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ICHGANS

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IH

 

 

 

 

 

This is to certify that the

thesis entitled

GENETIC LOADING FOR ALCOHOLISM:
NEW EVIDENCE FOR SUBTYPES

presented by

Deborah A. Wynblatt

has been accepted towards fulfillment
of the requirements for

M .A. degree in Psychology

 

 

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czkimMune-nt

 

GENETIC LOADING FOR ALCOHOLISM: NEW EVIDENCE FOR SUBTYPES

By

Deborah Ann Wynblatt

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

MASTER OF ARTS

Department of Psychology

1990

. ,v‘ - (1
wt?“ “/11

,/

ABSTRACT
GENETIC LOADING FOR ALCOHOLIS M: NEW EVIDENCE FOR SUBTYPES
By
Deborah Ann Wynblatt

Current research on the etiology of alcoholism suggests that genetic vulnerability
plays a role in the development of alcoholism. This study, using a population-based
sample and a broad set of independent variables, examined how genetic loading for
alcoholism affects developmental course of alcoholism and what moderating effects
various environmental variables might have on genetic load. Results confirmed that high
genetic loading for alcoholism was related to earlier onset and greater severity of drinking
difficulties and more frequent alcohol use. More importantly, alcoholic subtype was a
significant factor in predicting etiologic pathways into alcoholism. Among Type 2
alcoholics, genetic loading for alcoholism contributed strongly to later alcohol problems,
as did history of socialization to aggression. For Type ls, rearing in an alcoholic
environment was the only predictor of adult alcohol problems, suggesting that socialization

to using alcohol as a coping mechanism is most important for this subtype.

To Tom

iii

ACKNOWLEDGEMENTS

I am indebted to Robert Zucker for his guidance and support throughout the
development of this work. His knowledge of the alcoholism literature as well as his
theoretical conceptualization of the phenomenon were invaluable in broadening my
understanding of and approach to this work.

The other members of my thesis commitee, Frank Floyd and Ralph Levine, also deserve
my thanks for their support and help. Frank Floyd in particular contributed a significant
amount of time and energy to helping me with my data analyses; without his aid, my
understanding of path analysis would have been much more simplistic.

Finally, thanks go out to all the staff members of the M.S.U. family Project who so
assiduously collected the data I used, as well as to the project families who provide us with
so much information about their lives.

This work was supported in part by grants to R. A. Zucker, R. B. Noll and H. E.
Fitzgerald from the National Institute on Alcohol Abuse and Alcoholism (AA 07065) and
from the Michigan Department of Mental Health, Prevention Services Unit.

iv

W

LIST OF TABLES ............................................................................................................. vii
LIST OF FIGURES ........................................................................................................... viii
CHAPTER I: INTRODUCTION AND REVIEW OF THE LITERATURE

Alcoholism: A Generic Etiology? ........................................................................... 3

Genetics and Human Alcohol Consumption ........................................................ 5

Twin Studies ....................................................................................................... 5

Adoption Studies ............................................................................................... 9

What do Alcoholics Inherit? .................................................................................. l4

BiochemicalAbnormalities .......................................................................... 15

Brain Abnormalities ..................................................................................... 16

Temperament ................................................................................................. 18

Statement of the Problem ....................................................................................... 18

CHAPTERII: HYPOTHESES .............................................................................................. 21
CHAPTER III: METHODS

Subjects ..................................................................................................................... 23

Data Collection ......................................................................................................... 25

Measures ....................................................................... 25

Alcoholic Subtype ............................................................................................. 25

Drinking Measures ........................................................................................... 28

Genograrns ......................................................................................................... 29

Antisocial Behavior ............................................................................... ' ........... 30

Socioeconomic Status (SES) .............................................................................. 33

V

Environmental Exposure to Alcoholism ....................................................... 33

CHAPTER III: RESULTS

Relationship Between Family Expression of Alcoholism and Drinking

Variables ................................................................................................................... 35
Overall Relationships ....................................................................................... 35
Type 1 versus Type 2 Alcoholics .................................................................... 35
Relationship Between Lifetime Alcohol Problems Score and Other Life
Difficulties ................................................................................................................ 4]
Path Analyses ................................................................................................... 43
CHAPTER IV: DISCUSSION
Influence of Other Variables on the Developmental Course of
Alcoholism .............................................................................................................. 50
Future Directions .................................................................................................... 53
Summary .......................................................... ' ....................................................... 5 4
APPENDICES .................................................................................................................... 57
Appendix A: Full Models of Distal Predictors of LAPS for Type is and
Type 28 ...................................................................................................................... 57
Appendix B: Demographic Questionnaire .......................................................... 58
Appendix C: Diagnostic Interview Schedule ................. .................................... 64
Appendix D: Drinking and Drug History Questionnaire .................................. 75
LIST OF REFERENCES ..................................................................................................... 88

vi

W5

TABLE PAGE
1. Demographic Characterisrics of Subjects ...................................................... 24
2. Possible Family Illnesses .................................................................................. 26

3. Correlation Between Family Expression of Alcoholism and Alcohol
Involvement for Men ......................................................................................... 36

4. Differences Between Type 1(n=25) and Type 2 (n=60) Alcoholics on
Demographic/ Life Difficulty Variables ........................................................ 37

5. Correlation Between Family Expression of Alcoholism and Alcohol
Involvement for Type 1 versus Type 2 Alcoholics ....................................... 39

6. Correlation Between Family Expression of Alcoholism and Alcohol
Involvement for Type 1 versus Type 2 Alcoholics after Controlling
for Parental Alcoholism in the Rearing Environment ............................... 4O

7. Correlations among Life Difficulty Variables for Type 1(n=25) and
Type 2 (n=60) Alcoholic Men ............................................................................. 42

vii

W

FIGURE PAGE
1. Diagram for Classification of Alcoholic Subtype ......................................... 27
2. Coefficient of Relationship for Hypothetical Subject and His Extended
Family ................................................................................................................... 31
3. Sample Calculation: Family Expression of Alcoholism ................................ 32
4. Comparison of Path Models for Type 1 and Type 2 Alcoholism ................ 45
5. Extended Path Model for Type 2 Alcoholics .................................................... 46
6. Full Models of Distal Predictors of LAPS for Type Is and Type 2s ............... 57

viii

Introduction and Literature Review

Research into the etiology of alcoholism has been hampered by the lack of a widely
shared definition of alcoholism. Because of this lack of consistency, it is often difficult to
compare research across studies; one cannot be sure that the same populations are under
study.

The classical definition of alcoholism was formulated by EM. Jellinek in the 1950's.
He decried the broader medical profession's use of the word 'alcoholism' for any type of
heavy drinking. Instead, Jellinek (1952) distinguished two types of alcoholics (addictive
and non-addictive) in whom excessive drinking occured WW.
Using the medical model, he applied the disease conception of alcohol addiction nor to
excessive drinking per se, but to the 'loss of control' over drinking that accompanied it.
He considered this loss of control to be a disease condition that only occured in addicrive
alcoholics.

More modern formulations of the medical model of alcoholism include the diagnostic
criteria of DSM-IlI-R (A.P.A.,l987). As did Jellinek, DSM-III-R considers alcoholism to
be a disease with some unknown etiology. It defines peOple with alcohol dependence
syndrome as those who have any three of the following symptoms: a loss of control over
alcohol intake, a desire to cut down on intake, a great deal of time spent obtaining alcohol,
frequent intoxication or withdrawal symptoms which interfere with role obligations,
participation in important social or occupational aetivities reduced due to alcohol use,
continued use despite recognition of a problem with alcohol, tolerence of alcohol,
withdrawal symptoms, or intake of alcohol to avoid withdrawal. Because alcoholism is
thought to exist in differing degrees of severity, not all of these indicators need be present
to define a person as an alcoholic.

AnOther medical model of alcoholism which has recently been proposed is Edward
and Gross's (1976) Alcohol Dependence Syndrome. The seven facets of the syndrome

are narrowing of the drinking repetoire, salience of drink-seeking behavior, increased

2

tolerance to alcohol, repeated withdrawal symptoms, repeated relief of withdrawal
symptoms by further drinking, subjective awareness of a compulsion to drink and
reinstatement of the syndrome after abstinence. Edward and Gross' definition of
alcoholism differs from DSM-III-R in that social problems resulting from drinking are nor
included as indicators of alcohol dependence (Caetano, 1985).

The term 'alcoholism' has been used differently in various studies; n0t all use the
DSM-III-R criteria (or those of its predecessor DSM-III) to obtain samples of alcoholics.
Bohman (1978), for example, defined his sample of alcoholics based on law-breaking:
alcoholics were those who had been registered with local Temperence Boards set up to
regulate misuse of alcohol. Defining alcoholism in such a manner is problematic, since
criteria for being registered with the Temperence Board have changed over time. Cadoret,
Troughton and O'Gorman (1987) considered alcoholics to be those who had one or more
recorded social or medical problems because of drinking (i.e. lost a job due to drinking, got
a divorce due to drinking). In similar fashion, Schuckit (1984) defined alcoholism as the
occurence of one of several alcohol- related major life problems, such as dropping out of
school. One problem with such definitions is that they do not clearly differentiate
alcoholics from 'problem' drinkers, who may also have had difficulties functioning in
society due to excessive drinking. One way to distinguish between these two groups may
relate to Jellinek's (1952) original definition of alcoholism; 'problem' drinkers might well
be conceptualized as Jellinek's 'non-addiCtive' alcoholics, who do n0t lose control over
their drinking but may still drink to excess.

Mulford and Miller (1960) described alcoholism as a function of a set of social
norms which gave the individual a certain way of thinking about or defining himself,
alcohol, and the relationship between the two. Alcoholic drinking, in Mulford and Miller's
conceptualization, allowed an alcoholic to redefine himself and his relationship to Others in
a way that was more self-satisfying. Unlike those discussed previously, this definition

conceptualized alcoholism within a social learning theory framework.

3

One important question needs to be answered in order to produce a useful definition
of alcoholism: is alcoholism one end of a continuum that includes 'heavy' or 'problem'
drinkers? Goodwin (1979) has argued, based on his studies of Danish adoptees, that
alcoholism results from a different developmental path than does 'heavy drinking'.
However, research by Clark and Cahalan (1976) has indicated that more severe forms of
alcoholism merge gradually with problem and heavy drinking. A distinct, pathological
type of alcoholism does not appear to stand out on a population curve of those with
drinking problems (Peele, 1986). 8

Finally, the issue of whether there are several different kinds of alcoholism, each with
its own etiology, remains. Zucker (1987a) has proposed that four different alcoholisms,
each with its own cause and course, exist: antisocial alcoholism, developmentally limited
alcoholism, developmentally cumulative alcoholism and negative affect alcoholism.
Cloninger and Bohman's (1981) research also points to the need to develop definitions of

alcoholism which are specific to different alcoholic subpopulations.
”11"!5'5'1"

What kinds of evidence led to the idea that inherited factors might play a role in the
development of alcoholism? One of these was family studies. Such studies indicated that
rates of alcoholism were much higher among the families of alcoholics than among the
general population. Cotton's (1979) literature review encompases 39 studies of
alcoholics. She found that regardless of the nature of the non-alcoholic population used as
a comparison group, an alcoholic was more likely than a non-alcoholic to have a mother,
father or other close relative who was alcoholic. The fact that alcoholics were twice as
likely to report parental alcoholism as other psychiatric patients implied that a high rate of
familial alcoholism was mm; to alcoholics.

Two-thirds of the studies that Cotton reviewed found at least 25% of all alcoholics to

have alcoholic fathers. One third of alcoholics were found to have at least one alcoholic

4

parent. Corton noted that if anything, her figures erred on the side of conservatism due to
demonstrated underreporting of mental illness and alcoholism in the 39 studies.

Family studies also indicate that the rate of alcoholism is increased in the offspring of
alcoholics. Goodwin (1979) reported that sons of alcoholics were four times as likely as
were sons of non-alcoholics to become alcoholics themselves. Winokur, Reich, Rirrrrner
and Pitts (1970) also investigated the occurence of alcoholism in children of alcoholics.
They diagnosed 31% of the sons of male alcoholics to be alcoholic upon reaching
adulthood; an astonishing 51% of sons of female alcoholics were found to be alcoholic as
adults.

The fact that the rate of alcoholism is higher within families of alcoholics than in the
general population does not by itself prove that a genetic vulnerability to alcoholism exists.
An alternative explanation would be that similar environments are recreated within alcoholic
families, such that offspring in each generation are exposed to an alcohologenic
environment. But when coupled with results from animal research, the concept of a genetic
role in the development of alcoholism begins to be a plausible hyporhesis.

Animal studies have demonstrated strain and line differences in the acquisition of
alcohol preference, sensitivity, tolerance and dependence. Building animal models for
alcohol preference, for example, provides information about genetic mechanisms related to
voluntary excessive consumption in humans. Lumeng, Hawkins and Li (1977) were able
to use selective breeding to produce a true-breeding strain of rats that voluntarily consumed
large amounts of alcohol. However, it could be argued that the rats were drinking the
alcohol because they liked the taste or smell, rather than, like humans, for its mood altering
effects. To demonstrate that this was not the case, Waller, McBride, Gatto, Lumeng and Li
(1984) inserted devices directly into the stomachs of rats which provided the rats with
their choice of water or alcohol. Rats bred from the alcohol-preferrin g strain self-infused
with up to 9.4 g of alcohol per kilogram body weight each day as compared to the non-

alcohol preferring strain of rats which self-infused a maximum of .7 g per kilogram body

5

weight per day. Apparently, the rats bred for alcohol preference were seeking the
pharmacological effect of the alcohol. The fact that animals usually refuse to drink alcohol
(Petrakis, 1985) makes this research even more intriguing.

Genetics have also been shown to play a role in animals' sensitivity to alcohol.
McCleam and Kakihana (1981) developed two strains of mice which they called short sleep
(88) or long-sleep (LS) based on the duration of unconciousness after receiving a dose of
ethanol. Selective breeding over several generations produced large differences in
sensitiVity to alcohol. Quantities of ethanol that merely anesthetized SS mice were close to
lethal for LS mice. Mice selected for their genetically lower sensitivity to alcohol have also
been shown to develop alcohol tolerance more quickly during prolonged exposure to
alcohol (Gallaher and Gionet, 1988).

Lastly, two groups of researchers have developed animal models which demonstrate
a genetic contribution to alcohol dependence in rrrice. Crabbe, Kosobud and Young (1983)
and Allen, Petersen, Wilson and McCleam (1983) have selectively bred different strains of
mice which can be distinguished on the basis of the severity of their withdrawal symptoms
after alcohol is removed from their diet.

Therefore, indirect research evidence points to a genetic contribution to the
development of alcoholism in humans. More direct evidence from human genetic studies

will now be reviewed.
5 . 1H 5] 11C .
I. S 1'

There are several kinds of studies which allow conclusions to be drawn about the role
of inheritence in the development of alcoholism. One type is the twin study, where
drinking behavior in monozygous (MZ) twins (who are assumed to be genetically identical)

is compared to drinking behavior in dizygous (DZ) twins (who are related as normal

6
siblings). Higher rates of concordant drinking behavior in the monozygous twins can then

be attributed to their more similar genotype.

In one early twin study, Partanen, Brunn and Markannen (1966) investigated
drinking behavior in twins with 'normal' drinking patterns. The only inclusion criteria for
the study were that subjects be a member of a twin pair born in Finland between 1920 and
1929 and that they currently be living in Finland. After recruiting 902 male twin pairs, the
group found a significantly higher concordance rate in amount and density (i.e. frequency)
of drinking among MZ twins than among DZ twins. Heritability was calculated to be .36
for amount of drinking and .39 for density of drinking; Partanen et al. concluded that
genetic factors influence drinking patterns among normal individuals.

Similar research was conducted by Kaprio, Koshenvuo, Langinvanio, Romanov,
Sarna and Rose (1987) who also assessed 'normal' drinking behavior. They compared
879 male pairs of monozygous twins and 1940 pairs of dizygous twins from the Finnish
Twin Cohort. The Finnish Twin Cohort consists of all like-sex twin pairs born in Finland
in 1958 among whom both twins were living in 1967. Subjects used in this study
comprised nearly all surviving male twins in the 25-49 age range. Information was
requested on the frequency (number of days of alcohol use), quantity (amount of alcohol
used) and density (number of days of excessive use) of alcohol consumption per month
and the frequency of passouts in the previous year. Results confirmed genetic effects for
frequency, quantity and density of drinking, but not for passouts. Kaprio's group found
heritability rates that were similar to those of Partanen: .39 for frequency of beer
consumption, .38 for frequency of spirit consumption, .40 for density of consumption and
.36 for quantity of consumption.

Partanen's work was also confirmed by Gabrielli and Plomin (1985) whose sample
included 46 M2 and 44 DZ twin pairs as well as 46 unrelated pairs of subjects who were
raised together. 203 subjects were females and 143 were males; median level of schooling

was 14.5 years. Unrelated pairs of adoptees were included to assess the importance of

7

shared family environment in alcohol consumption, independent of genetic influence. The
Colorado Alcohol Behavior Questionnaire was used to assess amount, frequency and rate
of alcohol consumption. Gabrielli and Plomin found significantly higher correlations of
both amount and rate of alcohol consumption among MZ twins. Based on this data, they
calculated a 66% heritability for rate and 25% heritability for amount of alcohol
consumption. Gabrielli and Plomin concluded that genetic influences on drinking behavior
were more important than shared family environment.

