Person. indirid.

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Vol.

IO, No. 4, pp. 391-418.

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1989
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0191-8869

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1989 Pergamon

PERSONALITY IN THE THIRD DIMENSION: A PSYCHOBIOLOGICAL APPROACH*

MARVIN ZUCKERMAN Department of Psychology, University of Delaware, Newark, DE 19716, U.S.A.
(Received 19 February 1988; revised 8 April 1988)

Summary-An attempt is made to define the P dimension of personality in terms of its constituent traits, biological correlates, genetic bases, and relation to forms of psychopathology. Factor analyses revealed a coherent P supertrait incorporating the narrower traits of impulsivity. sensation seeking, lack of socialization and responsibility, autonomy, and aggression. Biological correlates of P dimension traits and some of the related types of psychopathology include poor conditionability, augmenting of the cortical evoked potential (EP), and low levels of the monoamine regulating enzymes monoamine oxidase (MAO) and dopamine-/?-hydroxylase (DBH), the serotonin metabolite (S-HIAA). norepinephrine in the cerebrospinal fluid, and cortisol. P is related to high levels of gonadal hormones in males. More than half of the variance in P psychological traits and more than 80% of the variance in the correlated enzymes MAO and DBH is determined by heredity.

Eysenck (1967, 198 1; Eysenck and Eysenck, 1985) has provided a three dimensional model of classification based on a psychobiological theory. Unlike many other personality theories this one has produced testable hypotheses and a great deal of research. The three dimensions are related to three of the problems of adaptation in primates that live in groups. The first is sociability or interacting in a positive, cooperative way with members of ones group in work, play, childrearing, and defense. Loners, rejected by primate groups, are in danger of being killed by predators or members of their own species. The second is emorionality, or general arousability in response to threats (fear or anger). An animal that is so unresponsive to threat that it cannot fight, flee, or freeze is not likely to survive in a hostile. environment. But an animal that is so frightened that it freezes for too long before fleeing or fighting is also doomed. Chamove, Eysenck and Harlow (1972) found a factor of intraspecies hostility and aggression in monkeys that they identify with the third major dimension of human personality, psychoticism (P), or tough-mindedness. Moderate aggressiveness is adaptive when involved with competition and dominance in males or maternal defense of the young in females. But the P dimension in humans seems to be more like irritable aggression in animals, or that type of aggression which does not seem to be tied to obvious survival or competitive motives and seems to have the infliction of maximal damage on the victim as its objective. The first two dimensions have received wide acceptance in all current personality classification systems for humans using Eysencks labels extraversion and neuroticism or the terms sociability and anxiety. But the existence or significance of Eysensks third dimension of personality, psychoticism, has been widely questioned (Bishop, 1977; Block, 1977a,b). In this article I will attempt to answer four questions: (1) Is there a coherent dimension and what traits does it encompass?; (2) Is there evidence of a biological basis for the dimension and the traits it subsumes?; (3) Is there a genetic basis for both the psychological traits and the biological traits which may be related to them?; (4) How might we conceptualize the interaction of biological and social determinants in forming the trait?
DEFINING THE BROAD P TRAIT

Pre-P scale evidence for the P dimension

Eysenck often cites two studies in support for his contention that there is a broad P dimension that includes both schizophrenic and affective psychoses as extremes on a continuum from the
*This article was presented as the presidential address at the third meeting of the International Society for the Study for Individual Differences, in Toronto, Canada, 18-22 June 1987. 391

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MARVIN ZLTKERMAS

normal to the clinical extreme. Trouton and Maxwell (1956) performed a factor analysis on 44 variables including current symptoms, family history, previous adjustment and symptoms and presumed causes and outcomes in 8 19 male psychiatric patients. The first two factors were labelled neuroticism (highest loading: anxiety symptoms, lifelong or episodic) and psychoticism (highest loading: delusions). Actually, a closer examination of the P factor shows that most of the highest loading items pertain to schizophrenia (e.g. schizophrenic thought disorder. socially withdrawn, catatonic type motor disturbances, hallucinations). Factor 3 contrasts symptoms of schizophrenia with those of affective disorder. Factor 4 was called inactivity-wirhdra~al, but actually seems to contrast the two poles of bipolar affective disorder. At one pole are the symptoms overactive excited mania or hypomanic . . . impulsive or aggressive . . . mood disturbances irritability and at the other pole are lacks confidence. . . retarded activity. . . socially withdrawn. The manic and hypomanic rating load much more highly on this factor than on the P factor. One could argue that manic ts depressive would be a better term for this dimension and schizophrenia would be a more appropriate lable for factor 1. However, this would suggest that the two disorders are independent instead of common components of a P dimension. This is not to deny that many symptoms, such as social withdrawal are not common to both disorders. There is a drawback to the use of symptoms as sole criteria for diagnosis. Social withdrawal, for instance, does not distinguish between a schizophrenic type of withdrawal based on fearful delusions, and a depressive withdrawal based on mood related feelings of inadequacy and guilt. In diagnosis of physical medical disorders non-specific symptoms like fever are of little use except in combination with other symptoms and laboratory tests. Eysenck (1952) was one of the first investigators to attempt to use objective behavioral laboratory tests in diagnostic classification. Using the statistical method of criterion analysis, that he developed himself, he attempted to test Kretschmers (1948) hypotheses that schizophrenia and manic-depressive psychoses are not qualitatively distinct, but lie on a continuum from normal to psychotic; and that the two psychoses represent a continuum from extreme schizothymics (schizophrenics), to schizoid personalities, to normal introverts, to normal extraverts, to cyclothymic personalities, to manic-depressives. Eysencks (1952) criteria for diagnostic distinction required that the same tests that differentiate one group from another should correlate positively in proportion to their discriminant power. The Ss consisted of three groups: normals, schizophrenics, and manic-depressives. The latter group was only tested during non-manic (presumably depressed) states. Ninety scores derived from a battery of 15 objective sensory-motor, perceptual, cognitive and attitude tests were obtained. This study was done during an inductive phase of Eysencks work, or at least before theories of the dimensions had been formulated, and this is probably why there was little rationale for the selection of the particular tests used. Twenty of the scores were selected for further analyses. The application of criterion analyses to the data supported the idea of a continuum between normalcy and psychosis, but did not confirm the hypothesis of a schizothymic-cyclothymic dimension. In the actual results, the scores of schizophrenics tended to be intermediate between the scores of normal and depressive groups, a counter-intuitive finding since most clinicians would regard schizophrenia as a more extreme kind of psychosis than manic-depressive disorder, assuming they do fall in the same dimension. A possible explanation is that many of the tests may measure speed, and depressives are generally slower than normals and even schizophrenics on most tasks. Looking at results of mirror-drawing, a timed test, depressives were considerably slower than schizophrenics who were slower than normals. However, speed of performance is only one aspect of psychoticism and may not be a crucial one at that. The fact that an objective test differentiates one group from another is no guarantee that it is a valid test of the basic dimension. Although the particular measures used in this study did poorly at differentiating major affective disorder from schizophrenia, more theoretically relevant measures might give a different answer. Trouton and Maxwells factor 3, based on ratings of affect, offered a possibility for discrimination of the two disorders. Zuckerman. Lubin, Rinck, Soliday, Abbott and Carlson (1986) applied a discriminant function analysis to diagnosis using affect scores from a self-report adjective check list. They found that the discriminant functions could correctly classify 72% of the patients with affective disorders with only 20% of the schizophrenics, 7% of substance abuse disorders, and 3% of normals misclassified as

