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1. Suicide, Aggression, and Depression
A Theoretical Framework for Future Research
FREDERICK zyxw
K. GOODWIN zyxw
Ofice of Scientific Director
Intramural Research Program
National Institute zyxw
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f Mental Health
Building zyxwv
10, Room 4N-224
Bethesda, Maryland 20892
I have been asked to provide some overview comments focusing on future directions
for research on suicide. First, we need to ask ourselves these questions: zy
( 1 ) What has
been firmly established by widely replicated studies? (2)What are the emerging areas
of consensus? (3) What are the remaining areas of complete ignorance? The field of
suicide research has, until recently, lagged behind the mainstream of advances in
clinical psychiatry-advances that have been so dramatic in the past two decades.
The papers presented in this volume are a healthy indication that the methods and
conceptsfruitful to research in psychopharmacologyand in the major mental disorders
(particularly, the affective disorders) can also invigorate suicide research.
In the past, the study of suicide has evolved in a peculiar way-that is, in two
separate intellectual traditions, each maintaining an isolation from the other. On the
one hand has been the psychosocial focus of the suicide prevention movement, and,
on the other hand, the clinical focus on suicideas an integral part of major psychiatric
illness. The suicide prevention focushas primarily derived its experiencefrom working
with people who threaten or attempt suicide, while the clinical-medical focus comes
primarily from dealing with completed or nearly completed suicide as part of psychiatric
illness, most often major depression. Although the domains of attempters and com-
pleters do overlap somewhat, by and large they represent distinctly different popu-
lations.’ Unfortunately, this distinction has too often been glossed over; a problem to
which others in this volume have pointed, as well. In my view, this important dis-
tinction should orient future research on suicide.
The presentations here serve to reemphasize what is already clear from the lit-
erature: the single most important risk factor for actual suicide is the presence of a
major mental disorder, particularly major depressionor manic-depressiveillness, and,
lessfrequently,personality disorders,alcoholism,schizophrenia and organic disorders?
It strikes me that one could conceptualize the affective disorders as conveying the
“core” vulnerability to suicide, while the other disorders contribute additional risk
factors such as impulsivity psychosis, and reduced cognitive function.
Another fundamental reality repeatedly emphasized here is that of genetic vul-
nerability. TABLE1 illustrates the data from the Schulsinger et a!. study: which
employed the adoption strategy, one of the better ways to tease apart “nature” from
“nurture.” What is most interesting about these results is that the association between
suicide in a subject and a family history of suicide in the biological parents (but not z
351

2. GOODWIN SUICIDE,AGGRESSION zyxwv
& DEPRESSION zyx
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limited by the kinds of patients who come to a particular treatment setting. The next
generationof clinical-biologicalstudiesin psychiatry should undertake sampleselection
using standardized epidemiological techniques. A relevant example of the need for
epidemiologicaltechniques derives from the reports of suicide ‘‘clusters.” It is not at
all clear that these reports will stand up to rigorous epidemiological replications. For
example, the initial reports of “cIusters’’ of leukemia were not substantiated by sub-
sequent, controlled epidemiologicalstudy.
Another critical conceptual issue highlighted in this volume is the distinctiqn
between “trait” and “state.” Even when one can demonstrate a trait variable, it is
difficult to assess the degree to which it may be influenced by overlying state effects.
To deal with this problem, I suggest that we focus on intensive, longitudinal studies
with small numbers of patients carefully selected as being in a high-risk group. Only
in this way can we accomplish the multiple simultaneous measures that will permit
a teasing apart of trait and state variables. Then one can tackle the larger populations,
with sharpened hypothoses and instruments more likely to yield results in which one
can have confidence. This longitudinalapproach should be at two levels: zy
(1) the entire
life course of an illness (which admittedly is not likely to be funded with the current
short-term oriented research grant policy); and (2) short-term longitudinal studies zy
within an episode of illness. Biologically, one has no reason to assume that the initial
phase of an illness episode is the same as later (compensated?) phases. For example,
with rapidly cycling manic-depressive patients, there are biological changes that ac-
cumulatewith an increasingnumber of episodes.Thesechangesimply that eachepisode
functions as a stress, with the development of a “sensitization” reaction. With relation
to suicide, Dr. Jamison asked when in the course of a particular illness is the risk for
suicide g:eatest? This question should be studied.
Dr. Asberg reviewed the common sources of variance in biological studies in
psychiatry. I think it is fair to say that none of us who work in these areas has
consistently been able to control for all of these variables in the same study at the
same time. Incidentally, one of the most interesting sources of variance is season?
FIGURE
1illustrates the seasonal peak in suicides, derived from a review of numerous
studies. This information should allow us to factor out some of the variance in the
literature and to focus high-risk studies at the appropriate time, i.e., early spring.
I would like to discuss briefly some newer approaches to enlarging our under-
standing of suicide. Important as the linkage between suicide and major diagnosis is,
it would, nevertheless, be helpful if more studies could focus on suicidal behavior as
the independent variable, relating it to a whole range of clinical, biological, and
psychologicalassessments.And there are many clinical questions to be answered. For
example, psychometric and psychophysiologicalcorrelates of aggression/impulsivity
would be of particular interest. Sensation seeking, the evoked response, reaction time,
field dependence, to name a few of the traditional measures, should all be explored.
It is very important to stick to a commonsensehypothesis. There are far too many
instances where an investigator becomes inundated by massive amounts of data ob-
tained without benefit of a coherent hypothesis. The data are then turned over to a
computer and a statistician, associations are produced, and then post hoc conceptual
formulationsare derived; this turns the process upside down. It is foolhardy to crunch
large numbers of observations through powerful discriminate function analyses so as
to produce “significant” associations and then to expect, de now, to extract biological
or clinical meaning. Any associations so generated should be considered meaningless
until replicated in a fresh sample. Unfortunately, the literature too often stops with
the interestinginitialassociation and we never see the replications.More commonsense
“eyeballing” of the data would allow us to make better use of powerful statistics.
Another issueis that of special populationsthat might advanceour suicideresearch.