The classic twin study which investigated alcohol abuse among twin pairs was Kaij's
(1960). Kaij's subjects were 292 Swedish twins. At least one member of each twin pair
had been registered with Temperence Boards set up to control excessive drinking. After
categorizing each twin in terms of alcohol consumption, Kaij found that the co—twin of an
index MZ twin was much more likely to fall into the same category of alcohol consumption
as his twin than the co-twin of an index DZ twin. For example, he found that among
chronic alcoholics, 71.4% of co-twins in M2 pairs fell in the same category as their index
twin, while this was only true of 32.3% of co-twins in DZ pairs. Based on these results,
Kaij concluded that alcohol abuse was largely an inherited trait.

Murray, Clifford and Gurling (1983), however, criticized Kaij's findings on several
grounds. One criticism was the low proportion of M2 twins in the study. This raised the
possibility that some MZ twin pairs were mistakenly labelled as DZ. How this would
lower the drinking concordance rate in the D2 group relative to the M2 group was not
explained, however. A more important criticism presented by Murray's group was that
Kaij's sample was not representative of alcoholics in general. For example, alcoholics
registered with the Temperence Board were much more likely to have been convicted of
alcohol-related criminal acts than most alcoholics.

A more recent study of twins with drinking problems was conducted by Hrubec and

Omenn (1981). Hrubec and Omenn accessed records of the VA to collect data on alcohol-

8

dependent twin pairs. They found MZ twins to be more concordant than DZ twins on rates
of alcoholism, cirrhosis of the liver, and alcohol psychosis.

Murray et a1. (1983) also criticized Hrubec and Omenn's methodology. They
pointed out that overall detection rate of alcoholics among veterans in the study was lower
than would be expected. They argued that the higher concordance rate among MZ twins
than among DZ twins could be explained away if alcoholic cootwins of M2 index alcoholics
were simply identified more often than alcoholic co-twins of DZ index alcoholics. Murray
and his coworkers felt that alcoholic co-twins of M2 probands were indeed more likely to
be identified by the armed forces because their relatedness was more noticeable than that of
DZ twins.

It has been argued that twin studies which find higher concordance rates for M2 than
DZ twins do so simply because MZ twins share a more similar environment than DZ twins
(Scarr, 1968). For example, parents may be more likely to treat their children alike if the
children look identical then they may be to treat their children alike if the children do n0t
resemble one another. Such factors could lead to more concordant drinking behavior
among MZ than among DZ twins in the absence of genetic loading for alcoholism.
However, several studies have disputed this argument by examining twins whose zygosity
was incorrectly classified (Scarr and Carter-Saltzmann, 1970; Matheny, 1979). Results
showed that true zygosity, not self-perceived zygosity or zygosity perceived by parents,
determined similarity of the twins' behavior. Loehlin and Nichols' (1976) research also
helped to resolve this issue. They correlated the similarity of twin pairs‘ social
environment in childhood with the similarity of their scores on the California Personality
Inventory and National Merit Test in adolescence. Results showed little or no correlation
between similarity of social environment as children and similarity of intellectual and
personality styles in high school.

Therefore, it appears that the higher concordance rates of drinking behavior for M2

twins are not an artifact. They cannot be explained away by assuming that MZ twins share

9
a more similar environment than DZ twins. However, the concordance rates for M2 twins
are not even close to the 100% one would expect if alcoholism was caused entirely by
genetic factors. In order to differentiate the effects of nature and nurture more clearly, it is

necessary to turn to adoption studies.
5 I . S 1'

Adoption studies allow researchers to more clearly separate the effects of heredity
from the effects of environment. Assuming that the child of an alcoholic biological parent
is separated from that parent shonly after birth, it is possible to see if the child's pr0posed
genetic predisposition for alcoholism affects him even in a family environment where.
alcohol abuse does not occur.

One of the earliest adoption studies on children of alcohol abusers was conducted by
Roe and Burks (1945). Roe and her associate found that non; of the adopted-away
sample of children of alcoholics and none of their matched controls showed any symptoms
of alcohol dependence. They concluded that heredity had no influence on the development
of alcoholism. However, these results may have been biased by the fact that children of
alcoholic biological parents were more often placed in rural homes (where the opportunity
to drink was infrequent) than children of non-alcoholic parentage (Cloninger et al., 1981).
Also, because Roe and Burks never personally interviewed the natural parents, questions
have arisen as to whether fathers of the index cases were really alcoholic (Goodwin et al.,
1973). Finally, Schuckit (1980) has questioned Roe and Burks' results on the basis of
small sample size.

The adoption study which began the modern debate over the contribution of genetics
to alcoholism was that of Goodwin and his colleagues in 1974 (Murray et al., 1983).
Goodwin et al.'s (1974) sample consisted of male Danish adoptees. The index group was
made up of sons of alcoholics raised by non-alcoholic foster parents while the control

group was made up of sons of non-alcoholics paired on age and circumstances of ad0ption.

10

Data on sons of alcoholics who were raised by their biological parents was also included.
Results showed that sons of alcoholic biological parents were four times more likely to
become alcohol abusers than sons of non-alcoholic biological parents, regardless of
whether or nor an alcoholic parent raised them. However, sons of alcoholics did not differ
from controls when the dependent measure was rate of heavy drinking. These results
strongly indicated that no matter what family environment sons of alcoholics were raised
in, some type of genetic factor made them more vulnerable to alcoholism (but not to heavy
drinking).

Murray et a1. (1983) thought it curious that widening criteria for drinking pathology
to include heavy drinking totally eliminated Goodwin's argument for a genetic diathesis in
alcoholism. Pointing out that this contradicts the evidence that heavy drinking and

alcoholism are closely related, they asked:

" Could it be that Goodwin's findings are simply an artifact
produced by the tlueshold for alcoholism accidentally di-
viding heavy drinkers in the index and control group
unevenly?"

In another criticism of Goodwin's work, Fillmore (in press) suggested that Goodwin
and colleagues' results were biased because of socioeconomic (SES) differences between
the control and index group. She proposed that children of alcoholic biological parents
would be more likely to be adopted out to lower class parents than children of normal
biological parents. There is substantial evidence for the existence of social class differences
in rates of alcoholism (Zucker, 1987a); (Cahalan and Cisin, 1976); more environmental
press for deviance (i.e. alcoholism and antisocial behavior) seems to exist in lower
socioeconomic groups. Given this fact, if adopted by lower SES parents, the index group

in Goodwin's study would have been at higher risk for alcoholism simply because rates of

11

alcoholism are higher in lower class families. There would be no need to include heredity
in an explanation of group differences.

A different adoption study by Cadoret and Gath (1978) involved 84 adoptive
families. Families were recruited through the 1939-1965 adoption records of the Iowa
Childrens' and Family Services Agency. In six cases, the biological parents of the
adoptive child were judged to have been alcoholic. A significant difference was found in
alcoholism rates in the two groups such that adoptive children with an alcoholic biological
parent were much more likely to become alcohol dependent. Questions about the validity
of this study have been raised because of the use of parental interview to diagnose
alcoholism in adoptees, the differential sample loss among families with alcoholic versus
non-alcoholic adoptees, the possibility of impressionistic diagnosis of alcoholism in
biological parents by adOption agency staff, and small sample size (Murray et al., 1983);
(Fillmore, in press). However, a follow-up study by Cadoret, Troughton and O'Gorman
(1985) was much more tightly controlled. The sample was drawn from Lutheran Social
Services records. Alcoholism in the adoptees was diagnosed using DSM-III criteria during
personal interviews. To assess sample loss, adoptive families who refused to participate
were evaluated for alcohol use and found to be equivalent to participating families. The
same type of results were found as before, indicating a genetic influence on the
development of alcohol abuse for both males and females.

Some of the best data from adoption studies comes from the research of C. Robert
Cloninger and Martin Bohman. One of their studies (Cloninger, Bohman and
Sigvardsson, 1981) involved 862 male Swedish adoptees, of whom 151 had some record
of alcohol abuse. Subjects were part of the Stockholm Adoption Study. The sample
included all persons born out of wedlock between 1930 and 1949 who were placed for
adoption. Each of the adoptees, based on his drinking behavior, was classified as
belonging to one of four groups. Data about both adoptive and natural parents was

collected as well. Analysis of Cloninger et al.'s data showed a significant correlation

12

between alcohol dependence in the biological parents and alcohol dependence in the
adoptees.

The researchers also wished to know if the biological parents of severely alcohol
dependent adoptees had differed from biological parents of mildly alcohol dependent
adoptees. They were able to demonstrate the existence of two types of alcoholism in the
alcohol abusing adoptees which were associated with psychological standing of the natural
parents. One type of alcoholism (male-limited or Type II) was proposed to be highly
heritable from father to son and to result in a moderate degree of alcoholism in the son.
Supporting this hypothesis, male-limited alcoholics were found to have no excess of
alcoholic mothers. In addition, Type II alcoholism was found to be associated with
criminality and severe alcoholism in the adoptees' natural father. Therefore, in the male-
limited alcoholic, antisocial behavior and alcoholism were found to be closely linked.
Cloninger, Sigvardsson and Bohman (1988) also found that personality traits associated
with antisocial behavior such as novelty-seeking behavior and harm avoidance which were
measured in a large sample of eleven year olds predicted early-onset alcoholism (i.e. Type
2) in adulthood. Such information is important in light of studies by Vaillant (1983) and
Mchd and McCord (1962) showing that childhood antisocial behavior is a good predictor
of later alcohol problems.

The Other type of alcoholism described by Cloninger et al. (milieu-limited or Type I)
was proposed to be somewhat heritable from either biological parent and was associated
with milder alcohol dependence and no record of criminality in the natural parents. In
addition, Type I alcoholism was thought to be influenced by post-natal environmental
factors, and to result in either a mild or severe degree of alcohol abuse depending on the
degree of post-natal environmental stress. In order to reconcile these findings with
Goodwin's (1974), which implied that family environment was not important in the
development of alcoholism, Cloninger et al. (1985) suggested that Goodwin's sample

consisted of male-limited, not milieu-limited, alcoholics.

1 3
A replication of the group's results among 913 female Swedish adoptees from the

Stockholm Adoption Study (Bohman et al., 1981) confirmed the initial findings. First,
there was a three-fold excess of alcohol abusers among adopted daughters of alcoholic
biological mothers as compared to daughters of non-alcoholics. Biological fathers with a
record of criminality and severe alcoholism had very few alcoholic daughters. This is
consistent with the prediction that male-limited alcohlism is mostly passed on to sons.
However, there was a high degree of alcohol abuse among. daughters of biological parents
who were not involved in criminal activity and whose alcohol abuse was mild, supporting
the idea that milieu-limited alcoholism is heritable by either sex. Bohman et al. concluded
that alcoholism in women generally fit the Type 1 pattern.

The work of Bohman and Cloninger is important for several reasons. It not only
replicated earlier findings of a genetic contribution to alcoholism, but it was one of the firsr
pieces of literature to suggest different degrees of heritability for different types of
alcoholism. Considered from this perspective, it is possible that adoption studies such as
Roe and Burks' (1945) found no evidence for a genetic contribution to alcoholism simply
because they studied children of 'milieu limited' alcoholics in adaptive family environments
(Cloninger et al., 1985).

As stated earlier, the validity of this research can be questioned because of its reliance
on registration with the Temperence Board to define alcoholism. The fact that legal criteria
for registration with the Temperence Board changed over time calls into question the
similarity of parental alcoholics to their alcoholic offspring (Fillmore, in press). At the very
least, it may limit how generalizable Bohman and Cloninger's results are to other alcoholic
populations.

Searles (1988) has also pointed out several flaws in the Cloninger studies. He nored
that in contrast to data from epidemiological studies, Cloninger and his colleagues found no
increased risk for alcohol abuse as a funCtion of age in their sample. This could be another

indication that their sample is atypical of alcoholics in general. In addition, Searles pointed

14

out that the group's system for classifying subjects as mild, moderate or severe was
inadequate; he suggested that their findings might simply be an artifact of their criteria for
abuse.

The evidence from b0th adoption and twin studies leads to similar conclusions.
Confirming the findings from twin studies which indicated that genetic factors influenced
the development of alcoholism, most of the adoption studies found higher rates of
alcoholism among adoptees whose natural parents had been alcoholics. Although some of
the studies were methodologically flawed, the fact that replications kept producing the
same pattern of results indicates that there is indeed a genetic component to the development
of alcohol abuse. However, as a caveat, it is important to remember that it is not at all clear
that parents who give their children up for adoption are representative of the general
alcoholic population; they may show more signs of antisocial behavior (Murray et al.,
1983). Lastly, there was little consensus among adoption studies about the degree to which
pOSt-natal family environment affects genetic loading for alcoholism.

There is obviously a need for well-controlled studies which define alcoholism in a
useful way and which also have large samples such as Cloninger et al.'s (1981). Also,
there is a need for research which makes even greater disrinctions between alcoholic
subpopulations and the degree of heritability of each.

If one assumes that alcoholism is indeed influenced by genetic factors, then what
exactly is being inherited? Factors from biochemical abnormalities to temperament

differences have been implicated. The evidence for such factors will now be reviewed.

1M 25111.11”,

Schuckit (1980), in a broad overview of possible biological mediators of alcoholism,
suggested five possible mechanisms through which a genetic predisposition for alcoholism
could express itself. The first of these was that individuals at risk for alcoholism could

inherit different acute responses to doses of alcohol. For example, alcohol might produce

15

more intense pleasure for alcoholics. The second of these was that high risk individuals
might inherit different subacute reactions to alcohol. As a third mechanism through which
a genetic predisposition could express itself, Schuckit proposed that high-risk individuals
might be more vulnerable to chronic alcohol exposure than other individuals. A fourth
proposed mechanism was differences in the way individuals at risk metabolize alcohol as
compared to individuals not at risk. Finally, Schuckit suggested that high-risk individuals

might inherit factors which affected psychological parameters such as temperament.

3.] .1” 1..

It is often hypothesized that alcoholics inherit a biochemical abnormality which
somehow affects their interactions with alcohol. Schuckit and Rayses (1979) proposed that
alcoholics produce higher amounts of acetaldehyde than non-alcoholics; because
alcetaldehyde is a breakdown product of alcohol metabolism in the liver, genetic variations
in the efficiency of alcohol-metabolizing enzymes would affect acetaldehyde concentrations
in the body. To prove that this was an inherited vulnerability, Schuckit and Rayses
compared non-alcoholic subjects with a positive family history of alcoholism to matched
controls with no family history of alcoholism. Results confirmed that after drinking
alcohol, the subjects with a positive family history had significantly higher breath
concentrations of acetaldehyde. Unfortunately, attempts to replicate this important finding
have been unsuccessful (Knop, Angelo and Christensen,1981).

Another biochemical abnormality which may be inherited by alcoholics is low levels
of monoamine oxidase (MAO), an mitochondrial enzyme that catalyzes the oxidative
deamination of biogenic amines. (Faraj, Lenton, Kutner, Camp, Stammers, Lee, Lolies
and Chandora, 1987). Monoamine oxidase is involved in brain neurotransmitter
metabolism, but is also found in blood platelets. (Alcohol and Health, 1987). Initial
research suggested that chronic alcoholics had MAO levels which were lower than normal

(Oreland et al., 1983); (Faraj et al., 1987). Puchall, Coursey, Buchsbaum and Murphy

1 6
(1983) were than able to demonstrate that MAO level was genetically determined. 75

subjects with either high or low MAO levels were chosen and MAO level was correlated
with that of their parents. Results showed significant and positive correlations.

Low MAO levels have been shown to be correlated with a tendency to increase or
'augment' stimulus intensity (Buchsbaum, Landau, Murphy and Goodwin, 1973);
alcoholics as a group are likely to be stimulus augmenters (Petrie, 1967). In addition, low
MAO levels are associated with the type of fast tempo and vigorous behavioral response
style which is typical of alcoholics (Tarter, Alterrnan and Edwards 1985).

Von Knorring, Bohman, Von Knorring and Oreland (1985), building upon the work
of Cloninger and Bohman, first showed that the male- limited (highly heritable)/ milieu-
limited (somewhat heritable) typology could validly differentiate alcoholics in a clinical
setting. The typology was used to classify 31 male and five female alcoholics treated
through a university outpatient psychiatric clinic. They then demonstrated that the MAO
levels of milieu-limited alcoholics did not differ significantly from those of healthy
controls, whereas male-limited alcoholics had significantly lower MAO levels than
controls. Findings of lower MAO levels among Type 2 alcoholics were confirmed by

Pandey, Fawcett, Gibbons, Clark and Davis (1988).

E . El 1..

Some researchers feel that alcoholics inherit an anomalous brain structure which leads to
some type of neurological dysfunction. Schuckit (1984) proposed that alcoholics were less
able than non-alcoholics to use internal cues to estimate their blood alcohol level (BAL)
after drinking. His sample consisted of 23 non-alcoholic male college students with either
a positive or negative family history of alcoholism. After consuming alcohol, subjects
with a family history of alcoholism had significantly lower self-ratings of intoxication than

controls. These results indicate that alcoholics may inherit a deficit in the ability to learn to

1 7
process cues about internal state, especially when the internal state experienced is alcohol-

induced.