Personality

in the third

dimension

393

x-

Genetic predisposition distribution ot being in the affected

predisposition

q Frequency q Frequency
Fig. I. Model of the diathesis
P Likelihwd

Genetic

population at a parficulor individuals level of x

distribution

of affected

stress theory of psychiatric disorder. Reprinted with permission.

From

Eysenck

and Eysenck

(1976).

affective disorder. Affect is of more obvious relevance to affective disorders than mirror-tracing or tapping tests. The point is that we cannot make definitive statements about the basic distinctions between disorders unless we can be sure we have included the most relevant types of variables in our analyses.
Group means on the P scale

According to Eysencks (Fig. 1) genetic model for P, the likelihood of an individual being psychotic or psychopathic increases as a function of the strength of the underlying genetic disposition, and the individuals who demonstrate the clinical disorder are drawn from the high end of the distribution. To the extent that the phenotype assessed by the personality scale reflects the genotype for P, those with the clinical disposition should score higher than a random sample of non-affected normal individuals. Another assumption is that all types of psychoses and antisocial personalities share the same broad latent genetic disposition. The first prediction can be roughly assessed by comparing mean P scores of clinical groups assumed to share a common genotype, with those of other clinical and normal groups (Table lj. Among the highest scoring groups for both sexes are German professional artists and English art students. In fact the German artists rated by critics as the most successful have the highest mean of all male groups and are higher than less successful artists on P. Creative writers in India also score high on the scale. Does this mean that artists have a strong disposition toward psychoticism? Although many people believe that creative artists are somewhat crazy, what they are really referring to is the unconventionally in their typical style of life. It is obvious that the P scale measures something broader than a pathological temperament. The fact that successful artists score even higher than non-successful ones may indicate greater aggressiveness, self-aggrandizement, and
Table I. Mean scores on P scale Males Studv G&z and G&z (1979a) Eysenck and Eysenck (1975) Eysenck and McGurk (1980) Mohan and Tiwana (1987) Eyxnck and Eysenck (1976) G&z and G6u (1979b) Eyxnck and Eyxnck (1976) Eyxnck and Eysenck (1975) Eysenck and Eyxnck (1976) Eysenck and Eyxnck (1976) Evscnck and Evsenck (1975) GIOUD Successful artists (German)t Art students (English) Delinquents (English) Creative writers (Indian): Prisoners (English) Professional artists (German) Psychotics (Schizophrenics) General students (English) Neurotics Endogcnous depressives General popularion n 37 27 614 100 1301 147 104 231 216 Mean* 8.14 7.67 7.48 7.05 6.55 6.53 5.66 4.84 4.19 4.10 3.78 n 41 Females Mean 4.52

58
2312

264 I10 72 203 332 68 3262

7.55 6.18 4.08 3.02 3.25 3.48 2.36

*Standard deviations range from 2.4 10 4.4, most around 3.0. tlncludes I female. :86 Male and 16 female, data nor broken down by xx.

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MARVINZUCKER.AIAN

an obliviousness to the needs of others, traits which combined with creative types of divergent thinking may make for success in the competitive art world. Eysenck (1983) has interpreted the Gotz and Giitz (1979a,b) data on German professional artists, as well as other studies showing relationships between creativity tests in normal populations, in support of the idea that creativity is a trait that links the P factor in personality and psychotic clinical disorders such as schizophrenia. While a case might be made for a link with manicdepressive disorder, I believe that anyone who has worked with schizophrenics would dispute the assumption that they are creative. Schizophrenics who have made contributions to the literary or visual arts are rare. The argument hinges on the meaning of the term creativity. Consider Rorschachs (1949) distinction between good original (0+) and bad original (0 -) responses on his test. 0+ responses, given frequently by artists but rarely by schizophrenics, are responses that construe the ink-blot in a way that is rarely, if ever, seen in the general population. However, if fits the form of the blot and thus represents the construing of reality in a unique way. Oresponses, given often by schizophrenics particularly chronic and paranoid types (Rapaport, 1946), are also unique but do not correspond to the form of the blot and combine elements of the blot in arbitrary and illogical ways. In most tests of divergent thinking a totally inappropriate response is not counted as an original response. Artists and other creative persons tend to be uninhibited and unconventional, but they do know the difference between reality and what they portray in their art. Writers like James Joyce do not talk to their friends in a word-salad or stream-of consciousness fashion. Schizophrenics are not creative, they are the unwilling victims of a mental disease that destroys their capacity for integrated information processing. Delinquents and prisoners also score very highly on the P scale, even higher than psychotics. If the P scale must be given in clinical label, these data would suggest that psychopathy would be more appropriate than psychoficism. Of course, it is possible that only one type of schizophrenic is characterized by high P scores. In fact, a study of psychotics (Verma and Eysenck, 1973) showed that paranoids scored higher than non-paranoid schizophrenics and affective disorders on the P scale. The highest correlate of P was a total score on a hostility inventory (rs = 0.74 for males and 0.65 for females). Much smaller but significant correlations for patients of both genders were found between P and staff ratings of paranoid projection and hostile belligerence. It appears that the hostile element of paranoid schizophrenia is what admits it to the P spectrum. Blaming the world for their problems is an attribution shared by paranoids and psychopaths.
Genetic studies

