Benoit article on Mesomorphosis.com

http://www.mesomorphosis.com/article...d-violence.htm

Chris Benoit Tragedy - Anabolic Steroids, Aggression & Violence

by Jack Darkes, PhD
Assistant Professor, Department of Psychology
Director of Interventions, Alcohol and Substance Use Research
Institute, University of South Florida

The following is an overview of the scientific literature on the
relationship between anabolic-androgenic steroids (AAS) and
aggression. It is intended as a brief informational review without
references to the larger literature from which it draws. A more in-
depth review of these issues can be found in a series of articles on
this topic I wrote several years ago that are available at
Mesomorphosis.com and include voluminous scientific references. An
expanded version of this review is likely to appear in a fully-
referenced form in the future.

The Chris Benoit Murder/Suicide - What It Can and Cannot Tell Us

In events like the Chris Benoit family tragedy the alleged
perpetrator's characteristics inevitably suggest hypotheses and the
search for confirming evidence begins. Anabolic steroids or anabolic-
androgenic steroids (AAS) were blamed before prescription AAS were
found, as researchers and commentators alike called forth the popular
AAS-'roid rage connection. Such narrow reasoning backward from the act
and actor to the cause shows that jumping to conclusions can seem like
reasonable inference. One commentator even noted her preference for
blaming steroids over accepting that a person could commit this act,
as if assuming that, in the absence of some drug influence, such an
act would be a conscious decision, that the only possible causes were
drugs or volition. It is likely that research and data will not change
these views; still they should not be forsaken.

The facts are: anabolic steroids are illegal. They are powerful drugs,
yet research shows the vast majority who use them do so without
physical or psychological harm. Some users show negative psychological
effects, although such symptoms' direct relationship to AAS is
unclear. This lack of clarity and the gap between science and society
makes it important at such times to look to science and question
reflexive assumptions; in doing so I do not advocate AAS use, but that
we pay attention to science.

Case studies, even tragic ones, may suggest associations among events,
like drug use and behavior, but are not proof of causality. Too many
idiosyncratic factors confound the observed associations; their
salience belies their scientific value. Scientific knowledge is built
over time with studies using groups that represent the population or
process, not the individual. Science looks for convergence among
findings. It uses experiments to examine cause-effect relationships.
Science often reveals that what seems to be so is not. These various
designs have been used to explore the AAS-aggression relationship and
no scientist can say absolutely that AAS did or did not cause this one
event.

There are no controlled scientific studies of "'roid rage", a popular
but not scientific term. The AAS-aggression relationship has been
studied and the research can be summed up as inconsistent at best and
largely unsupportive of the hypothesis. AAS do not inevitably cause
aggression. No critical dose that invariably triggers aggression has
been identified. When aggression is observed among AAS users, it is
within a minority, the effect is not uniform at any dose, and it is
not clearly related to blood levels of hormones (Hence, the
anticipated toxicology report will be insufficient in a scientific
sense to settle this question in the Benoit case).

At a mean level, users self-administering AAS may report higher levels
of irritability, hostility or aggressivity than non-users. But users
and non-users differ in many ways and AAS self-administration could be
influenced by pre-existing aggressive tendencies or a desire for
increased aggression, both of which can predict drug-related behavior.
Psychology has long known that the best predictor of future behavior
is past behavior, a fact that may be pertinent to this case. For
instance, on average AAS users have been reported to be more
aggressive than non-users whether taking AAS or not, suggesting that
such characteristics may predate/predict AAS use and that AAS could
facilitate the expression of existing tendencies. Unfortunately, the
true longitudinal data needed to answer this question of pre-existing
differences and AAS use are lacking.