Several studies have been conducted on the electroencephalograms (131305) of
persons at high risk for alcoholism. Propping (1977), in a study of 52 healthy twin pairs,
showed that the extent of alcohol action on the resting EEG was under genetic control.
After giving subjects a dose of ethanol, he recorded their EEG's; EEG's of M2 twins
reacted identically to alcohol loading whereas EBG's of DZ twins became more dissimilar.
Propping and his colleagues then conducted a follow-up study on relatives of alcoholics
and matched controls (Propping, Kruger and Nark, 1981). They found that non-drinking
females with a positive family history of alcoholism had a significantly poorer EEG
synchronization than female controls. No such effect was found for males, however.

Pollock, Volavka, Mednick, Goodwin et al. (1984) found that after consuming
alcohol, 44 subjects at high risk for alcoholism could be differentiated from 28 matched
controls by their EEG alpha frequencies. Subjects in the high-risk group showed
significantly greater increases in slow alpha frequencies and decreases in fast alpha
frequencies. The researchers interpreted the results to mean that EEGs could function as a
biological marker for an inherited central nervous system (CNS) sensitivity to the effects of
alcohol among alcoholics. Gabrielli, Mednick, Volavka, Pollock et al. (1982) found that 27
young high- risk children of alcoholics showed more beta wave activity in their EEG's than
27 matched controls.

Begleiter, Porjesz, Bihari and Kissin (1984) studied visually produced event-related
brain pctentials (ERPs) among 25 non-drinking sons of alcoholic fathers and matched
controls with no family history of alcoholism. They found significant group differences in
the P3 component of the ERP. Begleiter's group proposed that because P3 potentials
reflect processes involved in revising representations stored in memory, alcoholics might

inherit deficits in memory processing.

18

While this area of research is promising, a major problem exists. Although each
study on inherited brain wave abnormalities has found subjects at high risk for alcoholism
to differ from healthy controls, two studies have rarely found the same anomalous brain
wave patterns (Peele,1986). Therefore, findings may well be sample specific. Also, none
of these studies have discussed in depth how an inherited brain abnormality would lead to

alcoholism.

War

It is also possible that alcoholics inherit a temperament that makes them more
vulnerable to alcohol abuse. Tarter, Alterman and Edwards (1985), in an elegant
discussion, identified six temperament dimensions which might play a part in vulnerability
to alcoholism. These six factors were activity level, attention span /persistence,
soothability, emotionality, reaction to food and sociability. Tarter's group presented
evidence that at least some of these temperament dimensions had a genetic component and
then discussed possible underlying biological mechanisms. This piece of work is
important because it is one of the few papers which describes how inherited biological
dysfunctions could express themselves as factors which would hinder an alcoholic's

functioning in his environment.

Sratemenmflhefimblem

After reviewing the literature, it seems clear that some genetically-based vulnerability
to alcoholism exists. Animal models have been developed which show that true-breeding,
alcohol-preferrin g strains of rats can be produced with relative ease. The evidence from
twin and adoption studies also indicates that the children of alcoholic parents inherit some

factor which places them at risk for alcoholism. However, much of the research suffers

19

from poor methodology and problems with the way in which alcoholism is defined.
Therefore, generalizability becomes questionable.

Moreover, as previously discussed, although the best evidence which supports the
theory of genetic loading for alcoholism comes from adoption studies, it is not at all clear
that parents who give their children up for adoption are representative of the general
alcoholic population. If adoption studies have indeed used samples which tend to be more
heavily involved in antisocial behavior, it is possible that alcoholism is highly heritable only
among such groups. The present study addresses this issue by studying genetic loading
for alcoholism within a sample who were not adopted out by their natural parents.

Furthermore, few studies have investigated how genetic loading for alcoholism might
influence various different drinking-related variables; those which have done so have only
considered a limited range of factors, such as frequency and amount of drinking. This
study, using male subjects, examines the relationship between genetic loading for
alcoholism (as measured by family expression of alcoholism) and age of first drunkenness,
lifetime number of areas of drinking problems, percent of the lifespan characterized by
alcohol problems and quantity-variability and frequency of drinking. In addition, alcoholic
male subjects are characterized as Type I or Type II alcoholics in order to test whether
these different drinking-related variables are more heritable among male-limited alcoholics.
Such data are unique in that they provide information on the degree to which familial (and
ostensibly genetic) density of alcoholism affects the onset, duration and severity of alcohol
problems. They also help differentiate which aspects of drinking problems are under
genetic control.

Lastly, the study examines the role of other posited factors that moderate heritability
of alcohol abuse. While the effects of factors such as environmental press for deviance (as
defined by SES), exposure to an alcoholic caretaker and antisocial behavior have been
touched upon in various studies of genetic loading for alcoholism, they have been

addressed neither simultaneously nor systematically. Due to the nature of the sample,

20

findings from this study are only generalizable to a more impulsive population in which

drinking problems are already substantial.

Hypotheses

Hypothesis 1a: There will be a positive correlation between genetic loading for alcoholism
and problems with alcohol in adulthood (i.e. early onset of drinking-related difficulties,
longer percentage of the lifespan characterized by alcohol problems, high number of
lifetime problems with alcohol and heavy intake of alcohol as defined by quantity,

frequency and variability of alcohol use).

Hypothesis 1b: Genetic loading for alcoholism will only be positively correlated with the
variables listed in Hyporhesis 1a among Type 2 alcoholics.

Hypothesis 2: Current environmental press for deviance (as defined by adult SES) will
moderate the effects of genetic loading for alcoholism. Higher SES will be related to

fewer alcohol problems in respondents.

Hypothesis 3: Environmental press for deviance during childhood (as defined by
childhood SES) will moderate the effects of genetic loading for alcoholism. Respondents
with higher SES during childhood will have fewer alcohol problems in adulthood than will
respondents with lower SES during childhood.

Hypothesis 4: Exposure to an alcoholic environment as a child (e.g. being reared by an
alcoholic) will moderate the effects of genetic loading for alcoholism. Respondents who
were reared by alcoholic parents will have more alcohol-related difficulties than those who

WCTC DOt.

Hypothesis 5: Childhood antisocial behavior will moderate the effect of genetic loading for
alcoholism. Respondents who displayed childhood antisocial behavior will have more
alcohol problems than those who did nor.

Hypothesis 6a: Adult antisocial behavior will be highly correlated with alcoholism.

21

2 2
Hyp0thesis 6b: Adult antisocial behavior will be highly correlated with alcoholism among

Type 2 but not among Type 1 alcoholics.

Methods
Meets

This study utilized data from 125 men participating in the Michigan State University
Longitudinal Study (Zucker, Noll and Fitzgerald, 1986). The larger research project uacks
the deveIOpment of a group of families with children who are at elevated risk for conducr
disorders and alcoholism because of their male gender and because their fathers are
alcoholic. These alcoholic men are identified from the population of all males convicted of
drunk driving in the mid-Michigan Tri-County area. In order to meet selection criteria,
potential respondents must have had a blood alcohol concentration (BAL) of. 15% (150
mg/ 100ml) or higher when arrested (indicating the development of substantial alcohol
tolerance) or must have had a BAL of .12% but also have had a history of an additional
alcohol-related driving offense. In addition, potential respondents must have a male
offspring between three and six years of age and must be residing with the child's mother
at initial contact. After being approached by court probation officers about the study, those
men who agree to be contacted (currently 77%) are recruited into the M.S.U. Longitudinal
Study by project staff (the acceptance rate at this stage is 90%). Subjects are screened
using items from the SMAST (Short Michigan Alcohol Screening Test; Selzer, 1975)
shortly after recruitment and again later with items from the Diagnostic Interview Schedule
(DIS Version III) (Robins, Helzer, Croughan and Ratcliffe, 1980) to verify that they do
indeed meet the Feighner research diagnostic criteria (Feighner, Robins, Winokur, Guze et.
al., 1972) for either probable or definite alcoholism. Currently, 88% of fathers in the
study meet a definite diagnosis. Participating families are compensated at the completion of
each wave of data collection; families currently receive $250 for their involvement. For the
pruposes of this study, it is desirable to have a high degree of variance in the distribution of
subjects' current level of alcohol abuse. Therefore, a subset of men has been included

who come from families which function as matched controls for the alcoholic

23

24

 

Table 1
m hi h ° ‘ f

X ( s.d.) Range
Age 30.6 (4.6) 22-47
Years of
Education 12.7 (4.0) 7 -20
Number of
Marriages 1.2 (0.5) 0 -3
Annual Family
Income $26,983 (16,294) $2,000-$62,500
Number of
Children in 2.4 (0.9) 1-5

Household

 

25

These families reside in the same census tract as high risk families and are homogeneous
with them for age of target male offspring, family economic status and neighborhood;
however, neither parent may meet Feighner criteria for alcoholism or for other drug

abuse/ dependence (see Table 1 for sample demographics).
mm

Data are collected by trained project staff who are blind to family risk status. Because
of the large volume of data collected, a number of contacts with the family are necessary,
involving 18 hours of time for each parent and seven hours of time for the target child.
These contacts include quesrionnaire sessions, semi-strucrured interviews and interactive
tasks. Six of the data collection sessions take place in the family home, while two take
place on the M.S.U. campus.

Genograms are collected from the family during the last contact of the first
assessment phase. Subjects are first asked to produce a family tree which extends back to
the grandparental generation and which includes such second degree relatives as aunts,
uncles and first cousins. First names, sex, ages and/or birthdates of each relative are
recorded if known by the subject. Subjects are then given a list of various physical and
psychological disorders (Table 2) and, for each disorder listed, asked if any of the persons
recorded on the family tree suffered from it. Any additional information provided by
subjects about their family, such as disorders not included on the standardized list, is also

recorded.

mm
In order to determine whether alcoholic subjects fit a Type I or Type II classification, -
an algorithm (Figure l) was used which utilizes the criteria laid out by Cloninger's group

(Von Knorring et al., 1985; Cloninger, 1987). The measure uses questions from the

26

Tab1e2
E .1] E .1 II] a

 

Alcoholism

Allergies or Asthma

Anemia

Arthritis (Rheumatoid Arthritis)
Cancer/ Leukemia

Color Blindness

Depression

Diabetes

Drug Abuse

Emphysema

Epilepsy/ Convulsion Disorder
Gout

Heart Problems/ Heart Disease
High Blood Pressure (Hypertension)
Hyperactivity

Kidney/ Bladder Problems
Learning Disabilities

Liver Disease

Manic Depressive Illness (Bipolar Disorder)
Nervous Breakdown
Schizophrenia

Stroke

Suicide

Tuberculosis

Tumor

Other Illness

 

a List given to respondents during the genogram interview

2 7
Meets DSM-III Criteria No _
For Alcohol Dependence Nonalcohohc

\LYes

Three of the following Social Complications
(or two if DIS aQ #164 endorsed):

 

 

 

 

 

 

 

 

1. Arguments with family about drinking
DIS # 150

2. Absent from work due to drinking
DIS #160

3. Loss of job due to drinking
DIS #161

4. Legal Difficulties due to drinking
DIS #162, 163

5. Violent while intoxicated

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

DIS #164
\
No ,
Alcohol Problems
Began Before Age 25
One of the Following Psychological
Complications: \l/NO
1. Thought I was drinking too much No
DDHb #2 .
2. Felt guilty about drinking > I Indeterminate
DDH #6 Yes
Yes
Type I or Milieu-Limited l Type II or Male-Limi ted *
Figure 1
D' fiQ'fi' [€111.51

a
b

DIS #3 refer to questions from the Diagnostic Interview Schedule-III
DDH #5 refer to items from Drinking and Drug History

2 8
D18- Version III (Robins et al., 1980) and the Drinking and Drug History (Zucker and

N011, 1980) to determine alcoholic subtype. Both these instruments provide information
about problems associated with alcohol use. Subjecrs who met Feighner criteria for
probable or definite alcoholism, whose drinking had not incurred social consequences
(such as loss of a job) and who had suffered psychological distress over their drinking
were coded as Type I alcoholics. Subjects who met Feighner criteria for probable or
definite alcoholism, whose drinking began before age 25 and whose drinking had incurred

social complications were coded as Type II alcoholics.

£12.].

111]. ”112” 5 1,25:

In order to determine degree of alcohol related difficulty over the lifecourse, the
LAPS (Zucker, 1989) was used. Information from which LAPS is determined is
provided by the DIS, Drinking and Drug History and SMAST. LAPS is a composite
score derived from three different components: age of first drunkeness, variety of
alcohol problems and life percent involving alcohol problems These three subscores
are standardized and are calculated as 1) the squared reciprocal of age at which
respondent first reported being drunk 2) the number of areas in which drinking
problems are reported and 3) the number of years between respondents' first drinking
problem and most recent drinking problem multiplied by the squared reciprocal of his
age. The measure effecrively distinguishes between _ alcoholics and non-
alcoholics and is moderately to strongly correlated with a range of external measures

of alcohol-related difficulty.

WW
To determine quantity, frequency and variability of drinking, data from the

Drinking and Drug History (Zucker and N011, 1980) was utilized. This self-report

29

questionnaire assesses amount of alcohol intake in the past six months, using an
extended version of the standardized survey questions developed by Cahalan, Cisin and
Crossley (1969). Data are coded for quantity-variability and frequency of alcohol
consumption, where frequency is a yearly figure based upon number of drinking
episodes in the past six months (doubled) and quantity-variability taps both the modal
amount of alcohol consumed on any given drinking occasion and the maximum amount
consumed when there is variation in consumption. The measure used is a revised
version of Cahalan, Cisin and Crossley's Alcohol Consumption Index: the QFV-R
(Zucker and Davies, 1989), which provides a more extended range for the measure.
Alcoholics who are not currently drinking are not included in computations that

involve either of the current consumption measures.
CW

The measure used to obtain information on alcoholism in the families of subjects is
the genogram. The genogram utilizes an interview method known as the family history
method, where subjects provide data on psychiatric and physical disorders in other family
members. (Thompson, Orvaschel, Prusoff and Kidd, 1982). Several studies have
investigated the reliability and validity of the family history method. O'Malley, Carey and
Maisto (1986) compared young adults' reports of alcohol use and alcohol-related problems
in their parents to the parents' self-report; the two were found to be highly correlated (e. g.
the Pearson correlation between students' and fathers' estimates of average monthly
consumption was .72). Thompson et al. (1982) compared subjects' reports of various
psychiatric illnesses in their relatives to diagnoses made by psychiatrists during personal
interviews. They found that the family history method generated few false positives
(specificity = .96) for alcoholism, but that subjects often classified alcoholic relatives as
unaffected, producing many false negatives (sensitivity = .57). Offspring were found to

produce the most accurate reports of illness, as compared to spouses and parents.

3 0
Thompson et al. concluded that positive diagnoses generated by the family history method

are highly likely to be accurate, but that the true incidence of alcoholism in subjects'

relatives will be underestimated.

1 Luff..- '101' in o no ' n O; ‘ :. ‘.~ 0 --t- -' harm

The FEA score is not a true measure of genetic loading for alcoholism, as it
includes data from respondents' siblings (who contribute no genetic material to the
respondent). Rather, FEA indexes respondents' genetic loading for alcoholism by
reflecting the density of alcoholism in respondents' families as well as the degree of
relatedness of these alcoholic family members to respondents. In order to assign each
subject a FEA score, alcoholic family members were identified by using the subjects'
genograms. Although genograms provided data on cousins, only data about parents,
siblings, grandparents, aunts and uncles were used in the analyses, since it became
clear that in this data set, subjects' familiarity with more distant relatives was
insufficient to allow them to accurately label these relatives as alcoholic or n0t.

Next, the degree of relatedness between the subject and each alcoholic relative
was determined. The degree of relatedness between two family members can be
expressed by a value known in human genetics as the coefficient of relationship (Figure
2). Once coefficients of relationship were detemrined for the subject and each alcoholic
relative, genetic loading scores were calculated by 1) within each generation, summing
the coefficients of relationship for all alcoholic relatives 2) multiplying this sum
by the ratio of alcoholics in each generation to the total number of family members in
that generation and 3) summing the subscores across generations. A sample

calculation of FEA is shown in Figure 3.

25"111'

The NIMH Diagnostic Interview Schedule (DIS-Version III) ( Robins et al., 1980)

was used to measure childhood and adult antisocial behavior. The DIS is a semi-

31

 

 

 

 

 

 

 

 

 

 

O I O
Grandparent (.25) I
' Grandparent Great Uncle/ Aunt O
l (.25) (.125)
Unc e/ Aunt Parent Parent FirSt Cousin
(.25) (.50) (.50) Once Removed
(.0625)
Subject Sibling
(.50)

O = Common Ancestor
O = Relative by Marriage

 

Figure 2

- .. O- . ' ' ' ‘ 0 . o
.A. . x '. . I...) I‘k‘.’ '_ '. . 1.1.! a..'".' t."

