Hi! I'm Tetyana. I write the Science of Eating Disorders blog. This is the SEDs-associated tumblr. It is less formal. I post about eating disorders, mental health, psychology, neuroscience, skepticism, and reblog pretty art/photos.
Tryptophan is an amino acid found in food, and a precursor to serotonin.
Patients with AN have an “overdrive” in the serotonin system, producing/releasing more serotonin, as well as a different ratio of two receptors on the receiving end (“Neuron B”)
This overdrive leads to higher anxiety and harm-avoidant traits.
Reducing caloric intake results in less tryptophan —> less serotonin being made —> reduces the feelings that resulted from an overdrive of the serotonin system (anxiety, harm-avoidant temperament, etc..)
BUT, the nervous system is not static. It adapts to a reduced intake and compensates.
It compensates by putting MORE receptors on Neuron B, so that there are more opportunities for the limited serotonin released, to bind.
GIVEN THESE CHANGES
when an anorexic eats: suddenly there is more tryptophan —> more serotonin in the system —> EVEN more anxiety. Because now, there’s lots of serotonin, but there are also a LOT of receptors on “Neuron B”, and the more receptors serotonin binds to, the more changes occur that in the end may lead to heightened anxiety, harm-avoidance, etc…
when an anorexic continues restricting: changes in the neuropeptide systems (increase in stress-hormones for example, and many other things) drive restriction FURTHER, and contribute to changes in behaviour and cognition (prolonged starvation definitely changes the way one views themselves and the world),
This of course, perpetuates the cycle. Leading to MORE restriction, and so on..