Patients with affective disorders are sometimes given MAOI drugs. Unfortunately, there is a drug-food interaction with these drugs.
The Neurochemical Basis For Affective Disorders
Biogenic amines including serotonin and dopamine have been long suspected in affective
disorders. Various abnormalities of tryptophan have been reported. Low blood tryptophan has been reported. This could be explained if tryptophan was flooding the cells due to a transport error.
Serotonin has been linked to eating behavior in both humans and rodents. There is a theory that serotonin is deficient in affective disorders. If this was true, people with affective disorders (depression, mania, etc.) would eat constantly (hyperphagia). Some do, but most don’t.
One of my sources of information is a book called Psychopharmacology: Drugs, the Brain, and Behavior by Meyer & Luenzer. This book was published in 2005.
Tryptophan has long been suspected in depression. Delgado et al (1990) found that depression scores were negatively correlated with free plasma tryptophan levels. What this means is that patients were more severely depressed when the blood tryptophan was low.
Tryptophan in the blood “frequently appears low in depressed patients compared to controls” according to Meyer & Luenzer.
But what does this mean? It could mean that tryptophan is flooding the cells due to a transport error or mechanism.
Depression is a type of affective disorder. The glucocorticoid hypothesis is one theory for depression. There are stress-related endocrine abnormalities in this theory.
Unfortunately, many psychiatric drugs have resulted in a disastrous long-term side effect called “tardive dyskinesia”: Tardive dyskinesia occurs after years on the phenothiazine or atypical “antipsychotic”. This is an iatrogenic (man-made) form of Parkinson’s disease that can be permanent. The longer you are on the treatment, the greater your chances of getting it.
Orthomolecular treatments have good side effects.