Let’s start with a few givens (i.e. things that are well documented and known):
- Cortisol is the “stress” hormone. It is good in small amounts (getting you up in the morning, running away from lions) and bad in the chronic long term (immune suppression, abdominal “beer belly” obesity).
- Serotonin is the regulator of the six F’s: Fight, Flight, Food, Falling asleep, Feeling good, and… Sex. Too much is bad too little is bad. The same story as cortisol.
- Serotonin is involved in regulating cortisol secretion by the 5-HT(2a/2c) receptors (more serotonin, less cortisol)
Let’s step into the much neglected world of serotonin research on obesity. When’s the last time you’ve heard in pop culture about serotonin in any other way than depression? Maybe I’m reading the wrong news sites but the interplay here is important, however rarely talked about.
Serotonin has a strong entanglement with carbohydrate consumption. Additionally, carbohydrates significantly raise blood plasma levels of tryptophan. This tryptophan is then transported into the brain and is the precursor for serotonin. In a normally functioning system this would cause satiety, as it increases serotonin levels (and lowers cortisol).
It also turns out there are different polymorphisms for the serotonin receptor modulating cortisol. The lucky homozygotes for the -1438G allele had increased body mass and abdominal distribution of body fat along with less suppression of cortisol with dexamethasone than the other genotypes.
It seems serotonin could be a huge mechanism for failure. A disorder in producing serotonin could lead to the overconsumption of carbohydrates with little to no satisfaction (but the craving sensation would linger). An issue with the serotonin receptor modulating cortisol (or too little serotonin in the first place) could mean that despite a rich carbohydrate meal, the cortisol levels would never respond- leading to the unfortunate and unnecessary sequestering of fat. Dieting and food scarcity, while at first may seem like a good idea for dieting, does significantly boost cortisol levels and lead the vicious regain of weight once one strays from the path. Indeed, when given antidepressants that work on promoting serotonin bioavailability, it reduces food intake and circulating cortisol levels. One paper even concludes:
[...] there is evidence that some selective serotonin reuptake inhibitors are effective as antiobesity drugs.”
But before you rush out to get some Prozac, it’s important to realize that all of this is a function of eating carbohydrates. I have been searching, but it has been difficult to find and prove my theory here- that going low carb rehabilitates the serotonin system. This paper seems to have an extremely positive association between low carb diets and better sleep, mood, and memory (functions relating to serotonin). Also because most low carb advocates will stand by the idea of eating until you’re full- there is no starving cortisol mechanism kicking in- thus helping the body recover from cortisol overproduction.
It’s at least food for thought…
- 5-HT2A Receptor Gene Promoter Polymorphism in Relation to Abdominal Obesity and Cortisol, Rosmond, Bouchard et al. Obesity Research, Volume 10, Issue 7, pages 585–589, July 2002.
- Effects of normal meals rich in carbohydrates or proteins on plasma tryptophan and tyrosine ratios, Wurtman, Wurtman et al. American Journal of Clinical Nutrition, January 2003 vol. 77 no. 1 128-132.
- Long-term Effects of a Very Low-Carbohydrate Diet and a Low-Fat Diet on Mood and Cognitive Function, Brinkworth, Buckley et al. JAMA Internal Medicine. 2009;169(20):1873-1880. doi:10.1001/archinternmed.2009.329.
- Regulation of Appetite: Role of Serotonin and Hypothalamus, Sharma and Sharma. Iranian Journal of Pharmacology. Vol 11, 2, 2012.