Author's note: This article may make your brain hurt. Seriously, a criticism of this work is that it is too difficult. Well. Saving life is difficult. If it were easy, everyone would be doing it. Indeed, everyone is doing suicide prevention and "Where are we?" Historically high U.S. death rates and absolute numbers. Therefore, the traditional model must change.
"Natural selection will never produce in a being any structure [or process] more injurious than beneficial to that being..."
-- Charles Darwin
Patient A: "IT had me by the hair and wouldn't let go!"
Patient B: "IT was leading me to my execution!"
Patient C: "IT terrorized me!"
Mother of suicidal Patient D: "No one saw IT coming."
(IT = imminent self-toxicity)
In an attempt to provoke discussion, not bamboozle my well-mannered and insightful readers, I submit that an ominous trend in is the difficulty to engage in curiosity with higher order questioning. In a new process of unconventional suicide risk modeling, and utilizing the aforementioned cases, let's follow the first two steps of the scientific method.
Observation: The common elicitors of anaphylaxis are foods and drugs. However, some cases of high morbidity "" (IA) have been reported and defined by underlying psychological factors where other causes were excluded and no positive response to usual therapeutic intervention achieved.
Question: Counterintuitive to Darwin's above citation, can a unique subset of adjustment disorder (AD) be understood as a final common IA pathway involving stress induced programmed cell death (PCD), IT, and unforeseen suicide ("")? Anaphylactic suicide should not be confused with the exceptionally rare case of gruesome, self-intentioned of food or drug which the victim is aware they are allergic to.
What Did I Just Ask?
It is impossible to make progress in answering such complex and atypical clinical questions that impact the safety of patients when asking itself is often stifled. In particular, suicide research continues to lack an inquisitive or dimensional definition of suicide. As I will explore in the proceeding paragraphs, is suicide a consequence of rationality, a result of disordered thinking, or, on occasion, an act motivated by a heretofore unrecognized, genetically predisposed process?
For illustration, there is a strong temptation in violence assessment to emphasize depression, substance abuse, personality disorders, psychosis, and ideation. Moreover, the traditional evaluation is often reduced to simplification or generalization, to engage in dichotomous "either-or thinking," i.e., normalize a patient's aggression (false -) or construct dangerousness when absent (false +). Similar to moving beyond a two-plane x-ray of the chest with MRI, a deeper level of suicide risk study analysis is required.
How do we meaningfully weigh differences in and contributions of genetic underpinnings, epidemiological likelihoods, cross disciplinary observations, dysexecutive symptoms, and even serendipity in this calculation? Let's take a closer look.
Wait For the "IT" Factor
Although most of the questioning and analysis here is speculative, the prying hypothesis derives, in part, from scores of detailed statements of successfully resuscitated suicidal patients and recent, tantalizing research findings that independently confirm an trajectory.
Could abnormal PCD gene expression when experiencing acute interpersonal threats of humiliation, pandemic related problems at home, work, and school, or other psychological stresses, lead to atypical autoantibody defects? Is it possible for this once compatible, adaptive, and constrained PCD system to go terribly wrong with agonizing cries of apprehension and impending doom and the total destruction of the organism?
Intriguing clues have been reported recently. have demonstrated between suicide, inflammatory cytokines, and mediated pathways, for example, in the , a brain region involved in emotional and social behavior, inhibition of unwanted actions, and thus suicidal vulnerability.
What Might "IT" Look Like?
Could a salient or unanticipated stress be capable of provoking a heretofore "inside out" unrecognized ? Can the resultant kindling of be stopped once begun, or does it inevitably lead to critical and unusual autoantibody attack with often unobvious and grave neuropsychiatric symptoms in vulnerable persons?
Now, in the of suicide attempts to date, researchers have identified a region of the genome containing DNA variations that increase the risk of attempted suicide (SA). The study results suggest that the genetic underpinnings of SA are partially distinct from those of commonly cited psychiatric disorders associated with SA.
Rich in controversy as the medicalization of personal misfortune, a "distinct" and suicide-specific genetic subset.
Beyond criticism of classification and reimbursement, AD carries 12 times the rate of suicide as those without the diagnosis. Importantly, the genetic salience of the psychological trauma (permeable circuits) to the person, not its outwardly perceived severity, is determinative in symptom development and SA outcome. 2018 pre-pandemic CDC data and AD proximal suicide death associations range from to over .
The public health consequences of the pandemic and the potential association between stress responsive AD, atypical symptom development, and SA may become .
As a neuroscience example of the vulnerability, permeability, and rapidity of this atypical symptom expression, consider and compare the annoyingness (proximal stressor) of the song "It's a Small World (After All)" in healthy individuals. Within milliseconds of exposure, this innocent repetitive stress pattern "tricks" (situationally dependent epigenetic expression) the unpredictable yet susceptible mind into experiencing or "circus" movements, for moments or longer.
However, clinicians responsible for the evaluation and treatment of AD susceptible persons are often unable to understand, diagnose, or control correctly the acute disorganizing "circus" of IT development which often occurs within hours to days of the stressor. Transfixed "noisy" doom anxiety with dysexecutive function may transition quickly to often lethal and .
Whew! The Conclusion
Genetic failures in PCD decisions may also define a heretofore unrecognized role in a proportion of stress-responsive AD suicides. I have previously highlighted the evaluation and specific treatment of this group of patients, and proposed a neurological algorithm with bedside testing to expedite its diagnosis. I hope that continuing curiosity may help identify an implicated risk locus biomarker and pathway that contributes to understanding suicide vulnerability in this "IT" phenotype, not mediated by traditional immunologic or psychiatric disorders.
Russell Copelan, MD (Ret.), lives in Pensacola, Florida. He graduated from Stanford University and UCLA ľֱ School. He trained in neurosurgery and completed residency and fellowship in emergency department psychiatry. He is a reviewer for Academic Psychiatry and founder of , an originator and distributor of violence assessments. One of Copelan's four sons is an EMT/paramedic in Colorado Springs, and his daughter is a Denver-based physician assistant.