32

 

 

 

 

 

 

 

 

Grandfather Grandmother Grandfather
Alcoholism Asthma/ Allergies Heart Disease Grandmmhe"
Alzheimer's
.25
.25 .50 .50
I Mother 6
213111? lism Alcoholism
co 0
Aunt Uncle Uncle - Aunt Aunt Uncle
Kidney Problems 5 l a
J) 1.50 J] 4)
Sister Br0ther rother Sister
Alcoholism
I = alcoholic
Subject

Step 1: within each generation, sum the coefficients of relationship for all alcoholic
relatives
61: .25 + 0 = .25

G2: .25 + .50 + .50 = 1.25
G3: .50 + 0 = .50

Step 2: multiply this sum by the ratio of alcoholics in each generation to the toral
number of family members in that generation

61: (.25).25 = .06
G2: (1.25).38 = .48
G3: (.50) .20 = .10

Step 3: sum subscores across generations
FEA = .06 + .48 + .10 =.64

 

Figure 3

33

structured interview developed for use in a multisite study of rates of mental disorder in the
general population (Helzer, Robins, McEvoy, Spitnagel, Stolzmann, Farmer and
Brockington, 1985). It was designed to make diagnoses by three systems: DSM—III, the
Feighner criteria and Research Diagnostic Criteria (Robins, Helzer, Croughan and Ratcliff,
1980). Inter-rater reliability of the DIS has been reported to be high (k=.94) (Hesselbrook,
Stabenau, Hesselbrook, Mirkin and Meyer, 1982), as has its test-retest reliability
(Wittchen, Burke, Semler, Pfister, Cranach and Zandig, 1989). Validity of the DIS has
been tested by examining its concordance with the Schedule for Affective Disorders and
Schizophrenia-Lifetime (Endicott and Spitzer, 1978); agreement across diagnoses was
found to be quite high (k=.80) (Hesselbrook et al., 1982). The DIS was used to obtain a
count of the number of DSM-III symptoms of child and adult antisocial behavior

experienced by each subject.

E S . . S ESESI

Information used to rate socioeconomic status comes from the Demographic
Questionnaire (Zucker and Noll,1980). Childhood and adulthood SES of subjects was
calculated using the Duncan TSE12 Socioeconomic Index (Stevens and Featherman,
1981), an occupationally-based measure of social prestige. Significant evidence exists in
the sociological literature to suggest that occupation, not income or education, is the optimal
indicator of SES and that the perceived prestige of an occupation best captures its

underlying socioeconomic dimension (Mueller and Parcel, 1981).

WWW

To assess degree of exposure to an alcoholic environment (e. g. being reared by an
alcoholic parent or stepparent) as a child, the Demographic Questionnaire and

genograms were used. The Demographic Questionnaire identified people involved in

34

raising respondents, while genogram data provided a means for assessing drinking status
of subjects' parents and/or other primary caretakers. Degree of exposure to an alcoholic
environment was rated on a scale which assigned one point for each alcoholic involved in
raising the respondent (e.g. parents, stepparents, grandparents). An additional point was
added for any pairing of alcoholic caretakers (e.g. two alcoholic parents). Thus, a
respondent raised by an alcoholic mother would receive a score of one, whereas a
respondent raised by an alcoholic father and an alcoholic stepmother would receive a score
of three. Additional points were added for a pairing because of the potentiating effect of
having two caretakers who both agree about, rather than have conflict over, heavy

consumption (Reider, Zucker, Maguin, N011 and Fitzgerald, 1989).

Results

Pearson product-moment correlations between family expression of alcoholism and
alcohol involvement variables for the entire sample of men (including non-alcoholics) are
presented in Table 3. Correlations were significant between FEA and LAPS (p.32,
p<.001), age of first drunkeness (r,=-.28, p<.01), lifetime variety of alcohol problems
(1:.33, p<.001) and frequency of alcohol consumption in the last six months (1:.26,

p<.01).

W

Alcoholic males in the sample were further classified as either Type 1 or Type 2.
Some of these men (14%) were not codable as either type; they were excluded from these
analyses. Inspection of scatterplots of FEA and LAPS revealed distributions for Type ls
and 25 which were similar to that of the overall sample of men; no significant skewness
was found, justifying continued analyses of these two subtypes.

The two types of alcoholics were found to differ on a number of variables which
assess life difficulty. As shown in Table 4, t-tests demonstrated that Type 2 alcoholics had
significantly lower socioeconomic status (1: 2.58, p<.01). They also reported significantly
higher levels of child antisocial behavior (t=-5.86, p<.0001) and adult antisocial behavior
(1=-6.43, p<.0001) than did Type 1 alcoholics. Moreover, they experienced significantly
more separations/ divorces from their partners (t=-4.23, p<.0001). Type 2 alcoholics also
scored significantly higher on Lifetime Alcohol Problems Score (t=-3.28, p < .002).
However, the two groups did not differ significantly on consumpu'on variables such
as frequency of drinking in the past six months or quantity-variability of drinking in the

3 5

36

 

Table 3
0111'v'. _3 ' l 1.; '1 _ o ' i o ‘ thi r -_ 0 .1 chlo_ VOW 0 Mn.
MAW (n=124)
LAPS a .32 * *
Age First Drunk b --28 *
Variety C .33 * *
Life Percentd .07
WW (n=100)
Quantity-Variability .16
Frequency .26 *

 

11919.. Only current drinkers are included for the correlations involving consumption
indices.

a Lifetime Alcohol Problems Score

9 Age of First Drunkeness

C Lifetime Variety of Alcohol Problems

‘1 Life Percent Involving Alcohol Problems

e Quantity-Variability of Alcohol Consumption

fFrequency of Alcohol Consumption

*p<.01**p<.001

or..- or L ”roar-.- '

 

X (s.d.)

Typel

Socioeconomic Status
(Duncan TSE12) 35.5 (16.4)

Number of Child
Antisocial Behavior 1.7 ( 1.5)
Symptoms from DIS

Number of Adult
Antisocial Behavior 2.5 ( 1.0)
Symptoms from DIS

Number of Separations/
Divorces from Partner(s) .9 (1.0)

Lifetime Alcohol

Problems Score 9.8 ( 1.4)
QFV-R Frequency

Classification 6.2 ( 2.6)
QFV-R Quantity-

Variability Classification 13.4 ( 6.7)
Beck Depression

Inventory Score 2.6 ( 2.9)

Type2

26.2 (12.0)

4.4 (2.8)

4.4 (1.7)

2.2 (1.8)

11.2 ( 2.0)

5.9 (2.8)

15.0 ( 6.9)

3.8 ( 3.7)

2.58 *

-5.86 * * *

-6.43 * * *

-4.23 * * *

-3.28 * *

.54

-.84

-1.45

rpb

.50

.69

.71

.61

.55

.26

.32

.38

 

Note, Figures in parentheses are standard deviations.

*p<.05 **p<.01***p<.001

38

past six months. Current level of depression, as indexed by scores on the short form of
the Beck Depression Inventory (Beck and Beck, 1972) also did not differ between the two
groups.

The relationship between alcohol involvement variables and family expression of
alcoholism for Type 1 and Type 2 alcoholics is presented in Table 5. For Type 25, family
expression of alcoholism was found to be significantly positively correlated to overall
LAPS (1:.27, p<.05) and to the LAPS subscore assessing lifetime variety of alcohol
problems (p.30, p< .05). Frequency of alcohol consumption was also significantly
related to FEA (r:=.38, p _<_ .01). For Type I alcoholics, all correlations between FEA and
drinking variables were found to be non-significant. However, sample size in the Type 1
group is small; moreover, the magnitude of the relationships between FEA and drinking
variables was not significantly different in the Type 2 group than in the Type 1 group.
Therefore, initial analyses do not support the hypothesis that drinking difficulties are more
heritable among Type 2 alcoholics.

Because the FEA measure of genetic loading includes the contribution of alcoholic
parents, it is confounded with the environmental effects of being reared by an alcoholic
caretaker. In order to estimate the relationship between FEA and alcohol involvement
variables while adjusting for the effects of being reared by an alcoholic caretaker, partial
correlations were also calculated; alcoholic rearing environment was used as the control
variable.

Table 6 shows the correlations between FEA and the alcohol involvement variables
after the effects of being reared by an alcoholic were statistically controlled. For Type 2
alcoholics, the correlation between family expression of alcoholism and LAPS remained
significant (1:.28, p<.05), and virtually identical, as did the correlations between
family expression of alcoholism and lifetime variety of alcohol problems (I: .28, p<
.05) and between FEA and frequency of alcohol consumption (r: .36, p< .05). FEA and

age of first drunkeness were also found to be significantly negatively correlated ( r = -.27,

39

 

Table 5
0111’ ,9” :* gfi. ,3. Jo- 'o e A 001i gm. 10101VO’1V n 701' 0“
WW
Type 1 Type 2
WM (n=25) (n=60)
LAPS a .18 .27 *
Age First Drunk b --33 --23
Variety c .27 .30 *
we Pcrcentd ’.18 '20]
WW (n=20) (n=42)
Quantity-Variability -.14 .26
Frequency .03 .38 * *

 

151912, Only current drinkers are included for the correlations involving consumption

indices.

a Lifetime Alcohol Problems Score

b Age of First Drunkeness

9 Lifetime Variety of Alcohol Problems

‘1 Life Percent Involving Alcohol Problems

e Quantity-Variability of Alcohol Consumption
fFrequency of Alcohol Consumption

*p<.05 **ps.01

4O

 

Table 6
-02 ‘ltru =' "v.1! 1).. .u‘ or o a. on n 1.9. a- no ,rVVO'n'r 0 .40;
V T»; ‘ ochli L r onus in r '41 1A1 0011115 Ll ’ ‘- 'n
Enzircnment
Type 1 Type 2
1 1 1 1 ((1:25) (n=60)
LAPS a -.21'*' .28 * +
Age First Drunk b .13 -.27 *
Variety C _ -.01 .28 *
Life Percent d '35 -02
WWW (n=20) (n=42)
Quantity-Variability -.35 .17
Frequency -.15 .36 *

 

1191;, Only current drinkers are included for the correlations involving consumption
indices.

a Lifetime Alcohol Problems Score

9 Age of First Drunkeness

C Lifetime Variety of Alcohol Problems

‘1 Life Percent Involving Alcohol Problems

3 Quantity-Variability of Alcohol Consumption

fFrequency of Alcohol Consumption

*
p < .05
+ coefficients with this superscript differ significantly from each Other (p< .05)

41

p<.05). Therefore, these relationships are unaffected by rearing environment. In contrast,
for Type 1 alcoholics correlations between FEA and drinking variables remained non-
significant, but the direction of the relationship was now found to be Opposite from that
originally Observed. In addition, a significant difference was now found in the
magnitude Of the correlation between FEA and LAPS for Type 1 and Type 2 alcoholics (;=
2.00, p< .05). The fact that partialling out the shared variance between FEA and alcoholic
rearing environment differentially affected the relationship between FEA and LAPS for
Type 15 versus Type 25 is consistent with findings that a significant difference (7,: 2.14, p
< .05) existed in the magnitude of the correlation between FEA and rearing environment for

Type 15 (1:39, p < .01) and Type 25 (x=.74, p < .01).

31.1.] ”1.51112” 5
10! l'fiE'Efi 1.

Correlations between life difficulty variables for Type 2 alcoholics are presented in
Table 7 (figures below the diagonal). For these men, LAPS was found to be significantly
positively correlated with childhood antisocial behavior (p.39, p< .01) and adult antisocial
behavior (1: .41, p<.01) as well as with FEA (1:.27, p<.05). Childhood antisocial
behavior was also positively correlated with adult antisocial behavior (p.31, p<.05). NO
significant relationship between LAPS and socioeconomic status was found. However,
childhood antisocial behavior was found to be negatively correlated with adult SES (3:: -
.32, p<.05). Adult antisocial behavior was also negatively correlated with adult SES (1‘: -
.36, p<.01).

Table 7 also shows the relationships between life difficulty variables for Type 1
alcoholics (figures above the diagonal). Probably as a result Of low power, few correlations
were significant. Patterns were also different from those found in the Type 2 group.
For Type 1 men, LAPS was found to be significantly correlated only with being reared
in an alcoholic environment $.42, p< .05); neither childhood nor adulthood antisocial

42

 

Table 7

our tun tutor: f hi! - a Vat-1' f0 , n; = t u 1—01.
mm '

CASBa AASBb FEAC csr~:s<l A5556 LAPsf REARENVS

CASB .33 04 .20 - 15 .03 .17
AASB .31 "' .23 .04 -.26 .21 .23
FEA .16 .07 -.17 .14 .19 .74 * *
CSES .03 -.14 .01 .59 "' "' .04 .10
ASES -.32 * -.36 "' "' -.12 .14 -.28 .03
LAPS .39 * * .41 r r .27 * .10 -.19 .42 * *
REARENV -.01 -.19 .39 " "' -.09 -.09 .03

 

1191;, Correlations above the diagonal are for Type 1 alcoholic men; those below the
diagonal are for Type 2 alcoholic men

aNumber Of Child Antisocial Behavior Symptoms from DIS
bNumber Of Adult Antisocial Behavior Symptoms from DIS
CFamily Expression of Alcoholism

dChild Socioeconomic Status (Duncan Socioeconomic Index)
cAdult Socioeconomic Status (Duncan Socioeconomic Index)

1lifetime Alcohol Problem Score
8Alcoholic Rearing Environment

*p<.05 **p<.01

43

behavior were significantly correlated with LAPS. Childhood socioeconomic status was

positively correlated with adult socioeconomic status (1: .59, p<.01).

W

The analyses presented so far clearly point tO the appropriateness Of a developmental
conceptualization of more than one type of alcoholism, each with its separate causal
chain. In order to test this statistically, a stacked LISREL (Joreskog and Sorbom,1978)
analysis was performed. A stacked group analysis allows a statistical test of the
appropriateness of using different path models for two or more mutually exclusive groups.
A stacked LISREL model is first estimated with effect coefficients constrained to be equal
between groups (hereafter called the combined model); the model is then reestimated with
effect coefficients allowed to vary for groups (hereafter called separate models). The
difference chi-square for combined versus separate models then provides a test of the
goodness of fit when models for the two groups are allowed to differ.

The stacked groups analysis involved three of the most distal predictors of lifetime
alcohol problems: family expression of alcoholism, alcoholic rearing environment and
childhood antisocial behavior. In the combined model, childhood antisocial behavior, FEA
and alcoholic rearing environment were all used as predictors of LAPS. For the separate
models, alcoholic rearing environment was used to predict LAPS among Type 1 alcoholics
and FEA and childhood antisocial behavior were used to predict LAPS among Type 2
alcoholics; these submodels were chosen based upon preliminary LISREL analyses (see
Figure 6, Appendix A). LAPS was selected as the dependent variable for these analyses
rather than a dummy variable coded as alcoholic /nonalcoholic because it more adequately
characterizes the variation in extent of alcohol problems than does a binary characterization
schema; in addition, the score is highly correlated with alcohol dependence Inon-

dependence.

4 4
Figure 4 presents the results of this LISREL analysis. The difference chi-square for

combined versus separate models for Type 1 and Type 2 alcoholics is significant at the .05
level, indicating that the data fits significantly better when different models are allowed.
Moreover, the combined model explains only 13 percent of the variance in LAPS, while the
separate models respecrively account for 18 percent and 20 percent Of the variance in
LAPS. Type 1 alcoholism is best predicted by alcoholic rearing environment while Type 2
alcoholism is predicted by childhood antisocial behavior and FEA.

Because of small sample size in the Type 1 group, few life difficulty variables are
significantly related. Thus, the unitary path presented in Figure 4 remains the best model Of
Type 1 alcoholism; alcoholic rearing environment remains the only significant predictor of
later alcohol problems for this data set. An expanded path model for Type 2 alcoholics
which best fits the data is shown in Figure 5. The model shows that childhood antisocial
behavior has both a direct effect on alcoholism and an indirect effect through its relationship
to adult antisocial behavior. FEA misses significance at the .05 level in the path model, but
is retained because of its significance in the univariate correlations and because it remains a

trend (p< .10).

45
Combined model for Type 1 and Type 2 Alcoholics

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

r 2 = .13
Childhood Antisocial Behavior .26 e u
.10
.19 \ .
Family Expression of Alcoholism / LAPS
.04 ‘
52 "'
[Alcoholic Rearing Environment at: p < .05 III at- p < .01
Chi-Square with 7 d.f.= 11.57
Separate models for Type 1 and Type 2 Alcoholics
Type 1
1’ 2 = 18
.42 . l ,
Alcoholic Rearing Environment I \
l / . LAPS
Type 2
r2=20
1
Childhood Antisocial Behavior N
.16 LAPS
.21+

 

 

 

 

Family Expression of Alcoholism

 

 

+p<.10 *p<.05 **p<.01

 

Chi-Square with 3 d.f.= 1.40

Difference Chi-Square for combined versus separate models: X = 10.17, p < .05

 

Figure4

Wes

46

 

 

 

 

 

 

 

 

 

.25 “' \
Childhood ASB / Adult ASB
.31 * *
.16 $7 up at
- + .,.___.
I Family Expression Of Alcoholism I '21 ‘% LAPS @— r 2 = .27
I l , ,

 

 

 

 

 

+p<.10 *p<.05 **p<.01

Figure5
n lfr

Discussion

The research literature clearly points to a genetically-based diathesis in the etiology of
some forms of alcoholism. Although the Washington University group has begun to
addressthe que5tion of how inherited factors might affect the developmental course of
alcoholism (Cloninger, 1987), the role of other variables which might systematically affect
the relationship of genetic loading for alcoholism to alcohol related problems (e. g. onset,
density, severity) is still in its infancy. In addition, the role of Other variables which might
systematically affect the relationship of genetic loading for alcoholism to alcohol-related
problems has not yet been systematically addressed. The present study replicates those
earlier studies which implicate genetic factors in the etiology of alcoholism. In addition, it
specifies more clearly the domains of possible genetic influence during the lifespan and the
effects of variables such as socioeconomic status and antisocial behavior as they interact
with genetic loading for alcoholism.

