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Nl·:'l:l9 t'.88I04Ic Canada

 Potential Psyehologieal Markers

for the Predisposition to Aleoholism

Jordan Bernt Peterson

Department of Psyehology
MeGill University
Montreal, Quebee, Canada

Mareh 1991

A thesis submitted to the Faeu1ty of Graduate Studies and

Researeh in partial fulfillment of the requirements for the
degree of Doetor in Philosophy.

e J.B. Peterson, 1990

-7
, j

...
: .,
'

l
~Ialional Library Bibliothèque nationale
of Canada du Canada

Canadian Theses Service Service des thèses canadiennes

Ottawa. Canada
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ISBN 0-315-67484- 9

Canada
 Abstract
Sons of male alcoholics (SOMAs) are at incLeased risk
for the development of alcoholism, and are apparently
characterized by other a~normalities. It is possible that one
or more of these abnormalities might ~êrVe as a marker for
the alcoholic predisposition. Research described in thls
thesls, conducted ln the hopes of Identlfylng such a marker,
was designed (1) to separate the relatlve pharmacologlcal and
psychologlcal effects of acute alcohol Intoxlcation upon
neuropsychologica! functlonlng; (2) to Investlgate the
neuropsychologlcal functlon of SOMAs wlth a multlgeneratlonal
family history of male alcoholism; (3) to examlne the
relatlonship between SOMAs' neuropsychological functlon and
their cardlovascular hyper-reactlvity to threat of and
aversive stimuli; and (4), to investlgate the relatlonship
between a number of cardiovascular response patterns and
voluntary weekly alcohol consumptlon. These studles are
linked conceptually, wlthin the context of a general the ory
of informatlon-processlng and actlon.

2
 Résumé

Les fils non-alcooliques de péres alcooliques (SOMAs)

ont un risque élevé de développement de l'alcoolisme, et

sont caractérisés par d'autres anomalies. Il est possible

que certaines de ces anomalies puissent servir de marqueurs

pour la prédisposition à devenir alcoolique. La recherche

décrite dans cette thése, conduite dans l'es~nir.

d'indentifier de tels marqueurs, avait pour objectif (1) de

séparer les effets pharmacologiques et psychologiques

relatifs de la consommation aigue et toxique d'alcool du

fonctionnement neuropsychologique, (2) d'~tudier le

fonctionnement neuropsychologique des SOMAs ayant une

histoire multifamiliale d'alcoolisme dans la lignée

paternelle, (3) d'examiner la relation entre le

fonctionnement neuropsychologique des SOMAs et leur

hyperreactivité cardiovasculaire à la menace et à des

stimuli causant de l'aversion et (4) d'étudier la relation

entre un nombre de configurations de réponses

cardi.ovasculaires et la consommation volontaire hebdomadaire

d'al~ool. Ces études sont reliées conceptuellement dans le

contexte d'une théorie générale du traitement de

l'information.

3
 Acknowledgements
Dr. Robert O. Pihl supervised the research described in
this thesis. Dr. pihl took a calculated risk when he accepted
my original application to McGill. Biased perspective leads
me to much admire that calculation. His skepticism and
analytical ability helped me transform loose associations
into logically structured scientific arguments, and his
extensive knowledge of the general psychological literature
enabled me to place my theorizing within a proper, practical
context. Dr. pihl provided me with generous aggravation-free
financial support, and with time whenever l wanted it - which
was often. l believe that my association with him constituted
one of those fortunate working arrangements that everyone
wishes for, but seldom attains. l consider it a privilege to
have worked under his supervision.
l would also like to thank Dr. Peter Finn, with whom l
collaborated extensively. l believe that Dr. Finn, Dr. Pihl
and l formed a whole greater than the sum of its parts, and l
hope to continue working with both of them in the future.
The Douglas Hospital - McGill University Alcohol
Research Group provided me with financial support for five
years. A number of its members were of particular help. It
was a privilege to meet and to work with Dr. Frank Ervin, Dr.
Roberta Palmour and Dr. Maurice Oongier. It was a pleasure to
benefit from their collective experience and to make
acquaintance with their remarkable personalities.

4
 A number of other people also helped me complete the

research that led to my dissertation. Jennifer Rothflelsch,

..
- Philip Zelazo, and Debble Ross, undergraduates at the time,
are all pursuing graduate degrees ln psychology now, and made
substantlal contributions to the first study described in
this thesis. Jean Seguin, graduate student under Dr. Pihl,
collaborated with me to complete the third study. Rhonda
Amsel contributed invaluable statistical advice whenev2r l
contacted her. r found her interesting personally and helpful
professionally. Judy Young, Dr. Plhl's secretary, was always
extremely decent to me as well, and aided me whenever she
could. l would also like to thank the members of my
committee, Dr. Barbara Sherwln and Dr. Blaine Dltto, and the
staff of the McGlll Psychology Department. The six years l
spent here were perhaps the best in rny life.
My wife, Tammy, helped keep me upright and disciplined
durlng some trylng tirnes, and deserves recognition for her
patience. My rnother and father have always supported my
ambitions, and the relatlonship l have with thern ls a source
of unceasing comfort. l hope that l will have the opportunity
to reward thelr falth and patience.

5
 Table of Contents

TITLE PAGE 1

ABSTRACT 2

RESUME 3

ACKNOWLEDGEMENTS 4

TABLE OF CONTENTS 6

LIST OF FIGURES 9

LIST OF TABLES 10

NOTE REGARDING MANUSCRIPTS AND AUTHORSHIP 11

PREFACE AND STATEMENT OF ORIGINALITY 13

INTRODUCTION 16

Alcoholism: Consequences 16
Alcoholism: Familial Transmission 16

Characteristics of SOMAs 20

Behavioural characteristics 20
Cognitive characteristics 24
Psychophysiological characteristics 27
Reaction to alcohol 31
Biochemical characteristics 34

STUDY 1 & 2 37

Introduction to Study 1 38

Study 1: Acute Alcohol Intoxication and 39

Cognitive Functioning
Abstract 39
Introduction 39

Method 40
Subjects 40
Design & procedure 40
Results 42
Blood alcohol level 42
Subjective intoxication 42
Effects of expectancy 42

6
 Tests associated vitrr the 43
frontal cortex
Tests not directly associated 43
vith the frontal cortex
l Discussion 43
Table 1: Blood Alcohol Concentrations 42
Table 2: Subject Intoxication Measures 42
Table 3: Tests of Cognitive Function 44
References 45
Introduction: Study 2 48
Study 2: Cognitive Dysfunction and the Inherited 49
Predisposition to Alcoholism
Abstract 51
Introduction 52
Method 54
Subjects 54
Design and procedure 56
Results 63
Discussion 66
conclusion 70
References 71
Table 1: Tests of Cognitive Function 77
Table 2: Correlation Matrix 78
COMMENTS: STUDY 1 & 2 79

Theoretical Overview: Information Processing, 80

Neuropsychological Function and the
Inherited Predisposition to Alcoholism
Abstract 82
Introduction 83
Information processing, active exploration 84
and escape
Cortical structure and information processing 88

.. ,~ Characteristics of sons of male alcoholics 93

 The possible effect of alcohol on SOMAs 108

Conclusion 112

References 116

Table 1 134

Figure 1: Theoretical path 135

Figure 2: Neuropsychological path 137
Figure 3: Observable anomalies 139
Figure 4: Theoretical effect of alcohol 141

Discussion and Introduction to study 3 143

Study 3: Alcohol-Induced Heart Rate Change, 144

Family History, and Prediction of Weekly
Alcohol Consumption by Non-Alcoholic Males

Abstract 145

Introduction 146

Method 150

Subjects 151
Procedure 153

Results 155

Demographies and blood alcohol level 155

Psychophysiological measures 155
Prediction of drinking behaviour 160

Discussion 164

References 168

Table 1: Simple R(2) values 174

Table 2: Cross tabulation results 175

Figure 1: Per cent change in heart rate 176

Figure 2: Mean dr inks per week 178
Figure 3: Per cent change in heart rate 180

FINAL COMMENTS 182

REFERENCES 186

8
 List of Figures

Theoretical Discussion
t
~ Figure 1: Theoretical path 135
Figure 2: Neuropsychological path 137
Figure 3: Observable anomalies 139
Figure 4: Theoretical effect of alcohol 141

study 3

Figure 1: Per cent change in heart rate 176

Figure 2: Mean drinks per ~eek 178
Figure 3: Per cent change in heart rate 180

.~.

9
 List of Tables

study 1

Table 1: Blood Alcohol Concentrations 42

Table 2: Subject Intoxication Measures 42
Table 3: Tests of Cognitive F~nction 44

study 2
Table 1: Tests of Cognitive Function 77
Table 2: Correlation Matrix 78

Theoretical Discussion

Table 1 134

study 3
Table 1: Simple R(2) values 174
Table 2: Cross tabulation results 175

10
 Note Regarding Manuscripts and Authorship

Note: The McGi11 University Faculty of Graduate studies and

....::-
Research requires that rule 7 of their Guidelines concerning
Thesis Preparation be cited in full in those theses to which
it applies. Rule 7 is cited below, in accordance with this
requirement:

"The candidate has the option, subject to the approval of the

Department, of including as part of the thesis the text, or
duplicated published text (see belowl, of an original paper,
or papers. In this case the thesis must still conform to aIl
other requirements explained in Guidelines Concerning Thesis
Preparation. Additional material (procedural and design data
as weIl as descriptions of equipment) must be provided in
sufficient detail (e.g. in appendices) to allow a clear and
., .....
precise judgement to be made of the importance and
originality of the research reported. The thesis should be
more than a mere collection of manuscripts published or to be
published. l i must include ~ general abstract, ~ full
introduction and literature review and ~ final overall
conclusion. Connecting texts which provide logical bridges
between different manuscripts are usually desirable in the
interests of cohesion.
It is acceptable for theses to include as chapters authentic
copies of papers already published, provided these are
duplicated clearly on regulation thesis stationery and bound
as an Integral part of the thesis. Photographs or other
materials which do not duplicate weIl must be included in

11
 their original form. ln such instances, connecting texts are
mandat~ and supplementary explanatory material is almost
always necessary.
The inclusion of manuscripts co-authored by the candidate and
others is acceptable but the candidate is required to make an
explicit statement on who contributed to such work and to
what extent, and supervisors must attest to the accuracy of
the claims, e.g. before the Oral Committee. Since the task of
the Examiners is made more difficult in these cases, it is in
the candidate's interest to make the responsibilities of
authors perfectly clear. Candidates following this option
must inform the Department before it submits the thesis for
review."

:~
~-

12
 Preface and statement of Originality
This thesis presents information unique in a number of
manners. The literature reviev is extensive, and originally
structured. study 1 is unique because of its methodology, and
in its findings. A balanced-placebo design has never been
applied to the problem of determining the cognitive effects
of expectancy of and acute-alcohol intoxication. In addition,
the application of tests standardized on populations vith
knovn forms of brain damage to acutely alcohol-intoxicated
normals has never been attempted. Study 2 is unique primarily
because it tests the relationship betveen a particular
pattern of abnormal cognitive functioning, and cardiovascular
reactivity to threat of and aversive stimulation, and because
it examines this relationship vithin the context of the
.T.-
predisposition to alcoholism. This contrlbution ls
significant because it links tvo general phenomena normally
considered in isolation, applies them to a common, serious
form of psychopathology, and provides for the possibillty of
attributing both to a single factor. study 3 presents the
flrst hard evidence that a putative marker for the
predisposition to alcoholism actually is related to voluntary
veekly alcohol consumption, among individuals theoretically
at risk for alcohol abuse, and among normals.
In addition, the thesls contains a unique application of
a general model of neuropsychological functlon to the problem
of the alcoholic predisposition. This model unites the
studies contained in the thesis vith the relevant general

13
 literature, and contains numerous ideas for further
~.
investigation.
~
With regards to my specific contribution, and that of
others: the thesis introduction is based upon the latest
revis ion of a paper created during a intensive three-year
collaboration between Dr. Pihl, Dr. Finn and myself. Dr. Pihl
outlined the original structure of the pa,~=, published in
the Journal of Abnormal Psychology, wrote the introduction
and conclusion, and extensively edited each of perhaps twenty
successive drafts. Dr. Finn completed the review of
psychophysiological and biochemical characteristics of SOMAs,
and also edited each draft. l reviewed the relevant
literature on behaviour and cognitive function, edited each
draft, and attempted to stylistically unite the whole into
some form of literary unity.
study l, published in the Journal of Studies on Alcohol
(pages 114-122, volume 51(2), 1990), l designed, with Dr.
Pihl's guidance and direction. Jennifer Rothfleisch and
Philip Zelazo helped me select and organize the test battery,
and run aIl 72 subjects. l analyzed the data, and wrote the
paper. Study 2, in press in the Journal of Studies on
Alcohol, l designed and wrote, with Dr. Pihl's input, and
analyzed with Dr. Finn, who contributed data from hls earlier
studies on the cardiovascular reactivity of SOMAs. Study 3,
presently submitted for publication to Alcoholism: Clinical
and Experimental Research, l designed, analyzed and wrote,
with the help of Dr. Pihl, Jean Seguin, who set up the data

14
 bank used in analysis, and Dr. Finn, who contributed data
from his earlier studies, referred to previously. The
theoretical discussion, which has been accepted for
publication in Neuropsychology Review, is the result of
extensive discussions between Dr. Pihl and 1, influenced by
Dr. Finn, written by me and edited by Dr. Pihl.
1 certainly did not lack for help completing the
research described in this thesis. However, this help took
the form of collaboration and the work described herein can
accurately considered an original, personal contribution •

.'.-'"
.'>

15
 Introduction
Alcoholism ~ Consequences
Alcohol causes more problems than any other drug, vith
the possible exception of nicotine. Most people in North
America drink upon occasion, and 5 to 10 per cent of adults
can be considered alcoholic (Kamerov, Pincus and MacDonald,
1986). The vast majority of these are men (Adrian, 1984).
Alcohol abuse has serious personal and social consequences.
Chronic ethanol consumption heightens individual risk for
heart and 1iver disease, brain degeneration, and cancer, and
often seriously interferes vith normal fetal development.
Alcohol intoxication predisposes otherwise normal people to
engage in acts of interpersonal aggression, both as
perpetrators and as victims. Suicide is more common among
~
~. drunken individuals. Intoxicated drivers are involved in a
significant proportion of fatal traffic accidents. Finally,
alcohol abuse is the leading cause of potentially productive
vork-years lost. In 1983 alone, the Americans spent fifteen
billion dollars on primary treatment of alcoho1 abuse, and an
additional $116.7 billion dealing vith its secondary effects
(Pihl, 1983; Adrian, 1984; Harvood, Napolitano and
Kristiansen, 1984).
Alcoholism ~ Familial Transmission
The familial nature of a1coholism was noted by
Aristotle, Plutarch, and the authors of the 01d Testament.
Prior to the time of Darwin and Mendel, this familial
predisposition vas assumed to be the consequence of

16
 Lamarckian transmission of acquired traits. Researchers
working early in the post-Mendelian age, with an adequate
-1-
," ."
genetic model at hand, nonetheless generally attributed the
familial alcoholic pattern to learning (Goodwin, 1985). These
workers assumed that modelling, poor parenting, and various
additional environmental factors were responsible for the
development of alcoholism in children of alcoholic parents -
and indeed for the development of alcoholism in general. The
debate between nature and nurture continues to the present
day. While it is obvious that the effects of the environment
(most obviously, the availability of alcohol) help determine
the development of alcohol abuse, direct inheritance appears
to contribute as weIl.
A variety of adoption, family, twin and half-sibling
studies have investigated the degree to which familial
factors play a causal role in the etiology of alcoholism. The
adoption studies (Goodwin, Schulsinger, Hermansen, Guze and
Winokur, 1973; Cadoret and Gath, 1978; C1oninger, Bohman &
Sigvardsson, 1981j Cadoret, Cain and Grove, 1980) provided
support for the idea that genetic influences determine
predisposition to alcoholism, but have been subject, in
particular, to intense methodological criticism (Lester,
1988; Littrell, 1988; Murray, Clifford and Gurling, 1983;
Searles, 1968). These reviews have focused primarily on
criticizing the somewhat arbitrary criteria by which heavy
and moderate drinking by the experimental subjects were
distinguished from alcoholism, per se. Cotton (1979)
thoroughly reviewed the family studies, and concluded that

17
alcoholics were approximately 7 times more likely to have an
alcoholic parent than non-alcoholics. The relative
contribution of environmental and heritable factors could not
be determined in the course of this review. Researchers
involved in four twin studies (Kaij, 1960; Kaprio, Koskenvuo,
Langinvainio, Romanov, Sarna and Rose, 1987; Partanen, Bruun
and Markkanen, 1966; Pickens, Svikis, McGue, Lykken, Heston
and Clayton, 1991) concluded that pattern of alcohol
consumption, including normal social drinking, was
significantly affected by heritable factors. Two cited by
Gurling, Murray and Clifford (1981) did not support this
conclusion. Kaij (1960) and Hrubec and Omenn (1981) reported
that the twins in their studies were concordant for
alcoholism more often than would be dictated by chance, but
Gurling et al. (1981) and Partanen et al. (1966) did not
concur. It should be noted, however, that those twin studies
with the largest subject population produced evidence that
supported the supposition that heritable factors influence
transmission of alcoholism (Hrubec and Omenn, 1981) and
general pattern of alcohol consumption (Partanen et al.,
1966). Schuckit, Goodwin, and Winokur (1972) and Goodwin,
Schulsinger, Moller, Hermansen, Winokur and Guze (1974)
studied half-siblings raised with and without an alcoholic
parent. These researchers concluded that the environmental
effects of exposure to the alcoholic parent did net
additionally increase the heightened rate of alcohelism ameng
their subjects.

18
 In toto, it appears that familial influences indeed
helps determine predisposition to alcoholism. Murray et al.
(1983), who offered a balanced review of the relevant
literature, suggested that genetic factors comprise one such
influence, modest but significant. Sons of alcoholics, in
particular, appear to be at elevated risk. This increased
risk has been estimated at three (Goodwin, 1985) to nine
times (Cloninger, Bohman and Sigvardsson, 1981) that of sons
of non-alcoholics. The precise nature of the inherited
predisposition remains unknown, in part because many who are
interested in its determination derive their conclusions from
the study of seasoned alcoholics. Pihl and Spiers (1978)
determined that 93% of 270 sampled studies examining the
"addictive personality" assessed subjects already in
treatment, for addiction. This approach cannot help
distinguish between those factors that might distinguish
individuals predisposed to drug or alcohol abuse, and those
that results as a consequence of that abuse.
Non-alcoholic sons of male alcoholics (SOMAs) appear to
be more suitable subjects than alcoholics for those
interested in studying the predisposition to alcoholism.
Examination of their youthful idiosyncracies, if any, in
evidence prior to chronic alcohol ingestion, might lead to
the discovery of markers associated with the alcoholic
tendency, or to the identification of underlying causal
psychological or physiological factors. The results of the
experimental research on subjects at high risk for alcohol
abuse, for various reasons, have been reviewed with varying

19
degrees of completeness by Tarter, Alterman and Edwards
(1985; 1988), Schuckit (1985), Zucker and Lisansky-Gomberg
(1986), El-Guebaly (1986) and Cloninger (1987). Relevant
experimental and theoretical analyses presented in these
reviews, and other pertInent and more recent studies that
focus specifically on SOHAs are summarized below. This brief
summary includes research classified according to commonality
of flnding into five subsections: behaviour, cognition,
psychophysl010gy, reaction to alcohol, and biochemistry. The
theoEetical overview presented later in the thesis contains a
more detaIled descriptIon of the meaning of these findings,
and an elaborated critical dIscussion.
Characteristics of Sons of Hale Aicoholics
Behavioural Characteristics
SOHAs have most consistently been described as conduct-
disordered and hyperactive (Alterman, Searles & Hall, 1989;
Cantwell, 1972; Horrison & Stewart, 1971, 1973; Nylander,
1960 (part 1); Stewart, deBlols & Singer, 1978; Tarter,
Hegedus, Goldsteln, Shelly & A1terman, 1984); sole1yas
conduct-disordered (Aronson & Gilbert, 1963; Cadoret & Gath,
1978; Harden & Pihl, 1988; Nylander, 1960 (part 2); Nylander
& Rydelius, 1982; Rydelius, 1978, 1981, 1983a, 1983b); and as
impulsive (Aronson & GIlbert, 1963; Knop, Teasda1e,
Schulsinger & Goodwin, 1985; Saunders & SchuckIt, 1981;
Schuisinger, Knop, Goodwin, Teasda1e, & Hikkelson, 1986).
These descriptors have been most frequently applied during
childhood, but often remain applIcable in adu1thood as we11.

20
 They appear as valid even within those studies that provide
control for environmental influence (Cadoret & Gath, 1978;
1 Horrison & stewart, 1971, 1973; Nylander, 1960 (part 2);
stewart, deBlois, & Singer, 1978). This conduct-disordered/
hyperactive pattern of behaviour generally first presents a
serious problem in the early years of school, when it
disrupts the academic environment.
Children of alcoholics (male and female) have also been
frequently described as conduct-disordered (Chafetz, Blane &
Hill, 1971; Fine, Yudin, Holmes & Heinemann, 1976; Haberman,
1966). Such children frequently manifest behavioural patterns
associated with Attention Deficit Disorder and/or
hyperactivity (Fine et al., 1976; Sher & Alterman, 1988),
appear hypersensitive to auditory and visual stimulation
(Fine et al., 1976), and have difficulty in regulating
excitement and mood (Lund & Landesman-Dwyer, 1979).
Various longitudinal studies make the same points.
Children or adolescents who develop alcoholism later ln life,
as adults, are often antisocial and/or impulsive (Block,
1971; Hagnell, Lanke, Rorsman, & Ohman, 1986; Hechtman, Weiss
& Perlman, 1984; Hoffman, Loper & Kammeier, 1974; Jones,
1971; Loper, Kammeier & Hoffman, 1973; Hagnusson & Bergman,
1988; HcCord & HCCord, 1960; Nylander, 1979; Nylander &
Rydelius, 1973; Ricks & Berry, 1970; Robins, 1966; Vaillant,
1983), characterized by impoverished interpersonal ties
(Jones, 1968; HcCord & HCCord, 1962; Honely et al., 1983;
Robins, 1966), and hyperactive and/or aggressive (Hechtman et
al., 1984; Jones, 1968; Hagnusson & Bergman, 1988; HcCord &

21
 HcCord, 1960; Ny1ander, 1979). A comparative1y high
proportion of these vulnerable individua1s have a1coho1ic
parents (Ny1ander & Ryde1ius, 1973; Vaillant, 1983).
The families of SOHAs are often overt1y unstable (Knop
et al., 1985; Nylander, 1960 (parts 1 and 2); Rydelius,
1983a; Schulsinger et al., 1986; Tarter et al., 1984).
Chi1dren of a1coho1ics are often raised in severe1y disrupted
fami1ies (Chafetz et al., 1971), and heightened conf1ict
among parents or between parents and chi1dren (Jones, 1968,
1971; Hechtman et al., 1984; HcCord & HcCord, 1960; Hone1y,
Hart1 & E1derkin, 1983; Ricks & Berry, 1970; Robins, 1966;
Vaillant, 1983) is common1y reported, in the longitudinal
studies of chi1dren who 1ater become a1coho1ic. The precise
effect of this genera1 instabi1ity is not known, but it is
not difficult to imagine that it may exacerbate any pre-
existing tendencies to disordered conduct and hyperactive
behaviour.
Familial alcoholism has a1so been associated with male
sociopathy (Guze, Tuason, Gatfield, stewart & Picken, 1962;
Guze, Wolfram, HcKinney, & Cantwe11, 1967; Latcham, 1985;
Winokur, Rimmer & Reich, 1971) and chi1dhood conduct disorder
(Cadoret, Cain & Grove, 1980; Goodwin, Schu1singer,
Hermansen, Guze & Winokur, 1975; Rosenberg, 1969), childhood
hyperactivity (A1terman, Petraru10, Tarter & HcGown, 1983;
Goodwin et al., 1975) and overt familial disruption
(Rosenberg, 1969). Ha1e-1imited Type II a1coho1ism,

.~. theoretica1ly characterized by heightened severity (Oreland,

<!..•

22
 von Knorring, von Knorring & Bohman, 1985; von Knorring,
Bohman, von Knorring & Oreland, 1985; von Knorring, Palm &
1 Andersson, 1985), early onset, and Increased heritability
(Cloninger, 1987), is often preceded by chi1dhood conduct
disorder (Cloninger, Sigvardsson & Bohrnan, 1988; Hasin, Grant
& Endicott, 1988; Schaeffer, Parsons & Errico, 1988; von