The genetic overlap between the disorders thought to be on the psychotic spectrum is more crucial to Eysencks concept of P than the mean scores of the groups on the phenotype measure. Eysenck assumes a broad spectrum of the genotype for psychoticism that includes schizophrenia, psychopathy (antisocial personality), manic-depressive (bipolar affective disorder), and endogenous depressive (major depressive disorders), citing the Heston (1966) study as evidence. In this study biological children of schizophrenic mothers born in the psychiatric hospital were adopted shortly after birth. The Ss were followed up along with a control group of foster children. In addition to the greater number of schizophrenics in the adopted children whose biological mothers had that disorder, significantly more were judged to have sociopathic (antisocial) personalities, neurotic personality disorders, and criminal and prison records. However, another adoption study, using Danish adoptees (Kendler and Gruenberg, 1984; Kendler, Gruenberg and Strauss, 1981; Kety, Rosenthal, Wender, Schulsinger and Jacobsen, 1975), has been done since Hestons research and does not support this broad a genetic spectrum for schizophrenia. Biological relatives of schizophrenic adoptees have higher incidences of DSM II chronic, latent or uncertain schizophrenic diagnoses, and higher rates of DSM III diagnoses of schizophrenia, and schizotypal and paranoid personality disorders, but they do not differ from relatives of controls in the frequencies of other types of non-psychotic psychiatric disorders (Kendler, 1987). Research on family incidence (Kendler, Gruenberg and Tsaung, 1985) shows that schizoaffective, paranoid and atypical psychotic disorders are found with above chance frequencies in the families of schizophrenics, but major affective disorders, antisocial and borderline personalities are not. Crow (1986) has taken a position on the genetics of psychotic disorders that is more compatible with that of Eysenck in that affective psychoses and schizophrenia are seen as related to each other

Personality

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395

on a continuum that has a genetic basis, rather than as discrete disorders. This conclusion is partly based on the existence of the schizoaffective group in which there is a mixture of features of both disorders and partly it is due to the failure to find a bipolar distribution of symptoms. The existence of the schizoaffective category does indeed pose problems, particularly since it is found in the families of both affective and schizophrenic disorders. However, there is no reason why two separate or partially overlapping sets of genes could not combine in many cases with an intermediate symptomatic picture. The existence of something less than bipolarity is also not evidence that the two disorders are not primarily distinct. In one study cited a trimodal distribution was obtained suggesting that the intermediate type (schizoaffectives?) might actually constitute a third group. Many of the studies cited in the Crow review predate the DSM III and the use of more objective diagnostic interview and rating methods. It is possible that some of the overlap of the disorders is due to diagnostic errors or inadequate histories. The fact remains that the disorders do differ in typical age of onset, prognosis, and the success of different drugs with the two disorders. Although some schizophrenics may respond positively to lithium or antidepressants and some affective disorders may respond to phenothiazines, most respond best to the specific class of medications considered appropriate for their disorder. This fact suggests that the underlying biochemical basis of the two disorders is different. However, this does not mean that there may not be diversity in the drug-response characteristics within a group, particularly in cases with atypical symptomatology. Considering the general trend in these studies, it would seem that the schizophrenic genetic spectrum includes schizotypal and paranoid personalities but not affective disorders or antisocial personality disorders. Each of these three types of disorder seems to have its own genotype rather than sharing a common one, as suggested by Eysenck and Eysencks (1976) concept of P. Which one then would provide the best clinical model for P? Perhaps this question can be answered by better definition of the traits that make up the supertrait. Eysenck and Eysenck (1985, p. 14) have defined the subtraits in the broad P dimensions as: aggressive, cold, egocentric, impersonal, impulsive, antisocial, unempathic, creative and toughminded. These subtraits describe small clusters of items which ended up in the P scale after factor analyses. The definition of P in terms of its constituent traits might be more reliably achieved by a factor analysis of scales rather than items, using scales which have good internal reliability achieved through statistical item selection or factor analytic methods.
A trait factor analytic approach to the P dimension

In order to define the basic dimensions of personality we (Zuckerman, Kuhlman and Camac, 1988) factor analyzed 46 personality scales taken from 8 multiphasic tests and selected as potential markers for 7 hypothesized factors: activity, sociability, impulsivity, socialization, sensation seeking, emotionality and social desirability. Many of the scales and tests were selected because of their use in current research on the biological bases of personality (Zuckerman, 1979, 1983). Factor analyses were done and oblique rotations performed for 7, 5, and 3 factor solutions. Factor scores were correlated across levels providing a picture of how the higher order factors combine narrower factors (Fig. 2). Sociability and activity factors combined to form the broad E factor; anxiety and anger merged on the N-Emotionality factor; and impulsivity, unsocialized tendancies, aggression and sensation seeking factors combined to form the broad P, or ImpUSS (Impulsive Unsocialized Sensation Seeking) factor. The generalizability of the factors across genders were assessed by calculating two sets of factor scores for each individual, one based on a factor analysis of male data and the other based on a factor analysis of the female correlations. The greatest agreement in factor structure emerged at the 3 factor level. The P-ImpUSS factor scores correlated 0.98 for males and 0.91 for females; the E-Sociability factor scores correlated 0.98 and 0.78; and the N-Emotionality factor scores correlated 0.97 and 0.83 for men and women. Correlations between non-corresponding factor scores within or between men and women were low and mostly insignificant showing good discriminant validity. Figure 3 is a factor plot showing the relation between the P-ImpUSS and E-Sociability (E-Sy) factors. Note that the EPQ E scale has the highest factor loading on the E factor and the EPQ P scale lies right on the axis of the P-ImpUSS dimension among the highest loading scales: boredom

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MARWS ZUCKERMAN

3 Factor

0.91

0.59

-0.45

0.96

0.63

0.77

$ff

e[

Factor

0.99

0.94

0.65

0.93

0.71

0.91

0.97

fi

k]