Hypothesis la predicted that a positive correlation would be found between genetic
loading for alcoholism and problems with alcohol in adulthood. Supporting this
hypothesis, significant positive correlations were found for the overall sample between
family expression of alcoholism and LAPS. This finding reaffirms the role of genetic
vulnerability in later alcohol-related difficulties. The result also parallels findings from
adoption and twin studies. In addition, the present findings more clearly link respondents'
alcohol problems tO those in the respondents' extended families in addition tO those of their
parents.

Two Of the LAPS subscores, age of first drunkeness and lifetime variety of alcohol
problems, were also found to be positively correlated with family expression of
alcoholism. These findings imply that genetic factors play a role in determining both the
onset of alcoholism, that is, the age at which alcohol use first becomes problematic, and the

severity, or pervasiveness, of alcohol problems during the lifespan. Inherited factors

47

48

appear to affect the course of drinking problems over the lifespan by providing an
additional push toward earlier alcohol abuse; earlier use likely provides more Opportunity
for a wide range of alcohol problems tO develop. This finding is in contrast to those of
Vaillant (1989), who has suggested that age of onset of alcoholism is uncorrelated with
genetic load and is driven purely by environmental factors.

The correlation between the third LAPS subscore, life percent, and FEA was low
order and non-significant, lending no support to Hypothesis 1a. This subscore quantifies
the extent of invasiveness of alcohol problems; one possible explanation for the non-
significant correlation is that the length of time that alcohol-related difficulties persist is
impacred by numerous environmental factors which act to control drinking, such as family
pressure to stop drinking and court-ordered involvement in rehabilitation programs after
drunk driving arrests. These factors would be anticipated to affect duration Of drinking
problems much more directly than would genetic loading for alcoholism.

FEA was also found to be positively correlated with one of the alcohol consumption
indices: frequency. Earlier studies, such as those Of Kaij (1960), Partanen (1966) and
Kaprio et al. (1987) have indicated that there are genetic effects upon such drinking
variables as frequency and density Of alcohol consumption. However, family expression of
alcoholism is a lifetime measure whereas the frequency variable indexes current alcohol
consumption; consumption might be expected to fluctuate Over time and therefore to be
uncorrelated with FEA. Findings from the present study demonstrate that family
expression of alcoholism can in fact predict both current and lifetime drinking problems.

Hypothesis 1b predicted that once alcoholic males in the sample were divided by
subtype, genetic loading for alcoholism would only be positively correlated with alcohol
problem and consumption variables among Type 2 alcoholics. Before completing the
genetic analyses, comparisons were made between the two groups on other life difficulty
variables in order to confirm that Type 15 and Type 25 were distinctive enough and that

further analyses were warranted.

49

Comparisons between the two groups demonstrated that bOth types currently
experienced similar rates of current alcohol consumption. However, Type 2 alcoholics
reported significantly higher scores on LAPS. As expected, Type 2 alcoholics also
reported significantly higher levels of childhood and adult antisocial behavior, such as
difficulty maintaining stable relationships with partners. In addition, they had significantly
lower adult (i.e. achieved) socioeconomic status, although no differences were noted in
childhood SES (an index Of social class origins).

These data indicate that the alcoholic sample may seem homogeneous when
characterized by way of alcohol consumption, but that Type 1 and Type 2 alcoholics are
actually quite different in their life experiences. The data suggest that the course of Type 1
alcoholism is more benign, since the consequences of drinking do not invade as much of
the lifespace. The distinctiveness of Type 15 and 25 supports the concept Of different
etiological pathways into alcoholism, which is addressed in more detail by the LISREL
analyses.

Significant positive correlations were found for Type 2 alcoholics between LAPS, the
LAPS subscore lifetime variety of alcohol problems, current frequency of alcohol
consumption and family expression Of alcoholism. Although all correlations between FEA
and drinking variables were found to be non-significant for Type 1 alcoholics, power was
low in this group due to small sample size. Thus, the possibility that family expression of
alcoholism did in fact predict later alcohol problems among Type 15 cannot be ruled out. In
addition, the magnitude Of the relationship between FEA and drinking variables was not
significantly different between the Type 1 and Type 2 groups. Therefore, initial findings
provided no support for Hypothesis 1b, because they do not confirm that alcohol-related
problems are more heritable among Type 2 alcoholics. However, the FEA measure of
genetic loading is confounded by the effects of being reared by an alcoholic caretaker;

because the Cloninger et al. (1981) data indicate that post-natal environment differentially

5 0
affects Type 1 and Type 2 alcoholics, analyses were rerun while adjusting for the effect of

being reared in an alcoholic environment.

Hypothesis lb was now supported by the data; significant differences were now
found in the magnitude of the correlation between family expression Of alcoholism and
LAPS for Type 1 and Type 25. These findings suggest that the magnitude of the initial
correlation between LAPS and family expression of alcoholism for Type 1 alcoholics is
accounted for by the inclusion of alcoholic biological parents, who for the most part reared
the respondent, as well as contributing to his genetic makeup. Once the confounding
effects of rearing environment are controlled, the data clearly indicate that genetic loading
for alcoholism plays a much more important role in the development of alcoholism among
Type 2 than among Type 1 alcoholics. On the other hand, removing environmental effects
from the correlation between LAPS and FEA clearly shows the importance of alcoholic
rearing environment in the etiology of Type 1 alcoholism.

The differences which appear between Type 1 and Type 2 alcoholics on the genetic-
environmental continuum are similar to distinctions made by Zucker (1987a) in his
discussion of alcoholic typologies. He suggests that antisocial alcoholism (i.e. Type 2) has
a heavy genetic diathesis; moreover, he proposes that a history of socialization to
aggression, not necessarily to excessive alcohol consumption, is a necessary etiologic
factor. On the other hand, in developmentally cumulative alcoholism (i.e. Type 1) any
potential genetic diathesis is proposed tO be environmentally mediated; it is the role of
socialization involving exposure to an alcoholic parent and leading the future alcoholic to

regard alcohol use as a c0ping mechanism which is seen as vital.

li.t 0 .r‘ «_I-J' Hih‘v'um 1- 0-1x. 4 H091

Hypotheses 2 through 6 predicted that adult socioeconomic status, childhood

socioeconOmic status, alcoholic rearing environment, childhood antisocial behavior and

5 1
adult antisocial behavior would also affect the extent of lifetime alcohol-related difficulties.

These hypotheses were tested through univariate correlations and, in a more complex
manner, through path analysis.

Univariate correlations lend support to both Hypothesis 5 and HypOthesis 6b. Child
and adult antisocial behavior were found to be significantly related to LAPS among Type 2
alcoholics but not among Type 15. At one level, this is yet another confirmation of
widespread research findings which suggest that early onset antisocial behavior which
continues over the lifespan is systematically correlated with alcohol-related difficulty in
adulthood (McCord and McCord, 1962; Zucker and Gomberg, 1986). However, the fact
that the correlation between childhood antisocial behavior and LAPS is close to zero for
Type 1 alcoholics suggests that early delinquency is only one route into alcohol problems.
Other routes may a) not be as dependent upon childhood antisociality as they are upon
other childhood influences b) be susceptible to developmentally later influences or c)
involve some combination of these two sets of contributory effects. Further research
should investigate these other potential sources of effect.

Data from the univariate correlations also supported Hypothesis 4. Rearing by an
alcoholic caretaker was found to be significantly correlated with LAPS among Type 1
alcoholics, indicating, as previously discussed, the importance for this group of early
exposure to alcohol abuse.

No support was found in the univariate analyses for a direct effect of either adult
socioeconomic status or childhood socioeconomic status on lifetime alcohol problems
(Hypotheses 2 and 3). It should be noted that the general lack of significant relationships
between variables in the Type 1 group may well be due to small sample size, resulting in
low power. An alternative explanation, that variables which are etiologic in Type 1
alcoholism were not adequately addressed in this study, will be discussed later.

Both analyses of the relationship between family expression Of alcoholism and

drinking variables, and those involving LAPS and the non-drinking variables which might

5 2
have a potentiating effect on genetic loading for alcoholism, suggest that different factors

play a role in the development of alcoholism for Type 15 and 25. Supporting the hypothesis
that Type 15 and 25 are developmentally distinct, a stacked groups LISREL analysis
confirmed that in order to provide the best fit for the data, different models should be used
for the two groups. Out of four potential distal predictors of later alcohol problems (i.e.
family expression of alcoholism, childhood antisocial behavior, childhood SES and
alcoholic rearing environment), family expression of alcoholism and childhood antisocial
behavior are precursive to alcohol difficulties for Type 2 alcoholics. Exposure to an
alcoholic rearing environment is predictive of later alcohol problems for Type 15.

For Type 2 alcoholics, the preliminary path model can be expanded to included more
proximal predictors Of alcohol difficulties. In this expanded path model, both adult
antisocial behavior and LAPS were used as dependent variables. This approach was taken
because the direction of causality between antisocial behavior and LAPS was not indicated
by the LISREL analyses and also because other research in this area has failed to specify
which of these two variables is precursive (Cadoret et al., 1985). It is likely, in fact, that
antisocial behavior and alcoholism act synergistically, each driving the other. The
expanded path model also shows that childhood antisocial behavior continues to have a
direct effect on lifetime alcohol problems, but also influences these problems indirectly
through adult ASB. Thus, delinquent behavior as a child is predictive of antisociality in
adulthood, which as discussed above, drives alcohol problems.

The expanded path model for Type 25 indicates that family expression of alcoholism
makes a seperate contribution to LAPS which is not mediated by other variables. It also
shows that FEA makes a genetic contribution which is specific to alcoholism, as FEA does
not predict antisocial behavior. Therefore, although this data set does not elaborate the
mechanism through which genetic predisposition for alcoholism is expressed, it indicates

that the mechanism may well be alcoholism-specific for this subtype.

5 3
Therefore, path analysis provides further confimation of Hypotheses 5 and 6. Type

2 alcoholism, then, can be explained as a function of antisocial behavior over the life course
and genetic loading for alcoholism. These findings extend recent work by Cloninger,
Sigvardsson, and Bohman (1988) which suggests that in very young adolescents,
personality traits associated with antisocial behavior are predictive of Type 2, but not Type
1 alcoholism in adulthood.

For Type 1 alcoholics, exposure to an alcoholic rearing environment remains the only
variable which predicts later problems with alcohol use. One possible reason (besides low
power) why the data may not be capturing the developmental course of Type 1 alcoholism
is that variables etiologic to this form of alcoholism may not have been included in these
analyses. Zucker (1987a) suggests that adolescent problem drinking becomes
developmentally cumulative alcoholism (i.e. Type 1) when poor career and marital
adaptations occur, providing the alcoholic with fewer external resources upon which to
draw. Therefore, in order to properly capture the path to alcohol difficulties for Type 1
alcoholics, the nature of Type 15' intimate relationships and career satisfaction probably

need to be assessed.

E 13"

This study was able to replicate findings by a number of other researchers that genetic
loading contributes to the development of alcoholism. However, the nature of the data (i.e.
the genograms) used to measure familial alcoholism was somewhat imprecise and possibly
of lower reliability. Other familial-genetic researchers, such as Thompson et. al. (1982)
have gained access to populations where personal interviews with extended family

members can be conducted. Replication of results presented in this study with data

54

obtained from collateral informants would be another step which should be pursued by
investigators who are interested in the developmental role of genetics in alcoholism.

Although many variables which lead to the development of Type 2 alcoholism were
identified here, the available data set failed to adequately describe Type 1 alcoholism.
Further investigation is necessary to identify those developmental factors which push the
Type 1 alcoholic to experience drinking difficulties; intimate relationships in childhood and
adulthood as well as career satisfaction may well be fruitful areas for study. Differences in
the experience of depression may be anOther.

It is important to note that results from this study are limited to men. They do not
provided any information about the relationship between genetic loading for alcoholism and
drinking problems among women, nor about the developmental course of alcoholism in
women. Although Cloninger et al. (1987) suggest an etiologic process for alcoholic
women which is similar to that of Type 1 men, use of a broader variable domain may well
reveal a different path into alcohol problems for females. Future research should also
attempt to apply the antisocial alcoholic/ non-antisocial alcoholic dichotomy to women in
order to evaluate its possible relationship to an inherited predisposition to alcoholism across
both sexes.

Summary

Current etiologic research strongly suggests that genetic vulnerability plays a role in
the development of alcoholism. Studies using animal models have demonstrated that strain
and line differences exist in the acquistion of alcohol preference, sensitivity, tolerance and
dependence. Evidence which impinges more directly on alcoholism in humans comes from
family studies. Several sources have shown that alcoholics are significantly more likely
than non-alcoholics to have alcoholic parents, siblings and children. Both twin and
adoption studies, traditional behavioral genetic tools for analyzing heritability, have also

been used to investigate the etiology of alcoholism. Findings from these studies also

55

indicate that children of alcoholics inherit some factor which puts them at risk for
alcoholism.

However, few researchers have related genetic loading for alcoholism to a broad
range of drinking-related variables; thus, the issue of precisely what might be inherited
remains unclear. In addition, prior studies have only crudely assessed the effect of other
factors such as environmental press for deviance, antisocial behavior and exposure to an
alcoholic parent as these might moderate genetic vulnerability. Therefore, the present study,
which used a population-based sample and a broadly based set of independent variables,
was able to more clearly examine these potential contributory effects.

An addition question of significance was the extent to which earlier work on two
types of alcoholism (Cloninger's male-limited and milieu-limited types) could be replicated.
Should this be possible, the study also planned to model the contributory role of Other
psychosocial factors than those originally posited by Cloninger's group.

Results of the study confirmed bOth the effects of genetic loading for alcoholism and
the impact of other variables upon alcohol-related difficulties in adulthood. Positive
correlations were found between family expression of alcoholism and lifetime alcohol
problem score, as well as between FEA and two LAPS subscores: age of first drunkenness
and lifetime variety of alcohol problems. Frequency of alcohol use was also found to be
positively correlated with family expression of alcoholism.

The role of genetic loading for alcoholism in later alcohol problems was also found to
be different among Type 1 and Type 2 alcoholics. For Type 25, genetic loading for
alcoholism contributed strongly to the later development of alcoholism, whereas for Type
15, being reared in an alcoholic environment, rather than inheritance of a predisposition to
alcoholism, was key.

Finally, childhood and adulthood antisocial behavior were found to contribute
heavily to the etiology of Type 2 alcoholism; therefore, a history of socialization to

aggression, rather than to excessive alcohol consumption, is suggested as an etiologic

5 6
factor for this type of alcoholism. For Type 1 alcoholics, no variables other than alcoholic

rearing environment were found to be related to adult alcoholism. Thus, the role of
socialization involving exposure to an alcoholic caretaker, which leads to heavy use of
alcohol as a coping mechanism, was the only etiologic factor identified for Type 15.

This study replicates findings by a number of researchers which demonstrate that
genetic loading contributes to the development of alcoholism; at the same time, it specifies a
particular alcoholic subset for whom genetic predisposition to alcoholism is a necessary
etiologic factor. In addition, results more clearly link respondents' alcohol problems to
those in their extended families. Finally, the study demonstrates the importance of other
factors, such as being reared in an alcoholic environment and antisocial behavior, in the
etiology of alcoholism. It remains for future research to more fully chart these etiologic

pathways.

List of Appendices

Appendix A
Full Models of Distal Predictors of LAPS for Typels and Type 25

57

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

, r 2 = .22
[ Childhood Antisocial Behavior _.07
.04
-.30
.17 Farrrily Expression of Alcoholism > LAPS
.74 * *
Alcoholic Rearing Environment .65 o it
* * p < .01
r 2 = .20
.16 Childhood Antisocial Behavior 36\ \L
-_01 .23+
Family Expression of Alcoholism > LAPS
.39" *
-.06
Alcoholic Rearing Environment

 

 

 

+p<.10 **p<.01

 

Figure 6
Full Models of Digal Predictfi of LAPS for Tm 1 and Type; 2 Alcoholics

 

 

Appendix B
Demographic Questionnaire

58

 

 

 

OEHO ll/89
Respondent Number:
Given By:
Date:
ngHlGAN STATE UNIVERSITY Tl.0
FAMILY ERQJECT Ans. Chk:

 

East Lansing. Hichigan 48824

Background information

We would like to ask you a few questions about yourself. The questions ask
about your life during the time you were growing up as well as now. Please
answer gll of them as completely as possible. (PLEASE PRINT).

1. What is your date of birth?

 

 

 

MONTH DAY YEAR

2. Where were you born?

 

 

CITY/TOWN (COUNTY 1F RURAL) STATE COUNTRY (IF NOT U.S.)

3. Where did you live most of the time until you were 18?

 

 

CITY/TOWN (COUNTY lF RURAL) STATE COUNTRY (lF NOT U.S.)
4. Until you were 18. about how many times did your family move.
CIRCLE ONE 0 l 2 3 4 5 6 7 or more.

5a. Did you live together with both of your natural parents for most of the
time from birth to 18? ClRCLE ONE.

YES (if Yes. go to question 6) N0 (if NO. go to question 5b)

so. What was the main reason your parents did not live together with you
during that time? CIRCLE ONE

1. Hother died

2. Father died

3. Both parents died
4. Parents divorced or separated
5. Parents never lived together
6. Other (Please explain)

 

 

:59

So. Which adultis) did you live with most of the time from birth to 18?
CIRCLE ONE.