Randomly-assigned participants administered supra-physiological doses
of AAS in placebo-controlled experiments exhibit negligibly increased
aggressive responding; such assignment controls for potential
individual differences. Self-reported changes on aggression scales are
typically minimal if they do reach statistical significance. A
laboratory analog task (the Point Subtraction Aggression Paradigm;
PSAP) in which punitive responses to an alleged competitor's
aggressive responding index aggression has shown some reliable but
minor effects (and marijuana users in withdrawal scored similarly to
those administered AAS). Behavioral observations by significant others
note minimal behavior changes. Some increases in aggression have been
seen in participants administered placeboes, suggesting expectation
may influence AAS-related behavior. However, such human experiments
not only lack adequate active placeboes (normally using only inert
oils) to adequately determine AAS direct effects, but cannot ethically
administer "real world" AAS doses.

Animal studies allow for larger AAS doses to be used, but their
results often fail to generalize to the real world. For example, one
study (Ricci et al., 2007, in Behavioral Brain Research) cited in the
discussion of this tragedy administered AAS doses (e.g., a total 5mg/
kg/day of several AAS) over the complete adolescent period of animals
(30 days) and effects on aggression that lasted past cessation.
However, the equivalent treatment for a 100 kg human would be 3.5
grams of AAS per week non-stop for years. That regimen does not
reflect real world AAS use, either by typical dose or pattern of use,
nor does it conform to any known parameters in the current case. On
the other hand, consistent with human research, AAS-aggression in
animals differs as a function of individual characteristics. Steroid
administration increased overall aggression in existing non-human
primate groups, but the effect varied by social status; dominant
males' aggression increased while lower-ranking males' submissiveness
increased, suggesting an interaction between AAS and context/
characteristics.

It is clear that there is scant scientific evidence that AAS directly
cause aggression. What is often presented as evidence lacks external
validity. It is likely that any drug, illicit or prescription,
administered in high doses for a number of years would have
deleterious effects. Ultimately, a minority of self-selected AAS users
may show increased aggression, although the mechanism is not clear.
Experimental designs with random assignment control for self-selection
and find minimal if any evidence for a relationship. There is no
consistent relationship between symptoms and blood levels of AAS. The
discrepancies between the survey and experimental (including blood
levels) findings suggest a need to know more about how AAS interact
with individual characteristics and circumstances. That is the state
of the science on this issue.

There are an estimated 1 - 3 million AAS users in the US. Ghastly acts
such as the Benoit case are rare and, as science would predict, their
association with AAS use is virtually non-existent. Many other
characteristics are far more predictive of such events. It cannot be
said with certainty whether AAS contributed to this tragedy or not. If
they were involved, AAS were not a sole contributor but part of a
larger set of characteristics and circumstances. There is no
scientific evidence to suggest that AAS alone caused this behavior and
they are obviously not necessary for such events to occur. The
evidence does suggest that most AAS users do not become aggressive.
Nonetheless, science will, at best, play a small part in society's
verdict on Benoit and AAS in this tale and it will be another instance
where a drug is linked to a heinous act by association and, therefore,
the untested popular notions that dominate the headlines today will be
reinforced.

If blame were put aside for a moment, there are important lessons
unrelated to such simplistic notions that the Benoit tragedy can
impart to society. WWE officials say that Benoit tested negative for
AAS in April. If AAS is cast as a lone villain, then that was a clean
bill of health at that time. But, had society at large and the
surveillance program to which Mr. Benoit was subject been at least as
concerned with his emotional, familial, and social situation as with
his potential AAS use, this event may have been averted. Both science
and practicality suggest that, at most, AAS use should be one of
multiple foci here, as it should have been in April or before. No drug
test in April could have told us enough about this family's life nor
will any toxicology report that might follow.

If AAS are blamed and the richness of these lives ignored, then the
opportunity to prevent such rare events goes unrealized. Singling out
a drug to blame leads to fiery rhetoric, congressional hearings,
prohibition and scare tactics; none of these have succeeded in curbing
drug use, especially among those at greatest risk for harm. Most AAS
users do not experience negative effects and hence distrust the
message and the messengers, perhaps most notably among those who
should listen. Research has shown this many times. Blaming AAS diverts
focus from potential indicators of risk and predictors of harmful
outcomes. This is where science might be most helpful in dispelling
simplistic notions and in working toward more effective risk
identification, targeting of limited resources and reducing associated
harms.

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--
Curt