A&@ih

7Factor

Factor

score

correlations

across

levels

Fig. 2. Relations between factors derived from 3, 5 and 7 factor rotations of personality scales. From Zuckerman, Kuhlman and Camac (1988).

seeking. The factor is made up of almost all of the sensation seeking and impulsivity scales plus aggression and hostility at the positive pole. At the opposite pole we find socialization, responsibility, restraint and needfor cognitive structure. Figure 4 shows the relation between the P-ImpUSS and the N-Emotionality factor dimensions. This shows an interesting contrast between high and low P in the high N dimension. Hostility, anger, lack of control, and aggression are combinations of high P and high N, while succorance, conformity, and inhibition of aggression reflect a combination of low P and high N. In contrast, socialization and responsibility represent non-neurotic expressions of low P. The sensation seeking scales, in contrast to the aggression-anger cluster, represent non-neurotic types of high P since almost all of them fall in the high P-low N quadrant. This study provides an understanding of the P factor as a normal dimension of personality, since most of the traits that comprise it are normally distributed and only unusual at the extremes. If
P - ImpUSS

susceptibility, autonomy, risk taking and experience

J 0.7
SSS boredom SSS exps$ncr PRF
Buss

/ susceptibility JPIPirk taking .EASI seeking / stnsation seeking

SSS Dirlnhibltion aggression

hostility. Inhibitory control

KSP Monotony / avoidonce : EASX dscislon time .i SSS thrill 8 adventure seeking l KSP impulsivity PRF play . ST1 . flexibility est**m . EPQE

EASI ST1

activity. social energy

Jpl

adtptability

l EPO N . KSP detachment

JPI

level

l . CPI sociability

I
0.1 -0.1 0.2 0.3

E-Sy

l-o.4

-0.3

-0.2

-0.1

lKSP psychasthenia

. . 0.7 0.8 0.9 0.4 0.5 EASI sociability JPI social participation PRF PRF social . affiliation desirability
l

EASI fear
conformMy
l

-0.2

JPI KSP Inhlb.of

-0.3 . KSP social

Agg.. ,uccOrQce ST1

. EPQ L -0.5
l

desirability

r&aint
structue .

PRF cognitive

JPI

responsibility socialiratlon

-0.6
l

CPI

Fig. 3. Factor plot: P-ImpUSS vs E-Sociability dimensions.

Personality in the third dimension N - Emotionolity

l

397

EPON

KSP anxiety EASI emotionality

l

Buu

hortilify

9 EASI KSP Inhibition of aqqression EASI inhibitory .

anger control . PRF (Lock of1

aggression

. PRF

Cognitive

1lrc1re

CPI z0.6

rociollza?ion -0.5 -0.4 -0.3-0.2-0.1

I I
restraint

0.1 SSS boredom 0.1 0.2 0.2 0.4 KSP 0.5

I
.JPI

I -0.1

1 P,+F &.
EASI

i,bUbhity

responsibility . ST1

SSS dlsMibit~n sensation KSP -0.2 social der -0.3 .

seekIng:

l EPO L
. KSP

monol&y

EASI decision time

EPO E . JPI SSS th;l a

CPI sy
PRF so&L des :TI JPI r&y Self-esteem ST1 flexibility
l

.
PRF

susce~tibllity 0.60 0.7 1

~1mpUS-S

lEPO P
avoidance

. SSS erwrience seeking adventure o+:nomy . JPI Risk taking

level

~keffickncy -0.5 l ST1 emotional

control

Fig. 4. Factor plot: P-ImpUSS vs N-Emotionality

dimensions.

one must use a clinical label to describe this dimension, Psychopathy might be more appropriate than Psychoticism. The P factor is more complex than the E and N factors, encompassing traits of sensation seeking, impulsivity, non-conformity and a lack of restraint, responsibility, need to think in a structured way, and an unwillingness to live by the rules and norms of society (socialization). Taken together, these traits describe the classical picture of the psychopath. However, any one of the traits taken alone would not necessarily indicate an antisocial personality. The Gough (1957) Socialization (So) scale, which marks the negative pole of the factor, was first developed as a Delinquency subscale for the MMPI. It is remarkably effective in separating delinquent and felon groups from more socialized persons (Gough, 1957). Hare and Cox (1978) regard the So scale as the most discriminating questionnaire method for identifying clinical psychopathy and also useful in predicting psychophysiological aspects of the disorder (Hare, 1978). The SS scales Disinhibition, Experience Seeking and Boredom Susceptibility, which load highly on the P factor, also differentiate the primary psychopath from secondary psychopaths and other criminals (Emmons and Webb, 1974). BIOLOGICAL CORRELATES OF P-ImpUSS

The Eysenck and Eysenck (1976) hypothesis for the biological basis of the P dimension was derived from the fact of sex differences in P (males are higher) and aggressiveness as a component trait, suggesting that the hormone testosterone may play a role in the biological basis for the trait. Eysenck and Eysenck cite the greater incidence of first admissions among young males, although over all ages there is no gender difference in the number of hospitalized schizophrenics, and in one study data on community prevalence show more women with the disorder (Robins, Helzer, Weissman, Orvaschel, Gruenberg, Burke and Regier, 1984). Twice as many women as men have major depressive episodes although the incidence of bipolar disorder is not different for men and women. A better case can be made for antisocial personality disorder where males outnumber females about 7 to 1. Eysenck and Eysenck also consider Claridges (1967, 198 1, 1985) conception of psychopathology as based on a failure of modulation of central nervous system arousal, and Grays (1973)