 

2. Mother. but no adult male

3. Father. but no adult female
4. Mother and step-father
5. Father and step-mother
6. Other (Please explain)

 

 

6. Who was the main wage earner in your home while you were growing up?
CHECK ONE

(a) your father
(b) your mother
(c) someone else
What was their relationship to you

 

ABOUT YOUR NATURAL (BIOLOGICAL) Fxrggg

7a. Where was he born?

 

 

STATE COUNTRY (IF NOT U.S.)

ABOUT THE ADULT HALE WHO LIVED WITH YOU NOST OF Tߤ7TIHE UNTIL YOU WERE 18.
(This could be your natural father. or stepfather. or someone else).

7b. What kind of work did this adult male do (the adult male who lived
with you most of the time until you were 18?) That is.
what was his occupation?

 

 

(For example: electrical engineer. machinist. stock clerk. assembly line
worker. farmer)

7c. What were his most important activities or duties?

 

(For example: keep account books. filing. selling cars. operate printing
press. finish concrete)

7d. What kind of business or industry was this?

 

(For exarrple: TV and radio mfg.. Retail shoe store. Automobile
manufacturing [Oldsmobile]. State Labor Dept.. Farm work)

7e. What was the highest grade of school he completed?

CIRCLE THE HIGHEST GRADE COHPLETED.

None 0

Elementary l 2 3 4 5 6 7 8
High School 9 10 ll 12

College I 2 3 4 Degree?
Graduate School 5 6 7 8+ Degree?

6O

AGAIN, A QUESTION ABOUT YOUR NATURAL (BIOLOGICAL) FATHER

7f. How would you describe his primary cultural/ethnic heritage? CIRCLE ONE

(a) White (d) Native American (American Indian)
(b) Black (e) Asian/Asian American
(c) Hispanic/Hispanic-American (f) Other (describe)

 

 

AQOUT YOUR NATURAL (BIOLOGICAL) HOTHER

8a. Where was she born?
STATE COUNTRY--IF NOT U.S.

ABOUT THE ADULT FEEALE WHO LIVED WITH YOU HOST OF THE TIHE UNTIL YOU WERE ID.

(This could be your natural mother. or stepmother. or someone else).

 

 

so. What kind of work did this adult female do (the adult female who lived with
you most of the time until you were ID?) That is. what was her occupation?

 

 

(For example: electrical engineer. file clerk. assembly line worker
bookkeeper. sales clerk)

Be. What were her most important activities or duties?

 

(For example: keep account books. filing. selling clothing. teach fifth
graders)

8d. What kind of business or industry was this?

 

(For example: TV and radio mfg.. Retail shoe store. Automobile
manufacturing [Oldsmobile]. State Labor Dept.)

Be. What was the highest grade of school she completed?

CIRCLE THE HIGHEST GRADE COMPLETED.

None 0

Elementary l 2 3 4 5 6 7 8
High School 9 10 ll 12

College l 2 3 4 Degree?
Graduate School 5 6 7 8+ Degree?

AQAIN. A QUESTION ABOUT YOUR NATURAL (BIOLOGICAL) HOTHE :

Of. How would you describe her primary cultural/ethnic heritage?

ClRCLE ONE

(a) White (d) Native American (American indian)
(b) Black (e) Asian/Asian American

(c) Hispanic/Hispanic-American (f) Other (describe)

 

 

3 of 6

61

 

 

 

 

 

 

 

 

9a. Until you were 18. what religion was practiced in your home most of
the time? CIRCLE ONE
l. Protestant
2. Roman Catholic
3. Jewish
4. None. no religion
5. Other religion (please explain)
9b. What denomination? (please try to specify fully)
9c. Until you were 18. how often did you attend religious services?
ClRCLE ONE
1. several times a week
2. about once a week
3. 2-3 times a month
4. once a month or less
5. never
lOa. What is your religious preference 99!? CIRCLE ONE
I. Protestant
2. Roman Catholic
3. Jewish
4. None. no religion
5. Other religion (please explain
10b. What denomination? (please try to specify fully)
lOc. About how often did you attend religious services in the lastgyear?
CIRCLE ONE
l. several times a week
2. about once a week
3. 2-3 times a month
4. once a month or less
5. never
10d. Regardless of your attendance at religious services. how religious do

you consider yourself to be?

I.
2.
3.
4.

not religious at all
not very religious
fairly religious
very religious

4 of 6

62

ll. What was the highest grade you completed? CIRCLE THE HIGHEST GRADE

COMPLETED.

None 0

Elementary l 2 3 4 S 6 7 8
High School 9 ID II 12

Post High School

Voc-Tech School I 2 3
College I 2 3 4 Degree?
Graduate School 5 6 7 8+ Degree?

I2a. What kind of work are you doing (what is your occupation)?

 

 

(For example: electrical engineer. machinist. stock clerk. assembly line
worker. teacher. farmer)

12b. What are your most important activities or duties?

 

(For example: keep account books. filing. selling cars. operate printing
press. finish concrete. teach fifth graders. answer phone).

I2c. What kind of business or industry is this?

 

(For example: TV and radio mfg.. Retail shoe store. Automobile
manufacturing [Oldsmobile]. State Labor Dept.. Farm work)
IZd. Are you: CHECK ONE

an employee of a PRIVATE company. business or individual for wages.
salary. or commission?

a GOVERNMENT employee (federal. state. county. or local government?
self-employed in OWN business. professional practice. or farm?

own business not incorporated

own business incorporated

working WITHOUT pay in a family business or farm

IZe. Approximately what is your present annual family income?

CIRCLE ONE
I. under 54.000 6. $16.00I--$20.000
2. S 4.001-$ 7.000 7. $20.001--S30.000
3. 8 7.001--310.000 8. 830.00I-$S0.000
4. $i0.001-813.000 9. $50.00l--875.000
5. $13.001--316.000 IO. over 375.000

5 of 6

I3.

l4a.

14b.

lSa.

15b.

63

How many times have you been married? CIRCLE ONE
0 l 2 3 4+

What was the date of your marriage to your (present) spouse?

 

If married more than once. what was the date
of your first marriage?

 

List the children you have had from your present marriage or any
previous marriages. Please list all children. starting with the
oldest. and include birthdate. sex. and check ( '0 if the child

lives with you now.

FIRST NAHE ONLY BIRTHDATE SEX LIVING N91
(mo/day/Year) WITH YOU LIVING WITH
NOW YOU NOW

 

 

 

 

 

 

 

 

Now please circle the names of the children you listed in
Question ISa above who are from your present marriage. If all are
from your present marriage Just check a mark here .

THANK YOU FOR FILLING OUT THIS QUESTIONNAIRE

6 of 6

Appendix C
Diagnosdc Interview Schedule

64

DIAGNOSTIC INTERVIEW SCHEDULE DECK 01

Version III (5/81)

 

 

 

 

 

 

 

 

 

 

 

 

Emily Nuuber: '0 CODE
. . oooooooooo
3”” cm oooooooooo
mu H” “mm oooooooooo
mt: pasmmmpos: 3:3?“ i'v- 8888888888
.m: oooooooooo
“ 00 ooooeooooo
888888M°°
AM W
””“m"“' m ooooeooooo
, OM
ON
1. RECORD SEX A3 OBSERVED.
0 MALE ..................................... O
FEMALE ................................... Q 131
2. Howoldwereyouonyourlasibinhdey?
o
. o oooooooo W
“mma ooooeooooo

a What is your oil-thesis?

06
”WWE:] ggggoooooo
16/
“'[13 oooooooooo
ma ooooeooooo
[I] oooooooooo

a Areyoupmentlymernedorareyouwidowed.seperammivoroedmrheveyouneverbeenmarned?

Married .................................... <0 22/
Widowed ........ (sumi To a. s) .......... Q
sow-Ice ....... (SKIP TO 0. s) .......... O
Divan-o ........ (skip To 0. e) .......... G
mm....IskIPTo 0.5) .......... O
a Are you currently living with your (husband/wile)?
No .............. (SKIP To 0. '7) .......... 0 2:1
m ............. (SKIP To 0. 7) .......... 0

a Anyoueumnllyuvingwiihsomeoneuthoughyouweremarried?
No ........................................ 0 24/

IIF NEVER MARRIED. GO TO 0. 11 I

1

65

DECK 09
1 . Now i'd like to ask about your lite as a child. Let's begin with some questions about school. Did you ever
repeat a grade?
No .................. (SKIP To 0. 197)....0 in
Yes ..................... (ASK A) ........ 0

A. Did you get held back more than once?

No. only once ............................. 0 w
Yes. more than once ....................... 3

16?. How were your grades in school-better than average. average. or not so good?

Betterthaneverage ..(8KIP TO 0. 188).... 9 :s/
Average ............. (SKIP TO 0. 188).... 0
Notsogood ............. (ASK A) ........ 0
A. Did your teachers think youdidsboutsswell as youcouldordldtheythinkyouhadmeacilityto
do much better?
Didasweilascouid ..... (SKIP To a. its) 0 .0,
Could have done much better .(ASK a) ..... 0

B. How old were you when your teachers lirst felt that way?

an: *——‘ooooooooco
5333.33 .._._loooooooooo

Lmnwewsn: if R SAYS ‘DK": ASK c]

 

 

 

 

C. Do you think it was before you were 15 or later than that?

Drums ...... (RECORD 01 ABOVE) 23/
15 O! more ..... (RECORD es ABOVE)
Still DK ...... (RECORD 88 ABOVE)

160 Did you frequently get into trouble with the teacher or principal tor misbehaving in school?
(ELEMENTARY. JUNIOR HIGH. 08 HIGH SCHOOL)

No ................. (SKIP To a. tee)....0 24/
Yes ..................... (ASK A) ......... 0

A. How old were you when you first got into trouble tor misbehaving in school?

ENTEhAaes '— “0000000000
donates _JEoocooooooo

liNTERVlEWER: lF R SAYS “DK': ASK B I

I. Do you think it was beiore you were is or later than that?

 

 

 

 

Under 15 ...... (RECORD 01 ABOVE) 27/
iSormore ..... (RECORD es ABOVE)
Still DK ...... (RECORD es ABOVE)

$1

66

188. Were you ever expelled or suspended lrorn school? (ELEMENTARY. JUNIOR HIGH OR HIGH

_0 scuoou

No ........ (SKIP TO O. 200) ............ G
Yes ............ (ASK A) ................. 0

A. Howoid'wareyouwhenyouwereiirstexpelledorsuspended?

ENTERAGEl‘——‘ 0000000000
oomozoo (0000000000

Wis.”

B. DoyouthintltwasbeioreyouwereiSoriaterthenthat?

 

 

 

 

Underts ..... (RECORD 01 ABOVE)
iSormore ....(RECORD 6 ABOVE)
Still DK ..... (escono as AaoVE)

280. Didyoueverolayhookyiromschooletieesttwicelnoneyear?

DECK 09

31/

all

No ........ (SKIP To 0. 201) ............. 0
Yes ........... (ASK A) .................. 0
A. Was that only in your last year in school or before that?
Lastyearonly....(SKlP To 6. 201) ....... 0
Beiorelastyear ...(ASKaANo o) ........ 0
8. Did you play hookyas much as Sdayss year in at leasttwoachool years. not counting your last year
in school?
No ....................................... 0
Yes ................ . ..................... 0

C. Howoldwereyouwhenyoutlrstplayedhooky?

ENTEhAaes' *000000000
complain [1.1 0

90

 

 

 

00000000

 

D. Doyouthlnkltwasbeioreyouwereiiorlaterthanthat?

Under 15 ..... (RECORD 01 ABOVE)
15 ormore ....(RECORD 85 ABOVE)
Still Dix ..... (RECORD fl ABOVE)

2°01. Dldyouevergetlntotroubleatschooitorilghtlng?

No ............ (SKIP To a. sac) ......... 0

Yes ................ (ASK A) ............. 0
A. Did that happen more than once?

No ............ (SKIP To 0. 202) ......... 0

Yea ............ (ASK E AND c.) .......... 0

as!

67

 

 

DECK 09
S. Were you sometimes the one who started the light?
No ...................................... 0 so
Yes ..................................... 0
C. How old were you when you first gOI into trouble for fighting at school?
ENTERAGEII 0000000000
GOTOO.202 30000000000 “’
D. Do you think it was before you were 15 or later than that?
Under 15 (RECORD 01 ABOVE) 43/

15 or more (RECORD 85 ABOVE)
Still DK (RECORD 85 ABOVE)

81 Before age 15. did you ever get into trouble with the police. your parents or neighbors because of
fighting (other than for fighting at school)?

No...(SKIP TO INSTRUCTIONS BEFORE O. 202E) 0 «I
Yes ................... (ASK A) .................. 0

A Did that happen more than once?

No ............. .(SKIP To c) ............ 0 45/
Yes ............... (ASK B) .............. 0

8. Were you sometimes the one who started the fight?

N ...................................... 0
v; ..................................... 0 “I

C. At what age did you first get into trouble because of fighting (away from school)?

wenmemo—‘oocooooooo .1,
SKIP TO O. 203: _J

 

 

 

,0000000000

 

D. Doyouthlnkitwasbeforey‘ouwere15orlatarthanthst?

Under 15 ...(RECORD 01 ABOVE I SKlP TO 0. 203) eel
15 ormore .. (RECORD ’5 ABOVE l SKIP TO 0. 203)
SUII DK ..(RECORD 88 ABOVE A SKIP TO 0. 203)

 

 

INTERVIEW”: ARE BOTH O. 201 AND 202 CODED 1?

E No ............ (SKIP TO 0. 203) ........ 0 .0)
YES ................ (ASK E) ............. 0

  

 

E. Even though you didn't get into trouble for fighting. did you start fights more than once before you
were 15?

No ...................................... 0 st .
Yes ..................................... 0

53

°§

0.?

03

68

DECK oil
When you were a kid. did you ever run away from home overnight?
No ......... (SKIP To 0. 20s) ........... 0 am
Yes ............. (ASK A) ................ 0 -
A Did you run away more than once?
No. just once ............................. 0 ss/

Yea.morethenonce ....................... 0

B. How old were ya when you first ran away from home overnight?

ENTEAADEA‘__‘0000000000
ooroo.zoi,_) “’

 

 

 

_JOOOOOOOOOO

 

C. Doyouthlnkltwesbeforeyouwereisorlaterthsnthat?

Under 15 ....(RECORD 01 ABOVE) ss/
15 ormore ...(RECORD BS ABOVE)
Still DK .(RECORD BB ABOVE)

Ofcourse.nooneteilsthetruthalthetime.butdidyoutellslotoflieswhenyouwereschildor
teenager?

No .......... (SKIP To 0. 205) .......... 0 s71
Yes .............. (ASK A) .. . .~ ........... 0

A How old were you when you first told a lot of lies?

ENTERAGEA F— 0000000000
OOTOO.2osl_E|0000000000- 5"

B. DoyouthinltitwasbaforeyouwerelSorlaterthanB'Iat?

Under 15 ....(RECORD 01 ABOVE) as/
15 ormore ...(RECORD 85 ABOVE)
Still DK ....(RECORD SB ABOVE)

 

 

 

 

Whenyouweraschlld.didyoumorethan onceswipe thingsfromstoresortromotherchlldrenorstssl
from your parents or from anyone else?

No .......... (SKIP To a. zoo) ......... ..0 e11
Yes .............. (ASK A).......- ......... 0

A. Howoldwereyouwhanyoufirststolethlngs?

ENTERAdEa‘ _'0000000000
GOTOO.205E_0000000000 W

liNTERVIEWER: iF R SAYS "DK": A§K El

 

 

 

69

8 Do you think II was before you were 15 or later than that?

Under 15 ..... (RECORD 01 ABOVE)
15 or more . . . . (RECORD 95 ABOVE)
StIll DK ..... (RECORD DB ABOVE)

DECK 08

BEGIN DECK 10

206. When you were a kid. did you ever intentionally damage someone's car or do anything else to destroy or

200.
O

severely damage someone else's property?

No ........... (SKIP To 0. 207) .......... 0
Yes ............... (ASK A) ............... 0

A How old were you when you first did that?

ENTERAoeal_—'0000000000
cOToo.207_.J_.0000000000

limggyggggn; IF R §AY§ 2K": A§K E I

B. Doyouminkltwasbsioreyouwere15orlaterthantriet?

 

 

 

 

Under 15 ..... (RECORD O1 ABOVE)
15 or more ....(RECORD BS ABOVE)
Still DK ..... (RECORD BB ABOVE)

. Were you ever arrested as a juvenile or sent to Invenile court?

No ........... (SKIP TO 0. 208) ........ ..0
Yes ............... (ASK A) .............. .9

A. HOW Old ”'0 you the first (IMO?

ENTEAAse:‘——‘oocooooooo
cDTOO.200,._J__0000000000

(INTERVIEWER: iF R SAYS "OK": ASK BI

B. Do you think it was before you were 15 or later than that?

Under 15 ..... (RECORD 01 ABOVE)
15 ormore ....(RECORD 85 ABOVE)
Still DK .....(RECORD fl ABOVE)

 

 

 

Have you ever been arrested since 15 for anything other than traffic violations?

No ........... (SKIP TO O. 209) ..... ....0
Yes ...........(ASKAAND a) ------- ---0

A Have you been arrested more than once?

