"Suicide and Neuropsychiatric Adverse Effects of SSRI Medications: Methodological Issues"

Scientific Symposium

Marriott @ the Philadelphia Airport

Friday, October 4, 2002

10:45-11:30 a.m.



Distinguished Professor Emeritus, University of South Carolina

305 Sloan Bldg., 911 Pickens St, Columbia, S.C. 29208

Maris@sc.edu, 803-777-6870, http://www.suicideexpert.com/

ABSTRACT: This paper critically examines several methodological issues growing largely out of Daubert, pertinent to the question of whether or not SSRI medications can be said scientifically to cause suicide ideation, suicide attempts, and/or completed suicide.

There are several critical methodological issues involved in trying to determine scientifically, say, whether it is more likely than not that  any SSRI caused a particular suicide outcome.[1]  Many of these issues evolved out of Daubert v. Merrill Dow Pharmaceuticals (43 F.3d 1311, 1317 [9 th Cir., 1995]). 

In my own court experience (see curriculum vitae)[2] the drug companies invariably argue that depression (and often some other non-drug factors) causes suicide, never that their antidepressant does.  Thus, the question for the court, the trier of fact, or the jury is: “What objective, scientific criteria or empirical procedures would allow us to resolve the varying claims of plaintiff and defense experts?”

Some of the relevant methodological issues, criteria, or procedures that mainly grow out of Daubert are the following:

  1. The cases versus the controls normally (says Lilly) should have a relative risk (RR) or odds ratio of 2.0 or higher or other reliable methodologies.
  2. Whenever possible we must utilize double or triple-blind randomized clinical trials (hereafter “RCTs”) in our research designs.
  3. The evidence cited should be from relevant peer-reviewed scientific journals.
  4. Challenge/dechallenge/rechallenge studies are useful in suggesting drug or SSRI causation.
  5. We should do or cite epidemiological studies with adequate samples, controls, and appropriate statistical analyses.
  6. Theories or methods utilized should be generally accepted in the relevant scientific community or discipline.
  7. The investigator must make every effort to account for or rule out alternative explanations of the outcome.
  8. Testimony by scientific experts should be non-litigation driven.
  9. Purported outcome effects should be from similar purported causes.

(1)  The cases versus the controls normally should have a relative risk (RR) or odds ratio of 2.0 or higher (says Lilly) or other reliable methodologies.  For example, Donovan et al, 2000, studied 2776 deliberate self-harm (DSH) cases over 24 months.  In this study paroxetine (an SSRI) had a RR[3] of DSH of 1.9 versus Tofranil (imipramine) and a RR of 4.0 versus the tricyclic (TCA) Elavil (amitriptyline) (The RR for Prozac was 6.6).  In a related study of another selective serotonin reuptake inhibitor (SSRI), Jick et al., 1995, found that Prozac (flouxetine) had a RR for suicide of 2.1 versus Dothepin.  Fava and Rosenbaum, 1991, found the RR of emergent de novo suicide ideation was 2.7 in flouxetine users versus the non-flouxetine users (Cf., Mann and Kapur, 1991; Mann, 2000). Healy (2002) finds RRs ranging from 2.4 (suicidal acts) for the SSRIs v. placebo, from 4.3 (completed suicides for all SSRIs) to 10.0 for flouxetine (Cf., Healy, 2001).

Note: the Eli Lilly criterion of requiring a RR of 2.0 or higher is somewhat arbitrary (e.g., court appointed experts in Miller vs. Pfizer rejected an arbitrary “bright line” of 2.0 +) and was based on the assumption of a biological phenomenon with a single cause.  If there are multiple causes and a behavioral phenomenon, then the RR does not have to be as high as 2.0 to suggest a causal relationship (for example, Healy points out that in the case of  pertussis vaccine causing brain damage the acceptable relative risk was only 0.1 [Healy, 5/9/2002: ## 34 & 36; Cf., Healy, 2001]).  In sum, the cutoff point of a RR of 2.0 is arbitrary by the drug companies and is based on faulty generic assumptions; the required RR varies with one’s statistical design and assumptions.

