Commentary
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Simplistic explanations and convenient scapegoats belie the complexity of mass shootings.
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COMMENTARY
The recent horrific school shooting in Minneapolis has led, predictably, to widespread media coverage and much unwarranted speculation regarding the causes of mass shootings.1 The latter term has no single, universally accepted definition, but a frequently used definition is an event with a “minimum of 4 victims shot, either injured or killed, not including any shooter who may also have been killed or injured in the incident.”2 Many but not all school shootings qualify as mass shootings, though recent scholarship suggests that school shootings merit a distinct category, based on several distinguishing features.3
While mass shootings account for fewer than 1% of firearm deaths in the US, their frequency has increased in recent years.4 It is important to state that violence in general, and mass shootings in particular, do not lend themselves to single, monocausal explanations.5,6 Mass shootings are, however, disproportionately an American phenomenon, and are rarely seen at comparable rates in other industrialized countries.7 A comprehensive review of these background issues is beyond the scope of this article, but are covered in several recent articles.8-10
Our central concern here is to examine the claim that mass/school shootings are in some direct sense provoked or caused by the shooter’s use of antidepressant medication, particularly the selective serotonin reuptake inhibitors (SSRIs). We will focus on some of the more recent and methodologically sound studies. Our concerns were prompted by these recent remarks by the current US secretary of Health and Human Services (HHS), in response to a question about the Minneapolis school shooter1:
"At NIH we're launching studies on the potential contribution of some of the SSRI drugs and some of the other psychiatric drugs that might be contributing to violence. You know, many of them on there have black box warnings that warn of suicidal ideation and homicidal ideation. We can't exclude those as a culprit, and those are the kind of studies that we're doing."
We can dismiss at once the false claim that any currently available antidepressants in the US have black box warnings regarding “homicidal ideation.” However, since 2005, the US Food and Drug Administration (FDA) has required black box warnings regarding suicidal ideation among children, adolescents, and young adults—a controversial decision that remains a contested issue among psychiatrists and epidemiologists to this day. One recent (2024) systematic review concluded that the FDA warnings were associated with reduced physician visits for depression and increased suicide deaths.11
Further, it has been our experience that there is substantial confusion around the FDA’s Adverse Event Reporting System (FAERS). FAERS is a database maintained by the FDA that collects information about adverse events for the purposes of safety monitoring. However, adverse drug reaction reports are not verified and there is no certainty that the adverse drug reaction was caused by the medication. Thus, an adverse drug reaction may be due to underlying disease, other substances, or a host of other causal factors. We suggest here a careful consideration of the statement provided on the FAERS website: “Importantly, the FAERS data by themselves are not an indicator of the safety profile of the drug.”12
Our concern, however, is with the HHS secretary’s clear implication that SSRI antidepressants and some other psychiatric drugs may be contributing to violence and may be “a culprit” in the Minneapolis school shooting. Our focused review of several recent studies finds no credible evidence for this claim. Notably, the HHS secretary made his remarks before anything substantive was known regarding psychotropic medication use by the Minneapolis shooter.
Antidepressants and Violence
The term violence is obviously broad and ambiguous, in that it overlaps with several other terms in the literature, such as activation, irritability, anger attacks, and aggression. In our previous (2020) comprehensive review of this topic,13 we noted that “…A number of studies show an association between use of SSRIs and various forms of noncriminal aggression or violence,” while cautioning that “'association' does not demonstrate causation.” Specifically, we noted that,
“Sharma and colleagues published a large meta-analysis reporting a doubling in both suicidality and aggression in children and adolescents taking duloxetine, fluoxetine, paroxetine, sertraline, or venlafaxine. In contrast, an extensive review by Walsh and Dinan of all published papers linking serotonin, SSRIs, and aggression found "no convincing evidence to link the use of fluoxetine or other SSRIs with violent or suicidal behavior...On the contrary, there is a considerable body of evidence from the last decade to suggest that fluoxetine may be associated with improvement in anger and aggression both towards oneself and others."
We cautioned that,
“Many variables may explain these widely varying conclusions, including differing study methods; the particular drugs and drug dosages studied; use of concomitant medications; and perhaps most important, differences in underlying psychiatric diagnosis and psychopathology among participants.”
In brief, our 2020 review concluded that, “In weighing the existing evidence, we conclude that no direct connection between antidepressants and violence has been reliably established.”13 Since then, nothing in more recent studies have given us reason to alter our conclusion. That said, we should note that a study by Lagerberg et al found that SSRI treatment was associated with a modestly increased risk of violent crime (HR, 1.10)—particularly in those ages 15 to 25 years and ages 25 to 34 years (HR, 1.19 and 1.16, respectively).14
However, further analysis stratifying the cohort according to previous violent crime revealed that the elevated risk for violent crime convictions “seemed to be confined to the individuals with previous criminality,” compared to those with no criminal history (HR, 1.13 vs 1.07). In short, the study found that the elevated risk was almost entirely limited to the subset of individuals with a history of violent criminality.