NOJUBIOM eases eeeeeeee eeeeeeeeaeeeeeeeQ .
Yes.morethsnonce fl: 0

 

B. Have you ever been convicted of a felon”

No ................................... ....0
Yes 3 Q.

 

"I

12!

131

15/

15!

17/

1V

7O

 

 

 

coo: DECK 10

1 e 09 M ”D

2 - asto- cut 5 0 yes

a - enags or are
208. Have you had at least four traffic BcKets in your life for speeding or running a light or causing an
O accident?

No ...................................... 0 18'

VB. :0.

 

210. Now l'm going to ask you about your sexual experience. in general. has your sex life been important to
O you.orcouidyouhavegottenslongsswellwithoutlt?

Somewhat important ..................... 0 av
Gotten along as well without it ............ 0
No sexual experience ................... . . 0

 

SWIM USD: 11' NO SE! EDERIDICE OI REFUSES an QUESTIONS. am 1‘0 Q. 523.
ID SUPPLDENT: U IO SE! mmDICE, “I? TO Q. 215.
If REFUSES 5E1 DESTIGS SE1? TO CTIMS ABOVE . 216.

61:. Has having sexual relations ever been physically painful for you?
MD: - SELF: 9 Q 9 Q

21/

212. Has there been a period of several months in your life when having sex was not
pleasurable for you (even when it wasn't painful)?

MD: SELF: 0 Q 0 Q Q
a!

 

213. Have you had any (other) kind of sexual difficulties (FOR MEN. such as a period
0 of two months or more when you had trouble having an erection)?

up: SELF: 00000
as:

 

INSERT SUPPLEMENT HERE

217. Since age 15. have you been in more than one fightthat came to swapping blows (other than fights with
0 your [husband/wifelpsrtnerl)?

 

[INTEItvIswuc IF a VOLUNTEERS -ONLY AS REQUIRED sY JOB." coo: H

No .......................... 0
Yes A 0' w

V

85. HaveyouevermamlikesstictJtnifmorgun.inafightsincsyouwers15?

 

- INTERVIEWER: IF R SAYS ‘ONLY AS REQUIRED BY OCCUPATION.” CODE 1
IF R SAYS 'WIELDED BUT MISSED." CODE 5

NO eaeeeeaeeeee eeeeeeeeeeeeeeeeeeeeeeeeeee G ‘B/
V. :w.

618.

°§

°S

05!

71

 

 

ceDt DECK 11
l o no - d - med see
1 0 aero- enl 5 . yes
5 0 drugs or sit

 

 

Since you were 15. did you ever hold (three or more different lobawithln a five-year period?

INTERVIEWER: OMIT CHANGES VOLUNTEERED AS DUE TO JOB ENDING. RETURN TO
SCHOOL. iLLNESS OR MATERNITY. TRANSFER OF SPOUSE. BECOMING
HOUSEWIFE. COUNT CHANGES IN MAIN JOB ONLY.

 

 

NO................................; ..... 0 . 1"
Yes +0

v-

Have you beenfimsfrom more than one job?

No ................................. .....0 . 17/
YO. 4:0

. Since you were 15. have you an. bursa times or more before you already had another he lined up?

 

INTERVIEWBR: OMIT OUITTING VOLUNTEERED AS DUE TO RETURN TO SCHOOL. 1
ILLNESS OR MATERNITY. TRANSFER OF SPOUSE. BECOMING HOUSEWIFE.

 

 

 

No ....................................... Q . w
Y” :0

On any job you have had since you were 15. were you late or absehtan average of
5 days a month or more?

umaviewss: IF it SAYS "NO SET SCHEDULE”: CODE fl

 

RECORD ALC/MED: 0 Q . 15/
#0

 

How many months out of die last.fiva years have you been without a job?

ENTERIMONTHS:F"_'0000000000 10'
.L._u.0000000000

liNTERVIEVER: IF LESS THAN 0 MOS. SKIP TO 0. mj

 

 

 

 

IF 5 MOS. OR MORE. ASK B
IF R SAYS ”OK.” ASK A.

A Doyouthinltltwssisssthathonthsormorethanthat?

Less than 5 mos. ..... (RECORD OI ABOVE S SKIP TO O. 224) w
5 mos. or more ...... (RECORD 85 ABOVE l ASK B)
Still OK ............. (RECORD DB ABOVE A ASK B)

B. For how much of that time did you want to wont but were not able to find a job?

ENTER'MONTHS:l—T_' 0000000000 3’
_L_ 0000000000

LNTERVIEWER: IF s - s MOS. on MORE. SKIP TO F]
a:

 

 

 

 

223.

OE

05!

72

DECK ii
(Continued)
C. for how much of that time were you not looking for work because of emotional or mental problems
or because of problems with drugs or alcohol?

ENTEROMONTHS:'——@®@Q®@@@@@ ss/
[_JJcooooooooo

[INTERVIEWERz IF 5 . c - s MOS. OR MORE. SKIP To EI

 

 

 

 

D. How much time (besides that) were you Just not interested in working but not in school. or
physically ill (or retired or a housewife)?

ENTER MONTHS;‘_'—‘0000000000 ,
' ._O_Ji0000000000 ”

E. HTERVIE‘WER: DO B s C t D O B MONTHSOR MOREleIHOUT ,WORK?

NO ...................................... O 31
YES 4, 0"

 

 

 

Haveyoueverusadanaliasoranassumedname?

 

WmVIEY/ER: IF R VOLUNTEERS ONLY PEN on STAGE NAME- cooE 1.|
No ...................................... 0 . 30/
YO! - t 0

Have you thought that you lied, pretty often since you have been an adult?
NO ..................................... . G 31/

YBB .....................................

Have you ever traveled around for a month or more without having any arrangements ahead of time and
net knowing how long you were going to stay or where you were going to work?

 

[ lNTERVleER: IF R VOLUNTEERS "ONLY ON VACATION FROM JOB”: cooaj
No ...................................... 0 w
YRS f G.

Hasthereeverbean s periodwhanyouhadnoregulsrpiacetotive. for at Ieastamonthorso?

N ...... ............................ 0
Y; :0‘ w

73

DECK 11

 

INTERVIEWER: DOES R HAVE CHILD (O. 14 I 01 OR MORE)
OR

E HAS A AcTED As PARENT (D. 14A - 5)?

..(SKIP TO INSTRUCTIONS
BEFORE O. 202) .............. 0
YES ....... (AS): 0. 220) ................ o a.)

 

 

 

. Have you sometimes left young diiidreIRunder 5 years did home alone while you were shOpping or out

doing anyming else?

* lNTERVlswslt: IF R VOLUNTEERS -ONLY IN ENEROENOY: "FOR LESS
THAN so MINUTES.' OR -CI-llLD COULD sE HEARD OR
COULD cows THERE-z cops 1.

 

 

 

 

No . . . ....... . ........ . .................. 0 . a.
Yes :0
m "'00 VIE! CHIC ............... (SKIP TO

INSTRUCTIONS BEFORE O. 232) ....... 0

Have there been times when a neighbufedaail'd'mfyours/youwere caring for) because you didnt '
get around to snapping for food or cocking. or keptyour child overnight because no one was taking care
of him at home?

 

FINTERVIEwER: IF R VOLUNTEERS “ONLY IN EMERGENCY”: cooefi

No ...................................... 0 ss/
Yes ; Q.

. Has a nurse. or social worker or tssctlsr ever said that any child (of yourslyou were caring for) wasn't

being givanenouul beater wasn’t being kept clam encugh or wasnt getting medial carewhen it
was needed?

No ... ........... . ....................... 0 37/

money-onyourselforongoingout?

74

 

 

INTERVIEWER; I-low MANY ‘5"s" HAVE BEEN CODED IN Os. 200.231 (BEGINNING
ON PAGE 55)?
LL
NONE. ONE OR Two ..(SKIP TO O. 235) 0
TNREE OR MORE ...... (ASK O. 232) ..... 0 ...

 

232. Did you ever talk to a doctor about any of these things you did like (SPECIFY '5"s" WHICH HAVE

8:. Didyoudosny'ofth'ssedlingsbstwesntheageaofuanda?

0.?

BEEN CODED. BEGINNING WITH 0. 200. p. 55)

NO ...................................... 0 a
Yes ................................. 0

 

— INTERVIEWER: IS R OLDER OR YOUNGER THAN 25 YEARS OLD?

E ZBOROLDER ........ (ASK 0. sea) ...... 0
YOUNGER THAN25 .. (SKIP TO o. 204) . 0 41/

 

 

No .......... (ASK A) ............... - ..... 0 42/
Yes ....(SKIP TO 0. 204) ............... 0

A Was there some reason yOU couldn‘t have done these things between 15 and 25. for instance.
because yOu were ill in bed dist whole time (or in jail/not married/had no children)?

No ....(I-IAO OPPORTUNITY) ............ 0 43/
Yes ...(NO OPPORTUNITY) ............. 0

 

When is the last time you did any one of these things like (MENTION CODED '5"s" BEGINNING
WITH 0. 205)?

 

 

_ MthinlsstZweeks ......... '. ............ .8 “I
CODE “'05" WWW”‘Ii'IIIIIIIIIIIIIII'o b
RECENT "”5 Withinisstysar ....... ..0
POSSIBLE a Withlnlastayesrs ......... ...............0
Hommnayesrsago ....... .(ASK A)....0

I MORE THAN 2 YEARS ADD:
A Howpldwsreyouthelasttlmsyoudidanyofthossthings?

ENTERAGE'DJO000000000 45/
0000000000

 

W5...
.

Appendix D
Drinking and Drug History Form

75

(nfg:mgtiog_gg_ngigkigg gng Other Drug Us; R Number:

 

(6/I/B9) (I3 pages) Given By:

 

Date:

 

Ans. Chk:

 

This questionnaire takes about IS minutes to complete. All information
will be used for research only and will be kept strictly confidential.
If you are not sure Of the answer to a question please answer the best
you can. Please try to answer each item.

A. THE FOLLOWING QUESTIONS ARE ABOUT YOUR DRINKING OF ALCOHOLIC
BEVERAGES:

I. HOW OLD WERE YOU THE FIRST TIHE YOU EVER TOOK A DRINK? DO NOT
COUNT THE TIMES WHEN YOU WERE GIVEN A "SIP” BY AN ADULT.

 

 

years Old.
2. OVER THE LAST 6 QQNTHS. ON THE AVERAGE. HOW HANY DAYS A MONTH
HAVE YOU HAD A DRINK?
days a month.
3. OVER THE LAST §_fiQflIfl§. ON A DAY WHEN YOU ARE DRINKING. HOW

HANY DRINKS DO YOU USUALLY HAVE IN 24 HOURS? (A DRINK IS A I2
02. CAN. GLASS OR BOTTLE OF BEER: A 4 OZ. GLASS OF WINE: A
SINGLE SHOT; OR A SINGLE 'HIXED DRINK.”)

drinks per 24 hours.

 

4. OVER THE PAST 6 MONTHS. WHEN YOU GOT DRUNK. HOW BAD WAS YOUR

HANGOVER?
Never bad ______ Pretty Bad
Not bad Terrible
A little less than average Worst possible
Average Never drank enough to get
A little more than average hangover

CONTINUE ON THE NEXT PAGE.

Page l of l3

765

. THE FOLLOWING QUESTIONS ARE ABOUT YOUR DRINKING PATTERNS. IN

ANSWERING THE QUESTIONS. PLEASE TNIIK ABOUT WHAT YOU HAVE DONE
o__N_ THE AVERAGE OVER THE i_._A§T Six NONTNS.

WHEN ommw.
a. liOii OFTEN DO YOU USUALLY HAVE WINE OR A PUNCH

CONTAINING WINE?

3 or more times a day 2 or 3 times a month

2 times a day About once a month

Once a day Less than once a month.

Nearly every day but at least once a year

3 or 4 times a week Less than once a year

once or twice a week NEVER [If checked. go to
question 52a]

b. THINK OF ALL THE TIRES YOU HAD WINE OR A PUNCH CONTAINING
WINE RECENTLY. WHEN YOU DRINK WINE. HOW OFTEN DO YOU HAVE
ID OR MORE GLASSES?

Nearly every time: SKIP TO QUESTION 52 BELOW

Nore than half the time: SKIP TO QUESTION #2 BELOW
Less than half the time

Once in a while

NEVER

c. WHEN YOU DRINK WINE. llOil OFTEN 00 You HAVE As NANY AS 7 TO
9 GLASSES?

Nearly every time: SKIP TO QUESTION 52 BELOW

Nora than half the time: SKIP TO QUESTION 52 BELOW
Less than half the time

Once in a while

NEVER

6. WHEN YOU DRINK WINE. NOW OFTEN DO YOU HAVE AS HANY AS 5 to
6 GLASSES?

Nearly every time: SKIP TO QUESTION 52 BELOW

Nore than half the time: SKIP TO QUESTION 52 BELOW
Less than half the time

Once in a while

NEVER

e. WHEN YOU DRINK WINE. HOW OFTEN DO YOU HAVE AS HANY AS 3 to
4 GLASSES?

Nearly every time: SKIP TO QUESTION 52 BELOW

Nore than half the time: SKIP TO QUESTION 52 BELOW
Less than half the time

Once in a while

NEVER

2 of l3

'77

F. WHEN YOU DRINK WINE. HOW OFTEN DO YOU HAVE I TO 2
GLASSES?

Nearly every time

Nora than half the time
Less than half the time
Once in a while

NEVER
WHEN DRINKING BEER
0. HOW OFTEN DO YOU USUALLY HAVE BEER?
3 or more times a day 2 or 3 times a month

About once a month

Less than once a month.

but at least once a year

Less than once a year

NEVER [If checked. go to
question 53a]

2 times a day

Once a day

Nearly every day

3 or 4 times a week
Once or twice a week

b. THINK OF ALL THE TIRES YOU HAD BEER RECENTLY. WHEN YOU
DRINK BEER. HOW OFTEN DO YOU HAVE ID OR KORE CANS. GLASSES
OR BOTTLES?

Nearly every time: SKIP TO QUESTION 53 BELOW

Hore than half the time: SKIP T0 QUESTION 53 BELOW
Less than half the time

Once in a while

NEVER

' c. WHEN YOU DRINK BEER. NOll OFTEN DO YOU HAVE AS NANY As 7 To

9 CANS. GLASSES OR BOTTLES?

Nearly every time: SKIP TO QUESTION 53 BELOW

hore than half the time: SKIP TO QUESTION #3 BELOW
Less than half the time

Once in a while

NEVER

d. WHEN YOU DRINK BEER. HOW OFTEN DO YOU HAVE AS NANY AS 5 T0
6 CANS. GLASSES OR BOTTLES?

Nearly every time: SKIP TO QUESTION 53 BELOW

Nore than half the time: SKIP TD QUESTION 53 BELOW
Less than half the time '

Once in a while

NEVER

3 of l3

78

e. WHEN YOU DRINK BEER. HOW OFTEN DO YOU HAVE AS HANY AS 3 to
4 CANS. GLASSES OR BOTTLES?

Nearly every time: SKIP T0 QUESTION Q3 BELOW

Kore than half the time: SKIP TO QUESTION #3 BELOW
Less than half the time

Once in a while

AEVER

f. WHEN YOU DRINK BEER. HOW OFTEN DO YOU HAVE I TO 2
CANS. GLASSES OR BOTTLES?

Nearly every time

Nore than half the time
Less than half the time
Once in a while

NEVER
WHEN ORINKIQQ WHISKEY OR LIQUOR
a. HOW OFTEN DO YOU USUALLY RAVE WHISKEY OR LIQUOR (SUCH
AS HARTINIS. HANHATTANS. HIGHBALLS. OR STRAIGHT
DRUMS iNCLUDlNG SCOTCH. BOURBON. GIN. VODKA. RUN.
ETC.)2
3 or more times a day 2 or 3 times a month

About once a month

Less than once a month.
Nearly every day but at least once a year
3 or 4 times a week Less than once a year
Once or twice a week EVER [If checked. no to
question “I

2 times a day
Once a day

b. mm: or ALL THE mes YOU mo DRIiKS COITAININO :04:st:
OR OTHER LIQUOR neccmu. men YOU HAVE HAD THEN. How
OFTEN 00 YOU HAVE no on now: claims:

Nearly every time: SKIP TO OLESTION '4 BELOW

Kore than half the time: SKIP TO QlESTION #4 BELOW
Less than half the time

Once in a while

iEVER

c. WHEN YOU HAVE HAD WIMS CWTAINING WHISKEY G? OTl'ER
LIQDR. W “TEN DO YOU HAVE AS HANY AS 7 TO 9 DRUMS?

Nearly every time: SKIP TO QIESTION .4 BELOW

Bore than half the time: SKIP TO OLESTION #4 KLOW
Less than half the time

Once in a while

EVER

AUIS

U

79

d. WHEN YOU HAVE HAD DRIMS CONTAINING WHISKEY a? OTHER
LIQLDR. MW OFTEN DO YOU HAVE AS HANY AS 5 TO 6 DRIMS?

Nearly every time: SKIP TO QUESTION .4 BELOW

Kore than half the time: SKIP TO QUESTION (4 BELOW
Less than half the time

Once in a while

NEVER

e. WHEN YOU HAVE HAD DRIMS WAININ WISKEY m LIQLm. l'DW
NTEN no you HAVE 3 TO A DRIVKS?