3. 354 zyxwvutsrq
ANNALS NEW YORK ACADEMY OF SCIENCES zy
Especially important, in my view, would be a focus on first-degree relatives of those
who have committed suicide in the absence of a psychiatric diagnosis and/or the
absence of a family history of psychiatric illness. Or consider the normal subjects who
fall in the “suicide” range in an associatedbiological [e.g., 5-hydroxyindoleaceticacid
(5-HIAA)] or personality (e.g., impulsive) measure. For example, are the low 5-HIAA
normal controls more likely to have a trait of impulsivity?
One especially important population is the one with bipolar manic-depressive
illness-the subgroup at the highest risk for suicide. The data described here suggest
that for the bipolar patients, the serotonin-suicideassociation may not pertain. If true,
this suggests one of two possibilities: (1) The illness itself is so dominant as a risk
factor for suicide that it “overrides” the serotonin-impulsivity contribution seen in z
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18
16
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12
10
8
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2
J F M A M J J A S O N D
PEAK OCCURRENCE OF SUICIDE X MONTH
FIGURE 1. Monthly peak occurrences of suicide: a review of studies.
other diagnostic groups. (2) Serotonin alterations are imbedded in the pathophysiology
of bipolar illness itself, thus washing out serotonin-suicidecorrelations. There is some
evidencesuggesting that bipolar illness may involve serotonin disturbances more than
other subgroups of depressed patients. It is, therefore, possible that it is a lowered
serotonin function in bipolar illness that contributes to the high suicide rate among
these patients.
This volume has also reminded us that we need to look at the epidemiology of
treatment. These are not only scientific issues, but urgent public health questions. To
what extent does vigorous treatment of major depressive illness prevent suicide?What
has been the impact of successful lithium prophylaxis for bipolar disorder on the

4. GOODWIN SUICIDE. AGGRESSION zyxwvu
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suicide rate? Dr. Jamison presented some intriguing data from three major lithium
clinics indicating a substantial reduction in suicide in this population (lithium is also
known to enhance and stabilize central serotonin systems); controlled studies are
needed.
The horizons of biological research are expanding rapidly as a result of new
technology. Once we have carefully defined the appropriate questions and the appro-
priate populations, we will, no doubt, find these techniques of great potential benefit.
For example, brain-imaging strategies should allow us to evaluate whether the dis-
turbed areas of brain identified from postmortem examination might be reflected in
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in vivo measures. Not only can we now study regional metabolic activity, but
also we can now look at specific receptor types including serotonin receptors. Related
to these research questions is a robust literature on animal models of depression and
of aggressive behavior and even of self-destructivebehavior. Animal models are con-
venient because they allow us to ask a question that has always fascinated me: Not
only is there the more often asked question of what is the impact of a neurobiological
substrate on psychosocial change, but, further, what is the impact of psychosocial
change on a neurobiological substrate?
It has been encouraging to note here the beginnings of an apparent rapprochement
between psychosocial approaches to suicide and the clinical-biologicaltradition.
REFERENCES
1.
2.
3.
CLAYTON,
P. J. 1985. Suicide. Psychiatr. Clin. North Am. 8 203-214.
POKORNY,
A. D. 1964. Suicide rates in various psychiatric disorders. J. Nerv. Ment. Dis.
SCHULSINGER,
F., S. S. KETY,D. ROSENTHAL zyxw
& P. H. WENDER.
1979. A family study of
suicide. In Origin, Prevention and Treatment of Affective Disorders. M. Schou & E.
Stromgren, Eds.:277-287. Academic Press. London, England.
4. EGELAND,
J. A. & J. N. SUSSEX.
1985. Suicide and family loading for affective disorders. zy
5. GOODWIN,
F. K. & K. R. JAMISON.
Manic-Depressive Illness. Oxford University Press.
139 499-506.
JAMA 254 915-918.
New York, N.Y. (In preparation.)