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MARVIN ZUCKERMAN

identification of the P dimension with intraspecies aggressiveness in animals and with both testosterone and a fight-flight system centered in the medial hypothalamus and amygdala. However, as yet the Eysencks have not clearly formulated a biological model for P. Both the Eysencks and Claridge have looked to schizophrenic psychosis as one of the clinical models for the P dimension. Claridge (1981, 1985; Claridge and Clark, 1982) has shown reversals of the usual direction of correlation between measures of arousal and autonomic reactivity in both schizophrenic and high P score normal groups, and suggested that this shows the lack of modulation of arousal as a basis for P. However, the relationships between measures of arousal are often not predictable in any population and measures of arousal are often state dependent and therefore subject to immediate effects of experimental conditions. This literature is far too complicated to discuss in this paper. Support for Eysencks position viewpoint comes from the studies of Gattaz (1981) and Gattaz, Seitz and Beckmann (1985) with one particular human leucocyte antigen (HLA-B27). Gattaz (1981) says that HLA-B27 appears in about 36% of one type of schizophrenic, chronic paranoids, as contrasted with only 8% in a control group. Gattaz et al. (1985), pooling data from several studies, report an incidence of the antigen in the general schizophrenic population of 14% as compared to 6% in controls. While not an impressive marker for schizophrenia, the antigen assumes significance by the finding of Gattaz (198 1) that chronic paranoid schizophrenics with the antigen scored higher on the EPQ P scale than those without the antigen. There were no differences between the two groups on E, N or L scales. Gattaz et al. (1985) then extended the comparison to a psychiatrically normal group. This antigen is also found in increased frequency in one type of physical disease, arthropathic disorders. Gattaz et al. compared arthropathic patients with and without the antigen on the EPQ and again found that the antigen positive group scored higher on the P scale but not on the other EPQ scales. The results relating a variable that discriminates one group from another and also relates to differences within both groups on the dimensional measure fulfill Eysencks criteria for dimensionality. It is difficult, however, to see how a discontinuous variable, like the presence or absence of an antigen, would support a dimensional continuum hypothesis. Furthermore, the role of this particular antigen in schizophrenia, its specificity to schizophrenia as compared to other psychiatric disorders, and its behavioral significance, if any, is uncertain. It is encouraging that the antigen is not related to the other EPQ scores like N, because this suggests that the findings are probably not attributable to some general factor such as stress or stress susceptibility.
P as Psychopathy: a hypothesis

I would suggest that antisocial personality disorder represents the extreme end of the P dimension, and the clinical state of hypomania represents an episodic expression of P tendencies. Perhaps the dimension may also subsume hostile paranoid psychoses, including some schizophrenics, but as I would define the dimension, it would not include schizophrenics with negative symptomatofogy such as withdrawal, blunted emotions, and lack of interest and motivation. Kish (1970) found that such schizophrenics are particularly low on sensation seeking trait and sensation seeking is an important component of the P dimension, as shown by Zuckerman et al. (1988). Even the antigen in the studies of Gattaz is primarily found in chronic paranoids, and only in a minority of them. But if we define P in terms of a particular grouping of normal traits, such as impulsivity, sensation seeking, and socialization, then we can look for common biological correlates of these in normal, rather than clinical, populations.
Conditioning

Individual differences in classical conditioning have played an important role in Eysencks (1957, 1967) theory. According to the theory, introverts are likely to show better conditioning than extraverts because to their greater cortical arousal. Extraverts were thought to be more antisocial and prone to criminal behavior because socialization was mediated through conditioning (association of punishment with antisocial actions) and extraverts were less likely to learn conditioned avoidance and more likely to rapidly extinguish such conditioned responses. The study of Eysenck and Levey (1972) showed that only the impulsivity component of the E scale, and not the sociability one, accounted for variations in eyelid conditioning. This was no problem at that time because

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Eysenck and Eysenck (1963) held to the two-component theory of extraversion. With the construction of the P scale and its inclusion in the EPQ, the nature of the E dimension was changed. Most of the impulsivity items were discarded, found their way into the P scale, or became part of separate scales for impulsivity (Eysenck and Eysenck, 1977). This redefinition of the constructs in terms of the scales defining them required a reanalysis of the relationship between conditioning and dimensions of personality since impulsivity, which was most related to conditionability, was no longer part of the E dimension. Eysenck and Eysenck (1985) have argued that it is only narrow impulsivity (acting quickly without thinking) and nonplanning that relate primarily to P and not to E, while liveliness correlates mostly with E, and risk taking and total impulsivity relate about equally to E and P. Liveliness seems to be more of a measure of activity or energy level than of impulsivity; it correlates very lowly (around 0.2) with the other impulsivity scales. In the Zuckerman et al. (1988) factor analysis, none of the impulsivity scales had their primary loading on the E factor although many had equal or secondary loadings on this factor. Instead, nearly all of the impulsivity scales loaded primarily on P. Activity, however, was a component of E. Eysenck is still correct in saying that there is still some relationship between E and impulsivity traits. Frcka, Beyts, Levey and Martin (1983) found that while neither E or P showed main effects on eyelid conditioning there was a significant interaction between them. However, the interaction was somewhat difficult to interpret because both those high on both dimensions and those low on both showed superior conditioning to those high on either one and low on the other one. However, in a subsequent experiment using electrical stimulation, rather than an air-puff, as the UCS for the eyeblink, Beyts, Frcka, Martin and Levey (1983) found that P, but not E, showed a main effect for conditioning: high P Ss conditioned poorly compared to low P Ss. Neither of these studies showed a relationship between conditioning and new impulsivity scales developed by Eysenck and Eysenck (1977). In a more recent study, Frcka and Martin (1987) analyzed the conditioning data using short, factor analytically derived impulsivity (IMP) scales including: (1) a narrow IMP scale describing acting quickly without thinking; (2) a scale described as IMP in the broad sense, but which actually seems to consist almost entirely of items from the Disinhibition and Boredom Susceptibility subscales of various versions of the Sensation Seeking Scale (SSS, Zuckerman, 1979); (3) a Venturesomeness scale consisting largely of items from the Thrill and Adventure Seeking subscale of the SSS. Of these three subscales, only the narrow IMP scale yielded a significant main effect on conditioning; high IMP Ss showed less evidence of conditioning than lows. The final conclusion is that a narrow concept of impulsivity, consisting of fast, incautious decision making, is related to conditioning, but broad E and IMP and sensation seeking traits are not. OGorman and Lloyd (1987) found similar results in the personality correlates of cortical arousal as measured by the EEG: narrow rather than broad impulsivity or E is negatively related to cortical arousal. Revelle, Anderson and Humphreys (1987) also report that the effects of a caffeine-induced arousal on performance are related to narrow impulsivity but not to the sociability component of extraversion. Since Eysencks theory explains the differences in conditionability in terms of arousal, these results reinforce the conclusion that the relevant dimension is impulsivity of the narrow (fast decision time) type. The inconsistent findings with P may reflect the fact that narrow IMP is only one part of this factor. Also, eyelid conditioning may not be the optimal paradigm for assessing the relation with the broad personality dimension. Studies of psychopaths show poor skin conductance conditioning, particularly when electric shock is used as the UCS (Hare, 1978). Psychopaths are also poor at passive avoidance learning in tasks mediated by fear or anxiety, but they are as good as non-psychopaths when material rewards or punishments are involved (Schmauk, 1970). Augmenting-reducing of cortical Evoked Potentials (EPs)