Knorring, von Knorring, Smigan, Lindberg & Edholm, 1987! and

childhood hyperactivity (Tarter, McBride, Buonpane, &
Schneider, 1977). The notion that sorne relationship exists
between attention deficit disorder/hyperactivity and
a1coholism is further buttressed by the findings of Horton
(1985) and Wood, Wender and Reimherr (1983) who estirnate 30-
40\ of alcoholics qualify for the DSM-III diagnosis of
residual Attention Deficit Disorder.
Regardless of the source of information, despite
.....
.,.-

widespread differences in methodology and assumption across

studies, the same story emerges: SOMAs, and those more
generally at risk for alcoholism, are characterized by
conduct-disorder/antisoclal personallty, wlth or wlthout
hyperactlvlty/Attentlon-Deflcit Dlsorder. Such descrlptors
seem to be generally applied to those who are unable or
unwilling to adequately regulate thelr behaviour, in soclal
sltuatlons, ln accordance with prevaillng social standards.
There may be a heritable tendency for this pattern of
behavlour to emerge (Clonlnger et al., 1988), whlch might be
exacerbated by parental separatIon and neglect, which are
frequently assoclated wlth parental alcoholism (Jenkins,
1968; McCord, 1972; RydelIus, 1981), and which may form part

23
of the same long-term behaviour pattern.
In the general literature, hyperactivity and conduct
disorder overlap, although subgroups of children within these
domains appear to differ in important ways (Hinshaw, 1987).
Low socioeconomic status, intrafamilial hostility, parental
alcoholism and/or drug abuse, antisocial personality, and/or
hysteria tend to characterize the families of conduct-
disordered children, while cognitive and achievement deficits
(which are also typical of SOMAs) are often associated with
hyperactivity (Hinshaw, 1987). It is of interest to note that
August ~nd Stewart (1983) and August, Stewart and Holmes
(1983) have described the relationship between alcoholism and
childhood hyperactivity as secondary to that which exists
between alcoholism and childhood conduct disorder. However,
children displaying a combination o~ hyperactivity and
aggression suffer from the worst consequences of both, in
terms of observed behaviour, peer status, and outcome
(Hinshaw, 1987; Magnusson & Bergman, 1988). It appears
possible that SOMAs are often characterized by such a
combination. The presence of these behavioural patterns in
childhood appears to be strongly associated with increased
risk for alcohol abuse later in life.
Cognitive Characteristics
SOMAs have been consistently characterized by
comparatively poor performance on tests of linguistic ability
(Drejer, Theilgaard, Teasdale, Schulsinger & Goodwin, 1985;
Gabrielli & Mednick, 1983; Harden & Pihl, 1988; Hegedus,

24
 Alterman & Tarter, 1984; Knop et al., 1985; Noll & Zucker,

, .-
...~
1983; Schulsinger et al., 1986; Tarter et al., 1984; Whipple,
Parker & Noble, 1988). Reduced performance during tests
involving abstraction and/or problem solving are also
commonly reported (Drejer et al., 1985; Harden & Pihl, 1988;
Knop et al., 1985; Schaeffer, Parsons & Yohman, 1984;
schulsinger et al., 1986; Tarter, Jacob & Bremer, 1989).
comparative deficits in total Ia (Gabrielli & Mednick, 1983),
performance ra (Whipple et al., 1988), memory (Harden & Pihl,
1988; Hegedus et al., 1984; Tarter et al., 1984),
visuospatial ability (Hegedus et al., 1984; Tarter et al.,
1984), perceptual-motor capacity (Hegedus et al., 1984;
Schaeffer, Parsons & Yohman, 1984; Tarter et al., 1984) and
auditory/visual attention span (Hegedus et al., 1984; Tartcr
et al., 1984) llave been descr ibed ..,i th less consistency.
It is also important to note that SOMAs perform less
..,ell academically and have more trouble ..,ith school (Drejer
et al., 1985; Hegedus et al., 1984; Knop et al., 1985;
Rydelius, 1981; Schulsinger et al., 1986; Tarter et al.,
1984). Problems related to academic achiev.ment are also
reported in Many of the longitudinal studies, among children
and adolescents ..,ho later develop serious problems ..,ith
alcohol (see for example the revie.., by Zucker & Lisansky-
Gornberg, 1986). Such children are frequently characterized by
poorer school performance, more school truancy, and
completion of fe..,er years of schoel. The degree te ..,hich this
reduced performance can be attributed to impaired cognitive
ability per se is subject to debate. It could alse

25
 conceivably arise as a consequence of the behavioural

-
, abnormalities discussed previously, or for other reasons,
such as poor family life, or because of frequent transfer
from school to school (Knop et al., 1985).
This literature is not as consistent as that describing
the behavioural characteristics of SOMAs. Those studies that
find a link betveen cognitive differences and the alcoholic
family history generally examine sons of severely alcoholic
fathers, vho often have additional alcoholic relatives. Those
that do not are characterized by one of tvo methodological
veakness: they either include a preponderance of females, as
subjects or as the alcoholic parent, and do not offer
breakdovn of results by sex (Hesselbrock, stabenau, &
Hesselbrock, 1985; Wilson & Nagoshi, 1988; Workman-Daniels &
Hesselbrock, 1987) or they look for cognitive deficits among
SOMAs dravn solely from a university population (Alterman,
Bridges, & Tarter, 1986a; Alterman, Bridges & Tarter, 1986b;
Alterman, Searles & Hall, 1989; Schuckit, Butters, Lyn &
Irvin, 1987), vhose familial alcoholism is limited to a
mildly affected (one symptom in four to six diagnostic
categories) alcoholic father. With regards to the inclusion
of vomen: offspring of alcoholic mothers might suffer the
residual effects of fetal alcohol exposure, vhich can be
dramatic. In addition, a1coholism tends to be a male problem.
These tvo facts combine to make the nature of alcoholism
among females, and its potential mode of transmission, very
resistant to comprehension. With regards to the use of

26
 college students: SOMAs who attend university are those least

1··
likely to be characterized by cognitive deficits.
. -.'
Comparison of familial and no~-familial alcoholics
occasionally highlights weak group differences attributable
to family status (Schaeffer et al., 1984), vith the familial
alcoholics performing more poorly, particularly within
studies utilizing a large number of subjects (Schaeffer et
al., 1988), and sometimes fails to prcvide such
differentiation (Alterman, Gerstley, Goldstein & Tarter,
1987; Reed, Grant & Adams, 1987). Interpretation of these
studies in terms of predisposition is rendered difficult,
because the long-term effects of alcohol consumption upon
cognitive performance might vary according to family history.
Psychophysiological Characteristics
..',......
Most of the psychophysiological research conducted to
date upon SOMAs has concentrated on their cortical evoked-
response to stimuli. The cortical event-related potential
(ERP) ls derived from the electroencephalogram (EEG) recorded
during the presentation of a brief stimulus in any sensory
modality. First, it might be noted that there are two studies
(Schmidt & Neville, 1984; Neville & Schmidt, 1985)
demonstrating that SOMAs are characterized by decreased
amplitude of the N430 ERP component, linked to semantic
processing, during the course of two verbal tasks. These
studies are important in their own right, and are in
concordance with the studies described previously
demonstrating that SOMAs may be deficient in verbal
abilities. However, it is the p300 ERP compone nt that has

27
 been most commonly studied with respect to SOMAs. The
amplitude of P300 increases with the subjective motivational
relevance of stimuli (Begleiter, porjesz, Chou & Aunon,
19831; its latency varies with speed of identification and
processing (Donchin, Ritter & MCCallum, 1978). Eight studies
refer to SOMAs' production of P300 with reduced amplitude
(Begleiter, Porjesz, Bihari & Kissin, 1984; Beg1eiter,
Porj~sz, Rawlings, & Eckhardt, 1987; Elmasian, Neville,
Woods, Schuckit, & Bloom, 1982; O'Connor, Hesselbrock, &
Tasman, 1986; Steinhauer, Hill & Zubin, 1987; Whipple et al.,
1988) or increased latency (Hill, steinhauer, Zubin &
Baughman, 1988; Whipple & Noble, 1986) during the repeated
presentation of non-threatening, non-novel stimuli. This
pattern of p300 production also characterizes abstinent
....
j alcoholics (Begleiter, Porjesz & Tenner, 1980; Porjesz &
...
Begleiter, 1981). These abnormalities remain naticeable even
after periods of abstinence of up to 5 years, unlike deficits
in Brain Stem Auditory Response conduction velocity, which
characterize abstinent alcoholics (Porjesz & Beg1eiter, 1985)
but nat SOMAs (Begleiter, Porjesz, & Bihari, 1987).
It is important to note that these eight positive
studies are characterized by strl~t subject selection
procedures. Begleiter et al. (1984, 1987), Whipp1e and Noble
(1986), Whipple et al. (1988) examined non-drinking
adolescents or preadolescents and Hill et al. (1988),
O'Connor et al. (1986) and Steinhauer et al. (1987) young
adults whose fathers met Feighner criteria for alcoholism and

28
who often had additional alcoholic relatives. There are a
number of studies (Neville & Schmidt, 1985; Polich & Bloom,
1986, 1987, 1988; Polich, Burns & Bloom, 1988; Polich, Haier,
Buchsbaum & Bloom, 1988; Schuckit, Gold, Croot, Finn &
Polich, 1988) which report little or no differences in P300
production (amplitude and/or latency) between SOMAs and
matched controls. The majority of these (Neville & Schmidt,
1985; Polich & Bloom, 1986, 1987, 1988; Polich, Burns &
Bloom, 1988) report that such production is correlated vith
self-reported alcohol consumption, and/or by such alcohol
consumption in interaction with family history. Hovever,
these studies test university students, who are self-selected
for the absence of the kind of cognitive deficit that might
underlie P300 abnormalities (Begleiter, Porjesz & Tenner,
1980), and whose familial a1coholism is limited to a mildly
affected father (one symptom in four to six categories)
(Hill, Steinhauer, Park and Zubin, 1990). Given the
methodologica1 differences between the positive and negative
studies, it seems reasonable to conclude that SOMAs drawn
from the normal population, from families with extensive
histories of paternal alcoholism, may well be characterized
by abnormalities of the P300 ERP component. This pattern of
reaction might be considered an idiosyncratic cued
psychophysiological response.
There are four additional reports suggesting that
abnormalities in cued psychophysiological response might
characterize sober SOMAs. These studies differ
methodologically from the P300 studies described previously

29
in that they utilized stimuli whose motivational significance
might be described as inherent: Finn and Pihl (1987, 1988)
and Finn, Zeitouni and Pihl (1990) used 'countdown to shock,
electric shock, and presentation of novel tones; Harden and
Pihl (submitted) used mental arithmetic. These
investigations, conducted on individuals with extensive
multigenerational family histories of severe male-limited
alcohol abuse, demonstrated that SOMAs are characterized by
heightened cardiovascular reactivity to novel or avers ive
stimuli. Another study (Hennecke, 1984) notes that the
incidence of stimulus augmentation, characteristic of
alcoholics (Buchsbaum & Ludwig, 1978; Coger, Dymond,
Serafetenides, Lowenstam & Pearson, 1976; von Knorring,
1976), was significantly higher among children of alcoholics,
male and female, than among matched controls, while the
incidence of field-dependence, also characteristic of
alcoholics (Karp, Witkin & Goodenough, 1965), was not.
Stimulus augmentation might be considered a form of
perceptual hyper-reactivity.
Two studies have described EEG abnormalities as
characteristic of sober SOMAs. Gabrielli, Mednick, Volavka,
Pollock, Schulsinger and Itil (1982) demonstrated that the
EEGs of SOMAs were characterized by an significant excess of
high frequency beta activity. This pattern of response is
also typical of alcoholics (Mendelson & Mello, 1979). An
excess of fast beta activity has been associated with
psychological states of tension and anxiety (Kiloh &

30
Osselton, 1961). Begleiter et al. (1987) have also reported
that unspecified EEG abnormalities characterize SOHAs. It has
been commonly reported that alcoholics can be differentiated
from controls by their poorly synchronized brain wave pattern
(Begleiter & Platz, 1972), and Naitoh (1973) has argued as
weIl that individuals with such poorly synchronized EEGs are
predisposed to alcoholism. Propping, Kruger and Hark's (1981)
work, which showed that alcoholics and their first-degree
relatives shared EEG patterns, provides some support for this
notion, suggesting as it did that the EEG patterns
characteristic of alcoholics may be genetically determined.
However, the exact significance of these somewhat abnormal
patterns remains unspecified.
Finally, there are three studies (Hegedus, Tarter, Hill,
Jacob, & Winsten, 1984; Lipscomb, carpenter & Nathan, 1979;
Tarter et al., 1989) which suggest that sober static ataxia
characterizes SOHAs and three (O'Halley & Haisto, 1985;
Schuckit et al., 1987; Schuckit & Gold, 1988) that do not. It
is difficult to draw any final conclusions from these
studies. A pronounced lack of theory describing the
relationship between alcoholic predi:;position and increased
sober static ataxia complicates Interpretation and
Integration of these contradictory findings.
Reaction to Alcohol
SOHAs appear to be characterized most particularly by
increased susceptibility to what might be considered the
negatively and positively-reinforcing effects of alcohol
consumption. with regards ta putative negative reinforcement:

31
SOMAs appear hyper-sensitive to the dampening effect of
alcohol on cardiovascular and/or electrodermal reactivity to
aversive or novel stimulation (Finn & Pih1, 1987; Finn &
Pihl, 1988; Finn et al., 1990; Levenson, Oyama & Meek,
1987). A1coho1ics a1so seem to be characterized by some form
of susceptibi1ity to the stress-response dampening effect of
ethano1 intoxication. A1coho1ics manifest significant
reductions in e1ectroderma1 reactivity (Coopersmith &
Woodrov, 1967; Garfield & McBrearty, 1970) and to pain
reactivity (Brovn & cutter, 1977) after consuming alcohol. In
addition, alcoho1 consumption results in a shift from
stimulus augmentation to reduction in alcoholics (Buchsbaum &
Ludvig, 1978; Petrie, 1975), vhich might be considered a form
of dampening, and alcoholics vho are augmentors, like the
offspring of alcoho1ics (Hennecke, 1984), york harder for
alcohol than those vho are normalizers or reducers (Ludvig,
Cain & Wik1er, 1977).
With regards,to possible positive reinforcement: SOMAs
are characterized by significant1y increased baseline heart-
rate, vhen lntoxicated, during the ascending limb of the
b100d a1coho1 curve (Finn & Pihl, 1987; 1988; Finn et al.,
1990; Levenson et al., 1987). This increase appears of
importance, as Fov1es (1981; 1983) has described an
association betveen similar heart-rate elevations and revard.
More genera11y, a1coho1 intoxication appears to significant1y
reduce baseline muscle tension among SOMAs, (Schuckit,
Engstrom, A1pert & Duby, 1981), heightens their production of

32
 EEG waveforms associated with states of well-being (Pollock,
Volavka, Goodwin, Mednick, Gabrielli, Knop & Schulslnger,
,....
_.~

1983; Pollock et al. 1988) and normalizes their visual ERP

response to pattern-reversal (Pollock, Volavka, Goodwin,
Gabrielli, Mednick, Knop & Schulsinger, 1988). These latter
properties also appear potential1y associated with reward.
SOMAs are also characterized by Idiosyncratic subjective
response to ethanol challenge. They tend to self-report
reduced intoxication at low to moderate doses of ethanol
(O'Ma11ey & Maisto, 1985; Pollock, Teasda1e, Gabrielli &
Knop, 1986; Schuckit, 1980b, 1984a), and/or during the
descending limb of the Blood-A1cohol-Concentration (BAC)
curve (Moss, Yao & Maddock, 1989), although this effect seems
to disappear at higher doses (Finn & Pihl, 1987; 1988; Finn
et al., 1990; Schuckit, 1984b). Shuckit, Parker and Rossman
(1983), Schuckit (1984b), Schuckit, Gold and Risch (1987a,
1987b), and Schuckit (1988) also suggest that SOMAs manifest
greater decreases in plasma cortisol and/or plasma prolactin
after moderate alcohol consumption although Moss et al.
(1989), with a smaller sample size, did not concur. These
larger decreases are in logical accordance with SOMAs'
reduced subjective intoxication (Pollock, Gabrielli, Mednick
& Goodwin, 1988). The cause of these reduced se1f-reported
alcoho1 effects has not been estab1ished, although it is
tempting to specu1ate that increased experienta11y-based
to1erance among SOMAs might play a ro1e. Their significance
is a1so unknown, a1though New1in and Thompson (1990) have
suggested, after an extensive review of the 1iterature, that

33
SOMAs are more susceptible to alcohol's positive effects,
during the ascending limb of the blood alcohol curve, and
less susceptible to its negative effects, during the
descending limb. The potential consequences of this
differential sensitivity are obvious.
Finally, there have been two positive (Schuckit, 1980a;
Schuckit & Rayses, 1979) and one negative report (Behar,
Berg, Rappaport, Nelson, Linnoila, Cohen, Bozevich &
Marshall, 1983) that elevations in plasma acetaldehyde
characterize SOMAs after alcohol consumption. These results
may be unreliable due to difficulties in the accurate
measurement of blood acetaldehyde (Eriksson, 1980) although
elevated levels of blood acetaldehyde after alcohol
consumption are also characteristic of alcoholics (Korsten,
Matsuzaki, Feinman & Leiber, 1975).
Biochemical Functioning
Six studies describe what little is directly known about
the normal biochemistry of those with a positive-family-
history of alcoholism. Three studies of these 6 support the
most common finding, which is that family-history-positive
subjects are characterized by lower plate let monoamine

oxidase (MAO) activity than controls (Alexopoulos, Lieberman

& Frances, 1983; Schuckit, Shaskan, Duby, Vega & Moss, 1982;
Sullivan, Cavenar, & Maltby, 1979). The low plate let MAO
activity characteristic of such subjects has been correl&ted
with the frequency of alcoholism in their family pedigree

(Major, Hawley, Saini, Garrick & Murphy, 1985; Major &

34
Murphy, 1978; Sullivan, Stanfield, Schanberg & Cavenar,
1978), generally associated with alcoholism (Alexopoulos et
al., 1983; Brown, 1977; Gottfries, 1980; Major & Murphy,
1978; von Knorring et al, 1985) and specifically linked to
Type 2 alcoholism, which is considered highly heritable (von
Knorring et al., 1985). However, relatively decreased
platelet MAO activity also characterizes those suffering from
other psychiatrie disorders (Buchsbaum, Coursey & Murphy,
1976) and may not provide accurate measure of central MAO
function (stahl & Kravitz, 1986). Its precise significance is
therefore difficult to determine.
The three remaining studies variously describe the
biochemistry of individuals with alcoholic relatives. Moss,
Guthrie and Linnoila (1986) offered evidence that adolescent
SOMAs manifest an enhanced thyrotropin response to
thyrotropin releasing hormone. Swartz, Drews, and Cadoret
(1987) demonstrated that nonalcoholic adoptees with alcoholic
biological first or second degree relatives were
characterized by significantly reduced mental stress-induced
epinephrine release. This pattern is apparently also
characteristic of those with aggressive or hyperactive traits
(Swartz et al., 1987). Rosenthal, Davenport, Cowdry, Webster
& Goodwin, (1980) demonstrated that depressed first-degree
relatives of alcoholics are characterized by lower
cerebrospinal fluid levels of the serotonin metabolite 5-
hydroxyindoleacetic acid. Although the full significance of
these findings is not yet clear, the latter study may be of
particular interest, given the wealth of indirect evidence

35
suggesting that the dysfunctions of the serotonergic system

m~y be involved in the predisposition to alcoholism (Buydens-

Branchey, Branchey, Noumair & Lieber, 1989; Friedman,

Krstulovic, Severinghaus, & Brown, 1988; Murphy, MeBride,
Gatto, Lumeng & Li, 1988; Naranjo, Sellers, Sullivan,
woodley, Kaldec & Sykora, 1987; ROy, Virkunnen, Guthrie, &
Linnoila, 1986).

Conclusion
Non-alcoholic sons of male alcoholics have been most
consistently described as eonduct-disordered and as
hyperactive. They have difficulty in maintaining
concentratl'Jn and focus of attention, and can not or do not
regulate their overt behaviour in accordance with age-
approprlate structured social norms. They appear heir ta a
number of mild cognitive deficits, and manifest decrements ln
performance durlng tests of llngulstlc ability, abstract
thlnklng, and problem solving. Their academic performance is
often reduced. It has been demonstrated, with less
consistency, that SOMAs are characterized by abnormal
patterns of cued psychophysiological response. They appe~r to
hypo-react ta stimuli that require the allocation of

directed, voluntary attention, while hyper-reacting to

stimuli that might be considered intrinsically motivating.

Alcohol intoxication may be differentially reinforcing to

SOMAs: it decreases their exaggerated response to novelty and
aversive eues and increases their baseline heart-rate.

36
 Study 1 and 2
The pattern of behaviour, cognition and psycho-
...;,
physio1ogica1 response typica1 of SOMAs appears reminiscent
of that manifested by individua1s who have suffered sorne form
of mi1d pre frontal cortical trauma, in adulthood (Tarter,
Alterman and Edwards, 1985; 1988; Gorenstein, 1987). Sons of
male a1coho1ics and individua1s with minimal pre frontal
damage are characterized by increased impu1sivity,
attentiona1 deficit, impairments in the vo1untary regulation
of social behaviour, heightened levels of activity, poor

emotional modulation, deficits in organizatlon of information

and planning of behaviour, and various abnormalities of the
orienting response (Eslinger & Damasio, 1985; Luria, 1980;
Tarter et al., 1985, 1988). study 1 and 2, described below,
were completed in keeping with this general hypothesis.

,~.

37
 Introduction to study l
study 1 (Peter~on, Rothf1eisch, Zelazo and Pihl, 1990)
examined the effects of three different levels of alcohol
intoxication the neuropsychological functioning of 72 (6 X
12) undergraduate males, in the context of a ba1anced-placebo
design. This study was designed to examine the relative
contributions of expectancy and pharmaco1ogy to normal, but
alcohol-intoxicated neuropsychological functioning. The study
additiona11y allowed for the determination of the alcohol
dose sufficient to serious1y impair inte11ectual function.
This is a critically important point, as the use of many
different alcohol-dosing procedures in the relevant
literature excessively complicates comprehension of alcohol's
effects.

