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Psychological
Bulletin
2001,
Vol.
127,
No- 3,
291-324
Copyright
2001
by
the
American
Psychological
Association. Inc.
0033-2909/01/55.00
DOI:
10.1037//0033-2909.127.3.291
Testing
Hypotheses
on
Specific
Environmental
Causal
Effects
on
Behavior
Michael
Rutter
Institute
of
Psychiatry
and
Virginia Commonwealth UniversityAndrew Pickles
University
of
Manchester
Robin Murray
Institute
of
PsychiatryLindon
Eaves
Virginia
Commonwealth University
There
have been strong critiques
of the
notion that
environmental
influences
can
have
an
important effect
on
psychological
functioning.
The
substance
of
these criticisms
is
considered
in
order
to
infer
the
methodological
challenges that have
to be
met. Concepts
of
cause
and of the
testing
of
causal effects
are
discussed
with
a
particular focus
on the
need
to
consider sample selection
and the
value
(and
limitations)
of
longitudinal
data.
The
designs
that
may be
used
to
test
hypotheses
on
specific environmental risk
mechanisms
for
psychopathology
are
discussed
in
relation
to a
range
of
adoption
strategies,
twin
designs,
various types
of
"natural experiments." migration
designs,
the
study
of
secular
change,
and
intervention
designs.
In
each
case,
consideration
is
given
to the
need
for
samples that "pull-apart" variables that
ordinarily
go
together,
specific hypotheses
on
possible causal
processes,
and the
specification
and
testing
of key
assumptions.
It is
concluded
that
environmental
risk
hypotheses
can be
(and have been)
put to the
test
but
that
it is
usually
necessary
to use a
combination
of
research strategies.
There
is a
vast literature
on the
topic
of
environmental
influ-
ences
on
behavior,
and
especially
on
their
role
in the
causative
processes
leading
to
psychopathology (see, e.g., Birch
&
Gussow,
1970;
G. W.
Brown
&
Harris, 1978, 1989; Collins, Maccoby,
Steinberg, Hetherington,
&
Bornstein,
2000;
Goodyer,
1990;
E. E.
Maccoby,
2000;
Rutter.
1981b,
1999a,
2000b;
Wachs, 1992,
2000).
Researchers,
clinicians,
and the lay
public alike
all
have
come
to
accept
the
importance
of
environmental effects deriving
from
psychosocial deprivation,
stress,
and
adversity. Despite this,
studies
of
psychosocial influences have come increasingly under
attack from several different quarters
and for a
range
of
different
reasons.
In
this
article
we
consider
first
the
nature
of the
critiques
of
the
evidence
on
environmentally mediated
risks,
move
on to the
concepts
involved
in the
hypothesis
of a
causal
influence,
and
then
discuss
the
variety
of
designs that
may be
used
to
test hypotheses
on
environmental
risk
mediations.
Michael
Rutter, Social, Genetic
and
Developmental Psychiatry Research
Centre.
Institute
of
Psychiatry, London.
England,
and
Department
of Hu-
man
Genetics.
Virginia
Institute
for
Psychiatric
and
Behavioral Genetics.
Virginia
Commonwealth University; Andrew Pickles. Department
of
Med-
icine.
School
of
Epidemiology
and
Health Science, University
of
Manches-
ter. Manchester, England; Robin Murray, Department
of
Psychological
Medicine,
Institute
of
Psychiatry; Lindon Eaves, Department
of
Human
Genetics,
Virginia Institute
for
Psychiatric
and
Behavioral Genetics, Vir-
ginia
Commonwealth
University.
We are
most
grateful
to
George Brown,
Avshalom
Caspi. Eleanor
Maccoby, Barbara
Maughan.
and
Judy Silberg
for
their
helpful
comments
on an
earlier version
of
this article.
Correspondence concerning
this
article should
be
addressed
to
Michael
Rutter,
Social. Genetic
and
Developmental Psychiatry Research Centre,
Institute
of
Psychiatry,
De
Crespigny Park, London
SE5
8AF. England.
Electronic mail
may be
sent
toj.wickham@iop.kel.ac.uk.
Critiques
of
Environmental Mediation
Methodological
Critiques
The
first
critiques emphasized
the
problems inherent
in the
reliance
on
retrospective recall, with evidence calling into question
both
the
reliability
and the
validity
of
data
obtained
in
this
way
(Radke-Yarrow, Campbell,
&
Burton, 1970). Subsequent research
has
both confirmed
the
reality
of the
problem
and
shown that
the
biases
tend
to be
minor (Maughan
&
Rutter, 1997; Rutter,
Maughan, Pickles,
&
Simonoff,
1998). Nevertheless,
for
good
reason, researchers interested
in
testing causal hypotheses have
increasingly
turned
to
longitudinal
data
because
they provide
the
evidence
on
temporal sequence that
is
essential
for the
study
of
within-individual
change—see
below
(P. B.
Jones, Rodgers, Mur-
ray,
&
Marmot, 1994;
R.
Loeber
&
Farrington,
1994; Rutter, 1988,
1994;
Van Os,
Jones, Lewis, Murray,
&
Wadsworth, 1997).
Another
criticism
of
most studies
was
that they relied
on
between-groups comparisons.
This
meant that differences
in
group
characteristics
had to be
used
to
infer
risks
as
they applied
to
individuals.
This
is an
uncertain enterprise (see, e.g., Farrington,
1988).
The
testing
of
environmental risk mediation
is
greatly
enhanced
by
being able
to
examine
within-individual
behavioral
change
in
relation
to
changing environmental risk exposure.
Changes over time,
as
indicated
by
behavioral measures
ob-
tained
at
multiple time points spanning
the
developmental period,
might
seem
to be the way
forward. Longitudinal data providing
documentation
of
change
are of
immense value
in
testing causal
hypotheses (Wierson
&
Forehand, 1994). Nevertheless, attention
has
been drawn
to the
methodological hazards. There
are
numer-
ous
examples
in
which apparent change
is
little
more than mea-
surement error (Fergusson. Horwood, Caspi,
Moffitt,
&
Silva,
1997:
Moffitt,
Caspi, Harkness,
&
Silva. 1993).
A
further
challenge came from Bell's
(1968)
reexamination
of
socialization
effects, with
the
conclusion that many
findings
were
291
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