Furthermore, Paul F. Bouvy, MD, PhD, and Marieke Liem, PhD's study, "Antidepressants and lethal violence in the Netherlands 1994–2008," found a significant negative association between the use of antidepressants and rates of both homicide and suicide in the Netherlands during the studied period. The study analyzed nationwide data from 1994 to 2008 on antidepressant prescriptions (including total antidepressants, SSRIs, and venlafaxine) and rates of lethal violence (homicide, suicide, and homicide-suicide). In essence, as antidepressant use increased in the Dutch population, rates of lethal violence decreased. The authors concluded that the study provides no support for a significant role of antidepressant use in increasing lethal violence. On the contrary: the findings point towards a potential beneficial effect of antidepressants on these forms of violence.15
Antidepressants and Mass/School Shootings
Recent research by Ragy R. Girgis, MD, and colleagues suggests that there are “…several important differences between mass murders involving academic settings and mass murders in general…”3 For example, while mass school murders “are largely perpetrated by individuals without a history of psychotic symptoms,” this group of perpetrators is more likely to show psychotic symptoms than are mass murderers in general. In addition, perpetrators of shootings in academic settings “…take their own lives almost half the time, a higher rate than seen among mass murderers in general.” Notwithstanding these important findings, our discussion of antidepressants will generally not distinguish between mass shooters targeting academic settings from mass shooters in general.
The preponderance of recent research does not point to a link between antidepressants and mass shootings; ie, there is little or no evidence showing that perpetrators of mass shootings are more likely than those in the general public to have used, or to have been prescribed, antidepressants prior to the shooting. For example:
Based on an analysis of the Columbia University Mass Murder Database, the lifetime prevalence of antidepressant use among mass shooting perpetrators over the past 30 years is 4%; and for any psychiatric medication, it is 7%. The 4% lifetime antidepressant use among mass shooters is much lower than the estimated 11.4% of US adults who took antidepressants in 2023. Girgis—a professor of clinical psychiatry at Columbia—states that, "All the data suggest SSRIs are not the problem." He suggests that the misunderstanding that SSRIs are linked to violence comes from individuals conflating findings about suicidal ideation and irritability with violence.19 Girgis further argues that, “There is no evidence to suggest that antidepressants, or any psychiatric medications, play a role in mass shootings or homicide, and the black box warning has nothing to do with violence or homicidality.”20 Moreover, broader analyses from the Columbia database—examining 82 incidents of mass murder, by any means, involving academic settings—reveals that severe mental illness, such as psychosis, is a factor in only a small minority of mass shootings.3,21
Concluding Thoughts
In the face of horrific tragedy, it is only human to want to grasp potential solutions quickly. Yet this desire must be tempered by the risk of grabbing the problem by the wrong handle. The best research to date indicates that most school shooters were not previously treated with psychotropic medications—and even when they were, no direct or causal link was found. Given the absence of credible evidence that antidepressants are a causal factor, we must return to an analysis of the multifactorial nature of mass shootings.
Mullen (2004) was the first to point out that perpetrators of mass shootings seemed to be following some type of “western script,” and were influenced by previous mass murderers who received significant media exposure.22 While there is no evidence that antidepressants cause complex criminal behavior, there are numerous descriptive studies indicating that the common motives of the perpetrators include resentment, envy, revenge, overvalued ideological beliefs, and infamy.23 In search of more effective solutions, the results of the FBI’s Study of the Pre-Attack Behaviors of Active Shooters may provide some direction.24 Perpetrators displayed 4 to 5 concerning behaviors over time that were observable to others around them, including verbal or written communications. In contrast, the 2 most common responses of others who had concern about the perpetrators were to communicate directly to the shooter (83%), or to do nothing (54%).
In the light of these FBI findings, rather than repeatedly returning to the specious hypothesis that antidepressants are causing mass shootings, more ground may be gained through efforts to educate and encourage the public to report warning signs to law enforcement officials, as well as training law enforcement to investigate more effectively the concerning behaviors of potential perpetrators.25
Dr Knoll is a professor of psychiatry and director of forensic psychiatry at SUNY Upstate Medical University in Syracuse, New York. He is also emeritus editor in chief of Psychiatric Times and clinical director of Central New York Psychiatric Center in Marcy.
Dr Pies is professor emeritus of psychiatry and lecturer on bioethics and humanities, SUNY Upstate Medical University; clinical professor of psychiatry, Tufts University School of Medicine; and editor in chief emeritus of Psychiatric Times (2007-2010). Dr Pies is the author of several books, including several textbooks on psychopharmacology. A collection of his works can be found on Amazon.
Acknowledgments: We wish to thank Dr Ragy Girgis for his helpful comments, and MsElaine Mallon for her responsible reporting on this issue. The views expressed here, however, are those of the authors unless otherwise indicated.
References
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