Antidepressant-Induced Violent Behavior:
The Case for Pharmacogenomic Testing
At the Mind-Body Clinic personalizing treatment means much more than tailoring an intervention to each patient's unique history and symptom pattern. It also means, to the extent possible, matching every prescription, whether pharmaceutical, botanical, or nutritional, to the patient's individual genetic profile. (See the Laboratory Testing in Mental Health page for more details on the tests we run.) For example, genetic variations in the enzymes that comprise the cytochrome P450 (CYP450) system, which are involved in phase 1 detoxification of drugs and herbs, have a profound impact on whether or not a patient will derive a therapeutic benefit from a prescription, as well as the likelihood that he or she will have a significant adverse reaction. These reactions are not always relatively benign, like emotional flatness, amnesia, cognitive dysfunction, or reduced libido. They can include severe conditions like mania, psychosis, seizures, ataxia, paralysis, stoke, and suicidal and homicidal thoughts and behavior. While these more alarming adverse reactions are considered "rare," the latter term is defined by some (as in the article below) as a frequency of one in a thousand -- a rate of occurrence far too common for events that are so devastating.
This article by two Australian forensic psychiatrists is a deeply disturbing but compelling case review of a sample of patients diagnosed with medication-induced akathisia or serotonin toxicity who had been referred for evaluation and treatment. Eight of these patients had committed murder. Others had attempted suicide or engaged in serious violent behavior. The authors did a genetic profile on all of their 129 patients and found that when compared to a random sample of primary care patients, those referred to their forensic clinic had a much higher frequency of variant (under or over-functioning) genes for their CYP450 enzymes. All 10 of the most extremely violent had one or more genetic variations that are consistent with an impaired capacity to metabolize the drugs they had been prescribed. None of these patients had exhibited such behavior prior to being medicated. And all returned to their premorbid personalities upon discontinuing antidepressants. The tragic narratives contained in this study can be viewed as cautionary tales, reminding us all that sometimes the failure to address the biological uniqueness of each patient can have catastrophic effects.
Stephen J. Ducat, ND, PhD