38

,.~
Acute Alcohol Intoxication and Cognitive
Functioning*
JORDAN B. PETERSON, B.A., JENNIFER ROTHFLEISCH, B.A., PHILIP D. ZELAZO, B.A.
AND R.O. PIHL, PH.D.
Department of Psycholov. McGiII University. 120S Docteur Penfield Avenue., Montreal, Quebec H3A IBI, Canada
ABSTRACT. Acute a1cohol intoxication produces chanaes in the
coanitive functionina of normal individuals. Thc:sc chaniC3 appear
simiIar prima fade to those e:thibitcd by indhidu.ils who sustain
prd'ronl&1 lobe damaae durina adulthood. In order to test the
validity of this observation. and to conuol for the confoundina
effccu of ~tancy. 72 male subjeeu were adminiuered a
battery of neuropsycholoiÎcaJ tau. within the context of a
balaDced·placebo desisn. Eacb subjec:t rcecived one of three
T HE EFFECTS of acute alcohol intolÛcation upon
human cognition have been investigated for sev-
eral dccades. Jellinek and MacFarland (1940), who
first attempted to systematically integrate knowledge
about such effcets, hypothesized that alcohol hBd le"
impact upon simple than upon complex cognitive
functions. This hypothesis failed ta evoke unequivocal
support (Frankenbaeuser et al., 1962; Tart« et al.,
1971), at least in part because no accurate standard
for quantifying cognitive complexity exists. Attempts
ta clarify the confusion generated by this lack of
standardization have becn complicated bccausc meas·
ures of cognitive ability vary idiosyncratical1y. This
variance in approach makcs'comparison :~wccn dif-
ferent studies and integration of their findings dif·
ficult. Nonetheless, it has at lcast been demonstrated
that alcohol intoxication differential1y affcets different
aspects of cognition (Bimbaum et al., 1990; Ekman
et al., 1964).
The use of neuropsychological tests ta determine
the effects of alcohol intolÛcation could conceivably
help reduce such confusion. These tests offer the
po"ibility of clarifying the nature of the relationship
bClwecn intolÛcation and neuropsychologica1 dysfunc·
tian. Neuropsychologica1 testing offers the possibility
that alteration in functioning at the bohavioral level
Reœived: June 7, 1988. Revision: October l~. 1988.
• This wort wu supportcd in pan by the Medical Research
Counci1 or Canada.
39
Journal of Siudin 011 A/collot, Vol. JI .•,"'0. ]. /990
widely different doses of alcohol. Analysis of the rC3ulu of the
coJOitive test b&ncry clemonsuatcd that a h.iIh dose of alcobol
deuimenl&11y arfccu a numba' of funaions wociated with the
prefronl&1 and temporal lobes. includina pLannina. verbal Ouency,
memory and compla motor control. Espcctancy does not appear
to play a sianificant role in àeterminina this effcet. The impü·
cations of this panem of impairment ue ana.lyz.ed and disctwed.
(J. Stud. Alcohol 51: 114-122. 1990)
may be ascribed ta disruption of a specified cortical
system, rather than causaIIy linked ta impairment in
sorne rcified cognitive structure.
The research reported in this article was based
upon the hypothesis that the pattern of acute alcohol·
induced neuropsychological impairment is analagous
ta that characteristic of patients suffering from pre·
frontal damage. Two considerations guided the de·
velopment of this hypothesis. In the first place, many
so-called complex cognitive abilitics, apparently sus·
ceptible ta interruption by alcohol, are dependent
upon the activity of the prefrontal cortex (Luria,
1990). lndividuals who have suffered prefrontal injury
are impaired in the temporal organization of behavior
and reduced in the ability ta think abmactly. They
plan and/or implement courses of action poorly and
cannot modify such courses in accordance with their
consequences (Eslinger and Damasio, 1985). Similar
deficits-Most often described in terInS of l I abstrac.
tion l t and/or " planning"-are charaeteristic of acutely
intolÛcatod individuals (Jones and Vega, 1972; Wash·
bume, 1956; Zeichner and Pihl, 1979).
ln the second place, individuals with verified lesions
of the prefrontal area exhibit a pattern of overt
behavior reminiseent of that characteristic of intolÛ·
cated individuals. Damage ta the prefrontal cortex.
which synthesizes information about the state of the
extemal objective and internaI subjective worlds, im-
pairs the regulation of bohavior (Luria, 1980). Those
with such damage cannot JJe:fccivc errors in thcir
performance, fail ta ar.preciate the impact they make
on othe" and cannat criticize thcnuelves accurately
 .r PETERSON ET AL.
,:",
(Lezak, 1976). W..hbume (1956) poSlulated that al·
cohol intoxication simiIarly reduces people's aware-
ncss of thcir own actions, making them unable to
modify these actions in r~sponse ta environmentaJ
demands. Hull (19SI) has also proposed that alcohol
intoxication imcrferes with encoding processcs fun·
damentaJ to the state of self·awareness. These proc-
esses inc1ude the evaluation of self-relevant
information. including eues about appropriate forros
of conduct and evaJuation of behavior in the recent
pasto
Deficits in verbal ability have also been associated
with alcohol intoxication and with prefrontal impair-
ment. AJthouSh patients with left frontal lobe lesions
often appear 10 possess intact speech upon superficial
examination (Walsh, I97S). closer analysis reveals
impoverishment (Lezak. 1976), adynamia and persev.
eration (Walsh, 1978). Prefrontal patients often offer
cxtraneous associations during verbal tests (Luria et
al., 1967). Clinical studies show that patients with
left frontal dan",.e perform significantly worse than
controls on word-fluency tests (Bentan, 1968; Miller,
1988; Milner, 1964; Ramier and Hécaen, 1970). De·
crease<! verbal nueney is also characteriSlic of subjeets
acutely intoxicated by alcohol (Hanocollis and John·
son, 1956) and these individuals also alter their
responses to free·association tests (Weinganner, 1977).
In the present study, a variety of cognitive·behav.
ioraI tasks-some sensitive to panicular types of
neuropsychologica1 impairment-were administered ta
the subject population. Those more sensitive tO fron·
tal function were included to provide a direct test of
the hypothesis presented in this anicle. Nonfrontal
and miscollaneous tesL, were administered 10 deter·
mine the specificity or generality of alcohol-icduced
impairment. Tests with well-established !lorms or tests
that are apparently affected by highly specific forms
of damage were included as fltSt choices, but some
in use for other reasons (sensitivity to expectaney,
for example) were aise included.
Dose and expectaney confound the effeets of a
drug, and play crucial roles in determining its be·
havioral sequelae (Marlau and Rohsenow, 1981).
Variation in respanse due to dose and expectallcy
was ·,herefore directly measurd. Subjects randomiy
reeeived one of thr.. "'id.ly differing doses of al·
cohol, under two conditioll5 of expectalley, within
the confines of a baJanced-placebo d..,ign. A variety
cf teehniques have been designed to ensure that
subjeets remain naïve to condition and to therefore
maintain the validity of the balanced-placebo design.
Knight et al. (1986) have reeently criticized th...
wchniques. The present experiment was designed with
th... criticisms in mind, and w.. based on a modi-
fication of the baJanced-placebo design devise<! by
40
115
Ross and Pihl (1989). The present Sludy was addi·
tionally predicated upon the hypothesis that expec·
tancy detrimentally affects performance. This
secondary hypothesis was based on the assumption
that alcohol intoxication provides an excuse for in·
appropriate or substandard behavior (Graham. 1980:
Hull and Bond. 1986).
Metbod
S"bjects
Seventy·two male university students between the
agto of 18 and 34 were reeruited as paid subjects by
adverti:·;~r.1ent at McGiIl University. Moderate social
ùrinkers « 15 drinks/week) in good physical and
mental heaJtn were selected for panicipation. The use
of experienced drinke" in the sample ensured that
ail ,ubjects were farniliar with the effeets of alcohol
consumption. Exclusion criteria also included famil·
iarity with psychological experimentation, and medical
trcatment that contraindicated alcohol consumption.
Subjeets were asked to refrain from consumption of
alcohol for 24 hours and from food 4 hours before
the experimental session.
Design and Procedure
Upon arrivai at the laboratory. all subjects met
the first of four experimental personnel. They w.,e
then required to sign an informed consent form.
Each subject was then weighed and randomly ..."igned
to one of the following six sroups: told higl: dose.
reeeived high dose (THRH); told low dose, reeeived
high dose (TLRH); told high dose, reeeived moderate
dose (THRM); told low dose. reeeived moderate dose
(TLRM); told hir.h cto,",. rer.ived low dose (THRL);
'Uld told low dose, ",ccivO'j Ir>w dose (TLRL). High
dose consisted of 1.32 ml of 95'1. pure pharmaceuticaJ
alcohol per kilogram of body weight; moderate dose
of 0.66 ml/kg; and low dose. which was active
placebo. of 0.132 ml/kg. Drinks for the high doses
""ere mixed 1 pan alconel to 5 pans juic: (3 pans
grapefruit and 2 parts orange). The grapefruit juice
help,."!\ mask the presence or absence of alcohoL
Subjects in the moderate· and low-dose conditions
reeeived as much juice per kilograrn of body weight
as the subjeets who reeeived a high dose of alcohoL
Subjeets in each condition reeeived instructions de-
signed to maximize the effeetiveness of the balanced-
placebo design (Ross and Pihl, 19S9). Each subject
was given thr.. drinks, and was asked to finish them
within 20 ntinutes. Arter a 15·minute waiting period.
each subject was given the (;'3t of three subjective
intoxication scales and 'h-,' first of threc breath
analyzer tests. Subjeets completed their subjeetive
 116 JOURNAL OF STUDIES ON ALCOHOLIMARCH 1990
intoxication sca1es privatcly. to control for the effects
of experimcnter rlemand. The subjects wcrc then
taken to a separat!: testing area, where they were
introduced to th,~ remaining three experimenters, who
were blind to the subjects' condition.
The fallawing tests were divided equally amang
thesc three investigators. who administered them in
randam arder ta the subjects ta control for differ-
ences in performance due to praetice, fatigue, the
effcets of alcahal metabalism and central nervaus
system ~daptation to alcohol intoxication.
Tests assnciated wUh the frontal cortex
Parteus Maze Test, Extension Series. This test
measures planning and foresight (Parteus, 1959).
Subjccts are required to complete a series of Mazes
rankcd according ta difficulty. Individuals with le-
sions of the frontal lobes demonstrate impairments
in their ability ta correctly complete this test (Crown,
1952; Malmo, 1948; Meuler, 1952; Porteus and Kep-
ner, 1944; Porteus and Peters, 1947).
Rey-Osterreith Complex Figure, Copy (1). Rey
(1941) designed this comple. figure ta investigate
perceptual organization and visual memory in brain-
damagcd patients (Lezak, 1976). The subject is first
required to copy the figure Crom an original. Patients
, .,,>- with prefrantal damage copy this figure (and comple.
figures in general) poorly (Lezak, 1976; Luria, 1980).
Thurstone Ward Fluency Test. This test assesses
the ability ta generate words according ta an abstract
conceptual cat,egory. The subject must write as many
words as he can beginning with the letter S in 5
minutes. Individuals with left frontal lobe damage
consistently demonstrate significant impainnents in
ward flueney (Benton, 1968; Miller, 1989; Milner,
1967; Ramier and Hécaen, 1970; Tow, 1955).
Self-Ordered Painting Test, 12 Representational
Drawings. The Self-Ordercd Painting Test measures
arganizational ability and sequencing of responses
rather than the reproduction of sequences pre~organ­
izcd by the e.perimenter (Petrides and Milner, 1982).
Subjects must remember the location and sequence
of cach of 12 familiar pictures of abjects presented
12 different ways. Individuals with frontal damage
consistently maniiest deficits in performance on this
task. Individuals with temporal damage manifest def-
icits that vary with the severity of the lesion (Petrides
and Milner, 1982).
Wisconsin Card Sorting Test. This test was deviscd
ta study Uabstraet behavior" and Ushift of set"
(Berg, 1948; Grant and Berg, 1948). The subject is
given a dcck of 64 cards, and is requircd ta categome
th... according ta a plan establishcd by the investi-
gator. Individuals suffering from dorso-Iateral frontal
lesions perform poorly on this test (Milner, 1964).
Tests associated with the temporal cortex
Logical Memory, Immediate (1); Logica[ Memo,-,.
25-Minute Delay ID). These Wcchsler memary ,ub-
tests assess the immediate and delayed recall of verbal
ideas from an auditory presentation of two para-
graphs. Individuals with temporal lobe damage per-
farm poarly on these tests (Milner, 1975).
Rey~Osterreith Figure, Reproduction Iram .\femory
(2) & (3). After the subjcct has capied the Rey figure,
he is subjcctcd ta a delay of 3 minutes and is asked
ta duplicate the figure from memary. Th. subjcct is
then given a series of other tasks. and is finally
asked ta produce a final capy from memary 25
minutes later. Patients with right temporal lobe dam-
age (particularly those with hippocampal lesions) have
difficulty in completing this task (Milner, 1975).
Paired Associates, Difficult (D) and Easy lE). The
Paircd Associate subtest of the Wcchsler Memory
Scale assesses verbal retention (Lezak, 1976). The test
consists of la word pairs; six forming easy associa-
tions and four forrning word pairs not easily asso-
ciated. Individuals with left temporal lesions have
difficutly in completing this test (Milner, 1975). Ad-
ditionally, there is evidence that organic brain damage
panicularly impairs recail of the difficult pairs (Walsh,
1979).
Tests assaciated with the parieta/-occipital cortex
Albert's Simple Test of Visual Neglect. Subjccts
are given a pencil and a sheet of paper with a
number of short Iines printcd on it, and are asked
ta biscct each line with another short line. Subjects
who suffer from parietal damage perform panicularly
poarly on this test (Albert, 1973).
Apraxia Questionnaire. The apraxia questionnaire
provides a general measure of ideomotor, ideational
and buccofacial apraxia. Apraxia has becn opera-
tionally defincd by e.clusion as a disarder of skilled
movement not caused by weakness, akinesia, deaf~
ferentiation, abnormal tone or posture. movement
disordcrs, intellcctual deterioration, poor comprehen-
sion or lack of cooperation (Heilman and Valenstein,
1985).
Miscel/aneous tests
These tests were includcd in the battery for a
vanety of rcasons. The information and vocabulary
subtests of the WAIS provide a good measure of
general intelligence but are not generally affected by
frontal trauma in adulthood (Lezak, (976). Analysis
of the results of th... tests would help determine
whether alcohol affectcd the factor of "general in-
telligence" or if its action was more specific in nature.
41
 PETERSON ET AL. 117

The digit symbol subtest was included because il is T.uu: t. Blood alcohol concentrations
sensitive ta variations in motivation (Lezak, 1976),
Alcohol in high doses impairs certain aspects of DOSAGE GROUP
motor performance (Connors and Maisto, 1980; Hull High dose Medium dose Law dose
and Bond, 19S6; Lewis, 1969). A Reaction Time Test M~n SD Mean SD Mean SD
was included aJong with the Pursuit Rotor Test to
aid in clarifyins the nature of this impairment. Scores On. .093~·b .021 .044' .009 .00l .000'
Two .103a.b .027 .031" .008 .002 .0006
3rc assigned in tenths of a second for the reaetion Th,.. .083~·b .Oll .022' .009 .002 .000'
time test and in seconds for the Pursuit Rotor Test.
The Youns·Pihl Memory Test consists of a list of Nort: Ali rcponed differences are sianificant al p < .01.
40 words taken randomly from the Thorndike·Lorge Il Represenu a sianificant difference bctween the hiah- and 10w-

AA lim (1944) read by the examiner at a rate of dose conditions.

onc per second. Subjects are given 90 seconds to
recall and write down the words in any arder.
immediately after hearing the list. This test has proved
sensitive to the effects of expectancy in the past
(Young and Pihl, 19S0).
AlI subjects were given standardized instructions
relevant to the tests, and completed ail tests within
U hours. Subjects were administered the second and
third breath. analyzer tests and subjective intoxication
scales at the midpoint and conclusion of the tcsting
session. Each subject was then debriefed and, once
his blood alcohol concentration had fallen below
0.04, was paid S2S and allowed to leave. Subjects
were not allowed cigarettes during the testing session
to control for acy potential interaction between the
chemical, in cigarette smoke and alcohol.
Results
As the hypothesis to be tested varied according to
th~ test. univariate analysis of variance was employed
separately for each measure. No significant interaction
erfects emerged from any analysis.
Blood alcohol concentration . 2163 df, p < .OS) and Young·Pihl Memory Tests
Ali subjects in the high-dose condition maintained
BACs above the legal limit. Means, standard devia·
tions and sisnificance levels are presented ln Table
1. Significant differences between dosage groups were
found in the first (F = 2S6.S, 2/63 dt), second
(F = 217.S, 2163 dt) and final BAC reading
(F = 491.2, 2/63 dt).
Subjective intoxication
b Represenu a significant difference between the high- and
medium-dose condilions.
"Represenu a sianificant difference between the medium· and
low-dose conditions.
df, P < .07) approached significance. Further analysis
(Tukey Test) carried out on the subjective intoxication
ratinss indicated that the first ratings carried out by
subjects in the low-dose condition differed signifi·
candy from those completed by subjeclS in the
medium· (p < .01) and high-dose (P < .01) condi·
tions. Significant differences between the high· and
medium-dose conditions (p < .OS), high· and low.
dose conditions (p < .01) and medium· and low-dose
conditions (p < .01) also emerged from analysis of
the mid-session rating scale, although these differences
disappeared by the end of the testing period.
Ellecrs 01 expecrancy
Only two of more than 20 tests proved senslllve
to expectancy effects, albeit not as predicted. Subjects
told they were receiving a high dose of alcohol scored
significant!y higher on the Digit Symbol (F = sm,
(F = 11.16, 1/64 df, p < .001) than subjects who
were lold that they were receiving a low dose of
alcohol. For lhe sake of clarity, and since expectancy
TABLE 2. Subjective intollication measures
NUMBER OF BEER EQUIVALENTS SELF·REPORTED
Told high dose raid low dose
Minutes Mean SD Mean SD

Analysis of the subjective intoxication scale indi· High dose: lO l.71 1.19 l.5l 1.29
cated that the expectancy manipulation was success· 60 l.10 1.19 2.74 1.64
90 2.l5 1.06 1.86 0.67
fui. Means and stand~'sd deviations are listed in Table Medium dose: lO l.28 0.82 2.9l 1.22
2. Within dosage groups, subjects told that they were 60 2.6l 1.06 1.88 1.01
receiving a hiSh dose of alcohol rated themselves as 9(1 1.48 0.48 1.34 0.51
more intoxicated than subjects told they were receiv. Low dose: lO 2.71 0.75 1.77 0.71
60 1.62 0.91
ing a low dose. Initial (F = 4.IS, 1I6S df, p < .OS) 1.10 0.29
90 1.13 0.l2 1.00 0.00
and mid·session ratings (F = 4.38, 1/6S df, p < .OS)
were significant, whiJe final ratings (F = 3.2g, 1/6S Nott: 5ee Method section for I~els of sisnifi~.

42
1 118 JOURNAL OF STUDlES ON ALCOHOL/MARCH 1990
effects were othcrwise minimal. funher analyses wcre
carried out on means coUapsed within dosage groups.
Tests associaled with the frontal cortex
Four of six measures of frontal lobe functioning
proved sensitive to the effects of intoxication induced
by a high dose of alcohol. Means, standard deviations
and levels of significance are presented in Table 3.
The quantitative (F = 8.55, 2/64 df, p < .(01) and
qualitative (F = 6.79, 2164 df, p < .(02) score anal·
yses of the Porteus Maze demonstrated that perform-
ance on tlûs test was significantly impaired by the
effects of alcohol intoxication. The quantitative score
is awarded in tenns of mental age. Maximum score
is 17. Half a year is subtracted for each unsuccessful
trial. Lowest possible qualitative score is 100. Scores
on the Thurstone Word F1uency Test (F ~ 4.20, 21
62 df, p < .05) also were significantly negatively
affected by alcohol intoxication. Seores reported are
number of words generated. Intoxicated subjects also
demonstrated significant impairments in their ability
to repraduce the Rey-Osterreith complex figure (re·
producùon from copy: F = 4.85, 2163 df, p < .01).
Maximum possible score is 35. Tukey. Tests were
carried out subsequent to the ANOYA (sec Table 3).
The results of these tests indicated a strong detri·
".~.
mental high-dose effect of alcohol intoxication. The
".-::.?
Self·Ordered Pointing and Wisconsin Card Sort Tests
did not appear to be sensitive to the effects of
alcohol consumption. The Self-0rdered Pointing scores
reported are total errcrs in three trials. The Wisconsin
Card Sort scores are total errors.
Tests not directly ossociated with the frontal cane>:
Five of 14 measures of rtonfrontal' function also
proved sensitive to the effects of high-dose alcohol
intoxication. Analysis of the Logica1 Memory subtest
demonstrated that alcohol intoxication significantly
impaited delayed recall of verbal information
(F = 6.99, 2/64 df, p < .(02). Intoxicated subjects
were also impaired in thelr ability to repraduce the
Rey·Osterreith figure after a delay (3.minute delay:
F = 12.77, 2164 df, p < .001: 25-minute delay:
F = 15.21, 2164 df, p < .(01). Alcohol consumption
significantly impaired recall of the difficult pairs of
the Paired Associates (F = 3.32, 2164 df, p < .05),
while the level of impairment approached significance
for recall of the easy pairs (F = 2.52, 2164 df,
p < .09). The Pursuit·Rotor Test also proved sensi·
tive to the detrimental effects of alcohol intoxication
(F = 6.41, 2162 df, p < .(03). Mean.o, standard de·
viations and leve!> of sill'Ùficance for ail nonfrontal
tests except for the test of visua! neglect and the
Apraxia Questionnaire are presented in Table 3. No
43
subjects made any errars while carryÎng out the tasks
associated with these (wo tests.
Obcusslon
The present study tested two hypotheses: (1) that
a similar neuropsychological deficit pattern underlies
prefrontal lobe syndrome and alcohol intoxication.
and (2) that a1cohol expectancy detrimentally affects
neuropsychological perform~ce. The results provide
mixed support for the fim hypothesis at the high.
dose level, although it is apparent that a1cohol in.
toxication severely disrupts thase functions associated
with the temporal lobe as weU. The experimental
subjects demonstrated significant levels of impair-
ment, after consuDÙng a high dose of a1cohol, on
four of six measures of prefrontal lobe function and
on four of six measures of temporal function. Func·
tions associated with the parietal-occipital lobe re·
mainee! intact, as did those assessed by the
misceU:moous tests (with the exception of the Pursuit
Rotor Tes;). The second hypothesis did not receive
support. TI« expectaney manipulation employed dur·
ing tbis study wu successful. according to masures
of subjective intoxication. Nonetheless. expeetancy
played a minimal role in deterrnining the effect of
a1cohol upon neuropsychologica1 functioning and,
when it did play a role, it was in the opposite
direction to that predicted. The fact thal functional
tolerance to alcohol intoxication can be learned
(Hoffman and Tabuoff, 1995) May account for the
direction of the expectaney effect secn in this study.
If experienced drinkers receive accurate information
about the dose of alcohol they are consuDÙng they
May be able to adapt and adjust to that dose if
circumstances demand it.
The study is interesting because it demonstrates
that alcohol intoxication per se impairs cenain a3pects
of neuropsychological functioning. Cognitive skil!>
dependent upon the prefrontal cortex suffer deterio· .
ration. 5uch skil1s are crucial to successful cC"lmpletion
of the Porteus Mazes (Porteus, 1959), the Rey copy
(Lhermitte et al.. 1972) and to the copying of complex
figu,es in general (Luria and Tsvetkova, 1964). Al-
though individuals with parietal lobe damage aise
have difficulty copying complex figures (Walsh, 1978),
the pattern of impairments induced by alcohol intox·
ication is not suggestive of construetional apraxia.
AdditionaJIy, Albert (1973) found that constructional
apraxia was highly correlated with visua! negleet, and
alcohol intoxication did nol praduce visual neglect in
the present study. Impairments in word fiueney are
aIso associated with damage to the frontal lobe (Ieft,
anterior to Broca's area) (Benton, 1968; Milner, 1967;
Ramier and Hécaen, 1970; Tow, 1955). Since the
prefrontal cortex is responsible for the planning and
 PETERSON ET AL. 119

~
TAn! J. Test of coptitivc funaioninl
li( DOSAGE GROUP
Hia:h dose Medium dose Law dose
Mean SD M.an sb Mean SD

TUT3 A.UOClA TEl' WJTH

na; nOHT,U CO"TEX
Poneus Maze
Quantitative 12.780'tot 2.11 14.83 1.62 14.42 1.S6
Qualitative 7S.4O"tb· 23.4 Sl.6 26.3 49.6 26.9
Rey Osterrcith (1) JO. Salit 3.40 32.S0 2.40 33.23 2.6S
Ward Fluent)' 39.09"- 9.86 46.00 1\.63 48.46 10.82
Selr.ordered Pointina 3.S1 1.63 4.04 1.77 3.01 1.91
Wisconsin Card Son 20.33 11.49 17.63 11.78 17.20 II. t2
TEJn ASSOCIA TJiD wrrH'
TH1l l'DD"OJlAL COaTEX
loaical.. MemOry (l) 9.4] 2.84 1\.04 3.07 10.87 2.98
Loaical Memory (0) 6.86"th 2.74 9.27 3.11 9.91 2.69
Rey Osterrcith (2) 13.4O'jbt 4.6)- 20.28 6.40 21.78 6.62
Rey Ostcrreith Cl) IJ.06l1 tbt 3.87 19.93 6.60 21.71 6.40
Paired Associalcs (E) 16.51 \.92 17.45 1.32 16.96 1.35
Paired Associates (0) 6.53"· 3.00 7.9S 2.S1 8.64 2.77
MUCBLL,,1'lSOUS
TEST!
WAIS
Information 23.70 2.70 23.S9 2.82 23.23 3.3S
Vocabulary 57.27 7.36 S9.S4 6.23 S7.82 6.48
Oisit Symbol S8.09 7.74 6\.77 8.96 63.36 7.62
Reaction Time (1) 3S.46 S.84 34.33 6.19 33.SS 7.12
Reaction Time (2) 49.30 7.16 4S.20 S.89 46.23 6.79
Reaction Time (]) 57,24 8.11 S3.94 8.79 S4.86 8.13
Youna·Pihl Memory 6.42 \.79 7.31 2.67 7.64 2.10
(,ff'
Pursuit Rotor 9.S2"t 3.39 10.S4 3.00 12.S6 2.03
J
."'. 0' Reprcscnu a sÎanificant diffcrcnce between the ttiah. and low-dose conditions.
Il Represenu a siptifieant difference bctween the ttiah- and mt':lium-dose conditions.
• p < .05. t p < .01.