(2)  Whenever possible we must utilize double or triple-blind randomized clinical trials (“RCTs”) in our research designs.  Usually when I testify I hear repeatedly: “Dr. Maris, please cite the double or triple-blind clinical trials in which (the antidepressant in question, such as Prozac) had a relative risk of 2.0 or higher for suicide ideation (SI), nonfatal suicide attempt (SA), or completed suicide (CS) versus the control AD.”  All evidence should be as rigorous as possible (Note: When Lilly drafted the Beasely protocol to test Prozac and suicidality it rejected RCTs in facor of a challenge/dechallenge design). In a double-blind clinical trial neither the proband (i.e., the patient or research subject), nor the experimenter knows which drug is being taken or administered.  This method helps reduce any possible bias.  Drug companies are typically very critical of case studies; such as that of Teicher, Glod, and Cole (1990), in which six patients developed intense suicidal preoccupation after 2 to 7 weeks of flouxetine (Prozac) treatment.  The alleged problems in such case or “anecdotal” (as the drug companies like to call them) studies is that the drug is known beforehand and the sample is small and nonsystematic, with few (if any) controls. 

One serious problem with clinical trials is that almost all of them are being done (and practically sometimes can only be done, given the cost involved…to answer the question: “Do SSRIs cause completed suicide” one would probably need at least 10,000 patients on SSRIs and 2 to 3,000 controls on placebo) by the drug companies, who obviously have a financial interest in the outcome of the research and who alone tend to have the necessary resources to conduct  RCTs (Of course, non-drug company experts can and have done RCTs) .  In many cases rigorous proof of drug effect causation is just not available.  I am not aware of any RCT by a drug company that tests the hypothesis that SSRIs cause suicide (See Healy, 2002 @ 12).  Note that the drug companies championing of clinical trials is a two-edged sword.  That is, if (and I don’t concede this) plaintiff experts cannot prove, say, that SSRIs cause suicide; then neither can the defendant drug companies prove that they do not.

RCTs have other serious scientific faults.  For one by virtue of rules to protect human subjects and related ethical considerations, usually seriously suicidal subjects are eliminated from the samples (for example, for fear that being assigned randomly to a placebo group might induce a suicide).  Often an exclusionary criterion from an RCT of antidepressants and suicide is the proband having previously made a suicide attempt.  It follows that the research subjects in RCTs often, if not usually, are atypically healthy (e.g., not very suicidal or depressed to start with).

Another problem with RCTs is that they are not designed to detect rare outcomes (what Beasley calls the “needle in the haystack”; Espinoza v. Lilly, 11/8/00 @ 76), like suicides (which occur at the rate of about 1 in 10,000 in the U.S. general population).  Often the statistical significance levels in RCTs are 1 to 5 in 100.  Thus, rare events that could have occurred are often missed by RCTs (Teicher & Cole, 1993 @ p. 207). 

Allow me to elaborate this crucial point.  There is a generic problem in predicting any rare events; they tend to lead to “false positive” predictions.[4]  For example, we have seen above that suicides occur in the general population at rates of 1-3 per 10,000.  I know of no studies that indicate exactly how many US suicides were taking SSRIs.  I found in my random sample of Chicago suicides[5] that 47% were moderately to severely depressed, using the Beck Depression Inventory.  Today most treated depressives are started on one of the SSRIs.  But Srole et al.(1962) reminds us that only about 20% of those diagnosed (in NYC) with a mental disorder are ever treated.  Furthermore, the side-effects of SSRIs related to suicide outcome are also rare (See Teicher and Cole, 1993); viz., akathisia, emotional blunting, psychotic decompensation, etc.

You get the idea; since suicides and SSRI side-effects related to suicide outcomes are rare, it is difficult (but not impossible) to demonstrate scientifically, by the drug company’s scientific standards, that SSRIs cause suicide.  Usually a statistical significance level is 1 to 5 in a hundred (i.e., .01 or .05 probablility).  If, say, suicides taking SSRIs and having, for example, akathisia[6]  occurs at a rate of less than 1-5/100, then the drug companies can (and do) always claim scientifically that the side-effect and suicide could have occurred by chance alone.

