paper goes on offers an interesting view of obesity and food addiction.
“Brain imaging findings in humans who are obese are consistent with an enhanced sensitivity of the reward circuitry to food cues (for example, viewing images of high caloric food) that predict reward, but a decreased sensitivity to the rewarding effects of actual food ingestion (interoceptive stimuli)”.
Obese individuals are more sensitive to food and less sensitive to the reward of actual food ingestion (which can in turn lead one to overeat, seeking the expected level of reward).
You are more excited at the sight of food than a non-obese individual, yet you are less satisfied with ingesting of that food.
Thus, there is a mismatch between the reward that is expected from food, and the reward actually received from food as one explanation for obesity and food addiction. When exposed to food, the individual may then overeat in an attempt to correct the mismatch, and achieve the expected amount of reward.
Look at these cupcakes! If I eat one, I will be happy to the Xth degree!
Yet, after you eat one, you realize that you are only happy to the 0.5xth degree or even less. You then eat another cupcake, and possible another in hope to achieve the level of happiness (reward) you expected initially.
Yes, eating less would definitely solve the “obesity problem” (assuming there is a problem to solve). Calories-in-calories-out balance is the single biggest determinant of whether our weight gain or weight loss goals are successful. Yet… as an obese individual, you are starting at a major disadvantage.
And definitely puts a damper on oh-so-common advice of an overenthusiastic personal trainer to “just eat less”.
P.S. If this research deliciousness was not enough, I also learned a couple of new words:
- orexigenic = hunger generating
- anorexigenic = satiety generating (anorexia – get it???)
- mechanosensitive – omg, I’m giddy over here. Say it with me.
How much fun was this?