organization of behavior (Damasio, 1985), knowledge
that alcohol impairs ilS funetioning pharmacologically
sheds an interesting light on consideration of intox·
ication.
Skills associated classically with the temporal cortex
also deteriorate. Intoxicated subjects manifested def·
icilS in ail forms of delayed noncued memor}' (verbal
and spatial) during tbis study, as weU as perfonning
poorly on the Wechsler Paired Associates Test. This
pattern of impainnent, overall, suggcslS that alcohol
intoxication panicuJarly affects the funetion of the
hippocampus, which plays a key role in the transfer
of information from shon·term attention to long·
tenn storage and/or in ilS retrieval (Gray, 1982;
Luria, 1980; O'Keefe and Nadel, 1978). Extensive
support for tbis idea is available within the relevant
animal literature (Gray, 1982), which suggests that
the benzodiazepines, barbiturates and alcohol aet
primarily on the septal·hippocampal system. Recent
work by Begleiter and Porjesz (19g8) also lends
credence to tbis supposition. This is particuJarly
interesting given that the funetion of the hippocampus
is not limited tO memor}', and that it and the septum
play a role in elieiting a variety of eue-specifie states
of anxiety (Gray, 1982). These cues include novelty,
threat of punishment and threat of frustrative nonre-
ward (Gray, (982). An alcohol·impaired septal.hip·
pocampal system might weU show reduced sensitivity
to cues that would nonnally elicit anxiety and aid
an individual in maintaining safety. Alcohol intoxi·
cation may al10w people to engage in activities that
would nonnally produce anxiety, and may produce
cognitive impairmenlS that limit their ability to aet
adaplively even if they do become anxious. These
two factors May aeeount in pan for the pronouneed
tendeney of intoxicated individuals to become both
vietims and vietimizers.
Certain other aspects of this study deserve consid·
eration as weU. The detrimental effcet of alcohol
upon wbat bas bcen dcseribed as Hmotor" perform·
ance has been consistently demonstrated (Connors
and Maisto, 1980; Hull and Bond, 1986; Lewis, 1969;

44
120 JOURNAL Of STUDIES ON ALCOHOLIMARCH 1990
Vuchinich and Sobell, 1978). Researchers who study
the effcets of alcohol intoxication have described
bath the Pursuit Rotor and Reaction Time Tests as
indicators of "motar performance" (Williams et al.,
1981). However, in the present study, alcohol intox-
ication did not decrease reaetion time (in threc dif·
ferent paradigms) nor performance on the Digit
Symbol WAIS-R subtest, which is sensitive ta deficits
in motor persistence and response speed (Lezak,
1976). However, it did impair complex motor pero
formance, as measured with the Pursuit Rotor. Dif-
ferent pans of the central nervous system control
diffcreDt aspects of movcment. Recent research al
the Montreal Neurologica1 Institute suggests that the
frontal lobes are particularly imponant in goveming
complex aets of motor performance, but do not
determine motor specd (Leonard et al., 1988). Luria
(1980), in his discussion of the motor analyzer,
locatcd in the frontal conex, has made similar sugges·
tians. The", iaeas might help clarify the confusion
about alcohol's effcet on motor performance. Perhaps
intoxication has a more profound effeet upon the
sequencing, organizing and control of motor action,
rather than upon ilS spced of execution.
Alcohol intoxication did not produce deficits in
"verbal" or "general" intelligence per se, at least
insofar as these qualities are measured by the Weehs-
1er Adult Intemgence Scale Vocabulary and Infor-
mation subtests. These tests are robust in the face
of even extensive brain damage. and are often used
as indicators of premorbi" ability (Lezak, 1976).
Alcohol intoxication also had no effcet on perform-
ance during the Self-Ordercd Painting Test. This test
was validated on individuals with extensive and var·
iable lesions of the frontal conex (Petrides and
Milnor, 1982), and it may be that alcohol affcets a
system that docs not participate in the functions
neeessary ta complete this test successfully. There is
no evidence that alcohol intoxication detrimentally
affcets those functions associatcd with the occipital-
parietal lobes, insofar as the present study is con·
cemcd. Tests for the functioning of this region are
somewhat subjective in nature. but in all cases the
performance of the intoxicatcd and sober subjeets
was equally perfeet. No subjcets manifestcd any signs
whalSOCver of negicet, of apraxia associated with
Iimb and buccofacial gestures and manipulations, or
serial aets. In summary, it seems as though the
similarities between those behaviors associated with
alcohol intoxication and those associated with pre.
frontal damage are striking, but that the two con.
ditions are certainly not identical.
The fundamental hypothesis underlying this study
suffercd from a number of faults. The concept of
"frontal·lobe syndrome" itself bas bcen criticizcd as
45
a general descnptor for the dysfunction associated
with damage ta the prefrontal areas of the frontal
lobes. The concept is too simplistic. Locale of dam-
age, even within an area as specific and apparently
nonspecialized as the frontal lobes, still variably
affects behavior (Damasio, 1985). Althou8h dysfunc-
tion associated with circumscribed lesions may be
usefully described in terms of lobe location, it may
be mare aceurate ta attribute drug effects ta altera.
tions in neuropsychological systems, which are not
Iikely ta be lobe-specific. The prefrontal divisions are
supplicd with rich conncetions ta various Iimbic
structures, including the hippocampus (Luria, 1980).
The hippocampus plays a key raie in memory con-
solidation, and the memory deficilS demonstrated by
intoxicatcd subjects in the present study suggest that
its functions may be impaircd by alcohol consump-
tion. The orbital·frontal conex and various structures
in the Iimbic system act as an integratcd unit (Luria,
1980) and subsume many of the functions that scemcd
ta be impalrcd by alcohol during lhis study. This
thenry, admittcd1y post hoc, seems ta fit the facts
more accurately than the hypothesis offercd at the
beginning of the study. Nonetheless, the results of
the present study are interesting for a variety of
reasons. Research into the effcets of alcohol upon
behavior has lackcd a testable unifying hypothesis
since its inception-and the use of tests validatcd
clinically and experimentally offers the possibility for
dceper comprehension of intoxicatcd behavior. In
addition, the fact that alcohol affects cognition at a
purely pharmacologieallevel is striking, although Hull
and Bond (1986) suggestcd that the expeetaney effcets
associatcd with alcohol use primarily affcet social
behavior and not information processing per se. In
the present study, the effects of expectancy upon
cognitive functioning were minimal. Situations that
involve alcohol consumption May serve as an excuse
for indulging in cenain types of antisocial behavior;
nonetheless, il is evident that alcohol intoxication
pharmacologically induces neurop.ychologica1 impair.
ment. It docs not scem unreasonable ta suppose that
5uch impairment has serious behavioral consequences.
AckDowledcm.Dts
The authors would like to thank Debbie Rou and Or. Frank
Ervin for the eontribution of their time and knowlcd.e.
Ref.reDces
ALlEU. M.L. A simple test of vÎsuaJ nealect. NEURA. 13:
658-665, 1973.
8EOLEITEJ., H. AND POIJESZ. 8. NeurophysioloaicaJ dysfunetion in
aJeoholism. la: ROSE, R.M. AlfD 8AUlTT, J.E. (EdJ.) Alea-
hotism: Orilins and Outcomes, New York: Raven Preu, Pubs.,
1988, pp. IS7 -174.
 PETERSON ET AL.
BINTON. A.L. Differentia! behaviouraJ dfecu in frontal lobe
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BnoWAN. H .• 80&0, 5., Hnro.u.asH, T. t [OUTJ.Ow. C.-M• .uro
MCTz:!Ll. S. Computed·lom0lfl.phy of the brain and neuro-
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-.s.;..

47
 Introduction: Study ~

Study 2 (Peterson, Finn and Pihl, in press) applied the

neuropsychological battery utilized in study 1 to 22
nonalcoholic SOMAs who had, in addition to their father, an
alcoho1ic grandfather and unc1e or brother, at minimum, and
compared their performance to that of 22 matched nonalcoholic
family-history negative controls, drawn from Study 1. Half of
the probands and controls, 2 groups of Il, were tested
sober. The other half, the remaining 2 groups of Il, were
tested after the administration of a relatively high dose of
alcohol, sufficient to seriously impair normal intellectual
function. Study 2 also tested the relationship between
certain aspects of SOMAs' cognitive functioning (the planning
and organizational skills associated with the operation of
the pre frontal cortex) and their cardiovascular hyper-
reactivity and alcohol-intoxicated dampening of that hyper-
reactivity, previously demonstrated by Finn and Pihl (1987,
1988).

48
 Cognitive Dysfunction and the

Inherited Predisposition to Alcoholism

Jordan B. Peterson, B.A. (1) and Robert O. Pihl, Ph.D (3)

McGill University - Douglas Hospital

Alcohol Research Program

Montreal, Quebec, Canada

Peter R. Finn, Ph.D. (2)

Indiana University

Bloomington, Indiana

This research was supported in part by the

Medical Research Council of Canada.

Running head: COGNITIVE DSYFUNCTION AND RISK FOR ALCOHOLISM

49
 Cognitive Dysfunction
2

Cognitive Dysfunction and the

Inherited Predisposition to Alcoholism

Jordan Peterson

Department of Psychology

stewart Biology Building

1205 Dr. Penfield Avenue

Montreal, Quebec

CANADA

H3AIBl

,,,,,"';"

li

Key Words

Alcoholism, genetic risk, cognitive functioning,

neuropsychological performance, autonomie hyper-reactivity,

ff..... cued anxiety

50
 Cognitive Dysfunction
3

Abstract
A battery of neuropsychological tests was administered to 22
non-alcoholic sons of male alcoholics (SOMAs) from families
with extensive histories of male alcoholism and to 22 non-
alcoholic controls with no history of familial alcoholism.
Eleven subjects in each group were tested sober; eleven were
tested while alcohol-intoxicated. Analyses of the results of
this battery suggested (1) that SOMAs may be characterized by
comparative decrements in those cognitive functions
associated with the organization of novel information,
dependent in theory upon the prefrontal cortex; and (2) that
alcohol detrimentally affects delayed memory, associated with
the temporal cortex, equally across groups. Twenty of these
SOMAs had previously participated in either of two studies
that demonstrated their cardiovascular hyper-reactivity to
threat/stress and their increased sensitivity to the
reactivity-dampening effects of alcohol intoxication.
Correlational analyses of the results of the present and
prevlous studies demonstrated the existence of a highly
significant relationship between cognitive impairment,
cardiovascular hyper-reactivity, and susceptibllity to the
reactivity-dampening effects of alcohol.

51
 Cognitive Dysfunction
4

A variety of studies have demonstrated that the sons of

male alcoholics (SOMAs) are at heightened genetic risk for
the development of alcoholism. None of these studies are
above reproach methodologically (Lester, 1988; Searles, 1987;
Murray, Clifford, and Gurling, 1983), but taken collectively
they suggest that SOMAs are 3 to 9 times more likely to
become alcoholic than the sons of non-alcoholics (Cloninger,
Sigvardsson, & Bohman, 1981; Goodwin, 1985). The precise
nature of this increased risk remains unknown, but in recent
years a number of markers that appear in association with it
have been tentatively identified (Begleiter and Porjesz,
1988). These markers have been described critically, in
detail, by Pihl, Peterson and Finn (1990).
A number of studies have demonstrated that SOMAs perform
more poorly than controls on tests of linguistic ability,
abstraction, and problem-solving (Drejer, Theilgaard,
Teasdale, Schulsinger & Goodwin, 1985; Gabrielli & Mednick,
1983; Whipple, parker & Noble, 1988). Additiona1 evidence
exists suggesting that SOMAs hyper-react psychophysio-
logically to threat and novelty (Finn and Pihl, 1987, 1988;
Finn, Zeitouni and Pihl, 1990). Tarter et al. (1984, 1988)
have drawn a parallel between the cognitive and behavioural
styles of SOMAs and those with minor pre frontal cortical
trauma. Gray (1982, 1987), Luria (1980), Vinogradova (1975),
Nauta (1974), Sokolov (1969) and Granit (1977) reviewed
general neuropsychological informat.ion suggesting (1) that

52
 Cognitive Oysfunction
5

the pre frontal cortex provides the physiological substrate

for the cognitive functions associated with abstract
classification and planning; (2) that the prefrontal cortex
serves to inhibit or modulate the function of various
subcortical structures, including those governing threat or
novelty response; (3) that the hippocampus and hypothalamus
are critically involved in this threat response; and (4) that
alcohol intoxication might interfere with hippocampal
function.
Pihl, Finn and Peter son (1989) and Pihl, Peterson and
Finn (1990), integrating these sources of information, have
hypothesized that SOMAs have difficulty in abstractly
classifying and/or in modulating their reaction to

....;.'" threatening of novel information, perhaps because of mild

decrements in prefrontal function. They suggest alcohol
consumption might ameliorate the negative subjective
consequences of this difficulty - associated with increased
physiological reactivity - by interfering with the function
of the novelty/threat response system.
Three primary hypotheses were derived from thls theory,
for the purposes oi the present study. First: it was
predicted that sober SOMAs would perform more poorly than
controls on cognitive teots of classification and planning,
generally associated with prefrontal function; second, that
alcohol intoxication would interfere with the performance of
both groups on those neuropsychological tests that putatlvely

53
 Cognitive Dysiunction
6

assess transfer of information into long-term memory,

associated ~ith the hippocampus; and third that decrements in

pre frontal function among SOMAs ~ou1d be corre1ated ~ith

their çardiovascu1ar hyper-reactivity to threat. These

hypotheses ~ere to be tested in three parts. The first part

invo1ved assessment of the neuropsycho1ogica1 function of

stringent1y se1ected sober SOMAs and contro1s, in order to

he1p determine if and in ~hat manner their cognitive

abi1ities differed. The second part invo1ved a simi1ar

assessment, conducted upon intoxicated SOMAs and contro1s, in

order to he1p determine primari1y ~hat neuropsycho1ogica1

functions a1coho1 intoxication impairs per se and further, to

investigate ~hether SOMAs and contro1s differ in their

susceptibi1ity to a1coho1's effect on cognition. The third

part of the study invo1ved investigation of the re1ationship

bet~een the sober cognitive functioning of these SOMAs, and

their previous1y reported (Finn & Pih1, 1987, 1988)

cardiovascu1ar reactivity and sensitivity to dampening (Finn

& Pih1, 1987, 1988) of that reactivity by a1cohol

consumption.
Method

Subjects

T~o groups of 22 (N=44) non-a1coho1ic men participated

in this study. A11 subjects scored 5 or 1ess on the Michigan

A1coho1ism Screening Test (MAST) (Se1zer, 1971) and none

cou1d be characterized as a1coho1-dependent or abusing by the

54
 Cognitive Dysfunction
7

criteria set forth in the Diagnostic and Statistical Manual

~ Mental Disorders (DSM-III) (American Psychiatrie

Association, 1980). Subjects younger than 18 and older than

30 years of age were excluded from participation. Those who

completed the study had a mean age, equivalent across groups,

of approximately 24 years. Allsubjects were raised by their

biological parents; all were caucasian.

In the first of these two groups were SOMAs who had at

minimum, in addition to their father, a paternal grandfather

and brother or paternal uncle who were alcoholic according to

diagnoses made at a major Montreal psychiatrie institution,

where families of alcoholics are screened, interviewed,

referred for counselling, and recruited as potential subjects

for a number of interdisciplinary research efforts. At this

institution, extensive family histories are taken from as

many family members as possible. Diagnoses for the

interviewed members are based on the MAST and DSM-III

criteria. Unavailable family members are diagnosed according

to the Family History Research Diagnostic Criteri~ (FH-RDC)

(Endicott, Andreasen & Spitzer, 1975). Subjects are selected

according to these stringent criteria in order to increase

the likelihood that they truly are at increased genetic risk

for the inheritance of alcoholism. This increased risk is

reflected in the fact that 76% of the first and second-degree

male relatives of subjects selected in this fashion are

alcoholic (Finn & Pihl, 1987). SOMAs had an average of 13.4

55
 Cognitive Dysfunction
8

years of education, and drank between 5 and 15 drinks a week.

Mean age of onset of paternal alcoholism was 20 years.
Probands with alcoholic mothers, with mothers who drank
during pregnancy, or with psychotic relatives were excluded.
In the second group were 22 men recruited by newspaper
advertisement as paid controls. Healthy non-alcoholic
moderate social drinkers (5 > x < 15 drinks/week) with
between 13 and 14 years of education were selected for
participation. Control subjects had no identifiable
alcoholism (MAST and DSM-III criteria) in the past two
generations of their pedigree. Control subjects familiar with
psychological experimentation, or who had psychotic
relatives, were excluded from participation. An augmented
group of these subjects also served as controls in the
concurrently run Peterson, Rothfleisch, Zelaza and Pihl
(1990) study.
AlI subjects were asked ta refrain from the consumptian
of alcohol for 24 hours and from food for 4 haurs before the
experimental session. Subjects were paid $5/hour for their
participation.
Design and Procedure
Parts One and Two
Upan arrivaI at the laboratory, subjects were
farniliarized with the experimental procedure, and were
rp.~1Jirp.n to Rign nn inEormed consent form. Each subject was

then randomly assigned to receive either 1.32 ml/kg of 95%

56
 Cognitive Dysfunction
9
pharmaceutical alcohol mixed 5:1 in orange juice, or to
receive an equivalent amount of juice by body weight and
0.132 ml/kg pharmaceutical alcohol, to provide "active
placebo" (Ross & Pihl, 1989) control for subject and
experimenter expectancy. All subjects were then submitted to
a battery of neuropsychological tests. An independent-groups
design with random group assignment was chosen specifically
to control for the effect of practice on the
neuropsychological test battery.
It should be noted additionally, that although

expectancy and dose generally confound the effects of a drug

(Marlatt and Rohsenov, 1980), previous experience vith the
test battery used in this gtudy, within the confines of a
multiple-dose balanced-placebo design, lndlcated that it vas
insensitive to the effects of expectancy and sensitive ta the
pharmacological affects of a 1.32 ml/kg dose of 95\ pure
pharmaceutical alcohol (Peterson, Rothfleisch, Zelazo & Pihl,
1990).
Each subject was given 3 drinks, and was asked to finish
them within 20 minutes. After a 15 minute waiting period,
each subject was given the first of 3 subjective intoxication
scales, and the first of three breathalyzer tests. The former
were completed privately, to control for the effects of
experimenter demand. Subjects were then taken to a separate
testing area, where they were administered the following
tests in random order by 3 experimenters blind to the

57
 cognitive Dysfunction
la

subject's risk status and assigned condition. These tests

were chosen for heuristic 9urposes, and were classified

accordingly, because the cognitive abilities they test have

been experimentally associated with the function of

relatively specifie cortical areas. It should be noted,

however, that there is no simple one-to-one relationship

between cortical locale and cognitive function. Nonetheless,

since the neuropsychological approach allows in part for

analysis of cognitive functioning per se, and further,

provides for the possibility of clarifying the nature of the

relationship between cognition and cortical functioning, its

utility outweighs the inherent risk of oversimplification.

Tests of cognitive function often associated with the

~ ..
Ct pre frontal cortex

Porteus Maze (extension series). Subjects are required

to complete a series of mazes ranked according to difficulty.

Individuals with les ions of the frontal lobes demonstrate

impairments in their ability to correctly complete this test

(Crown, 1952; Malmo, 1948; Mettler, 1952) which was designed

to measure planning and foresight (Porteus, 1959).

Rey-Osterreith Comp1ex Figure: Copy. Subjects are

required to copy a complex spatial figure from an original.

Individuals with pre frontal damage copy this figure (Lezak,

1976) and complex figures in general (Luria, 1980) poorly,

although parietal damage may a1so produce performance

deficits (Lezak, 1976) of a more severe sort.

if. '

58
 Cognitive Dysfunction
11

Thurstone Word Fluency. Subjects are required to ~rite

as many ~ords beginning ~ith "S" as possible in 5 minutes.

Individuals ~ith left frontal damage consistently demonstrate

impairments in ~ord fluency (Benton, 1968; Ramier and Hecaen,

1970), ~hich measures the ability to generate ~ords according

to an abstract conceptual category.

Self-Ordered Pointing: 11 representational dra~ings.

Subjects must point to a different one of 12 pictures of

familiar objects, prcsented in 12 different arrays.

Individuals ~ith frontal damage consistently manifest

defictts in performance on this task, ~hich requires the

abllity to organize information conceptually. Individuals

~ith temporal damage also manifest deficits, that vary ~ith

the severity of their les ion (Petrides and Milner, 1982),

although temporally-damaged individuals tend also to suffer

from severe memory loss.

Wisconsin Card Sort. Subjects are presented sequentially

with 64 cards, and are required to categorize them according

to feedback provided by an investigator. Individuals

suffering from dorso-lateral frontal les ions perform poorly

on this test, which is sensitive to perseveration (Grant and

Berg, 1948; Milner, 1964).

Tests ~ memory often associated with the temporal cortex

Wechsler Logical Memory: Immediate and ~ minute delay.

Subjects are required to repeat t~o stories, in sequence,

.~ . once immediately after presentation and once (unknown to them

.. ~

59
 Cognitive Dysfunction
12
. a priori) 25 minutes 1ater, after comp1etion of a number of

other tasks. Individua1s with temporal (particu1ar1y

hippocampa1) damage perform poor1y on these tests, especia11y

after a de1ay (Mi1ner, 1975).

Wechs1er Paired Associates: Difficult and easy pairs.

Subjects are orally presented three times with ten word

pairs, and are required to remember the second word in each

pair. Six pairs are easy and four difficult to associate.

Individuals with le ft temporal (particularly hippocampal)

damage have difficulty in completing this test, and there is

additional evidence that organic brain damage particularly

impairs recall of the difficult pairs (Walsh, 1978).

Rey Osterreith Figure: Reproduction from memory.

~,

"i
~-
~ -,
Subjects are required to redraw the figure copied earlier 25

minutes later, with no a priori knowledge that they are to do

50, after completing several other tasks. Patients with right

temporal (particularly hippocampal) damage have difficulty in

completing this task (Milner, 1975).

Tests Qi cognitive function often associated with the

parietal-occipital cortex

Albert's Test Qi Visual Neglect. Subjects are given a

pencil and a sheet of paper with a number of short lines

printed on it, and are asked to bisect each line with another

short line. Subjects who suffer from parietal damage perform

particularly poorly on this test (Albert, 1973).

GO
 Cognitive Dysfunction
13

l Apraxia Questionnaire. Subjects are required to

originate and/or duplicate a number of simple motor

operations. This questionnaire provides a general measure GE

ideomotor, ideational and buccofacial apraxia, which has been

operationally defined by exclusion as a disorder of skilled

movement not caused by weakness, deafferentiation, abnormal

tone or posture, movement disorder, intellectual

deterioration, poor comprehension, or lack of cooperation

(Heilman & Valenstein, 1985).

Miscellaneous tests.

The Information subtest of the Revised Wechsler Adult

Intelligence Scale (WAIS-R) provided a measure of accumulated

verbal knowledge. The Digit Symbol WAIS-R subtest vas

.: ...;-
included because it is sensitive to variations in motivation

(Lezak, 1976) and as a measure of performance IQ. A Reaction

Time Test, with three subtests of increasing complexity, vas

included to assess motor speed.

Tests were completed within 1 1/2 hours. Subjects vere

given a breathalyzer test and a subjective intoxication sca1e

half-vay through and at the end of the test session,

debriefed and, upon regaining sobriety (BAL < 0.04), vere

paid $25.00 and alloved to leave.

Part Three

Tventy of the 22 SOMAs who volunteered for the present

study had previous1y participated in one of tvo projects that

demonstrated their augmented cardiovascu1ar hyper-reactivity

• .,!-

61
 Cognitive Dysfunction
14

to threat/stress and their increased sensitivity to the

reactivity-dampening effects of alcohol, in comparison to

matched controls (Finn and Pihl, 1987, 1988). Participants

in these studies were subjected to a number of successive

electric shocks (1.85 mA for 0.25 seconds), whose onset was

signal1ed by a ID-second countdown, once while sober and

once under the influence of either 1.00 or 1.32 ml of 95%

pure pharmaceutical alcohol per kg of body weight, in

counterbalanced arder. In these studies, sober SOMAs from

families with extensive male familial alcoholism reacted ta

the shock procedure with significant increases in heart-rate

(HR) and significant decreases in digital blood volume

amplitude (OBVA) (cardiovascular reactivity) in comparison ta

f
~- contraIs, while when alcohol-intoxicated this characteristic

cardiovascular hyper-reactivity was essentially eliminated

(cardiovascular reactivity-dampening).

Since the theory presented by Pihl et al. (1989, 1990)

and discussed earlier predicts that deficits in the cognitive

functions associated with the prefrontal cortex should be

accompanied by increased cardiovascular reactivity ta threat,

and that alcohol intoxication should eliminate that

reactivity, exploratory correlational analyses comparing

prefrontal function, cardiovascular reactivity, and alcohol-

induced reduction of reactivity were completed.