Buchsbaum and Silvermans (1968) method of using EPs in relation to stimulus intensity has been a very useful technique linking personality variation in the normal range of sensation seeking and impulsivity to clinical manifestations in affective disorders, schizophrenia and antisocial tendencies (Buchsbaum, Haier and Johnson, 1983; Zuckerman, Buchsbaum and Murphy, 1980). Essentially, the method consists of presenting stimuli sampling a range of stimulus intensities, and measuring one of the early EP components (PI-Nl, lOO-140msec post-stimulus), and assessing

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ZUXERMAS

24 r

Low disinhibiters

10

I
2 Stimulus

I
4 intensity

I
6

I
16

Fig. 5. Mean visual evoked potential amplitudes (EP Amp) of PI-N1 component for Ss scoring high and low on the Disinhibition subscale of the Sensation Seeking Scale (form IV) at each of five stimulus intensities (Joules/cm* per pulse at I = 0.08, 2 = 0.12. 4 = 0.17, 8 = 0.20. 16 = 0.25). Amplitudes are in arbitrary mm deflection units. Each mm unit = 0.42 pV. From Zuckerman, Murtaugh and Siegel (1974). Reprinted with permission.

the relationship between stimulus intensities and the averaged amplitudes of response at each intensity for each S. The relationship may be expressed as a slope. High positive slopes are usually called augmenting and negative or very low positive or zero slopes are called reducing, although measures of the function have yielded an essentially continuous and normal distribution (Buchsbaum et al., 1983). The term augmenting-reducing was carried over from Petrie (1967) where its operational measure was a psychophysical (width-judgements) task rather than an actual measure of brain reactivity. The use of Petries term was unfortunate on two counts: first, it carried over surplus meanings attached to Petries concept, sometimes diametrically opposed to the actual results with the EP method (Davis, Cowles and Kohn, 1983, 1984; Zuckerman, 1986); second, it created the idea of a typology rather than the actual fact of a dimension. Buchsbaum (1971) first reported some evidence of a positive relationship between EP augmenting and sensation seeking. Zuckerman, Murtaugh and Siegel (1974) found a relationship between visually evoked EP augmenting and one of the sensation seeking scales: Disinhibition, the subscale most consistently related to psychopathy and hypomania. Figure 5 shows the relationship for the visual EP (Zuckerman, Murtaugh and Siegel, 1974). Although the high disinhibitors showed a generally accelerating EP in reaction to increasing stimulus intensity and the lows showed a decelerating function, the difference between the groups occurred primarily at the highest stimulus intensity where the highs showed marked augmentation and the lows showed clear reduction. Since that study, the Disinhibition subscale and sometimes the General SSS have been positively related to visual EP augmenting in three more studies (Lukas, 1987; von Knorring, 1981; Zuckerman, Simons and Como, 1988). One study (Haier, Robinson, Braden and Williams, 1984) failed to find a relationship between visual EP augmenting and Disinhibition, probably because it did not use the extreme stimulus intensity level which usually yields the difference between high and low sensation seekers. The Disinhibition or General SS scales have also been related to auditory EP augmenting in 5 studies (Coursey, Buchsbaum and Frankel, 1975; Lukas and Mullins, 1985; Mullins and Lukas, 1984; Orlebeke, Kok and Zeillemaker, 1984; Zuckerman et al., 1988). Figure 6 shows the relationship between Disinhibition and auditory EPs in the study by Zuckerman et al. (1989). A study by Lukas and Mullins (1983) did not find a relationship between the SS scale and auditory EP augmenting because (they say) they did not require the Ss to attend to the stimuli as they did in their later studies. In the Zuckerman et al. study (1974) EPI E and N scales were not related to EP augmenting. I know of no studies using the P scale. However, Barratt and Patton (1983) found a relationship between their scale of impulsivity and visual EP augmenting. Clinical groups characterized by impulsivity, sensation seeking, and antisocial behavior tend to show augmenting EP patterns. Augmenting is characteristic of manic-depressive disorders (Buchsbaum, Landau, Murphy and Goodwin, 1973; Gershon and Buchsbaum, 1977) alcoholics (Coger,

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401

8.0

P
a
8 7.5

Low disinhibiterr 6.5

6.0

50

I
65 Stimulus intensity IDSI

I
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J 9s

Fig. 6. Mean auditory evokedpotentialamplitudes (EP Amp) of PI-N1 component for Ss scoring high and low on the Disinhibition subscale of the Sensation Seeking Scale (form V) at each of 4 stimulus intensities (SO, 65, 80 and 95 dB). Amplitudes are in NV units.