However, and this is important, just because drug effects or suicides are rare, does not mean that they were not caused by the drug,  It just means that by the drug company’s criterion or standard, we may (and sometimes we can prove a causal relationship by the drug companies own standards) not be able to prove that suicide was caused by their SSRI drug.  Note: neither can the drug company prove either that their SSRI drug did not cause the suicide (unfortunately, usually the plaintiff has the burden of proof here).  In short, the pristine, unreasonably lofty criterion (e.g., RR or significance levels) championed by the drug companies may be the problem, not that SSRIs don’t cause suicide.

Healy et al. (1999:107) points out:

“the use of RCTs by pharmaceutical companies is largely determined by registration requirements for evidence of some treatment effect.  The patients recruited to such studies are samples of convenience, which need not represent either the general population or any vulnerable population (such as suicides) within it.  These trials are not designed to answer the question of whether the drug on occasion can trigger an emergence of suicidality.  To date there have been no such trials (emphasis mine)….Quite simply, beneficial effects on suicidality in a majority of depressed patients do not outrule (i.e., rule out) drug-induced problems.” 

(3)  The evidence cited should be from relevant peer-reviewed scientific journals.  The peer-reviewed journal articles that plaintiffs cite in  SSRI court testimony are among the most respected in the scientific community and tend to have high rejection (low acceptance) rates for the articles reviewed by the best consulting editors.  For example, Donovan, 2000 appeared in the British Journal of Psychiatry; Jick et al., 1995  was in the British Medical Journal; Teicher et al, 1990 was in the American Journal of Psychiatry;  David Healey’s 1990 book, The Antidepressant Era was published by the Harvard University Press; the Fava and Rosenbaum 1991 article appeared in the Journal of Clinical Psychiatry. Mann & Kapur, 1991 was in the Archives of General Psychiatry.   These journals’ editorial boards are among the most rigorous and respected in the world (Cf., Healy, 2002: 41). 

One problem here is the sponsorship, even ghost writing, of purported scientific articles by the drug companies, who obviously have biases or at least preferences for the research outcomes (See Healy, passim).

(4)  Challenge/Dechallenge/Rechallenge studies are a useful and reliable methodology in suggesting drug or SSRI drug causation.  In a challenge/dechallenge/rechallenge study patients or subjects are given specific ADs /SSRIs (See Rothchild & Locke, 1991; King, Riddle, Chappell et al., 1991; Beasley rechallenge protocol for Lilly, 1991).  If an adverse reaction occurs, the drug may then be discontinued.  The adverse side-effect may also stop.  Finally, the AD drug may then be readministered and the adverse side-effect may reoccur.  Other things being equal, it is scientifically sound to posit in such circumstances that this drug was a proximate cause of the adverse side-effect (See Grounds et al., 1995; Teicher et al., 1990; Mann, 2000: 100).

(5) We should do or cite epidemiological studies with adequate samples, controls, and appropriate statistical designs.  “Epidemiology” is the study of the distribution and determinants of diseases and injuries (such as of suicide) in human populations (Cf., Healy, 2002: 17 ff).  One of the primary tools in epidemiology is the case-control method.  In a case-control design the probability of making a “type I” error (false positives; See Maris et al., 1992, Chapters 1 and 32) is called the “level of significance” (a or p) and the probability of making a “type II” error (false negatives) is represented by b, where 1 - b is called the “power” of the study.

In a case-control study ((say, of flouxetine or paroxetine suicides versus Tofranil (imipramine) and/or Elavil (amitriptyline) suicides)) the required size of cases (sample) is determined by:

The following table  (from Maris, 1981) provides an example of a simple explanatory statistic:

Beck Dep. Inventory Natural Deaths % Suicides%

None (0)

Mild (1-20) 

Moderate (21-25)












Mean BDI score


(n = 71)


(n = 266)


t-test for significant differences of means = 5.6, p = < .001

In this table we ask: Do the two death types (natural versus suicidal) differ significantly on depression levels?  Typically we assume that there is no difference (the “null” hypothesis or Ho) and then actually test for significant differences given certain assumptions.  If the test statistic (here a t-test, but other tests might include X 2, gamma, alpha, Z or F) reaches a certain level (e.g., p = .05, .01, or .001 = the probability of a type I error in rejecting Ho), then we reject Ho (with a known error factor, such as 5 times out of 100 for p = .05) and assume based on the test that there are statistically significant differences (here) in the two depression scores.