..
( ,

62
 Cognitive Dysfunction
15

Results

Parts One and Two

The nature of the relationship betveen risk, alcohol

intoxication and neuropsychological performance vas explored

statistically by two (SOMA/control) X tvo (alcohol/no-

alcohol) analyses of variance (ANOVA), employed separately

for each measure. Post-hoc tests of simple main effects were

employed in the single case of the Thurstone Word Fluency

Test, where interaction effects reached significance.

Subjects of both risk status maintained equivalent mean

blood alcohol levels of approximately 0.10 for the duration

of the test period, and rated themselves as equally

intoxicated on aIl three scales of subjective intoxication.

No subjects in either group or condition made any errors

while carrying out the tasks associated with Albert's Test of

Visual Neglect or the apraxia questionnaire. Nevertheless,

the analyses demo~strated tvo primary effects (Table 1).

- INSERT TABLE 1 HERE -

One can be attributed to risk status, the other to the

consequences of intoxication.

With regards solely to risk status: SOMAs manifested

comparative decrements in performance on the Rey-Osterreith

(copy) (F(1,40l = 5.2, p < 0.05), Self-Ordered Pointing

(F(1,40) = 11.3, p < O.OOll, Difficult Paired Associates

(F(1,40) = 5.87, P < 0.05) and Information tests (F(1,40) =

4.8, P < 0.05l. With regards solely to intoxication: Alcohol

63
 Cognitive Dysfunction
16

consumption impaired the performance of individuals in both

risk categories, on the Porteus Maze (F(I,40) = 4.1, P <

0.05), Rey copy (F(I,40) = 5.2, p < 0.05), Wisconsin Card

Sort (F(I,40) = 4.1, P < 0.05), Easy Paired Associates

(F(1,40) = 5.3, P < 0.05), Difficult Paired Associates

(F(1,40) = 8.2, P < 0.01), Delayed Rey Osterreith Figure

(F(1,40) = 24.7, p < 0.001) and Delayed Logical Memory

(F(1,40) = 15.6, p< 0.001) tests. Additionally: SOMAs and

controls ~ere differentially affected by alcohol, whi1e

completing the Thurstone Word Fluency test (F(I,40) = 5.5, p

< 0.05), in that the controls were significantly impaired

(F(1,40) = 6.3, p < 0.05) while the SOMAs w"re not.

Part Three

In order to examine the relationship between pre frontal

function/planning and cardiac hyper-reactivity/ alcohol

dampening, scores on the five tests associated with the

pre frontal cortex (Porteous Maze, Rey Osterreith (Copy),

Self-Ordered pointing, Wisconsin Card sort, and Thurstone

Word Fluency) were included in a Pearson Product-Moment

correlation matrix along with 2 indices of sober

stress/threat reactivity (HR increase and DBVA decrease) and

2 indices of alcohol-intoxication-induced stress/threat

reactivity dampening (HR increase-reduction and DBVA

decrease-reduction). A number of correlation coefficients in

this matrix approximated or exceeded the alpha 0.0025,

determined by Bonferroni correction for matrix size (alpha

64
 Cognitive Dysfunction
17

(0.05) divided by the number of correlations of interest

(20)). These correlations are presented in Table 2. Tt is of

- INSERT TABLE 2 HERE -

interest to note that the correlation bet~een weST

performance and HR increase improves ~hen only those ~ho

completed the weST sober (N=ll) are considered (r = 0.75, p <

0.009), and falls for those ~ho took the test drunk (r =
0.49, P < 0.18). This is an important consideration from the
methodological vie~point, because alcohol detrimentally

affected weST scores for both groups. It is also interesting

to note that HR reactivity (increase) is highly correlated

~ith HR (r = 0.92, p < 0.0001) and DBVA (r = 0.85, p <

0.0002) dampening, and that DBVA reactivity (decrease) is

highly correlated ~ith DBVA (r = 0.94, p < 0.0001) and HR (r

= 0.88, p < 0.0001) dampening.
T~o separate canonical correlation analyses ~ere also

conducted, to further aid in exploring the nature of the

relationship·bet~een neuropsychological performance and

cardiovascular reactivity, and to provisionally determine how

much of the variance in the latter could be accounted for by

the former. The first of these analyses examined the

relationship bet~een the neuropsychological variables SOP and

weST and HR and DBVA reactivity; the second examined the

relationship bet~een sOP/WeST and HR/DBVA dampening.

Significant correlations emerged in the former case (lst

canoni~Q~ correlation r = 0.75; R-square = 0.57; Wilk's

,:-.t.•

65
 cognitive Dysfunction
18

lambda F(4,32) = 4.2; P < 0.008) and in the latter (lst

canonical correlation r - 0.81; R-square = 0.65; Wilk's

lambda F(4,32) = 6.4; P < 0.0004).

Discussion

Parts One and T~o

Sober SOMAs could be distinguished from controls by their

performance on four cognitive tasks: the Self-Ordered

Pointing, Rey copy, Difficult Paired Associates, and WAIS-R

Information tests. Successful completion of the Self-Ordered

Pointing test requires the generation of a workable strategy

for memory, and intact memory itself (Petrides and Milner,

1982). Although temporal damage, and subsequent memory 1055,

can interfere per se ~ith performance on this test, tests

most sensitive to temporal damage (delayed recal1) did not

distinguish SOMAs from controls. This suggests that

comparative lack of organization accounts for their poorer

performance. Accurate copying of the Rey figure requires

intact spatial perception, a putative function of the

parietal cortex (Luria, 1980), and the ability to organize

comp1ex novel non-verbal visual information into 10gica1 sub-

groups (Lezak, 1976; Luria, 1980). Although both parietal and

frontal damage can interfere ~ith performance on this test

(Lezak, 1976), the fact that SOMAs performed weIl on the

tests for apraxia and neglect, ~ut comparatively poorly on

other frontal tests, suggests that lack of organization,

rather than impairment in spatial perception, accounted for

(
66
 Cognitive Dysfunction
19

1 their minor, but statistically significant, performance

decrement.

The development of a mnemonic device or another similar

strategy for aiding memory also seems crucial to success on

the Difficult Paired Associates subtest, although it

obviously also involves recall per se. The easy ~ord pairs

are matched according to inherent association (e.g. baby-

cries), and one ~ord serves as a cue for the other during

memory trials. No inherently meaningful associations exist

for the difficult pairs (e.g. crush-darkl and must therefore

be invented. The fact that SOMAs performed at par, ~ith

regards to the easy pairs, but comparatively poorly on the

difficult pairs, suggests once again that SOMAs are

characterized by decrements in the ability to organize or

categorize information. Although none of these individual

tests can be considered conclusive in isolation, the overall

pattern of results suggests that sober SOMAs may be

characterized by deficits in the ability to organize and

categorize novel information. This ability has been most

commonly associated ~ith the function of the pre frontal

cortex (Luria, 1980). The deficit in accumulated kno~ledge,

demonstrated by the Information subtest of the WAIS-R , is a

possible consequence of this primary dysfunction, ~hich may

~ell have existed in sorne form since birth.

Three tests of those cognitive abilities associated

~ith the pre frontal cortex proved mildly sensitive to the

67
 Cognitive Dysfunction
20

debilitating effects of alcohol intoxication (Porteus Maze,

Rey copy and Wisconsin Card Sort Test). Hovever, those
cognitive abilities associated with the functions of the
temporal cortex - particularly of the hippocampus - were even
more severely affected. Subjects who had consumed alcohol
vere impaired in their recall of word pairs (Easy and
Difficult Paired Associates), in delayed recall for a
narrative (Delayed Logical Memory) and for non-verbal
informatioi (Delayed Rey Osterreith Figure). This pattern of
results, equal for both groups, is in keeping with that
suggested/reported by Gray (1982). Direct evidence supporting
the contention that alcohol interferes vith hippocampal
function has also recently been reported (Lovinger, White &
Weight, 1989).
The sIngle interaction effect detected by the Thurstone

Word Fluency Test is interesting and suggests perhaps that

SOMAs are less sensitive ta the detrimental effects of

alcohol on word fluency than controls. It ls not unreasonable
to suppose that those who are predisposed to abuse alcohol
benefit maximally from its positive attributes and suffer
minimally from its drawbacks, at least in the short term.
Part Three
Two particularly interesting patterns of correlations
emerged, with regards to the theoretical relationship betveen
cognitive performance and cardiovascular reactivity: Scores
on the Wisconsin Card Sort Test (WCST) were highly correlated

68
 Cognitive Oysfunction
21

with sober HR increase and OSVA decrease ta signalled shock.

This means that those who made the most errors during the

WCST were most reactive ta the signalled shock. Scores on the

Self-Ordered Painting Test (SOP) were correlated similarly

with sober HR increase and OSVA decrease, although not as

strongly. Performance on both tests was dlso correlated with

alcohol-induced HR and OSVA reactivity-dampening, most

significantly for SOP and HR dampening. This means that t~ose

who made the most errors during the SOP were most susceptible

ta the HR reactivity-dampening effect of alcohol. This

general line of reasoning is supported by the results of the

canonical correlation analysis. Although this analysis should

be considered exploratory because of the small sample size

involved, it adds credence ta the notion that poorer

cognitive performance and increased cardiovascular-

reactivitY/alcohol-dampenlng are significantly related in

multigenerational SOMAs.

With respect to the relationship between general

cardiovascular reactivity and cardiovascular-reactivity-

dampening: sober HR increase was highly correlated wlth

alcohol-dampening of t~at increase and similarly, sober OSVA

decrease was highly correlated with alcohol-dampening of that

decrease. Sober HR increase was also highly correlated with

OSVA dampening, and likewise, sober OSVA decrease Wd5 highly

correlated with HR dampening. This combinat ion of results

suggests that those SOMAs most reactive to the signalled

69
 Cognitive Dysfunction
22
shocks were also most susceptible ta alcohol's ability to
eliminate that reactivity.
Conclusion
This study provides tentative support for the hypothesis
that sober SOMAs from families with extensive
multigenerational male alcoholism are characterized by
comparative decrements in the ability to classify or to
attribute meaning to novel information. This ability has been
classically associated with prefrontal cortical function. It
also demonstrates the existence of a significant relationship
between certain aspects of this cognitive deficit and the
cardiovascular hyper-reactivity and alcohol-reactivity-
dampening characteristic of such SOMAs, and that such
reactivity and dampening are integrally related. In addition,
demunstration that alcohol intoxication severely impairs the
transfer of information from short-term storage into
permanent memory in SOMAs and contrals lends additional
credence to Gray's (1982, 1987) idea that alcohol
intoxication particularly impairs hippocampal function.

70
 Cognitive Dysfunction
23
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76
 Cognitive Dysfunction
29

1 TABLE ONE: Tests of Cognitive Function

Mean Scores (Standard Deviations)

TESTS ASSOCIATED WITH Sons of Alcoholics ContraIs

THE PREFRONTAL CORTEX No Alcohol Alcohol No Alcohol Alcohol

Porteus Maze Age 13.9 ( 3 . 4 ) +12.7 ( 3 .1) 14.9 (1. 3 ) +13.0 (1. 8)

Rey Osterreith Copy *31. 7 ( 4 .6) *+26.9 ( 6 . 2 ) 32.7 ( 3 . 3 ) +31. 9 (2.4)

Thurstone F1uency ~38.4(13.1) ~42.1(10.7) ~50.0 ( 9 .3) '39.0 ( 8 . 2 )

Self Ordered Pointing * 5.4 ( 1. 4 ) * 5.8 ( 3 . 8 ) 3.3 ( 1. 9 ) 3.2 (1. 4)

Wisconsin Card Sort 20.4 ( 9 .5) +23.7 ( 6 .7) 14.9 ( 7 . 7 ) +22.9(11.4)

TESTS ASSOCIATED WITH Sons of A1coho1ics Contro1s

THE TEMPORAL CORTEX No Alcohol Alcohol No Alcohol Alcohol

Logical Memory 9.4 ( 2 .8) 8.0 ( 3 .1) 10.6 ( 3 .6) 8.9 ( 2 . 7 )

Logical Memory Delay 8.9 (3.2) + 4.7 ( 2 . 4 ) 9.4 ( 3.1) + 6.6 ( 2 . 9 )
-;-;:.
Paired Associate (E) 17.0 (1. 5) +15.4 ( 2 .0) 17.0 ( 1. 5 ) +16.1 ( 2 . 2 )
Paired Associate (D) * 7.1 ( 1. 5 ) *+ 4.7 ( 3 .3) 8.9 ( 2 .1) + 6.7 ( 3 .2)
Rey Osterrieth Delay 20.2 ( 6 . 6 ) +13.0 ( 5 .9 ) 22.1 ( 5 . 8 ) +12.4 ( 3 . 8 )

MISCELLANEOUS TESTS Sons of Alcoholics Con troIs

No A1cohol Alcohol No A1cohol Alcohol

Information *20.5 ( 4 . 7 ) *20.7 ( 4 .3) 22.8 ( 3 . 3 ) 23.4 ( 2 . 2 )

Digit Symbol 59.9 ( 9 . 6 ) 54. 4 ( 6 .4) 59.3 ( 7 . 4 ) 60.0 ( 8 .0)

Reaction Time 34.7 ( 5 . 8 ) 37.7 ( 5 . 8 ) 34.8 ( 6 .7) 33.5 ( 5 . 7 )

RISK EFFECT: * p < 0.05

DRUG EFFECT: + p < 0.05
INTERACTION: p < 0.05

NOTE: Scores for the Self-Ordered Pointing are reported as total

errors in three trials of 12. Scores for the Wisconsin Card Sort are
reported as total errors in 64 trials.

77
 Cognitive Dysfunction
30

TABLE TWO: Correlation Matrix

Pearson Correlation Coefficients

N = 20

HR HR DBVA DBVA Self-Ordered Wisconsin

Increase Dampen Decrease Dampen Pointing Card Sort

HR 0.86 0.83 0.73 0.57 0.69

Increase 0.0001 0.0001 0.0002 0.0082 0.0007

HR 0.79 0.73 0.77 0.54

Dampen 0.0001 0.0003 0.0001 0.0137

DBVA 0.88 0.52 0.69

Decrease 0.0001 0.0192 0.0010

DBVA 0.42 0.54

Dampen 0.0673 0.0140

Self-Ordered 0.53
Painting 0.0169

.
.~--

:1

/·'",.f
"

78
 Comments ~ Study 1 and ~

What conclusions can be drawn from the results of these

two studies? Study l demonstrated (a) that a high dose of
alcohol detrimentally affect~ cognition at the pharmaco-
logical level, and (b) that the cognitive functions most
severely affected seem to be dependent upon the operation of
the intact, closely integrated prefrontal-limbic system,
particularly upon the hippocampus. Study 2 demonstrated (a)
that SOMAs from families with extensive histories of male
alcoholism were characterized by deficits in planning and the
organization of information, scoring more poorly than matched
controls on tests classically associated with the functioning
of the pre frontal cortex, and (b) that the severity of sorne
of these cognitive deficits were associated with SOMAs'
~ .. heightened cardiovascular reactivity to threat of and
aversive stimulation, and with their susceptibility to
alcohol-induced dampening of that reactivity.
How can the results of these two studies be understood,
and integrated with the relevant literature, in order to
clarify the potential nature of the inherited predisposition
to alcoholism? More specifically, how is it that the cogni-
tive deficits and associated cardiovascular hyper-reactivity
characteristic of SOMAs might predispose them to alcoholism,
given what is known about the general pharmacological effects
of alcohol consumption, and SOMAs' specifie reaction to
alcohol intoxication? The following paper provides a
provisional answer to these questions, presented in
,,--:,.
discussion centred upon 4 figures.

79
 Information Processing, Neuropsychological Function, and the
Innerited Predisposition to Alcoholism

J.B. Peterson and R.O. Pihl

Department of Psychology
McGill University
Montreal, Quebec

_.
1.

80
 Predisposition to Alcoholism

l Jordan Peterson
Department of Psychology
McGill University
1205 Dr. Penfield Avenue
Montreal, Quebec
CANADA
H3AlBl

.. 0:.'

Key Words
alcoholism, heredity, neuropsychology, cognition,
psychophysiology, conduct disorder, hyperactivity, alcohol
intoxication

81
 Predisposition to Alcoholism
3

ABSTRACT

Sons of male alcoholics are at particularly heightened risk

for the development of alcoholism. This heightened risk
frequently appears in association with increased incidence of
conduct-disorder/hyperactivity, with deficits in abstract
thinking and poor school performance, with abnormalities in
cued psychophysiological response, and with increased
sensitivity to the putatively stress-response-dampening
effects of alcohol intoxication. This risk and its associated
features are discussed within the context of a
neuropsychological theory, predicated on the ùotions (1) that
deficits in cognitive functions theoretically dependent upon
the intact functioning of the pre frontal cortex could
underlie manifestation of the idiosyncracies commonly
attributed to sons of male alcoholics, and (2) that acute
alcohol intoxication could relieve the subjective discomfort
associated with the consequences of such deficits.

82
 Predisposition to Alcoholism
4

Society pays a heavy price for alcohol use. Five to 10

per cent of adults might reasonably be considered alcoholic
(Kamerow, Pincus and MacDonald, 1986). Alcoholism ranks third
nationally in terms of its detrimental effects on public
health, narrowly trailing heart disease and cancer (Kamerow
et al., 1986). Treatment for alcoholism is often expensive
and 1ess than successful (Emrick and Hansen, 1983; Miller and
Hester, 1986; Polich, Armor and Braiker, 1980).
The etiology of alcoholism is poorly understood. This
makes matching treatment regimen to individual alcoholic
difficult (Miller and Hester, 1986), and prevention of
a1coholism next to impossible. Studies designed to rectify
this state of ignorance have generally been conducted upon
.- alcoholics in treatment (Pihl and spiers, 1978). Conclusions
concerning etiology drawn from such investigations are
severely limited by the confusion of cause and effect
characteristic of retrospective analyses.
Such confusion might conceivably be overcome by
examination of non-alcoholic individuals at elevated risk for
the deve10pment of alcoholism. Balanced reviews (Murray,
Clifford and Gurling, 1983) of a number of older adoption
(Bohman, 1978; Cadoret, Cain and Grove, 1980; cadoret and
Gath, 1978; Goodwin, Schulsinger, Hermansen, Guze and
Winokur, 1~73; Goodwin, Schu1singer, Moller, Hermansen,
Winokur and Guze, 1974), family (reviewed in cotton, 1979)
and twin (Hrubec and Omenn, 1981; Kaij, 1960) studies have

83
 Predisposition to Alcoholism
5

concluded that heritable factors play a role in determining

such ~isk. More recent work (Heath and Martin, 1988; Kaprio,
Langinvainio, Romanov, Sauna, and Rose, 1987; Pickens,
Svikis, McGue, Lykken, Heston and Clayton, 1991) supports
this general conclusion. Sons of male alcoholics appear
particularly susceptible to the development of alcoholism
(Cloninger, 1987).
It is interesting to note, in this regard, that men in
general abuse alcohol more frequently than women (Adrian,
1984), especially between the ages of 18 and 25, and that
sons of male alcoholics have consistently been differentiated
from males with no family history of alcoholism on various
behavioural, psychophysiological, cognitive and biochemical
measures (Pihl, Peterson and Finn, 1990; Tarter, Alterman and
Edwards, 1985, 1988). It appears therefore that the intensive
study of nonalcoholic sons of male alcoholics could lead to
deeper understanding of the etiology of alcoholism. In
consequence, this paper is devoted ta 'Jescribing the most
commonly described characteristics ofthese individuals,
within the framework of an information-processing/
neuropsychological theory, devised to provide a testable
hypothesis linking diverse findings.
Information Processing, Active Exploration, and Escape
INSERT FIGURE 1 HERE
Lt is necessary to consider the manner in which
information is generally analyzed, per se, before attempting

84
 Predisposition to Alcoholism
6

to describe how abnormalities ~n information processing might

underlie sons of male alcoholics' (SOMAs) predisposition to
alcoholism. Figure 1 has been G~~igned to offer a general,
highly simplified, schematic description of this process.
This figure is based up0n evidence suggesting that integrated
mu1timoda1 sensory input is categorized according to
expectancy, after being subjected to intensive, specialized
analytic/synthetic processing, which has as its end product
identification and amplification of the meaningful aspects of
the sensory field, and their separation from irrelevant
sensory detai1s (Luria, 1980; Sokolov, 1969; Vinogradova,
1975). Expectancy, for th~ purposes of this discussion, is
the active component of pre-established knowledge. Just as
T
perception itself is an active process, wherein sens ory data
l
is processed withln a context defined by previous experience,
and not merely the static, passive re-representation of the
"outside world", expectancy is a complex context-specific
activity guided in its development by previous experience,
directed towards a particular set of circumstances (Luria,
1980). An expectation is the act of predicting dynamically
what should happen on the basis of what is presently
occuring, according to verbal (explicit) and nonverbal
(implicit) assumptions predicated in their development upon
analysis of past sequences of events (Luria, 1980; Sokolov,
1969; Vinogradova, 1975).

85
 Predisposition to Alcoholism
7

A complete model of what should occur is presently

impossible to generate, and is likely to remain so.
Mismatches between expectancy and the integrated sens ory
field are therefore unavoidable. Such mismatches occur
unexpectedly, by definition. These unexpected, unpredictable
or novel occurences might be considered the most meaningful
elements in the field of human experience. It is only through
constant analysis of novelty that human models of reality
(expectancies) are originally developed, continually updated
and transformed in structure. This process of constant
modification is necessary, because the appearance of the
unexpected signifies unspecifieà potential (in its simplest
form, for reward or for punishment). Detection of the
unexpected, unpredictable or novel therefore must play a key
role in human information processing (Sokolov, 1969;
Vinogradova, 1975).
The occurence of such detection appears to have been
generally interpreted within the literature in two manners:
as anxiety, and as the orienting response. Anxiety appears to
oe the subjective interoceptive process associated with the
response to novelty and threat (Gray, 1982, 1987; Heath,
1986; Maclean, 1986; Reiman, Fusselman, Fox & Raichle, 1989),
while the orienting response, the involuntary gravitation of
attention to novelty, measured in a variety of different
manners, appears to function as the first stage in an
objectively observable analytic/motor process that has as its

86
 Predisposition to Alcoholism
8

function the classification of the unexpected (Sokolov, 1969;

Vinogradova, 1975; Luria, 1980).
This analytic/motor process appears to occur in three
stages, once the stage is prepared for classification by
involuntary focus of attention. The first stage involves
(psychophysiological) preparation for nonspecific action, in
readiness for contingent, appropriate response, in the
(general) form of approach or avoidance (Granit, 1977;
Panksepp, 1986). The second stage occurs with the
participation of socially-determined verbal and non-verbal
processes associated with higher forms of abstract cognition
(Luria, 1980). Abstract classification places the unknown
provisionally within a pre-existent, experientially-
determined social context, and can be usefully considered a
phylogenetically advanced, human-specific substitute for the
third stage, action (Granit, 1977; Luria, 1980). Abstract

classification offers rapid categorization with minimal

exposure to physical risk (Granit, 1977). If abstraction
fails, for whatever reason, then action itself provldes
escape (which offers safety at the cost of knowledge), or
increased access to sens ory information, attendant upon
active exploration. This process either transforms the
unexpected into the expected (in the case where abstract
classification or active exploration was successful), .hich
means that appropriate behavioural measures are established

...
.~;
for next contact, or leaves the unexpected in its

87
 Predisposition to Alcoholism
9

automatically established anxiety-inducing - threatening -

context (in the case of escape).
Cortical structure and Information Processing
INSERT FIGURE 2 HERE
Figure 2 presents putative neuropsychological
localization of the information processing sequence detailed
in Figure l, and serves as an overlay for that figure. It is
based upon propositions set forth by Sokolov (1969), and upon
work completed in a similar manner by Vinogradova (1975),
Luria (1973, 1980) and Gray (1982, 1987). Luria (1973)
proposed a general theory of neocortical function, ba~ed upon
the division of the neocortex into two functional units; the
sensory unit, which includes the parietal, temporal and
.""fI-
,1 occipital lobes, which subsume the organization and
...
integration of multimodal sensory input, and the mot or unit,
discussed in detail later. Underlying these cortical units is
the limbic system, responsible for the addition of affective
tone to experience and for modulation of autonomic and
visceral response, as weIl as for the governance of many
other complicated functions, such as hunger and thirst.
The more complex operations of the system which reacts
automatically to the unexpected appear to be based
physiologically in the limbic system, particularly in the
hippocampus. This subcortical structure, which is critically
involved in the transfer of information from real-time
experience to sensory memory, appears to operate &s a library

