The mental disorders that are typically all put under the category of anxiety disorders are not all of one kind in terms of functioning of the serotonergic system, new research suggests. A team of researchers from the University of São Paulo; the Imperial College of London; the University of Western Australia and the University of Toronto, reanalyzed the results of six other studies.
The studies had looked at effects of acute reductions in tryptophan, the precursor of serotonin, a substance that makes the communication between neurons, in patients who had received successful treatment for their disorder, with either a serotonergic antidepressant action or cognitive-behavioral therapy for individual anxiety disorders.
Such treatment can bring about sudden lowering in serotonin levels in the body, giving information about the role of this neurotransmitter in many disorders and psychological functions.
Sub-clustering Anxiety Disorders
The reanalysis confirmed, in subjects with disorders psychiatric, predictions from a theory developed by researchers Bill Deakin and Frederico Graeff.
According to this theory, acute reductions in serotonergic levels would cause worsening of symptoms in patients with a subgroup of disorders more related to fear, but not in those with psychiatric disorders more related to anxiety, even though all of them are grouped under the single term “anxiety disorders” and treated with serotonergic antidepressants.
Lead author Felipe Corchs, of the University of São Paulo, says:
“The idea of responses to threatening stimuli causing feelings and emotions related to fear and anxiety, as well as a myriad of subgroups within these responses, is not new. However, our study gives an important step towards sub clustering of disorders once it is based on one of the most important neurotransmitters involved in these reactions and in the fact that it was tested in actual psychiatric patients”
According to the authors, this distinction is important to the ongoing efforts to re-categorize psychiatric disorders based on etiological variables. It could also help give direction to the development of new treatments.
“Importantly, the data must be interpreted in the light of the fact that our results are a reanalysis of studies that had as main objective the assessment of the effects of acute tryptophan depletion in samples grouped by disorders. Further studies need to be developed with specific methodology to identify the exact clinical characteristics of patients who have these two pharmacological profiles independently of the current diagnostic criteria of the DSM and ICD. This may contribute to future etiology-based diagnostic criteria”, notes Corchs.