Of course, more sophisticated statistics can involve multivariate analyses and causal model testing (especially logistic regression and log-linear analyses); including estimating interaction effects among several independent variables in the models.

At issue in scientific studies and the law is what is the requisite degree of scientific certainty.  Often this boils down to the best available facts or data (Cf., M. Angell, Science on Trial, 1997, NY: Norton; See Healy, 2002:41: “Drug companies are commandering the appearances of science.”).

(6)  Theories or methods utilized should be generally accepted in the relevant scientific community or discipline.  One of the methods used to argue for suicide causation is the “psychological autopsy (PA).”  The PA can be defined as “a procedure for reconstructing an individual’s psychological (or “biopsychosocial”) life after the fact of death…in order to better understand the circumstances contributing to a death.”  Combined with the physical autopsy, the PA is a generally recognized and accepted method in the scientific community (See Maris et al, 2000: 66; Cf., Maris, 1969 and 1981).  I myself learned and applied this method originally from 1968 to 1973, as a Deputy Medical Examiner in Baltimore, Maryland and as a post-doctoral fellow and Associate Professor in Psychiatry at the Johns Hopkins School of Medicine.

(7)  The investigator must make every effort to rule out alternative explanations of the outcome.  Any bona fide scientific investigation should make every effort to rule out possible alternative explanations.  A scientific “rule-out” is not always possible (e.g., Mann, 2002, admits that suicide is multi-factorial; and I agree, see my general model of suicide in Maris et al., 2000: p. 58), but every effort should be made nevertheless (that is one reason why the scientific paradigm requires control groups).  For example, in arguing that an SSRI causes suicide, a scientist must try to control for the possible independent or interactive causative effects of depressive disorder, alcoholism, prior suicide attempts, other psychotropic drugs the patient may be taking, a positive history of suicides among their first-degree relatives, etc. (See Maris et al, 1992: Chapter 1).  Note, the law usually allows that a drug effect can be “a”  proximate cause of an outcome.  It does not require that the drug be the proximate cause.  A drug may be a “necessary condition” for an adverse or untoward outcome (i.e., “that without which not”), but it need not be a “sufficient condition (i.e., the only required condition).

(8)  Testimony by scientific experts should be non-litigation driven. Although I cannot speak for other experts, my own testimony is non-litigation driven,  I have written widely about the causes of suicide (e.g., See Maris, “Suicide,” Encyclopedia of Human Biology, Volume 8, 2 nd edition, pp. 255-268, 1997, NY:Academic Press and Maris, “Suicide,” The Lancet, 2002)  in an academic, non-court context.  I have authored 20 books and numerous peer-reviewed scientific journal articles.  I was Editor-in-Chief of the only American scientific suicide journal for 16 years.  When I do appear in court I have testified roughly equally for plaintiff and defense (viz., 53% for the plaintiff and 47% for the defense in 123 lifetime forensic cases).  Since I do believe and opine that SSRIs can cause akathisia, emotional blunting, and/or psychotic decompensation (among other suicidogenic side-effects) and ultimately can be a proximate cause of suicide; none of the drug companies have ever asked me to testify on their behalf.  My testimony over about forty years averages only about 20% of my professional time.  I have turned down many court cases .

(9)  Purported outcome effects should be from similar purported causes.  Finally, any alleged drug effects methodologically should result from generically similar drugs.  GSK (then SKB) argued in Tobin that paroxetine was a unique SSRI with a unique side-effect profile.  Although paroxetine, flouxetine, sertraline, etc. do have some relatively distinctive effects (e.g., paroxetine is more sedating than flouxetine and can have serious withdrawal effects), they are all nonetheless “SSRIs” (Cf., Healy, 2001: 28 and 36).