88
 Predisposition ta Alcoholism
10
or coding system (Teylor and Discenna, 1985, 1986) for the
1 higher cortical structures. Each pattern of sensory
experience is accompanied by the activation of ~idespread,

relatively unique cortical structures (the cortical modules

(Goldman and Nauta, 1977»), particularly in the sensory unit.
The hippocampus theoretical1y forms an index which documents
the spatial and temporal pattern of activation of these
cortical moè.ules during a given experience (Teylor and
Discenna, 1985, 1986). When an unexpected experience occurs,
which produces a pattern of cortical activation which differs
from any in the past, the orienting response (Sokolov, 1969;
Vinogradova, 1975; Luria, 1980) centres attention
invo1untari1y upon the mismatch. Evidence, direct and
.,'....
indirect, that the hippocampus is critically involved in
production of this orienting response continues to accumulate
(Halgren, Squires, Wilson, Rohrbaugh, Babb, and Crandall,
1980; Okada, Kaufmann and Williamson, 1983; Porjesz and
Begleiter, 1985; Sokolov, 1969; Vinogradova, 1975). As well,
a variety of studies demonstrate the existence of specific
cells, which concentrate primarily in the hippocampus, that
can be induced ta respond ta a variety of complex situations
involving the unexpected, unpredictable or novel, regardless
of sensory modality (Vinogradova, 1975; Watanabe and Niki,
1985) .
Several processes combine in the orienting reflex.
Concomitantly with signalling of mismatch cornes physiological

89
 Predisposition to Alcoholism
Il
activation: preparation for activity, via the
hypothalamus/pituitary adreno-cortical system, partially
under the inhibitory control of the hippccampus and frontal
cortex (Luria, 1980). Such physiological activation, elicited
prior to engagement in situation-relevant behaviour, might be
considered non-specifie, in that it is not necessarily
directed tovards any particular end (Panksepp, 1986). It is
interesting to note, hovever, that in the absence of
appropriate specifie goal eues, hypothalamic stimulation
evokes not only arousal, in its more general sense, but
generalized searching responses, vhich are amplified if there
are novel objects in the sens ory field of the animal
(Panksepp, 1986). It is for this reason that it may be more
generally use fuI to consider the hypothalamus central to the
integration of physiological state and psychobehavioural
function (Panksepp, 1986), rather than merely responsible for
autonomie regulation. The fact that hypothalamic stimulation
results in generalized searching behaviour (in the
appropriate context) makes it appear reasonable to regard the
cooperative activities of the structures presented in Figure
2 as truly systematic, and integrated in activity.
In addition to physiological activation, mismatch
activates vhat Luria (1973) described as the motor unit
(Gray, 1982), which is composed primarily of the prefrontal,
premotor and motor cortices. The pre frontal cortex, the
primary neocortical representative of the limbic system

90
 Predisposition to Alcoholism
12
(Nauta, 1971) provides the physiological basis for the
voluntary, abstract organization of motor behaviour (Granit,
1977) and experience (Luria, 1980), and for the voluntary
direction of attention (Damasio, 1986; Es1inger & Damasio,
1985; Luria, 1980). The premotor and motor cortices appear to
hierarchically arrange intentions into mot or programs, and
execute them in behaviour (Luria, 1973). Intention is thereby
transformed sequentially into action, in the motor unit.
The role of the motor unit in the analysis of the
unexpected can take two parts. Comp1ex non-primates depend
primarily on the action of the premotor/motor cortex to
provide them with additional sensory information, about
unexpected circumstances, or to remove them from danger
(Granit, 1977). The application of search programs, drawn
primarily from the reservoir of learned and instinctual
behaviour, involve behavioural alterations (exploration,
play) and subsequent transformations of sensory input. When
an animal actively explores something new, it changes the
sensory aspect of the object under observation. This change
provides the animal with the opportunity to observe the novel
thing under a variety of circumstances. This adds to its
know1edge about the new situation, transforming the novel
into the known (Gray, 1987). If the unexpected occurs, too
dramatica11y (which means it varies in too many dimensions
simultaneous1y, and/or too quickly), then the animal flees,

..-,-...,

91
 Predisposition to Alcoholism
13

to avoid permanently, or to cautiously approach, from a safer

distance (Gray, 1987).
Primates, with a deve10ped prefrontal cortex (Nauta,
1971), are more capable of performing such exploration at the
abstract (non-motoric) level. Humans possess such cortical
development that is structurally unique, as weIl as unique in
mass (Lurla, 1980). The human prefrontal cortex is integrally
involved in control of the speech system, and in the
regulation of activation processes that are under the
complete or partial control of that system (Luria, 1980). It
appears abstract analysis (verbal and non-verbal) of the
unexpected or novel plays a much greater role for man - a
role that may in fact be primary (Gray, 1987). It seems
.~
q
~
~.
possible that it is only when this system fails partially or
completely in man - or when it plays a paradoxical role
(arnplifying the significance or potential danger of the
unknown) - that active exploration (or active avoidance) with
its limitations and dangers, becomes necessary (Granit,
1977). The apparent purpose of abstract classification and
motoric exploration is to transform the unexpected into the
expected, and to increase the behavioural repertoire, in
permanent memory.
The limbic system that registers unexpected phenomena
only registers that a phenomenon is of potential significance
(because its properties are as of yet unknown, or only
relatively known); it àoes not and can not describe how it is

92
 Predisposition to Alcoholism
14

significant or to what system (reward or punishment, broadly)

it is significant. Simple habituation might take care of what
is irrelevant and predictable, but active exploration (in
lower animaIs) and/or active exploration and the use of
higher order abstract cognitive processes must be involved in
the determination of the specific relevance of novel
phenomonen.
Characteristics of Sons of Male Alcoholics
INSERT FIGURE 3 HERE
Figure 3 presents characteri~tlcs of SOMAs that have
been described most frequently, categorized within the schema
offered in Figures land 2. These characteristics have been
described and/or are discussed at the theoretical and
neuropsychological levels, in the following text, in keeping
vith the presentation of the first two figures. Evidence
suggesting that SOMAs may exhibit abnormalities in the
function of the system that compares actuality with
expectancy can be derived most directly from studies which
concentrate on the cortical event-related potential (ERP)
and/or upon general psychcphysiological response to specific
stimuli. The literature concerning ERPs and SOMAs is
described in sorne detail in the following section, (1)
because the use of this paradigm, which can objectively
measure subjective reactions to complex stimuli, appears
promlsing from a theoretical and practical viewpoint, (2)
becùuse the ERP, especially the P300 component, is extremely

93
 Predisposition to Alcoholism
15
sensitive to experimental variation and (3) because there is

substantial controversy about the meaning of the relevant ERP

research com~leted to date.

The cortical ERP is a waveform with a duration of

approximately half a second, produced by the electrical

response of the brain to a brief, sensory stimulus of any

modality, derived from the EEG by signal averaging

techniques, which extract the time-locked electrical activity

(Porjesz & Begleiter, 1981). The P300 component of the ERP,

which has been most commonly studied with regards to SOMAs,

can be elicited when active attention is directed towards

discrimination (when decision or response depends upon that

discrimination) and/or when the specified targets, eliciting

response, occur infrequently (Porjesz, Begleiter and

samuelly, 1980). The latency of the P300 appears to depend

upon the speed with which a given stimulus is identified and

processed (Donchin, Ritter, & Mccallum, 1978). The amplitude

of the P300 has been related to the subjective determination

of the meaning of an event, and not to its sens ory modality

or inherent qualities (Halgren et al., 1980). The process

underlying manifestation of the P300 is initiated only

whenever the stimuli presented to the individual is

"motivationally significant" (Begleiter, porjesz, Chou &

Aunon, 1983). Unpredictable or unexpected events, which are

motivationally significant because of their novel quality

(Gray, 1982) therefore elicit large P300 amplitudes (Duncan-

94
 Predisposition to Alcoholism
16

~..
Duncan-Johnson & Donchin, 1977; Tueting, Sutton & Z11bln,
'~
1971). From the neuropsychological viewpoint, it is
interesting to note that the P300 component has also been
described as an electrophysiologlcal manifestation of the
orienting reflex (Donchin, 1981; Porjesz & Beg1eiter, 1985),
with its probable origin in the hippocampus and amygdala
(Ha1gren et al., 1980; Okada, Kaufmann & Wllliamson, 1983).
Those studies examining the P300 production of SOMAs
have generally analyzed ERPs recorded during the course of a
visual or auditory "oddball" task. During this task,
participants are elther required to count infrequently
presented stimuli (such as high tones), embedded in a context
of more frequently presented, irrelevant but somewhat slmilar
j' stimuli (like low tones) or to make a judgeme~t regarding the
.. ~ ...

nature of sorne object or sequence of objects presented on a

TV screen. The P300 compone nt is generally analyzed as the
average response evoked durlng repeated expesure te several
blocks of a large number of such stimuli. A variety of
studies utilizing thls methodology have determined that SOMAs
are characterized by reduced me an P300 amplitude and/or
increased mean P300 latency. These studies are listed in
Table 1A-I.
INSERT TABLE ONE HERE
There exists reason to uelieve, however, that this
conclusion might lack specificity. ·As noted previously, P300
response is affected by predictability and novelty. This

if..
'~ ...-
means that P300 evoked at the beginning of a task might

95
 Predisposition to Alcoholism
17
differ from that produced at or near the end. Conclusions
dravn from studies examining P300's averaged over a large
number of trials are limited by their failure to examine this
potentially important possibility. The single study in Table
lA-I vhich presents data bearing directly on this issue in
fact suggests that stimulus novelty and family history
interact to affect P300 production (Elmasian, Neville, woods,
Schuckit and Bloom, 1982). Detailed examination of the data
presented in this study reveals that sober, lov-drinking
SOMAs are actually characterized by increased P300 amplitude,
and by decreased or at least equivalent P300 latency (and
overall reaction time) during the first block of stimulus
presentation (vhen the task is still novel), and by more
rapid deterioration of these responses during presentation of
later blocks and/or vhile under the influence of alcohol.
It is interesting to consider the recent york of Hill,
Steinhauer, Park and Zubin (1990) in the light of this more
detailed analysis of Elmasian et al. (1982). These authors
analyzed the ERP reactions of children of family-history
positive alcoholics and controls, obtained during the course
of an auditory oddball task, according to the conditional
probability of target stimuli appearance. Children of
alcoholics vere actually characterized by the production of
significantly larger mean P300 amplitudes and smaller P300
latencies than their controls, vhen exposed to the most
unpredictable target stimuli, and by cc~trast produced

96
 Predisposition to Alcoholism
18

smaller P300 amplitudes and increased latencies to the more

predictable targets.
The general conclusion that SOMAs are characterized by
decreased amplitude and increased latency of p300 production
may therefore have to be replaced by the specific conclusion
that this response is typical only when they are not
processing novel or unpredictable stimuli (or when their
response to novelty is rnasked by analysis of ERP averaged
over a large number of trials). It ap'pears probable that
participants in oddball tasks like those used in the ERP
experiments pay attention or respond to appearance of the
target stimuli because of social demand (since they have
agreed to follow the experimenter's instructions) and because
of the intrinsic motivational significance of the task. One
of the factors that determines the intrinsic motivational
significance of a task is its relative unpredictability or
novelty. It appears reasonable to conclude from the ERP
literature discussed so far that the motivational
significance of a task undertaken in accordance with social
demand appears to deteriorate because of decreases in novelty
or increases in predictability more rapidly among SOMAs than
among matched controls. This conclusion is potentially of
extreme importance, because success in a vast number of real
world tasks obviously depends on the ability to do weIl,
because someone else requires it - especially in childhood,
in situations such as school - regardless of the novelty or

97
 Predisposition to Alcoholism
19
unpredictability of the task.
As outlined previously, the hippocampus appears to
determine the intrinsic fascination of novel and/or
threatening ~henomena. By contrast, it appears to be the
prefrontal cortex that regulates the voluntary application of
cognitive resources (attention) in situations like those
described previously, where the significance of a stimuli is
merely dependent upon its social or individual labelling as
significant (Luria, 1980). In other words, those with a
highly functioning pre frontal cortex can concentrate on
performing a task for reasons other than its novelty, or
because it poses a threat. Given this argument, it appears
reasonable to provisionally attribute the differences between

.•.::1;.-•.
those with alcoholic fathers and controls in the experiments
described in Table lA-I to the effects of a specifie type of
attentional deficit characteristic of SOMAs, which makes
itself evident in situations that are boring, defined for the
limited purposes of this discussion as neither novel
(unpredictable) nor threatening, and to further posit that it
is a deficit in those abilities dependent upon the prefrontal
cortex that underlie this attentional deficit. Supportive
evidence for this latter claim will be reviewed later in the
manuscript.
Before these general hypotheses can be accepted as
useful, it is important to examine the minority of ERP
studies whose conclusions differ in part or whole from those

98
 Predisposition to Alcoholism
20

that fit straighforvardly into the theoretical structure

outlined above. Neville and Schmidt (1985), Polich and Bloom
(1987) and Polich, Burns and Bloom (1988) found that P300
amplitude decreased and/or P300 latency increased vith
increases in self-reported alcohol intake per occasion among
SOMAs, but not among control subjects. Polich and Bloom
(1988) attempted to duplicate the placebo manipulation of
Elmasian et al. (1982), but failed to find differences
betveen the P300 response of SOMAs and controls. These
authors did de termine that P300 latency increased
significantly vith increased self-report alcohol intake per
occasion among SOMAs and controls. Polich, Haier, Buchsbaum
and Bloom (1988) failed to find differences betveen the P300
responses of a very small sample of SOMAs and matched
controls, and did not find that self-report alcohol intake
per occasion correlated vith P300 latency or amplitude, in
this and a larger sample of university undergraduates.
Schmidt and Neville (1984) and Neville and Schmidt (1985)
determined that young adult SOMAs vere characterized by
decreased amplitude of the N430 ERP component, during the
course of a visual language task. The N430 has been related
to proficiency in language processing.
It is difficult to drav general conclusions from these
more ambivalent or negative studies, but it is important to
note that they can be differentiated methodologically from
the more positive studies described previously. AlI the

99
 Predisposition to Alcoholism
21

studies described in Table l-AI, ~ith the exception of

""T"""'r
-..'
Elmasian, Neville, Woods, Schuckit, and Bloom (1982), ~ere

either conducteà upon adolescents or preadolescents ~ho had

not yet begun to consume alcohol (Begleiter, Porjesz, Bihari

and Kissin, 1984; Begleiter, Porjesz, Ra~lings and Eckardt,

1987; Whipple and Noble, 1986; Whipple, Parker and Noble,

1988) or upon young adults (Hill, Steinhauer, Zubin and

Baughman, 1988; O'Connor, Hesselbrock and Tasman, 1986;

steinhauer, Hill and Zubin, 1987) ~ho ~ere not selected

specifically from a university population, and ~ho aIl had at

minimum fathers ~ho had been in active treatment for their

drinking and/or ~ho met strict Feighner criteria for

alcoholism. Many of these studies additionally limited their

subjects to those ~ho had families ~ith extensive histories

of alcoholism, to increase the probability of testing

individuals truly at heightened risk for developing

alcoholism (Steinhauer et al., 1987; Hill et al., 1988;

Whipple and Noble, 1986; Whipple et al., 1988). Polich's

group, by contrast, classified subjects as family-history

positive if they reported that their fathers ~ere

characterizeà by a single symptom of alcoholism (Hill et al.,

1990). In addition, Polich's subjects only required one

alcoholic relative - the father - rather than the extended

family history, or at least severe alcoholism, required by

Begleiter et al., (1984), (1987), Whipple and Noble (1986),

Hill et al., (1988), (1990) and Steinhauer et al. (1988).

100
 Predisposition to Alcoholism
22

Polich's group also tends to test university students, who

might comprise a subject population self-selected against the
type of cognitive deficit proposed in this paper as the
factor underlying susceptibility to the negatively-
reinforcing properties of alcohol.
Given these methodological issues, it seems reasonable
to conclude that non-university educated SOMAs with well-
defined and extensive histories of paternal-lineage familial
alcoholism are characterized by their production of
attenuated or delayed P300 response to stimulus presentation
requiring voluntary, directed attention and/or higher-order
cognitive or linguistic processing (those stimuli that are
predictable), and may produce enhanced P300 responses to
stimuli that are novel or threatening.
Begleiter, Porjesz and Tenner (1980) have suggested that
it is the inability to distinguish between what is relevant
and what is irrelevant that distinguishes abstinent
alcoholics' and, by implication, the sons of male alcoholics'
P300 component from that of nonalcoholic controls. In keeping
with this idea, it appears that SOMAs manifest reductions in
P300 amplitude and/or increases in P300 latency only during
situations where they must voluntarily allocate attentional
resources to maintain the motivational significance of the
target stimuli. When they are faced with involuntarily
motivating stimuli (like novelty or threat), however, the
situation seems to be reversed.

101
 Predisposition to Alcoholism
23

"
This latter pnssibility is reinforced by the conclusions
of four additional studies, utilizing a different
methodology, demonstrating that SOMAs may be characterized by
increased psychophysiological response to novel and/or
avers ive stimuli. Finn and Pihl (1987, 1988) demonstrated
that young adult nonalcoholic SOMAs vith extensive
multigenerational family histories of paternal alcohnlism
vere characterized by increased heart-rate and decreased
(OBVA) whe~ anticipating and receiving mild electric shock.
Finn, Zeitouni and Pihl (1990) discovered the same pattern of
cardiovascular hyper-reactivity among SOMAs faced vith and
receiving avoidable and unavoidable signalled electric shock,
and furthermore demonstrated that SOMAs vere characterized by
larger electrodermal orienting responses, shorter orienting
response latencies, and slover rates of habituation vhen
presented vith a short course of novel non-avers ive tones.
Harden and Pihl (submitted) extended the range of this
demonstration, determining that pre- and early adolescent
SOMAs vith extensive multigenerational histories of paternal
alcoholism vere characterized by increased heart-rate and
decreased OBVA during the course of a mental arithmetic task.
It is interesting to note, in this rega~d, that the
hypothalamus appears to be responsible for modulating
physiological preparation-for-activity (such as increased
heart-rate and decreased OBVA) and for integrating such
preparation vithin the context of stimulus-relevant

102
 Predisposition to Alcoholism
24
behaviour, and that the hypothalamus is partially under the
inhibitory control of the hippocampus and pre~rontal cortex.
It is directly relevant to this notion that a majority of
the studies designed to address the issue have concluned that
FH+ subjects are characterized by comparatively poor
peLformance on tests of linguistic ability, abstraction and
problem solving. Comparative deficits in total IQ,
performance IQ, memory, visuospatial ability, perceptual-
motor capacity, and auditory/visual attention span have been
described less frequently (Pihl, Peterson, and Finn, 1990).
Those studies which describe such differences are presented
in Table 1-B. SOMAs have often been characterized by reduced
academic achievement, as weil, in many of these reports, and
in various longitudinal studies of children and adolescents
who later develop serious problems with alcohol (see for
example Rydelius, 1981; and the review by Zucker and
Lisansky-Gomberg, 1986). This reduced achievement includes
poorer school performance, more truancy, and completion of
fewer years of school.
The minority of studies which have not provided support
for the notion of reduced cognitive capacity among FH+
subjects can be grouped into three categories. In the first
category are those reports that include a preponderance of
females as subjects or as the alcoholic parent and do not
offer analysis of results by sex (Hesselbrock, Stabenau and
Hesselbrock, 1985; Wilson and Nagoshi, 1988; Workman-Daniels

103
 Predisposition to Alcoholism
25

and Hesselbrock, 1987). These can be excluded from this

discussion, which is centred on the sons of male alcoholics,
by definition. In the second category are those that look for
cognitive deficits among SOMAs drawn from a university
population and who have at best familial alcoholism limited
to a mildly affected father (characterized by the presence of
one symptom in four to six categories) (Alterman, Bridges and
Tarter, 1986a, 1986b; Alterman, Searles and Hall, 1989;
Shuckit, Butters, Lyn and Irwin, 1987).
In the interests of complet ion, it might also be noted
that comparison of familial and nonfamilial alcoholics
sometimes demonstrates mild group difference that can be
attributed to family status (Schaeffer, Parsons and Yohman,

.:.;;,.
1984), especially within larger studies (Schaeffer, Parsons
and Errico, 1988) and sometimes does not provide such
differentiation (Alterman, Gerstley, Goldstein and Tarter,
1987; Reed, Grant and Adams, 1987).
Many of the studies listed in Table 1-B utilized tests
drawn from the neuropsychological literature. This approach,
with aIl its flaws, allows for the production of inferences
based on the relationship between brain function and
behaviour, and such inferences, with regard to SOMAs, have
indeed been drawn (Tarter, Alterman and Edwards, 1985, 1988).
Although the cognitive deficits characteristic of SOMAs have
been defined and measured in a relatively heterogeneous
manner, the abilities many of the most commonly reported

104
 Predisposition to Alcoholism
26
apparently share one important feature in common: their
dependence on the proper functioning of the prefrontal
cortex, described in detail by Luria (1980). As noted
previously, this cortical subunit is primarily responsible
for the abstract classification of stimuli and the
organization of behavinur. Tarter et al. (1985, 1988), Pihl,
Peterson and Finn (1987) and Gorenstein (1987) have aIl
observed that the pattern of cognitive impairment typical of
males at increased general risk for alcoholism is similar to
that demonstrated by individuals ~ho have suffered somé form
of mild prefrontal cortical trauma. In addition, the non-
cognitive characteristics of SOMAs and such individuals share
certain features in common. These characteristics include

those discussed previously - abnormalities of the orienting

response and heightened sympathetic reactivity to novelty
(Vinogradova, 1961) and reduced ability ta engage or

participate in goal-directed behaviour under normal

circumstances (Damasio, 1986). It is interesting to note, in

this regard, that Peterson, Finn and Pihl lin press) have
demonstrated highly significant correlations bet~een SOMAs'
performance on t~o tests characterized by their sensitivity
to disruption by prefrontal trauma (the Self-Ordered Pointing

Test (Petrides and Milner, 1982) and the Wisconsin Card Sort
Test (Milner, 1964)) and their susceptibility to bath aspects
of the cardiovascular hyper-reactivity to anticipation and
receipt of signalled electric shock demonstrated by SOMAs in

105
 Predisposition to Alcoholism
27
Finn and Pihl's (1987, 1988) studies. It may be relevant as
well that Whipple et al. (1988) showed that the performance
of SOMAs and their fathers on various tests of "visuo-
perceptual" performance correlated with the average amplitude
of their ERP production to target stimuli. Parsons,
Sinha and Williams (1990) have replicated the latter finding
in a population of FH+ male alcoholics.

Individuals who sustain damage to the prefrontal cortex

in adulthood are also characterized by behavioural
abnormalities, which include impulsivity and the inability to
regulate their behaviour in accordance with social demands
(Luria, 1980j Damasio, 1986). This pattern of behaviour has
been described as "acquired sociopathy" (Eslinger and
Damasio, 1986). If such damage is sustained early enough in
life, it can lead to the development of what Eslinger and
Damasio (1986) describe as a "pervasive developmental
abnormality of social and affective behaviours" or what
Ackerly and Benton (1948) refer to as a "primary social
defect" - the inability to accomodate "social impulses into

the total personality structure." It is inte~esting to

consider the studies contained in Table le, given this line

of reasoning and the evidence described previously supporting
the notion that deficit in the functions of the prefrontal
cortex might characterize SOMAs. These studies provide
consistent support for the notion that SOMAs are prone to
conduct-disorder and/or hyperactivity/impulsivity, especially

106
 Predisposition to Alcoholism
28

during childhood, but often in adulthood as ~ell. SOMAs

manifest impairments in the ability to control their
behaviour ~hen required to (particularly in heavily
structured situations), concentrate and pay attention poorly,
and appear comparatively quick to resort to aggression in
social situations. These behavioural idiosyncracies generally
cause trouble in the early years of school, when they tend to
disrupt the academic and social environment. SOMAs act out
more frequently, and often break rules, and although they may
appear gregarious, they are more likely to get into trouble
with others. This combination of traits, rather contradictory
at the surface, has been noted among children characterized
by their peers as aggressive (Hinsha~, 1987). School
misbehaviour and social problems undoubtedly puts SOMAs at
risk as well for increased conflict with authority, and for
all the second-order problems such conflict breeds.
Supportive evidence for this general line of reasoning can
also be derived from numerous experimental and longitudinal
studies detailing similar behavioural and attentional
abnormalities among children and lesser relatives of
alcoholics (Pihl, Peterson and Finn, 1990).
The model described in this paper is predicated upon the
notion that SOMAs are characterized by increased impulsivity
and motoric activity because their motor systems tend to
become activated by novelty and threat. Instead of relying on
their comparatively poor ability to abstract and verbally

107
 Predisposition to Alcoholism
29
reason, SOMAs may tend to use search or avoidance strategies,
1···.
.
or to resort (when aIl else fails) to aggression. It i5
interesting to note in this regard that Pihl and Harden
(submitted) have demonstrated that a single group of

preadolescent SOMAs, from families with extensive histories

of paternal alcoholism, per[orm more poorly on tests of
prefrontal function, manifest more cardiovascular reactivity
(increased heart-rate and decreased OBVA) to threat, react
impulsively during objective testing and are more hyperactive
by parent rating, when compared to controls matched for age,
socioeconomic status, education level and full scale IQ.
The Possible Effect of Alcohol on SOMAs
INSERT FIGURE 4 HERE
The model described in the present manuscript suggests
that SOMAs characterized by deficits in pre frontal function
might dlso manifest hyper-reactivity to threat and novelty
and lessened ability to maintain attention for the sake of
social demand. It appears possible that such individuals
might also be differenttally susceptible to the negatively-

reinforcing effects of acute alcohol intoxication.

