Why We Like Chocolate Cake: The Interaction Between Dopamine and Metabolic Hormones
By Taylor Mitchell Brown
There are certain foods that a large percentage of Americans enjoy eating. Things like bacon, ice cream, and barbecue sauce fill our lives. But why is it that so many of us enjoy eating these foods? and why do we often choose to eat them over more healthy alternatives?
The mesolimbic dopamine pathway in the brain is largely responsible for feelings of and motivation towards pleasure. For instance, every drug known — and probably even those unknown — to man work on this pathway. We give rats and mice amphetamine, and this pathway lights up. We give humans amphetamine, and this pathway lights up. As it turns out, if we give somebody chocolate, this pathway also lights up.
The mesolimbic pathway begins in the mesencephalon of the brain stem in a nucleus called the ventral tegmental area. From there, it projects signals of dopamine to the nucleus accumbens. The nucleus accumbens has both a core and a shell, each of which project further to other brain regions. The core is thought to fire in response to the anticipation of pleasure, while the shell the consummation of pleasure.1
But what about when we get full?
Our desire for sugary or salty foods seems to diminish (depending, actually, upon what we are eating) with appetite. In other words, the less hungry we become, the less appetitive that ice cream begins to look. This simple fact leads us suspect that maybe the hormones and other molecules that help govern or guide our feelings of hunger and satiation are moving the pieces within the dopaminergic system.
The ventral tegmental area has receptors for both leptin and insulin. Leptin is released in proportion to fat stores while insulin after meals in response to escalating glucose levels. It makes sense that these two molecules, then, that in a rather significant way suppress our desire to feed, interfere with the pleasure we can derive from our food.
Explicit evidence for this suspicion is seen when we inject leptin straight into the ventral tegmental area. When we do this, the desire to eat sugary foods is diminished. The same goes for insulin: If we inject insulin straight into the ventral tegmental area, the rats become satiated — they illustrate no intent to reach for the sucrose.2
There are a handful of other molecules as well that project to the ventral tegmental area. These molecules originate in the lateral hypothalamus, a brain region strongly implicated in our ability to feel satiated.
Another way in which this relationship can be elaborated is though the deletion of the receptors that receive the signals. In effect, we can make the cells deaf.
When we do this to insulin, and break the receptors that it works on in the mesolimbic pathway, an obese phenotype emerges. This entails that the insulin was helping dull the pleasurable aspect of different foods, and thereby putting some brakes on eating. Without insulin to exert this effect, the pleasurable experience of eating drove at full speed, and showed no signs of stopping.
So it appears that the interaction between certain satiating hormones and the dopaminergic pleasure pathway is quite acute. The hunger molecules work to dampen our desire for sugary foods after we have ingested a meal, and the mesolimbic pathway subsequently remains inert. So your mom was right: eat your dinner before your desert.
More info at:
1. Kalivas, Peter W., and Nora D. Volkow. “The Neural Basis of Addiction: A Pathology of Motivation and Choice.” Foc Focus 5.2 (2007): 208–19. Web.
2. Khanh, Doan V., Yun-Hee Choi, Sang Hyun Moh, Ann W. Kinyua, and Ki Woo Kim. “Leptin and Insulin Signaling in Dopaminergic Neurons: Relationship between Energy Balance and Reward System.” Frontiers in Psychology Front. Psychol. 5 (2014): n. pag. Web.