As such the literature and research on flouxetine is generically relevant to paroxetine (and vice-versa)  and all SSRIs.  They don’t call them “SSRIs” for nothing.  This is important, because a great deal more scientific study has been made of flouxetine than of other SSRIs at this point in time.

Although a great deal more could and probably needs to be said about SSRIs and suicide, allow me to close with a few observations about SSRI neuropsychiatric side-effects and my general model of suicide (See slide Figure 2.6).

The traditional suicidogenic triumvirate of psychotropic drug reactions are (1) akathisia, (2) emotional blunting, and/or (3) psychotic decompensation (Healy, 1990; Healy Rule 26 statement in Tobin v. SmithKline, 2001; Maris in Coburn v.GlaxoSmithKline, 2001; Teicher and Cole, 1993 (who note 9, not just 3 reactions), and Healy, Langmaak, and Savage, 1999; Cf., Beasley’s (2000: p. 37 ff.) “signature” suicidal SSRI drug reaction pattern, which he calls, following Teicher, “ego-dystonic”).

Teicher and Cole (1993) delineate 9 “clinical mechanisms” by which SSRIs can induce or exacerbate suicidal tendencies by: (1) energizing depressed patients, (2) paradoxically worsening their depression , (3) inducing akathisia, (4) inducing panic attacks, (5) switching patients to mania or hypomania, (6) causing insomnia or interfering with sleep architecture (esp. with REM sleep), (7) inducing an organic obsessional state, (8) promoting personality disorder with borderline traits, or  (9) producing EEG or other neurological disturbances.

(1) Akathisia is a diffuse psychomotor restlessness which affects the patient’s entire body (van Putten, 1975; Griest  and Jefferson, 1992; Raskin, 1972; Teuth, 1993; Healy, 2002:32).  Akathisia occurs in some patients taking antipsychotic and/or antidepressant drugs (especially, the SSRIs; See Healy, 2002: 13 – “About 5% of subjects drop out of RCTs due to agitation or akathisia.”).  Patients experience akathisia as a profound inner disquiet and sometimes commit impulsive violent acts [like assault, murder, suicide, or murder-suicide] while under its influence.  Often these violent acts are totally out-of-character for the patient (See Forsyth v. Lilly, 1997).

In normal individuals akathisia is a little like drinking many consecutive cups of black coffee on an empty stomach.  It is a very real, often terrifying experience, which has prompted some patients to murder, suicide, or commit murder followed by suicide.  For example, in 1991 (Haffercamp/Sorg v. Lilly) I testified in the Prozac case of Sandra Sorg, a nurse in Madison, Wisconsin who actually requested she be put in a straightjacket while akathisic, to keep her from being able to hurt herself.

She eventually suicided.

(2) Emotional blunting is when the patient reacts to a drug with feelings of flat affect, listlessness, and/or apathy (Healy, Langmaak, and Savage, 1999; Mann & Kapur, 1991).  Patients with emotional blunting often become anhedonic (also a trait of major depression); that is, they develop an inability to take pleasure in life experiences that they would normally have found pleasurable or stimulating.  Emotional blunting can cause one to feel depersonalized or have difficulty concentrating.

(3)  Psychotic decompensation.  Here the investigator needs to ask if the subject became psychotic after taking an SSRI.  For example, did they know the difference between reality and fantasy or delusion?

Another important point in countering SSRI drug companies is that depressive disorder is not the sole proximate cause of most suicides. Lilly likes to argue that depression, not Prozac, causes suicide (Cf., Healy, 2001: 35-36; Healy, 2002: 39).  Real life is not that simple.  Unfortunately, Prozac can make depressed patients worse, especially early on in the treatment (e.g., by causing akathisia, emotional blunting, psychotic decompensation, increased anxiety (at times Lilly suggested in clinical trials that an anxiolytic or beta blocker be given concomitantly with Prozac (Fawcett, 1992, 2002, argues that anxiety is highly suicidogenic), decreased impulse control (which can be a induced state of any serotonergic drug), increased anger, increased aggression…See Brown, Linnolia, and Goodwin, 1992).  