Four studies, contained in Table 10, describe SOMAs'

hyper-sensitivity to the dampening effect of alcohol upon
psychophysiological reactivity to threat and/or novelty.
Levenson, Oyama and Meek (1987) determined that alcohol
intoxication reduced sorne aspects of cardiovascular

reactivity (ear pulse transit time) and general somatic

·1··'
" -,

108
 Predisposition to Alcoholism
30

activity to self-disclosing speech and electric shock among

SOMAs. A male personality control, composed of "outgoing,
aggressive, impulsive and antisocial individuals " (Sher and
Levenson, 1982), was characterized by increased baseline
heart-rate after admi~istration of alcohol, and by decreased
heart-rate acceleration to the stressors. The latter aspect
of this study essentially replicated Sher and Levenson's
(1982) study. Similarly, the sober cardiovascular hyper-
reactivity characteristic of the SOMAs in the Finn and pihl
(1987, 1988) and Finn et al. (1990) studies was virtually
eliminated by acute alcohol intoxication (Peterson, Finn and
Pihl, submitted) and such intoxication also significantly
increased their baseline heart-rate.
A comparable pattern of response to alcohol appears to

characterize alcoholics and/or stimulus augmentors. Alcohol

consumption decreases electrodermal reactivity (Coopersmith
and Woodrow, 1967; Garfield and Mc8rearty, 1970) and
sensitivity to pain (Brown and Cutter, 1977) among
alcoholics. Additionally, alcohol intoxication transforms
alcoholic stimulus augmentors into reducers (Buchsbaum and
Ludwig, 1978; Petrie, 1978). This transformation might be
considered a form of dampening. Furthermore, alcoholics who
augment, like the offspring of alcoholics (Hennecke, 1984),
will work harder for alcohol than those who normalize or
reduce (Ludwig, Cain and Wikler, 1977).
Figure 4 provides a schematic view of the potential

109
 Predisposition to Alcoholism
31
...
~.,~"
effect of alcohol upon SOMAs, within the framework provided

by Figures 1-3. It appears possible that alcohol-induced

cardiovascular reactivity-dampening takes place because acute

alcohol intoxication interferes with the functioning of the

subcortical unit that governs the orienting reflex and

produces the acute psychophysiological response to threat

and/or novelty (Gray, 1982, 1987). The hippocampus, part of

that subcortical unit, appears particularly sensitive to the

acute and chronic effects of alcohol ingestion (Gray, 1982,

1987; Lovinger, White, and Weight, 1989; Freund and

Ballinger, 1989; Peterson, Rothfleisch, Zelazo and Pihl,

1990) and to the action of the other anxiolytics

(barbiturates and benzodiazepines) as well (Gray, 1982,

1987). It might be recal1ed, at this point, that alcohol

intoxication reduces the amplitude of the P300 response,

which is produced by the hippocampus, in SOMAs and

controls (Elmasian et al., 1982). Generalized alcohol-induced

alcohol-reduction of hippocampal response could conceivably

be negatively and positively reinforcing to SOMAs, given (1)

that increased activity in the hippocampus and/or temporal

cortex is apparently accompanied by states of anxiety and

negative affect (Gray, 1982; Reimann et al., 1989),

especially when it accompanies threat and/or novelty, and (2)

that such activity inhibits the operation of those limbic

centres that provide the physiological basis for the

sensations of pleasure and wel1-being (Heath, 1986). The

no
 Predisposition to Alcoholism
32
theory presented in this manuscript suggests that it is
reduction in the hippocampal response to threat and novelty
that decreases subsequent physiological preparation for
activity, like that described by Finn and Pihl (1987, 1988),
Finn et al. (1990) and Levenson et al. (1987) and which also
reduces the necessity for action in the face of threat, as
described by Levenson et al. (1987).
It also seems possible that SOMAs are more susceptible
to what might be the positively reinforcing effects of
intoxication. Pollock, Volavka, Goodwin, Mednick, Gabrielli,
Knop and Schulsinger (1983) and Pollock, Gabrielli, Mednick
and Goodwin (1988) described SOMAs' comparative1y increased
production of EEG waveforms associated with pleasure and
well-being during alcohol intoxication. This is particularly
interesting given that SOMAs aiso produce more high frequency
beta activlty when sober (Gabrielli, Mednick, Volavka,
Pollock, Schulsinger, and Itil, 1982), like alcoholics
(Mendelson and Mello, 1979), and that these beta waveforms
have been associated with psychological states of tension and
anxiety (Kiloh and Osselton, 1961). Finn and Pihl's (1987,
1988) and Finn, Zeitouni and Pihl's (1990) observation that
the baseline heart-rate of SOMAs increases signlficantly,
when compared to controls, within twenty minutes of alcohol
ingestion could conceivably be indicative of a positively-
reinforcing effect, as drug-related increases in heart rate
have, under sorne clrcumstances, been linked wlth reward (Wise

111
 Predisposition to Alcoholism
33
and Bozarth, 1987; Fowles, 1983). Recent research conducted
by Peterson, Pihl, Seguin, and Finn (submitted) suggests that
alcohol-induced heart-rate hyper-react~vLty dampening and
alcohol-induced baseline heart rate increase are associated,
significantly, with increased weekly alcohol consumption.
This is sorne indication that a link exists between putative
markers of alcoholic tendencies and actual drinking behavior.
Conclusion
Sons of male alcoholics are at heightened risk for the
development of alcoholism. This risk is associated with
various observable abnormalities in psychophysiological
response, cognition, behaviour and reaction to alcohol. SOMAs
appear to be characterized by increased amplitude and
decreased latency of the P300 ERP component to stimuli that
are new and/or and unpredictable, and by decreased P300
amplitude and increased latency to stimuli that have lost
their novelty and/or threat. They are aiso characterized by
increased cardiovascular response to novelty and threat, by
decreased performance on tests of verbal ability, problem
solving and abstraction, and by increased rates of conduct
disorder and hyperactivity. SOMAs aiso appear hyper-sensitive
to the cardiovascular-response reducing effect of alcohol
intoxication, to aicohol-intoxication induced reductions in
P300 response to novelty, and to alcohol-induced increases in
baseline heart-rate.
The theoretical model described in the present

112
 Predisposition to Alcoholism
34
manuscript is predicated on the notion that deficits in the
function of the pre frontal cortex cou Id underlie
manifestation of aIl these abnormalities. The prefrontal
cortex is responsible for the maintenance of voluntary
attention under conditions of social demand, for the
regulation of psychophysiological response to threat and
novelty, and for many aspects of verbal reasoning,
abstraction and problem solving.
It therefore appears possible that SOMAs are hyper-
reactive to threat and novelty because they are characterized
by deficits in pre frontal function. Their difficulties with
prefrontal function may render them (1) less able to use

~.-.
abstraction to inhibit preparation for activity in the face
~L of novelty and threat, ( 2 ) more likely to revert to action
itse If when confronted with novelty and threat, and ( 3 ) less
likely to maintain attention to stimuli that are no longer

intrinsically relevant, under the pressures of social demand.

The combination of these proclivities might account for the
tendency of SOMAs to become labelled as conduct-disordered or
hyperactive. Furthermore, the the ory posits that what might
be inherited in familial alcoholism is actually a pattern of

hyper-responsiveness to the new and anxiety-provoking, which

can be alleviated temporarily by alcohol intoxication. In
general, alcohol intoxication appears to interfere with the

activity of the system that initially signaIs the presence of

the new and anxiety-provoking - the hippocampus. It seems

113
 Predisposition to Alcoholism
35
. "".,.

......
:~
possible that such interference might be negatively
reinforcing, particularly to those characterized by
hyperactivity of this system.
This the ory makes a' number of specifie and testable
predictions. These include the hypotheses that SOMAs with
well-defined extensive histories of paternal alcoholism will
manifest increased sober reactivity (increased heart-rate,
decreased digital blood volume amplitude, increased P300
amplitude, decreased P300 latency, increased somatic
activity) to unpredictable or novel stimuli or to stimuli
that serve as a eue for punishment and that alcohol-
consumption at or above legally intoxicating doses will
significantly reduce or even eliminate this reactivity. The
theory also predicts that aIl these indices of reactivity
will be correlated, and that such reactivity should be
correlated with alcohol-induced reactivity dampening (no
reactivity, no elimination of that reactivity). The ability
of SOMAs to abstract should be correlated with this increased
reactivity, as weIl, if abstraction is defined as performance

on tests dependent upon the function of the intact pre frontal

cortex. It must be remembered, however, that it may be

difficult to determine which particular tests will actually

predict such reactivity, given that prefrontal function is

very complex. In addition, SOMAs descrlbed by their teachers

as hyperactive and/or conduct disordered should also be those
characterized by decreased abstracting ability, decreased

114
 Predisposition to Alcoholism
36

ability to maintain attention after multiple repetitions of

simple, nonthreatening tasks, and by increased reactivity to
novelty and threat.
The the ory is ~rimarily limited by its failure to take into
account any potential directly positively-reinforcing effect
of acute alcohol intoxication. However, it is possible that
different individuals might manifest independent,
idiosyncratic sensitivity to different aspects of alcohol's
effects. Sorne might be more sensitive to alcohol's negatively
reinforcing properties, sorne to its positively reinforcing
properties, and sorne to both. These differences in
sensitivity may be accompanied by variable patterns of
heritability, and by the presence of different markers or
risk factors. The the ory described in the present manuscript
concentrates on the potential effect of negative
reinforcement. This does not necessarily mean that the
authors believe this is the only reinforcing property of
alcohol.

il5
 Predisposition to Alcoholism
37

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133
 Predisposition to Alcoholism

TABLE 1

A. ELECTROPHYSIOLOGICAL ABNORMALITIES
I. Reduced P300 ERP Amplitude II. Psychophysiological
and/or Increased P300 ERP Latency Hyper-reactivity
E1masian et al. (1982) Finn & Pihl (1987)
Begleiter et al. (1984) Finn & Pihl (1988)
Whipple & Noble (1986) Finn et al. (1990)
O'Connor et al. (1986) Harden & Pihl (submitted)
Begleiter et al. (1987)
Steinhauer et al. (1987)
Whipple et al. (1988)
Hill et al. (1988)

B. DECREMENTS IN COMPARATIVE NEUROPSYCHOLOGICAL PERFORMANCE

AND/OR REDUCED ACADEMIC ACHIEVEMENT AMONG SOMAS

Rydelius (1981) Drejer et al. (1985)

Gabrielli & Mednick (1983) Peterson et al. (in press)
Noll & Zucker (1983) Harden & Pihl (submitted)
Hegedus et al. (1984) Whipple et al. (1988)
Tarter et al. (1984) Tarter et al. (1989)
Schaeffer et al. (1984)
Knop et al. (1985)
Schulsinger et al. (1986)

C. CONDUCT DISORDER, HYPERACTIVITY AND/OR IMPULSIVITY AMONG SOMAS

Nylander (1960) Rydelius (1981)

Aronson & Gilbert (1963) Nylander & Rydelius (1982)
Cantwell (1972) Rydelius (1983a)
Morrison & Stewart (1971) Rydelius (1983b)
Morrison & Stewart (1973) Tarter et al. (1984)
Cadoret & Gath (1978) Schulsinger et al. (1986)
stewart et al. (1978) Knop et al. (1985)
Rydelius (1978) Harden & Pihl (submitted)
Saunders & Schuckit (1981)

D. ALCOHOL-INDUCED REACTIVITY-DAMPENING AMONG SOMAS

Levenson et al. (1987) Finn & Pihl (1988)

Finn & Pihl (1987) Finn et al. (1990)

.,~

134
 Figure 1: Theoretical Patll of Information Processing

SENSORY INFORMATION

Mu~imodal Sensory
Integration

COMPARISON OF ACTUALITY Ta EXPECTANCY

UNEXPECTED EXPECTED
Unspeuified Potential Specified Potential
Reward-Neutrality-Punishment Reward-Neutrality-Punishment

ABSTRACT
CLASSIFICATION

~,!'~
~,

Unable to Classily

RELEVANT IRRELEVANT
RewardlPunishment Neutral

ACTION INACTION

Approach
(active exploration)
or
Avoidance

135
 Predisposition to Alcoholism
56

l FIGURE 1. THEORETICAL PATH OF INFORMATION PROCESSING:

Classification of sens ory information, in stages, from top of

diagram to bottom. Arrows indicates flow schematically;

barred line indicates inhibition. The following figures can

be overlaid sequentially.

136
Figure 2: Neuropsychological Path of Information Processing

SENSORY ORGANS

SENSORY UNIT

HIPPOCAMPAL SYSTEM

Access 10 Cortical Modules Access 10 Cortical Modules

(Memory Slorage) (Memory Storage)

PRE FRONTAL
CORTEX

PREMOTOR
AND
MOTOR CORTEX

137
 Predisposition to Alcoholism
57
......
,
FIGURE 2: NEUROPSYCHOLOGICAL PATH OF INFORMATION PROCESSING:

This diagram indicates major cortical areas hypothesized to

underlie those cognitive functions indicated in the

isomorphic boxes of Figure 1.

138
 Figure 3: Observable Anomalies in Information Processing

P300 ABNORMALITIES MEMORY DEFICITS (?)

POO· Performance on Tests

of Abstract Reasoning

Increased
Motorlc Actlvlty
Increased
Distractlbllity

139

.'!1 '
(,1."
 Predisposition to Alcoholism
58

FIGURE 3. OBSERVABLE ANOMALIES IN INFORMATION PROCESSING:

This diagram localizes some abnormalities perhaps

characteristic of sons of male alcoholics.

140
 Figure 4: TheoreticaJ Effect of AlcohoJ on Information Processing

INTERFERENCE WITH
HIPPOCAMPAL FUNCTION

141

if......
' "'"
 Predisposition to Alcoholism
59
FIGURE 4: THEORETICAL EFFECT OF ALCOHOL ON INFORMATION

PROCESSING: This diagram localizes the putative effect of

alcohol - an effect to which sons of male alcoholics may be

particularly sensitive.

142
 Discussion and Introduction to Study l
The theory outlined above does not provide a simple
explanation for the potentially positively-reinforcing
elevations in heart-rate characteristic of SOMAs during the
ascending limb of the blood alcohol curve, after consumption
of a relatively high dose of alcohol (Levenson et al., 1987;
Finn and Pihl, 1987, 1988; Finn et al., 1990).In addition,
there is no direct evidence linking cardiovascular
reactivity-dampening to negative-reinforcment, or to its
putative consequence - increased voluntary alcohol
consumption. The data analysis (Peterson, Pihl, seguin and
Finn, submitted) designated below as study 3 was designed to
rectify these shortcomings. It provides an examination of the
relationship between alcohol-induced basline heart-rate
increase, cardiac hyper-reactivity to threat of and aversive
stimuli, susceptibility to alcohol-induced elimination of
that reactivity, the multiplicative interactions of these
effects, and voluntary self-reported weekly alcohol
consumption by 36 SOMAs with a multigenerational family
history of alcoholism, 14 SOMAs with alcoholic fathers only,
and 33 sons of nonalcoholics wlth no familial alcoholism.

143
Alcohol-Induced Heart Rate Change, Family History, and
Prediction of Weekly Alcohol Consumption by Non-
Alcoholic Males

Jordan B. Peterson
Robert O. Pihl
Jean R. Séguin
Department of Psychology
McGill University
Montréal, Québec, Canada

Peter R. Finn
Department of Psychology
Indiana University
Bloomingdale, Indiana

Running Head: PREDICTION OF WEEKLY DRINKING

144
 Alcohol-Induced
2

Abstract
A number of investigations have demonstrated that sons
of male alcoholics with multigenerational family
histories of male alcoholism are characterized by
cardiac hyper-reactivity to avers ive stimuli, by
susceptibility to alcohol-induced elimination of that
reactivity, and by increased baseline heart-rate while
intoxicated. Although it has been assumed that these
characteristics, and others like them, might serve as
markers for the inherited predisposition to alcoholism,
the relationship between their presence and actual use
of alcohol remains unknown. The analyses conducted in
the present paper, completed in an attempt to reduce
this lack of knowledge, demonstrate that all three
psychophysiological factors, and their interactions,
are significantly associated with self-reported weekly
alcohol consumption by 83 non-alcoholic males: 36 who
had at minimum, an alcoholic father, grandfatQer and
uncle or brother; 14 whose familial alcoholism was
limited to the fathcr; and 33 whose familles were not
characterized by alcoholism.

145
 Alcohol-Induced
3

Alcohol-Induced Heart Rate Change, Family History, and

Prediction of Weekly Alcohol Consumption by Non-
Alcoholic Males
A number of adoption (Bohman, Sigvardsson &
Cloninger, 1981; Cadoret, Cain & Grove, 1980;

Cloninger, Bohman & Sigvardsson, 1981; Goodwin,

Schulsinger, Hermansen, Guze & Winokur, 1973), family
(reviewed in Cotton, 1979) and twin (Hrubec & Omenn,
1981) studies have demonstrated that genetic factors
play a role in determining predisposition to
alcoholism. Such studies have fallen prey to extensive

methodological criticism (Lester, 1988; Searles, 1988)

but balanced reviews of the literature support the
notion that a heritable predisposition to alcoholism

exists (Murray, Clifford, & Gurling, 1983). Sons of

male alcoholics (SOMAs) appear particularly to be at
heightened risk for alcohol misuse - from 3 to 9 times
that of sons of nonalcoholics (Cloninger et al., 1981;
Goodwin, 1985).

This increased propensity for alcoholism id ~ne

putatively phenotypal characteristic, common ta ,3

subset of SOMAs. Other relatively unique quallties of

146
 Alcohol-Induced
4

SOMAs have been tentatively Identified. SOMAs are more

likely than the sons of non-alcoholics to be conduct-
disordered and/or hyperactIve during chIldhood (Pihl,
Peterson & Finn, 1990; Tarter, Alterman, & Edwards,
1988). They appear heir to a variety of cognitive
deficits and psychophysiological abnormalities, and
react idiosyncratically to alcohol intoxIcation (Pihl
et al., 1990). It is often assumed, and more often
devoutly desIreà, that these other quaiities might
serve as markers for the aicoholic predisposition,
since that characteristic seems particularly
problematic, from the personal and social viewpoints.
Nonetheless, the nature of the reiationship between
these additional, supposedly phenotypal features and
alcohol use and misuse remains unknown. This lack of
association between marker and disorder substantially
decreases the practicai and theoretical utIlity of the
relevant literatu:e.
DemonstratIon of a relationship between any of the
cognitive, behavioural or psychophysiological
differences characteristic of SOMAs and their genera1
level of alcohol consumption would provide a certain

147
 Alcohol-Induced
5

degree of evidence linking that difference to their

alcoholic predisposition. Such a demonstration vould
have, as a consequence, identification of vhat might be
a true marker for at least one form of abusive
drinking. The Ideal marker might be expected to
function as a simple, plausible mediating factor,
midvay betveen the (unknovn) heritable factors, per se,
and development of the complex behavioural pattern
described as alcoholism.
In accordance vith this line of logic, Finn and
Pihl (1987, 1988) and Finn, Zeitouni and Pih1 (1990)
have demonstrated that SOMAs vith extensive
multigenerational family histories of alcoholism (MFH)
are characterized by sober cardiovascular hyper-
reactivity (significantly increased heart-rate and
vasoconstriction) to threat of and signalled electric
shock. This hyper-reactivity theoretically appears in
association vith heightened preparation-for-activity
(Pihl and Peterson, in press), in keeping with the idea
of cardiac-somatic coupling (Obrist, 1976). SOMAs
appear sensitive as well to the virtual elimination of
this cued reactivity after consumption of a lega1ly-

148
 A1coho1-Induced
6

intoxicating dose of a1coho1 (Finn & Pih1, 1987, 1988;

Finn, Zeitouni & Pih1, 1990; Levenson, Oyama & Heek,
1987). Levenson et al., (1987) and Pih1, Finn and
Peterson (1989) have proposed that alcoho1-induced
e1imination of reactivity to threat might prove
negatively reinforcing. Those susceptible to such
elimination shou1d, therefore, consume a1coho1 in
greater amounts, or with greater regularity, all other
factors being equa1. This is a testable hypothesis,
4"'"
':j
and such a test comprises part of the data analysis
....;"."
reported in thls paper.
Finn and Pih1 (1987, 1988), Finn et al. (1990)
and Levenson et al. (1987) have a1so reported
significant a1coh~1-induced resting baseline heart-rate
increase among their respective high-risk subjects.
This effect is too consistent and too striking to
ignore, given (a) that a1coho1 has been consistent1y
demonstrated to produce resting heart-rate increases,
of unknovn significance (Sher, 1987); (b) that
increases in base1ine heart-rate have been assoclated
under certain conditions vith increased magnitude of
reward and heightened incentive (Fow1es, 1980; 1983),

149
 Alcohol-Induced
7

and (3) that ·,tse and Bozarth (1987) have suggested all
drugs of abuse might share psychomotor stimulant
actIons, and assoclated posltively relnforcing
propertles. Accordlngly, it seems plausIble to poslt
that SOMAs are differentlally susceptible to what might
be the dlrectly relnforclng effect of alcohol, deflned
operationally as heart-rate increase, as weIl as to its
negatlvely-relnforclng propertles. The results of thls
equally testable hypothesis are also reported in this
paper, along wlth an analysls based upon the
Interaction of the two putatively relnforclng effects,
and lts relatlonshlp to alcohol consumptlon.
Method
Data analysed and presented ln thls paper were
collected as part of a continuous high-rlsk project
sponsored by the Douglas Hospital-McGlll UnIversIty
Alcohol Research Project. Various aspects of this
project have been descrlbed ln prevlous communIcatIons
(FInn & Plhl, 1987, 1988; Finn, Zeltoun1 & Pihl, 1990),
and the data lncluded ln the analyses reported herein
have been drawn, from these studles, and from others
completed slnce. However: aIl the analyses descrlbed

150
 Alcohol-Induced
8

in this paper, detailing the relationship betveen

cardiovascular reactivity and drinking history have
been conducted presently, as the theoretical reasons
for doing 50 have become evident, and since the project
sample size has become sufficiently large.
Subjects
Data analyzed vas gathered from 83 non-alcoholic
males betveen the ages of 18 and 35. All subjects
scored 5 or less on the Michigan Alcoholism Screening
Test (Selzer, 1971) and vere neither depel.dent upon or
abused alcohol according to criteria described in the
third edition of the Diagnostic and Statistical Manual
of Mental Disorders (DSM III, American Psychiatrie
Association, 1980). Each of 36 of these subjects had a
multigenerational family history (MFH) of alcoholism:
at minimum, an alcoholic biological father, paternal
grandfather, and paternal uncle or brother. Fourteen
had a unigenerational family history (UFH) of
a1coho1ism: limited, in the past tvo generations, to
the father. The remaining 33 had no family history
(FH-) of alcoholism in the previous tvo generations.

151
 Alcohol-Induced
9

Subjects in the MFH and UFH group were recruited

from a subject pool maintained by the Douglas
Hospital - McGill University Alcohol Research Centre.
This subject pool is composed of families of
alcoholics, who are willing to participate in a variety
of multidisciplinary research projects. Extensive
family and psychiatric histories are obtained from the
participating family members, according to DSM-III
criteria for those interviewed, and Family History
~.
Research (FHR) Diagnostic Criteria (Endicott,
Andreasen, & Spitzer, 1975) for those who are
unavallable.
Subjects in the FH- group vere recruited through
newspaper and posted advertisements. Subjects were
screened by telephone, after indicating their
willingness to participate, and vere subsequently
intervieved according to FHR Diagnostic Criteria.
Subjects vith no alcoholism in their family for tvo
generations vere assigned to the FH- group.
Subjects were excluded from the experiment if
their mother drank heavily, and if any of their
relatives had suffered a psychotic episode at any time.

