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"Remember the country mouse's encounter with the town mouse, and the flurry and agitation into which it threw him." Marcus Aurelius, Meditations Book 11, c22

Introduction to Observations That Inspire

The Roman poet and philosopher Lucretius (c. 94 – c. 55 BC) left us with some remarkable observations on his only known work (On the Nature of the Universe). I suggest that his most remarkable perception of all is his description of dust particles in verses 112-140 of Book II. He invites readers to observe what happens to dust particles when sunbeams enter a building and cast shafts of light illuminating their random, accelerated motion (i.e., perturbation). Roman emperor Marcus Aurelius, writing two centuries later, would extrapolate this construct by warning the philosopher not to exchange the quiet of his own soul for the perturbation of the world.

And it does not stop there. I have often opined on a new quantitative theory of the deep brain's irresistible perturbation of self-destruction in specific acute psychological and physical states. This is beyond a qualitative "process of the mind" offered by so many in the field of suicidology quarreling over their territory.

A Grandmother's Perspective

Permit me to explain this new, unfamiliar concept in relatable and easy-to-understand terms.

My Russian maternal grandmother would prepare hot tea in a glass. Before pouring the steaming water, she would place a clinking metal spoon into the little beaker and then let the boiling water flow from the pot. "You see, child, the spoon protects the glass from cracking."

Now, it goes without saying that my grandmother had no understanding as to "why" the glass didn't break. Of course, we didn't discuss the relationships of temperature, volume, and pressure, or the random fluctuations of water molecules and positioning, or the forces of constant wall bombardment, more on one side than another, leading to hitting and breaking of the glass.

Yet, my bubbe (Yiddish for "grandmother") did understand "how" to prevent it from breaking. She knew perfectly well how to foresee and reduce an agitated, boiling liquid to improve the outcome, a favorable risk-benefit equation.

At this point, my readers may understandably ask, "what does this have to do with suicide?" It has to do with the relationship of "why" (i.e., etiologic causes, origins, and course of an illness or disease) to "how" (i.e., preclinical, and clinical foreseeability to avoid or reduce the occurrence of negative outcomes).

The Importance of "Why" and "How" in Suicide Research

The principles of "why" etiology and natural history of disease -- suicide among these -- are essential to recognizing opportunities for "how" prevention. The success of prevention lies in understanding both "why" and "how." This applies across the phenotypic illness spectrum.

In teaching, I often consider a few examples of "why," where a disease state is clinically perceived, suspected, and occasionally unrecognized, however likely to appear at later stages. This is the strategy of foreseeability, optimal standards of assessment, that includes the interplay of social, environmental, and biologic factors, from onset to resolution, which can either be recovery or eventual death:

1. Malignancy, hypercoagulability, migratory thrombophlebitis, leading to pulmonary embolus
2. Temporal cranial trauma, acute extradural hematoma, resulting in brain stem herniation
3. Borderline personality, micro-psychoticism, responding by repeated, deliberate self-harm
4. Iron deficiency anemia, non-pharmacologic akathisia, motivating intense suicidal behavior
5. Acute adjustment (stress) disorder, dysexecutive function with quantitative perturbation, precipitating imminent suicide

Of course, ideal prevention and treatment "how" strategies in any of the cases above include health promotion focused on social determinants and early clinical recognition, including pre- and post-test observations, to reduce pre-pathogenic, pathogenic, and latency period modifiable/antecedent risk factors.

"How" in Acutely Perturbed States

My work continues to evaluate, through effective screening, the impact of acute stress/adjustment disorder phenotypic expression on youth attempt rates within this natural history and thus preventing later stage demise. It has been through innovative statistical methodology in the integrated and intricate application of risk factor analysis, effective communication, integrated modeling, and utilizing Bayes' likelihood ratios and Markov one-step transition reverse probabilities. This requires the strict application of of strength, consistency, specificity, dose response, epidemiological plausibility, coherence, temporality, and so on, narrowing the correlation/causality relationship and improving the coefficient of determination.

Additionally, it requires the practice of a concept I refer to as "1 + X" in suicide phenotype "why" etiology, suggesting that one primary risk factor ignites the acceleration of the suicidal death, while other factors kindle its development. Recent retrospective analyses of my earlier published data confirm that the presence of neuropsychological dysregulation and polymorphic akathisia-like deficits (i.e., perturbation, alone or in combination, in the presence or absence of a pure youth stress disorder diagnosis, with or without ideation) accelerates a one-step suicide transition to extreme risk in these cases, anticipated and confirmed utilizing intricate Bayes' likelihood ratio and Markov chain probabilities.

The "how" in acutely perturbed suicidal crises involves understanding the immediate neuromodulation of noradrenergic, glutamatergic, and GABAergic system activation in these often unrecognized, unconventional cases. The main neural networks antecedent to and involved in these neuroimmune, excitotoxic/neuroinflammatory reactions must be treated with a "spoonful" of aggressive, yet judicious beta-blockade, anxiolytics, and nonsteroidal inflammatory medications in emergency department treatment.

It is often impossible in suicide research to make progress in answering such complex and atypical clinical questions that impact the safety of patients. Why? The "asking" by administrators and researchers alike is often stifled. Suicide research continues to lack an inquisitive or dimensional discussion of the interplay between "why" and "how."

Try putting a spoon in it!

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