The SSRIs affect the patient’s vegetative symptoms of depression (viz., their sleep patterns, appetite, libido, vital signs, and energy) first, before (note, too, that about 30% of Prozac takers have no  antidepressant response to it) they raise the patient’s mood or lower their suicide ideation; thereby energizing some patients who are still depressed and suicidal (Healy, Langmaak, and Savage, 1999; Maris, 2002; Anderson et al., 1995; Fisher et al., 1995: Mann and Kapur, 1991).

In some cases ingesting Prozac has been associated with de novo, emergent suicide ideation after treatment (Fava and Rosenbaum, 1991; Teicher et al., 1990; Healy, 2002; King, Riddle, Chappell et al., 1991).

If the disease of depression causes suicide (as Lilly tends to argue), then why would it cause a suicide early on in the treatment with Prozac (Cf., Healy, 2002: 39)?

Although suicide has a complex, multifactorial aetiology, SSRIs can be a trigger of suicide. See my general model of suicide (Maris et al., 2000: 58, Figure 2.6, attached).  Most suicide have depressive episodes, which among other factors helps put them in what I call the “suicide zone” (column # 4); viz., at the threshold of committing suicide.

They are then usually medicated with an SSRI (column # 3),  and then most of them (remember RCTs are not appropriate for detecting rare outcomes) improve over the next 4 to 8 weeks and never commit suicide (remember, too, that about 30% of patients taking Prozac have no therapeutic response and are usually switched to alternative or combined treatments (“cocktails”), like other SSRIs, ECT, anxiolytics, etc.).

However, some of those patients treated with SSRIs,  have adverse reactions (including but not limited to akathisia, hypomania,, emotional indifference or blunting, psychotic decompensation, heightened anxiety, sleep disturbances (especially terminal insomnia), rashes, etc.) which in turn may paradoxically (raising brain and body 5HT or 5-HIAA is supposed to lower suicidality; See Äsberg, 1976) increase their suicidality and thrust them back into the suicide zone and sometimes over the threshold into suicide.

As Healy et al. note (1999):

“One problem with such side-effects early in treatment may be a risk of misattribution by the patient to a worsening of their illness.”

The bottom line is that SSRIs can and do change patients, sometimes for the worse.  It never ceases to amaze me that drug companies can argue (with a straight face) that their SSRIs are powerful enough to alter the course of a deadly, recalcitrant depressive disorder, but never (to hear them tell it) adversely affect the delicate psychological and physiological balance of seriously ill individuals.  Their claim flies in the face of commonsense and much of the scientific evidence that has accumulated.  The truth is that SSRIs do change many ill people.  Often they save their lives; however, occasionally, SSRIs kill people who would not have died otherwise.


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[1] For my general position on suicide see R.W. Maris, Suicide, The Lancet 2002 (July 27) 2002; 360:319-26.

[2] Since 1991 I have testified in or about eleven SSRI cases: (1) Wesbecker v. Lilly, 1991 (2) Haffercamp/Sorg v. Lilly, 1991 (3) Saines v. Lilly, 1994, (4) Greer/Rosenbloom v. Lilly, 1995, (5) Gianguilio v. Lilly, 1997, (6) Forsyth v. Lilly, 1997, (7) Williamson v. Lilly, 1998, (8) Hartman v. Pfizer, 1998, (9) Madison v. Pfizer, 1999, (10) Coburn v. GSK, 2001, and (11) Lown v. Lilly.

[3] A “relative risk”  is how many times more likely the event in question (e.g.,  suicide or akathisia) is likely to occur in the experimental group (e.g., SSRI  users) versus the comparison or control group (e.g., non-SSRI users) under controlled, scientific conditions or assumptions (e.g., randomized double-blind clinical trials).

[4] See Maris et al., 1992, Assessment and Prediction of Suicide.  NY: Guilford Press, pp. 6-7.

[5] See Maris, R.W., 1981, Pathways to Suicide.  Baltimore: John Hopkins Press.

[6] “Akathisia” is diffuse psychomotor restlessness which affects the patient’s entire body and mind.