152
 Alcohol-Induced
10
AlI subjects were paid $5.00 per hour for their
participation.
Procedure
The majority of the subjects who part~cipated, to
date, in the Douglas Hospital-McGill Univer~ity Alcohol
Research project (and aIl of those described in the
present analysis) were subjected to a standard
procedure, described in detail in Finn and Pihl (1987,
1988) and outlined briefly below. upon arrivaI at the
lab, subjects were required to read and sign an
informed consent form, were weighed, and asked to
complete a self-report questionnaire concerning age,
education, and frequency and quantity of alcohol
consumption. This form of self-report has been
demonstrated to be a valid measure of alcohol
consumption (Sobell & Sobell, 1986). With regards to
freguency: all subjects were asked to estirnate how
often they consurned alcohol per week, on average.
Those who consumed upon less than one occasion weekly
were asked to estimate monthly, or yearly frequency.
With regards to quantity: aIl subjects were asked to

153
l
Alcohol-Induced
11

estimate average number of drink& (one beer = one mixed

drink = one small glass of wine) consumed per occasion.
After complet ion of this self-report
questionnaire, each subject participated in the
physiological recording session, once sober and once
while alcohol-intoxicated. Each subject was seated in
a reclining chair, attached to a polygraph, and asked
to relax. Baseline measures of heart rate, digital
blood volume amplitude, skin conductance, and frontalis
muscle tension were taken during the following ten
minutes. After baseline recordings vere established, a
small concentric shock electrode was attached to the
inside of the subject's right e1bov, and headphones
were placed on his head. Betveen three and ten trials
of countdown to and signalled electric shock began.
Countdown to and signalled shock consisted of the
presentation of a lov frequency l stone followed by a
countdown from 10 to 1, presentation of a second, ls
tone concurrent1y vith onset of a 1.85 ma 0.25 s shock.
Subjects assigned to the alcohol condition were given
three drinks of 95\ pure USP alcoho1 mixed 5:1 vith
orange juice fifteen minutes before the experimental

154
 Alcohol-Induced
12
procedure began. Each subject whose data was included
in the present analysis was tested while under the
influence of either 0.75, 1.00, or 1.32 ml/kg of
alcohol. Alcohol administered at these doses
consistently produces measurable psychophysiological
alterations in functioning in MGH SOMAs (stewart, Finn
& Pihl, 1988). Order of participation was not
consistently counter-balanced, as Finn and Pihl (1987)
and Finn, Zeitouni and Pihl (1990) showed no order-
effect.
Results
Demographies and blood alcohol level (BAL)
One-vay analysis of variance revealed that
subjects in th~ three risk groups did not differ
significantly in mean age (M = 23.12, SE = 0.50),
years of school1ng (M = 14.09, SE = 0.21), or BAL (~ =

0.091, ~ = 0.002).
Psychophysiological measures
Results from the first three countdown to and
signalled shock trials are included in the present data
analysis, since a minimum of three trials were
conducted upon every subject. Only one

(..... ~.

155
 Alcohol-Induced
13
psychophysiological measure (heart-rate) and one
measure of weekly alcohol consumption are included in
the following analyses. Heart-rate was selected for
sole inclusion (a) because it has varied in previous
investigations conducted upon SOMAs in terms of
~ea~tivity to threat, and merely as a function of
alcohol consumption, as outlined in the introduction;
(b) because its psychological concomitants are
comparatively well-understood, with regards to positive
reinforcement (Fowles, 1983) and preparation-for-
activity (Obrist, 1976); and (c) because it is easily
and reliably assessed, and baseline measures are
comparable within and between subjects (in distinction
to DBVA, which is only comparable within subjects
(Jennings, Tahmoush, & Redmond, 1980). Multiplication
of average weekly frequency and average quantity
provided a simple, easily comprehensible composite
measure of total weekly alcohol consumption. As weIl,
comparison of only two straightforward measures
heightens the parsimollY, utllity and statistical power
of the analyses.

156
 Alcohol-Induced
14

Blood alcohol level, which varies as a function of

alcohol dose, is not included as a covariate in any of
the following analysis. Correlational analysis,
completed because three dose groups were included in
this investigation, indicated that the effect of BAL
upon the psychophysiological measures included in the
following analyses was minimal (less than a non-
significant 2 per cent).

Insert Figure l about here

Per cent change in heart-rate, means and standard

errors, for all three risk groups, are graphically
presented in Figure 1. Per cent change scores were
selected for use as dependent variables because they
account for proportionality, unlike simple change
scores, and because they can be easily understood in
teras of the original data, unlike residuals. Per cent
sober heart-rate reactivity (\SOB-HRR) was calculated
by subtracting mean sober baseline heart-rate (recorded
during the ten-minute rest period prior to the shock
trials administered to sober subjects) from heart-rate

157
 Alcohol-Induced
15
recorded from sober subjects during the signalled shock
procedure (from the tone signalling trial onset to 7
seconds after shock), divièing that figure by the sober
baseline heart-rate, and multiplying the end result by
100. FH- subjects vere characterized by a mean 6.23%
increase (~= 1.92); UGH subjects by a mean 1.29%
increase (~= 2.87); and HGH subjects by a mean 13.07%
increase (SE = 1.79). One-vay ANOVA revealed
significant differences betveen the groups (~(2,78) =
...
-.
7.11, R< .0015. Post-hoc Fisher's LSD indicated that
the HGH and UGH, and HGH and FH- groups differed
significantly, R< .05.
Per cent a1cohol-induced heart-rate reactivity
change (%ALC-HRRC), also graphically presented in
Figure l, vas calculated by subtracting mean
intoxicated baseline heart-rate (recorded during the
ten-minute rest period prior to the shock trials
administer~d to intoxicated subjects) from heart-rate
recorded from intoxicated subjects during the signalled
shock procedure (from the tone signalling trial onset
to 7 seconds after shock), dividing that figure by the
intoxicated baseline heart-rate, multiplying by 100,

158
 Alcohol-Induced

16

and subtractlng the end result from \SOB-HRR. FH-

subjects were characterlzed by a mean 2.71\ decrease

(~ = 1.81) ln reactlvlty; UGH subjects by a mean 2.61\

lncrease (~ = 2.70); and HGH subjects bya mean 14.00\

decrease (~ = 1.68). One-way ANOVA revea1ed

signlflcant dlfferences between the groups (E(2,78) =

17.75, ~< .0001). Post-hoc Fisher's LSD lndlcated that

the HGH and UGH, and HGH and FH- groups differed

significantly, ~< .05.

,
d.·
Per cent alcohol-1nduced baseline heart rate
.....
;'I

change (\ALC-BLHRC), presented as well ln Figure 1, ls

mean alcohol-intoxicated base1ine heart-rate, minus

mean sober basellne heart-rate, dlvided by mean sober

base1ine heart-rate, aultiplied by 100. The baseline

heart-rate of FH- subjects increased 3.83\ (~ = 1.98)

while lntoxlcated; of UGH subjects decreased 1.32\ (~

= 3.03); and of HGH subjects increased 13.46\ (a& =

1.89). One-way ANOVA revealed slgnificant differences

between the groups (E(2,BO) = 10.87, ~< .0001). Post-

hoc Fisher's LSD indicated that the HGH and UGH, and

HGH and FH- groups dlffered signiflcantly, ~< .05.

159
 Alcohol-Induced
17
~rediction of drinking behaviour
Squared inter-correlations betveen mean drinks per
veek, risk, \SOB-HRR, \ALC-HRRC, \ALC-BLHRC and the
interaction products of the latter three variables are
included in Table 1. Weekly alcohol intake is
significantly correlated vith all the factors and vith
their interactions. As vell, each factor correlates
significantly vith each other factor. This means that
drinking is associated vith sober heart rate
reactivity, alcohol-induced change in that reactivity,
and with alcohol-induced baseline heart rate change.
The multiplicative interaction between sober heart-rate
reactivity and alcohol-induced baseline heart rate
change is assoclated vith drinking almost as well as
the multiplicative interaction between alcohol-induced
heart-rate reactivity change and alcohol-induced
baseline heart rate change.

Insert Table 1 about here

Automatic stepvise regression analysis makes it

clear, however, that weekly alcohol intake is best

160
,
•1

Alcohol-Induced
18

predicted by the interaction between \ALC-HRRC and

\ALC-BLHRC Cdenoted from here on in the text as
ALCOHOL-EFFECT). This outcome also makes sense from
the theoretical viewpoint, as it is the combined
alcohol-effect that is potentially rewarding. Each of
the remaining variables adds almost no additional
predictive power Cless than 3.0 per cent for the
interaction between \SOB-HRR and \ALC-BLHRC, less than
0.5\ for all others), once ALCOHOL-EFFECT is included

~.-
in the model. ALCOHOL-EFFECT, entered in multiple
1
~.

regression analysis as the single predictive variable,

accounts for 20.03 per cent of the variance of weekly
drinking CEC1,79) = 19.79, ~< .0001).
The actual effect of the interaction between
alcohol-induced heart rate reactivity change and
alcohol-induced baseline heart rate increase CALCOHOL-
EFFECT) can be seen by examining the drinking behaviour
of two arbitrarily created groups: one consisting of
those subjects who scored above the Mean CR =34), in
terms of the Most predictive interaction, as described
above CHigh Alcohol Effect), and the other of those who
scored below CN =47) CLow Alcohol Effect). The first

161
 Alcohol-Induced
19
ANOVA of these tvo examined alcohol consumption purely
as a function of the primary division. The high
ALCOHOL~EFFECT group consumed significantly more drinks
per veek ,M = 9.68, ~ = 0.65) than the lov ALCOHOL-

EFFECT group (~ = 5.26, SE = 0.80) (~(1,79) = 12.71, ~<

.0006). Means and standard errors are presented in the

"No-Covariate" group in Figure 2. The second examl.ned
veekly drinking vithin these tvo groups, as a function
of ALCOHOL-EFFECT, vith the effect of rl.sk (~(1,78) =
0.67, ~< .4139) covarl.ed out. The removal of the rl.sk
effect made little difference to the outcome: members
of the hl.gh ALCOHOL-EFFECT group stl.ll consumed more
alcohol (~= 9.37, ~ = 0.95) than members of the lov
ALCOHOL-EFFECT group (M = 5.48, ~ = 0.81), ~(1,78) =
7.64, 2< .0071. Means and standard errora are also
presented in Figure 2, under the heading "Riak
Covaried". The third ANOVA examl.ned the effect of rl.sk
upon veekly alcohol consumption, vith ALCOHOL-EFFECT
(E(1,77) = 6.04, ~< .0163) covaried out. Risk dl.d not
remain significantly associated vith drinking under
these conditions: members of the FH- group consumed a
mean 6.51 drinks per veek (SE = 1.00); members of the

162
.j
".\..

Alcohol-Induced
20
UGH a Mean 6.58 drinks per week (SE = 1.491; and
members of the HGH a Mean 7.84 drinks per week (SE =
0.931, [.(2,771 = 0.39, 12.< .6767.

Insert Figure 2 about here

These arbitrarily created groups differ very much

from each other in terms of their Mean cardiovascular
response: per cent sober heart rate reactivity (LOW
ALCOHOL EFFECT ~ = 4.32, ~ = 1.54; HIGH ALCOHOL EFFECT
~ = 14.09, SE = 1.81), ~(1,791 = 17.02, ~< .00011, per

cent a+cohol-induced heart rate reactivity change (LOW

ALCOHOL EFFECT ~ = 0.55, ~ = 1.39; HIGH ALCOHOL EFFECT
K = 15.46, ~ = 1.641, ([.(1,791 = 48.13, 12.< .00011, and

per cent alcohol-induced baseline heart rate change

(LOW ALCOHOL EFFECT K = 0.01, ~ = 1.31; HIGH ALCOHOL
EFFECT ~ = 17.78, ~ = 1.541, ([.(1,79) = 77.58, 12.<
.00011. Heans &nd standard errors for these measures
are presented in Figure 3. Distribution of subjects in
these two groups, by risk, is shown in Table 2. For
the FH- group, X2(1, N = 331 = 4.8, ~< .05; for the
UGH, X2(1, N = 141 = 7.0, 12.< .01; and for the HGH,

163
 Alcohol-Induced
21

X2(1, N = 36) = 13.5, R< .001. For the entire aample,

X2(2, N = 36) = 25.28, R< .0001. As this analysis
demonstrates, significantly fewer UGH and FH- subjects
and significantly more FH+ subjects are found in the
high ALCOHOL-EFFECT group, than would be expected if
random assortment accounted for the division.
--------------------------
Insert Figure 3 about here

Insert Table 2 about here

Discussion
This study demonstrates most importantly that a
significant relationship exists between three measures
of cardiovascu1ar response and week1y a1coho1
consumption, among non-a1coho1ic social drinkers.
Individua1s characterized by sober heart rate
acce1eration to signa11ed electric shock, by alcohol-
dampening of that acceleration, and/or by heart-rate
acceler~tion to a1cohol consumption consume more
alcoho1 on a week1y basis than those who are not
characterized by these responses. Additionally, those

164
 Alcohol-Induced
22

who manifest any two of these ~haracteristics

simultaneously consume even more, especially if they

are susceptible to alcohol-dampening of cardiovascular
reactivity and to alcohol-induced baseline heart rate
acceleration. Furthermore, males from families with
multigenerational histories of male alcoholism are more
likely to be those who are characterized by the
particular cardiovascular response patterns that occur
in association with increased weekly alcohol
consumption. The MGH males who do not manifest these
responses do not drink more than subjects in the UGH
and FH- groups.
Positing that increased sensitivity to the
reactivity-dampening and baseline heart-rate-
accelerating effects of alcohol might predispose to
alcohol abuse appears reasonable from the theoretical
viewpoint, as weIl. These two alcohol effects could
vell be negatively and positively reinforclng,
respectively, and therefore serve as plausible
lntermedlaries between the heritable factors that
underly susceptibility to alcoholism, and the emergence
of the alcoholic behavioural pattern per se.

165
.--'.-
.. ..;;;

Alcohol-Induced
23

Additionally, it is a telling fact that more HGH

subjects manifest sensitivity to alcohol's effect, than
UGH or FH- subjects. This appears to suggest that the
haightenr-à cardiovascular response is linked to
familial risk, rather than consequential to alcohol
consumptlon, slnce rlsk Itself Is strongly llnk~d to
the cardiovascular response and poorly linked to weekly
alcohol consumption. It ls also Interesting to note
that estim~tes of the he~itability of alcohol use have
been deteL.lned to range between 0.22 and 0.58 (Kaprio,
Koskenvuo, Langinvainio, Romanov, Sarna & Rose, 1987;
Partanen, Bruun, & Harkkanen, 1966). If It is assumed
that a moderate-to-1arge percentage of the alcohol-
effects descrlbed in the present paper are in fact
genetically deterained, the results reported here
appear in keeping with these estlmates.
Of course, the mere existence of an association
between one factor and another does not prove that one
causes the other. Regardless of the logic of the
prevlous arguments, on1y longltudinal follow-up could
determine whether the pattern of helghtened
cardlovascular response llnked ln thls study to

166
 1
".;..

Alcohol-Induced
24

increased alcohol consuaption actually predisposes to

alcohol abuse and/or dependence.

,,'r
.....

167
1
Alcohol-Induced
25
References
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statistical manual of mental disorders (3rd ed.).
Washington, De: Author.
Bohman, M., Sigvardsson, s., & Cloninger, c. R. (1981).
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Cadoret, R. J., cain, C. A., & Grove, W. H. (1980).
Deve10pment of a1coholism in adoptees raised apart
from alcoholic biological relatives. Archives of
General Psychiatry, 11, 561-563.
cloninger, C. R., Bohman, H. & sigvardsson, S. (1981).
Inheritance of alcohol abuse: A cros5-fostering
analysls of adopted men. Archives of General
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Cotton, N. S. (1979). The familial incidence of
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116.

Endicott, J., Andreasen, N., & Spitzer, R. L. (1975).

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168
 Alcohol-Induced
26

Finn, P. R., Zeitouni, N. C., & Pihl, R. o. (1990).

Effects of alcohol on psychophysiological

hyperreactivity to nonaversive and aversive stimuli
in men at high risk for alcoholism. Journal of
Abnormal Psychology, ~, 79-85.

Finn, P. R. & Pihl, R. o. (1987). Hen at high risk for

alcoholism: the effects of alcohol on cardiovascular

response to unavoidable shock. Journ~l of Abnormal
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Finn, P. R. & Pihl, R. o. (1988). Risk for alcoholism:

A comparison betveen tvo different groups of sons of

alcoholics on cardiovascular reactivity and
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Fovles, D. c. (1980). The three arousal model:

Implications of Gray's tvo-factor learning the ory

for heart rate, electrodermal activity, and
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Fovles, D. C. (1983). Hotivational effects of heart

rate and electroderaal activity: Implications for
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of Research in Personality, 11, 48-71.
~
~

169
 Alcohol-Induced
27
Goodwin, o. W. (1ge5). Alcoholism and Genetics.
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Goodwin, o. W., Schulsinger, F., Hermansen, L., Guze,
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 Alcohol-Induced
28
Levenson, R. W., Oyama, O. N., & Meek, P. S. (1987).
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Peterson, J. B., Finn, P., & Plhl, R. O. (in press).
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,r•
.-
171
 Aleohol-Indueed
29
Pihl, R. O., Finn, P., and Peterson, J. B. (1989).
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.-.....
.•
Pihl, R. O., Peterson, J. B., & Finn, P. (1990) .
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. ..
~

172
 Alcohol-Induced
30
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173
 Alcohol-Induced

31

Table 1: Simple R-Sguared Values

B C 0 E F G H 1

A (R2) .078 .192 .125 .140 .212 .212 .186 .034

(,,-< ) .0115 .0001 .0010 .0006 .0001 .0001 .0037 .0954

B (R2) .754 .072 .450 .085

(,,-< ) .0001 .0155 .0001 .0080

C (R2) .185 .707 .164

(,,-< ) .0001 .0001 .0002

D (R2) .129 .066

(,,-< ) .0010 .0192
..
- ";-
E (R2) .131
--'" (12.< ) .0009

F (R2) .199
(12.< ) .0001

G (R2) .200
(12.<> .0001

H (R2) .183
(12.<> .0001

A=Risk F= B*D
B=Sober Heart Rate Reactivity G= C*D
C=Alcohol Induced Heart Rate Reactivity Change H= B*C*D
D=Alcohol Induced Baseline Heart Rate Change I=Drinks/Week
E= B*C

174
 Alcohol-Induced

32

Table 2

Cross tabulation resu1ts

LOW A-E HIGH A-E

FH- (Actua1 Number) 24 7
(Percent of risk group) ( 77%) (23%)

(Predicted NUmber) 18 13

UGH (AN) 13 1

(%) (93%) (07%)

< (PN) 8 6
1
.....

HGH (AN) 10 26

(%) (28%) ( 72%)

(PN) 21 15

175
,'......
Per Cent Change
.:.
en
.:.
N o <Xl

0
;,g
0
l'al
;,g
0
•
-,g
0
»
r
»
r
Cf)

." () ()
0
, , ,
CD
I1 CD :c :c
r ::Il ::Il
:c ::Il ::Il
::Il ()
()

..
c
~
Ci)
I

s::
Ci)
I

176
 Alcohol-Induced
33

Figure Caption
Figure 1. Per cent change in heart rate. SOB-HRR =
sober heart rate reactivity. ALC-HRRC = alcohol-induced
heart-rate reactivity change. ALC-BLHRC = alcohol-
induced baseline heart-rate change .

.~
'1
'~

177
 Mean Drinks/Week

o Cl

m
ï
0
•
:r:
cci"
::E :::r
z
o
» »
C")
0 ë'ï
a :::r 0
:::r
o Q. 0
m
01
~.
:::::
CD
m
:::::
CD
p> .....
C")
.....
C")

éD

-<'.....

JJ
tf)
;;s:;;-
a
o
<
m
::"1.
cr>
Q.

178
 Alcohol-Induced
34

Figure Caption
Figure 2. Mean drinks per veek (self-report) by high
and lov susceptibillty to ALCOHOL-EFFECT (AE).

r
...

179
 21 1 1

18 • %SOB-HRR

15
lm %ALC-HRRC
12

9
o %ALC-BLHRC
ID
0> 6
c
~ o
..c 3 co
o ri

....... 0+1---'
C
al
o..... -3
al
a.. -6

-9

-12

-15 ;

.,." : 1

LOWAE HIGH AE

, (
 Alcohol-Induced
35

Figure Caption
Figure 3. Per cent change in heart rate, by high and
lov sUBceptibility to ALCOHOL-EFFECT (AE). SOB-HRR =
sober heart rate reactivity. ALC-HRRC = alcohol-induced
heart-rate reactivity change. ALC-BLHRC = alcohol-
induced baseline heart-rate change.

181
 Final Comments
According to the extant literature, sons of male
alcoholics (SOMAs) are characterized by conduct
.~.

disorder/hyperactivity, deficits in cognitive function,

abnormalities in psychophysiological response and by
susceptibility to alcoholism. The first two studies
presented in this thesis support the notions (1) that
alcoho1 intoxication suppresses the function of the
integrated fronta1-limbic system, particu1arly of the
hippocampus; (2) that sober SOMAs are characterized by
deficits in the functions associated with operation of
the pre frontal cortex; and (3) that these deficits are
linked to SOMAs' cardiovascular hyper-reactivity to
threat of and aversive stimuli. Theoretica1
consideration of the general literature, and of these
two studies, allowed for the formulation of a general
model (1) detaili~~ the potential negatively-reinforcing
properties of acute alcohol intoxication and (2)
describing the increased susceptibility of SOMAs with a
core deficit in abstraction and subsequent
cardiovascular hyper-reactivity to novelty and threat,
to this property of negative reinforcement. The third
study demonstrated the existence of a relationship
between alcohol consumption, cardiovascular hyper-
reactivity, dampening of that reactivity by alcohol
consumption, and the potential positively-reinforcing
effects of acute alcohol-intoxication, evident from
alcohol's effect on baseline heart-rate.

182
 The literature examined in the introduction to this
thesis suffers from a number of general faults. Too many
studies use subjects vhose familial alcoholism is
limited at best to the father, and many do not conduct
their analyses by sex. The presence of male alcoholism
in at least tvo concurrent generations of a given
proband's pedigree vould increase the likelihood that
the proband is in tact characterized by the familial
alcoholic predisposition. The nature of alcoholism in
the family, and the long- and short-term patterns of
alcohol use among experimental subjects must be more
carefully specified. Description of alcohol use should
involve investigation of consumption and consequences.
Frequency, duration, intensity and onset of alcohol use
are critical variables. The nature of complications
arising from alcohol use must be clarified in as much
detail. Duration and severity of detrimental effects
upon physical, social, and occupational functioning
should be described. Demographie variables must be given
careful consideration. With regard to age, for example,
the likelihood that a given subject is actually
characterized by an alcoholic predisposition decreases
as he or she ages, vithout actually abusing alcohol.
Younger subjects are therefore more suitable. Finally,
comparison of SOMAs to sons of fathers vith other
psychiatrie disorders vould aid in determining the
specificity, and therefore the utility, of any
·r
183
 distinguishing markers. Implementation of these

methodologica1 improvements would elimlnate much of the

- confusion that present1y obscures comprehension of the
.' nature of the a1coho1ic predispositlon.
The three studies described in this thesis were
a1so f1awed in varlou8 ways. study 1 employed the m08t
sophisticated design - but its hypothesis was somewhat
prlmitive and lts results were probab1y the 1east
important of the three. Study 2 attempted too much, with
too few subjects (a1though it shou1d be said that Harden
and pih1 (submitted) essentia11y rep1icated its resu1ts,
with younger subjects). Study 3 was not real1y a study
at a11, but a data ana1ysis. On1y longitudinal fo11ow-up
of the subjests inc1uded in this ana1ysis would
demonstrate whether its findings were accurate: whether
the putative markers it identifled actual1y indicate
the a1coho1ic predisposition. The thesis itse1f is
heavi1y theoretica1. This is problematlc: ln that lt i8
dangerous to theorize, without rep1ication. In addition,
there are gaps in the story it presents. Fll1ing these,

however, is a matter for future endeavour.

On the plus side, the work this thesis represents a
significant portion of has 1ed to the identification of
two plausible markers for the alcoho1ic predispoBition:
the cognitive dysfunction/cardiovascu1ar hyper-
reactivity that may under1ie susceptibi1ity to the
negative1y-reinfùLclng, anxiu1ytic properties of
alcoho1, and the a1coho1-induced basellne heart rate

184
 increase that may be indicative of susceptlbllity to
positive reinforcement. Assessment for presence of these
markers or risk factors promises to be relatively
straightforward, and non-invasive. In addition, these
markers are plausible intermediary factors, either from
the viewpoint of heredity or environment.
The story presented in this thesis is predicated
upon a number of assumptions, which may or may not be
grounded ln facto Research conducted upon assumptlon
cannot be made rlsk-free. Over-interpretation of data
may lead to the pursuit of knowledge, where knowledge
does not in fact exist. However, in scientific
endeavour, as elsewhere, the willingness to risk Is
everything.

r
1
.~.

185
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