Dymond, Serafetinides, Lowenstein and Pearson, 1976; von Knorring, 1976), and male delinquents (Silverman, Buchsbaum and Stierlin, 1973). In contrast to these groups, acute schizophrenics tend to be reducers for visual (Landau, Buchsbaum, Carpenter, Strauss and Sacks, 1975) and somatosensory EPs (Davis et al., 1979). However, chronic schizophrenics tend to be augmenters (Asarnow, Crowell and Rennick, 1978; Schooler, Buchsbaum and Stierlin, 1976) and acute schizophrenics who do show an augmenting pattern tend to have a poorer prognosis than those who show a reducing pattern (Landau et al., 1975). What this suggests is that reducing of cortical activity in schizophrenia represents a protective adaptation to some more basic biological disturbance. Acute schizophrenics are often characterized as overwhelmed by stimulation and intolerant of high intensity or complexity of stimuli, a condition known as an input dysfunction (McGhie and Chapman, 1961; Payne, Matussek and George, 1959; Venables, 1964). Acute schizophrenics in an overaroused state may avoid stimulation in order to reduce their levels of arousal (Broen, 1968; Epstein, 1970; Mednick, 1958). Indeed, schizophrenics, particularly those who are more behaviorally retarded, have low scores on the Sensation Seeking Scale (Kish, 1970). The EP augmenting-reducing phenomenon has also been found in cats and the behavioral correlates of individual differences in the biological trait are suggestively similar to those found in humans. Hall, Rappaport, Hopkins, Griffin and Silverman (1970) and Lukas and Siegel (1977) found that augmenting cats were judged to be more exploratory, active, and emotionally responsive to novel stimuli while reducer cats were more socially avoidant and unreactive to novel stimuli, These findings, based on observational behavior, were replicated in a recent experiment by Saxton, Siegel and Lukas (1987). Augmenter cats were more active in the behavioral chamber, tended to show more exploratory behavior and approach the stimuli, were more easily adapted to the experimental situation, and more rapidly learned a fixed interval bar-pressing task. Reducer cats were more emotional and tense, and tended to withdraw from the stimuli. However, reducers were more successful in controlling bar pressing behavior during an inhibitory DRL task suggesting a relationship between EP augmenting and impulsivity, and between EP reducing and restraint. von Knorring and Perris (198 1) found correlations linking the augmenting-reducing phenomena in humans to certain neurotranmitter metabolites and enzymes which will be discussed next. Augmenters were characterized by low levels of serum dopamine-/I-hydroxylase (DBH), 5-hydroxyindoleacetic acid (5-HIAA, a metabolite of serotonin) in the cerebrospinal fluid (CSF), homovanyllic acid (HVA), and /3-endorphins in the CSF. Negative correlations have also been found between EP augmenting and the enzyme monoamine oxidase (MAO) in blood platelets (Buchsbaum et al., 1973; Haier, Buchsbaum, Murphy, Gottesman and Coursey, 1980) in depressive patients and students showing indications of affective disorders, but not in normal students. These findings bring us one step closer to the genotype for the P-ImpUSS dimension, for genes are more directly involved in the building of enzymes and neurotransmitters than in behavior or psychophysiology.

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Monoamine neurotransmitters,

enzymes and metabolites

The monoamines are classified as such because of the similarity of their molecular structures. One subsclass is called the catecholamines and includes the neurotransmitters dopamine, norepinephrine (NE), and epinephrine (Epi). Although some Epi is found in the brain, dopamine and NE are the principal neurotransmitters there. The second subclass is the indoleamines of which serotonin is the principal one in the brain. The biosyntheses of the neurotransmitters are regulated by enzymes that convert precursor compounds along a number of steps to the final form of the neurotransmitter. Other enzymes are involved in the degradation of the neurotransmitter yielding metabolites, or breakdown products, which are eventually eliminated from the body. Figure 7 shows the primary steps in the biosyntheses and breakdown of NE and serotonin. The sequence in the dopamine neurons is not shown because up to the point of conversion of dopamine to NE it is the same as that for NE. Looking first at the noradrenergic processes, we see that tyrosine, an amino acid ingested in certain foods, is converted by the enzyme tyrosine hydroxylase to L-DOPA. L-DOPA is converted by DOPA decarboxylase to dopamine, which is the final neurotransmitter in that system. In the NE neurons the enzyme dopamine-fl-hydroxylase (DBH) attaches a hydroxyl group to dopamine, which becomes NE. This last process takes place within the vesicles containing the neurotransmitter. Low levels of DBH would mean that NE would also be low since it would be depleted by activity in the NE system and would not be replaced at an adequate rate. In the serotonergic system, the amino acid trytophan is converted by the enzyme tyrosine hydroxylase to 5-hydroxytryptophan which in turn is transformed to 5-hydroxytryptamine (serotonin). Monoamine oxidase (MAO) and catechoi 0-methyltransferase (COMT) are enzymes involved in the degradation of the monoamines. MAO is contained within the mitochondria of the neurons and acts on neurotransmitter that is taken up into the neuron. MAO is the principal agent of inactivation of intraneuronal catecholamines, while COMT is the principal extraneuronal mode of catecholamine inactivation. The metabolites, or breakdown products, of the neurotransmitters provide one of the main ways of estimating the activity in the neurotransmitter systems. While NE and dopamine may be assayed in the cerebrospinal fluid (CSF), much of the research on humans depends on assays for the NE metabolite 3-methoxy4hydroxyphenygfycol or MHPG, the dopamine metabolite homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). Both MHPG and the enzyme DBH, involved in the biosynthesis of NE, can be sampled in CSF and from blood plasma. MHPG is also obtained from urine but urinary MHPG seems to be inferior to CSF and plasma MHPG as an index of brain NE activity; most of it is derived from peripheral NE turnover. MAO is usually sampled from blood platelets.
Dopamine-/I-hydroxylase (DBH)

DBH measures from CSF and plasma correlate highly (Ballenger, Post, Jimerson, Lake, Murphy, Zuckerman and Cronin, 1983; Lerner, Goodwin, von Kammen, Post, Major, Ballenger and Lovenberg, 1978) suggesting either a common source like brain DBH or the possibility that the peripheral and central NE systems work synchronously. In the Ballenger et al. study plasma DBH was negatively correlated with sensation seeking trait, and this result was also found in other

Fig. 7. Biosynthesis

and breakdown

of norepinephrine

and serotonin.