Nearly every time: SKIP TO QUESTICRI t4 BELOW

Here than half the time: SKIP TO QLESTION #4 KLOW
Less than half the time

Once in a while

NEVER

f. WHEN YOU HAVE HAD DRI'KS CONTAINING WHISKEY (I? LIQUOR. i'DW
NTEN DO YOU HAVE I TO 2 DRIMS?

Nearly every time

More than half the time
Less than half the time
Once in a while

NEVER

I I .CI‘ECKl'OdOFTENYOU HAVE ANYDRII’K
CONTAINING ALm. WETHER IT IS WINE. BEER. WISKEY OR ANY
OTI'ER DRIM. HAKE SURE THAT YOUR ANSWER IS MT LESS FREMNT
THAN THE FREQIENCY REPORTED CW ANY OF THE PRECEDING QJESTIUIS.

Once or twice a week

2 or 3 times a month
About once a month

Less than once a month.
but at least once a year
Less than once a year

3 or more times a day
2 times a day

Once a day

Nearly every day

3 or 4 times a week

Now a Question about earlier in your lifg: l‘DW OLD WERE YOU THE
FIRST TINE YOU EVER DRAM EIDUGH TO GET DRUM?

years old.

Sofl3

80

6a. WE ARE ALSO INTERESTED IN THE OCCASIONS THAT HAY BE RARE (OR
NOT). WHEN PEOPLE DRINK A LOT HORE THAN THEY USUALLY DO. I!
THE LAST SIX HONTHS. THINK OF THE 24 HOUR PERIOD WHEN YQQ DID
Iflfl HOST DRINKINQ: THIS WOULD BE A DAY SOHEWHERE iN THE PERIOD
BETWEEN . AND NOW.
(month) (year)

On that day. how many drinks did you have? (A drink is a (2
oz. can. bottle. or glass of beer. a 4 oz. glass of wine. a
single shot. or a single mixed drink).

30 or more drinks
25 - 29 drinks
20 - 24 drinks

IS - l9 drinks
l0 - I4 drinks
7 — 9 drinks
5 - 6 drinks
3 - 4 drinks
I — 2 drinks
none
6b. APPROXIHATELY WHEN DID THIS HAPPEN? . .
(month) (year)
.6c. Now ANSWER THIS QUESTION FOR W
W- W “*1 24 m PERIOD W

DRINKING. HOW HANY DRINKS DID YOU HAVE?

3D or more drinks
25 - 29 drinks
20 - 24 drinks

I5 - l9 drinks

in - I4 drinks
7 - 9 drinks

5 - 6 drinks

3 - 4 drinks

I - 2 drinks
none

6d. APPROXIHATELY WHEN DID THIS HAPPEN? 9
(month) (Vlmr)

6 of I3

 

)0.
I).

)2.

III

ANSWER KEY FOR QUESTIONS BELOW:

 

 

 

I 2 3-5 6-l0 11-20 21-50 Sl-IOO

301-250 251-500 SDI-I000 I000+ (more than 1000) .

 

 

C. NOW SOHE QUESTIONS ABOUT OUTCOHES PEOPLE SOHETIHES HAVE BECAUSE OF
DRINKING. HAVE YOU EVER HAD ANY OF THE FOLLOWING HAPPEN BECAUSE OF

YOUR DRINKING?

  

1§§ 59 HOW ANY AGE AGE

(check one) TIHES first most
(approx.- time recent
see key)“ time

Hissed school or time on Job

Thought I was drinking too
much

Gone on a binge of constant
drinking for 2 or more days

Lost friends

My spouse or others in my
Family (my parents or children)
objected to my drinking

Felt guilty about my drinking
Divorce or separation

ToOk a drink or two first
thing in morning

Restricted my drinking to
certain times of day or week
in order to control it

or cut down. (like after SPH.
or only on weekends.

or only with other people)

Been fired or laid off

Once started drinking,
kept on going till
completely intoxicated

Had a car accident when l

was driving _—:i-i;:

 

 

' SELECT YOUR ANSWER FRO" KEY AT THE TOP OF THE PAGE

 

 

 

Questions continue on the next Page.

7 of i3

82

 

 

 

 

I3.

14.

I7.

I9.

20.

2‘.

22.

ANSER KEY FQ ggg‘rig gig:
i 2 3-5 6-10 ll-20 Zl-SO 5i-I00
l0I-250 251-500 50i-l000 I000+ (more than I000)
HOW NANY ADE AGE
TINES first most
1§§ N9 approx- time recent
(check one) see key)' time

Kept on drinking after
i promised myself not to

Had to go to a hospital
(other than accidents)

Had to stay in a hospital
overnight

Had the shakes “the
morning after”

Heard or saw or felt things
that weren't there.
hallucinations) several

days after stopping drinking

Had blackouts (couldn't
rail-ember later what
you'd done while drinking)

Been given a ticket fer
drunk driving (DWI or DUIL)

Had a Jerking or fits
(convulsions) several days
after stopping drinking

Been given a ticket for
public intoxication. drunk
and disorderly. or other
nondrlving alcohol arrest

Had the D.T.'s (delirium
tremens. shakes. sweating.
rapid heart. etc.)

within 2 - 3 days

after stopping drinking

 

 

‘ SELECT ANSWERS FROH THE KEY

 

 

AT THE TOP OF THE PAGE

 

B OF 13

83

D. THE LAST SECTIONS OF THIS QUESTIONNAIRE DEAL WITH VARIOUS DRUGS OTHER THAN
ALCOHOL. THERE IS STILL A LOT OF TALK THESE DAYS ABOUT THIS SUBJECT. BUT VERY
LITTLE ACCURATE INFORHATION. PARTICULARLY ABOUT PATTERNS OF USE OF THESE SUBSTANCES
IN ADULTHOOD. THEREFORE. WE STILL HAVE A LOT TO LEARN ABOUT THE ACTUAL EXPERIENCES
OF PEOPLE YOUR AGE.

WE HOPE THAT YOU CAN ANSWER ALL QUESTIONS: BUT IF YOU FIND ONE WHICH YOU FEEL
YOU CANNOT ANSWER HONESTLY. WE WOULD PREFER THAT YOU LEAVE IT BLANK.

REHEHBER THAT YOUR ANSWERS WILL BE KEPT STRICTLY CONFIDENTIAL AND THEY ARE
NEVER CONNECTED WITH YOUR NAME. THAT IS WHY THIS QUESTIONNAIRE IS IDENTIFIED ONLY
WITH A CODE NUMBER.

THE FOLLOWING QUESTIONS ARE ABOUT CIGARETTES (CHECK THE BEST ANSWER):
la. HAVE YOU EVER SHOKED CIGARETTES?

Never (60 TO QUESTION 3)

Once or twice

Occasionally but not regularly
Regularly in the past
Regularly now

lb. HAVE YOU SMOKED CIGARETTES DURING THE PAST 12 MONTHS?

Never (60 TO QUESTION 3)

Once or twice

Occasionally but not regularly

Regularly for a while during this year. but not now
Regularly now

 

2. HOW FREQUENTLY HAVE YOU SMOKED CIGARETTES DURING THE PAST 30 DAYS?

Not at all

Less than one cigarette per day

One to five cigarettes per day

About one-half pack per day

About one pack per day

About one and one-half packs per day
Two packs or more per day

Will

E. THE FOLLOWING QUESTIONS ARE ALL ABOUT NON-PRESCRIPTION USE OF DRUGS. E THER FOR
RECREATION OR FOR SELF-MEDICATION. é

(HARK ONE SPACE FOR EACH LINE).

3.

ON HOW HANY OCCASIONS (IF ANY)
HAVE YOU USED HARIJUANA
(GRASS. POT) 0R HASHISH

(HASH. HASH OIL)

More than 1000

I
g
g

10~19 Occasions

0 Occasions
1-2 Occasions

In your lifetime? (
During the last

l2 months?
During the last 30 days? ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) (

wv
AA
wv
AA
vv
AA
v”
AA
VV
AA
«v
AA
vv
A»
vv
AA
haw

\J

(HARK ONE SPACE FOR EACH LINE).

4.
ON HOW NANY OCCASIONS
(IF ANY) HAVE YOU USED
LSD (ACID)

In your lifetime?
During the last

i2 months?
During the last 30 days?

5.

ON HOW HANY OCCASIONS
(IF ANY) HAVE YOU USED
PSYCHEDELICS OTHER THAN
LSD (LIKE HESCALINE.
PEYOTE. PSILOCYBIN. PCP)

In your lifetime?
During the last

I2 months?
During the last 30 days?

6.
ON HOW HANY OCCASIONS
(IF ANY)

HAVE YOU USED COCAINE
(COKE OR CRACK)

In your lifetime?
During the past

12 months?
During the last 30 days?

7.
AHPHETAHINES ARE SOHETIHES
PRESCRIBED BY DOCTORS TO
HELP PEOPLE LOSE WEIGHT OR
TO GIVE PEOPLE HORE ENERGY.
THEY ARE SONETIHES CALLED
UPPERS. UPS. SPEED. CRYSTAL.
CRANK. BENNIES. DEXIES. PEP
PILLS. AND DIET PILLS.

ON HOW HANY OCCASIONS (IF ANY)
HAVE YOU TAKEN AHPHETAHINES ON
YOUR OWN--THAT IS. WITHOUT A
DOCTOR TELLING YOU

TO TAKE THEN

In your lifetime?
During the last

I2 months?
During the last 30 days?

Occasions

0

l-ZlOccasions

1-2 Occasions

3-5 Occasions

3-5 Occasions

'10 of 13

6-9 Occasions

6-9 Occasions

10-19 Occasions 10-19 Occasions

10-19 Occasions

10-19 Occasions

20—39 Occasions

20-39 Occasions

40-99 Occasions

40—99 Occasions

100.1000 Occasion:

100-1000 Occasions

More than 1000 More than 1000

More than 1000

More than 1000

(HARK ONE SPACE FOR EACH LINE).

8.
ON How HANY OCCASIONS (If ANY)
HAVE YOU USED QUAALUDES g
(QUADS. SOAPERS. HETHAQUALONE) ...
ON YOUR OWN-- THAT IS. WITHOUT

A DOCTOR TELLING

YOU TO TAKE THEN o

In your lifetime? ( )

During the last ( l
12 months?

During the last 30 days? ( )

9.

BARBITURATES ARE SOHETIHES PRE-
SCRIBED BY DOCTORS TO HELP PEOPLE
RELAX OR GET TO SLEEP. THEY ARE
SOMETIMES CALLED DOWNS. DOWNERS.
GOOFBALLS. YELLOWS. REDS. BLUES.
RAINBOWS.

ON HOW HANY OCCASIONS g
(IF ANY) HAVE YOU TAKEN «4
BARBITURATES ON YOUR OWN -- 3
THAT IS. WITHOUT A DOCTOR 8
TELLING YOU To TAHE THEN o

In your lifetime? (
During the last

I2 months?
During the last 30 days? (
I0.

TRANQUILIZEPS ARE SOHETIHES
PRESCRIBED BY DOCTORS TO CALH
PEOPLE DOWN. QUIET THEIR NERVES.
OR RELAX THEIR HUSCLES. LIBRIUH
VALIUH. AND NILTOWN ARE ALL
TRANQUILIZERS.

ON HOW HANY OCCASIONS (IF ANY) 3
HAVE YOU TAKEN TRANQUILIZERS 3
ON YOUR OWN -- THAT Is.

WITHOUT A DOCTOR TELLING YOU 8
TO TAKE THEN o

In your lifetime? (

During the last (
l2 months?

During the last 30 days? (

1—2 Occasions

85

1-2 Occasions

3~5 Occasions

II Of 13

6—9 Occasions

10—19 Occasions

A

10-19 Occasions

10-19 Occasions

20-39 Occasions

20—39 Occasions

40-99 Occasions

" 40-99 Occasions

40-99 Occasions

100-1000 Occasions

T‘T‘ 100-1000 Occasions

A

loo-1000 Occasions

More than 1000 More than 1000

More than 1000

 

 

 

(BARK ONE SPACE FOR EACH LINE).

II.

ON HOW "ANY OCCASIONS (IF ANY)

HAVE YOU USED HEROIN (SHACK.

HORSE. SKAG)

In your lifetime? (

During the last (
I2 months?

During the last 30 days? (

I2.

THERE ARE A NUHBER OF NARCOTICS
OTHER THAN HEROIN. SUCH AS NETH-
ADONE. OPIUH. HORPHINE. CODEINE.
DENEROL. PAREGORIC. TALWIN. AND
LAUDANUH. THESE ARE SOHETIHES
PRESCRIBED BY DOCTORS.

ON HOW MANY OCCASIONS (IF ANY)
HAVE YOU TAKEN NARCOTICS OTHER
THAN HEROIN ON YOUR OWN--

THAT IS. WITHOUT A DOCTOR
TELLING YOU TO TAKE THEN

In your lifetime? (

During the last (
12 months?

During the last 30 days? (

‘3.

ON HOW MANY OCCASIONS (IF ANY)
HAVE YOU SNIFFED GLUE. OR
BREATHED THE CONTENTS OF
AEROSOL SPRAY CANS. OR INHALED
ANY OTHER GASES OR SPRAYS IN
'ORDER TO GET HIGH

0 Occasions

0 Occasions

In your lifetime? (

During the last (
I2 months?

During the last 30 days? (

’1-2 Occasions

86

Si .3
§ 3
8
E 1?.
l I I
l I
) I
I) I)
.§ .5.
U) I)
g 8
8
E 3

3-5 Occasions

12 of 13

6-9 Occasions

6-9 Occasions

10-19 Occasions

10—19i0ccasions

10-19 Occasions

20—39 Occasions

20-39 Occasions

40-99 Occasions

40—99 Occasions

40-99 Occasions

100~1000 Occasb

100b1000 Occaéions

. 100-1000 Occas.

More than 1000

More than 1000

Here than 1000

87

F. NOW SOHE OTHER QUESTIONS ABOUT NONPRESCRIPTION USE OF DRUGS. HAVE YOU EVER HAD
ANY OF THE FOLLOWING OUTCOHES BECAUSE OF YOUR USE OF THE NONPRESCRIPTION DRUGS
ASKED ABOUT IN SECTION E (THE LAST SECTION)?

ANSWER KEY FOR QUESTIONS BELOW:

  

 

 

' I 2 3-5 6-10 ”-20 21-50 51-100
101-250 251-500 500+ (more than 500)
1§§ N9 HOW HANY AGE AGE
TIHES first most recent
(approx) TIHE TIHE
(see key)‘

I. Hissed school or time on Job

 

Lost friends

 

3. Been divorced or separated
4. Been fired Or laid off

 

 

5. Had a car accident when
you were driving

6. Had to go to a hospital
(other than accidents)

 

 

7. Had to stay in hospital
overnight

8. Had to see a doctor because
of drug use (unintentional
overdose) or had a doctor
say drugs had harmed your health

9. Gone through physical with-
drawal from drugs

 

 

 

IO. Been arrested for
possession or sale
of drugs other than marijuana

_—“--—--———————{T:TSELECT YOUR ANSWER FROH KEY AT THE TOP OF THE PAGET]

Ila. Have you ever taken drugs intravenously (using a needle)? Don't count shots
you were given by a doctor or nurse or shots you may have taken for treatment of
diabetes.

 

 

 

NO YES

Ilb. IF YES. WHAT DRUGS HAVE YOU TAKEN INTRAVENOUSLY (IV)?

 

IIC. AT WHAT AGE DID YOU FIRST TAKE AN IV DRUG? years old.
lld. AT WHAT AGE WAS THE HOST RECENT TINE? years old.
13 0F 13

List of References

88

List of References

Allen, D. L. Petersen, D. R., Wilson, J. R., McCleam, G. E. and Nishimoto, T. K.
(1983). Selective breeding for a multivariate index of ethanol dependence in mice.
results from the first five generations WW

Researchl. 443- 337

 

American Psychiatric Association (1987). b 2.. '4; .. ' ' ' ° . a I :.
WW Edition-Revised). Washington, D. C. A. P. A.

Beck, AT and Beck, R. W. (1972) Screening depressed patients in family practice: A
rapid technique WM? 81 ~85

Begleiter, H., Porjesz, J., Bihari, B. and Kissin, B. (1984). Event-related brain potentials
in boys at risk for alcoholism. M 1493-1496.

Bohman, M. (197 8). Some 6g9en2eti6c aspects of alcoholism and criminality. mm
Wham. 2 - 7 -

Bohman, M. Sigvardsson, S. and Cloninger, C. R. (1981). Maternal inheritance of
alcohol abuse: Cross- -fostering analysis Of adopted women. W

W 265 -269

Buchsbaum, M. S. Landau, S., Murphy, D. and Goodwin, F. (1973) Average evoked
response in bipolar and unipolar affective disorders: Relationship to sex, age

of onset and monoamine oxidase. WM, 199- 212.

Cadoret, R. J. and Gath, A. ( 1978) Inheritance of alcoholism 1n adoptees. British
WM 252- 258

Cadoret, R. J. O'Gorman, T. W., Troughton, E. and Haywood, E. (1985). Alcoholism
and antisocial personality: Interrelationshipz, genetic and environmental factors.
WM 161 1 7

Cadoret, R. J. Troughton, E. and O'Gorman, T. W. (1987). Genetic and environmental
factors In alcohol abuse and antisocial personality. W

AlthLAfil-8

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