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studies (Kulcsar, Kutor and Arato, 1984; Umberkoman-Wiita, Vogel and Wiita, 1981; but not in the study by Murphy, Belmaker, Buchsbaum, Martin, Ciaranello and Wyatt, 1977). Ballenger et al. also found a negative correlation between sensation seeking and NE in the CSF, consistent with the idea that low levels of DBH mean that less NE will be produced. Low DBH has been associated with certain types of deviance in disturbed populations. Major, Lerner, Goodwin, Ballenger, Brown and Lovenberg (1980) found that patients in an alcohol rehabilitation center with low CSF DBH were higher than those with high DBH on a number of MMPI scales including: hypochondriasis, hysteria, psychopathic deviate, paranoia, psychasthenia and schizophrenia. Rogeness (1984) compared case records of emotionally disturbed boys with near zero levels of plasma DBH and the records of boys from the same psychiatric facility with normal or high DBH. Two diagnoses were characteristic of the boys with low DBH: undersocialized conduct disorder, and borderline personality disorder. The high DBH boys were more likely to be diagnosed socialized conduct disorder. There was no difference in the incidence of diagnoses of schizophrenia in the two groups. The low DBH group differed from the highs in terms of a greater frequency of symptoms involving firesetting, cruelty to animals, homicidal threats with knives or guns, and severe problems of impulse control in general. Those in the low DBH group were also characterized as failing to establish any kind of meaningful relationships with others. The absence of significant amounts of DBH in the plasma is associated with a syndrome that closely resembles the Eysencks concepts of P. However, in the Ballenger et al. (1983) study of normals no relationship was found between the P scale and CSF or plasma DBH suggesting that the relationship may only exist among deviant groups and at extremely low levels of the DBH distribution.
Monoamine oxidase (MAO)

In contrast to DBH, the enzyme MAO, involved in the breakdown of the monoamines, is fairly stable, resistant to stress and extreme alterations in clinical conditons like the change from mania to depression in a bipolar disorder (Murphy, Wright, Buchsbaum. Nichols, Costa and Wyatt, 1976). However, certain demographic differences are apparent. Females are higher than males in platelet MAO (Murphy et al., 1976) and MAO increases with age in human brain, platelets and plasma (Robinson, Davis, Nies, Revaris and Sylvester, 1971). Individual differences related to platelet MAO appear shortly after birth. Sostek, Sostek, Murphy, Martin and Born (1981) obtained blood from the newborns umbilical cords at birth for platelet MAO and plasma amine oxidase (AO) determinations. Low MAO babies were awake and active more than high MAO babies. They also were rated more highly on motor maturity and facility scales and on two signs of autonomic lability. The significance of these correlates for later personality development is ambiguous but the fact that such behavioral differences are related to MAO or A0 before the social environment has had a significant impact suggests a primarily genetic influence on these aspects of temperament. Two large scale studies, one done in America (Coursey, Buchsbaum and Murphy, 1979) and one in Sweden (von Knorring, Oreland and Winblad (1984), have compared male Ss from the extremes of the platelet MAO distribution (upper and lower deciles). Both studies showed more alcohol, tobacco and illegal drug use in low MAO Ss. The American study also showed more time spent in social activities and more convictions for criminal offenses in the low MAO Ss. The Swedish study also found higher sensation seeking scale scores on an abbreviated version of the SSS (omitting all of the Disinhibition and part of the Experience Seeking subscales). The largest difference was on the Boredom Susceptibility (BS) subscale. Although the P scale was not used in this study, it should be remembered that the BS scale was the scale loading most highly on the P-ImpUSS factor in the study by Zuckerman et al. (1988). E and N scales showed no relationship to MAO. Apart from the negative relationship between sensation seeking and MAO in the von Knorring et al. (1984) study, significant negative correlations have been found in studies by ArquC, Segum and Torrubia (1985) in groups of normals and patients and Murphy et al. (1977) and Schooler, Zahn, Murphy and Buchsbaum (1978) in two groups of male students and one out of two groups of female students. The correlations in the studies by Ballenger et al. (1983) and Schalling, Edman and Asberg (1983) were also negative but did not reach significance. While the typical correlations

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in these studies are not high, the number of significant findings and the fact that all correlations are negative show that the association is not produced by chance alone. Low platelet MAO levels have been found in bipolar (manic-depressive) affective disorders (Murphy and Weiss, 1972) but not in unipolar major affective disorders (Wyatt and Murphy, 1976). Among depressives, MAO is lower in primary than secondary depressions or those associated with borderline personality, lower in retarded than agitated depressions, and lower in delusional and endogenous depressions than in other types (Davidson, McLeod, Turnbull, White and Feuer, 1980). The low MAO levels are found in the non-affected relatives of bipolar disorders as well indicating that low MAO is a genetic marker but not a sufficient explanation for the disorder itself (Leckman, Gershon, Nichols and Murphy, 1977). Low MAO levels are also found in alcoholics (Major and Murphy, 1978; Sullivan, Cavenar, Maltbie, Lister and Zung, 1979; Sullivan, Stanfield and Dackis, 1977) and marihuana users (Stillman, Wyatt, Murphy and Rauscher. 1978). In a meta-analysis of the results of eight studies comparing paranoid and nonparanoid schizophrenics, Zureick and Meltzer (1989) found that while paranoid and hallucinating schizophrenics had lower levels of MAO than controls, other types of schizophrenics had values higher than those of normal controls. Both DBH and MAO enzymes seem to be related to the P-ImpUSS dimension, as indicated by trait scale correlations (sensation seeking, impulsivity), and to activities such as drinking, drug abuse, and criminal infractions. Furthermore, some of the clinical disorders most highly involved in the P dimension, manic-depressive, alcoholism, drug abuse, antisocial personality and paranoid schizophrenia, also tend to have low levels of one or both of these enzymes. While DBH is specifically involved with the noradrenergic system, MAO is a regulating enzyme in all of the monoamine systems and therefore tells us little about which of these systems may be involved in the lack of behavioral control and the seeking of sensation in the face of risk that seems to characterize those persons with low MAO levels. The metabolites of the monoamine neurotransmitters in CSF has been used in a few personality studies. While the results are still tentative, some suggestions of P related findings are discernible.
Serotonin

The serotonin metabolite 5-HIAA is usually obtained from CSF and therefore little is known about its reliability. Schalling, Asberg and Edman (1984) correlated CSF 5-HIAA with various trait measures in normals, depressed patients, and non-depressed patients. The P scale was negatively and significantly correlated with 5-HIAA in the normal and non-depressed groups; neither E or N correlated with this serotonin metabolite. Monotony avoidance correlated negatively with 5-HIAA in both patient groups but not in the normal group. A negative correlation of 5-HIAA with impulsivity and a positive correlaton with socialization were only found in the non-depressed patient group. Four of the six significant findings occurred in this group. While the diagnoses are not given for this group, one would suspect that it contained a large number of personality disorders of an acting-out type because these are the only patients in which depression is not usually a problem. Members of a group of personality disorders were assayed for CSF 5-HIAA and their htstones were rated for relative degrees of aggressiveness by Brown, Goodwin, Ballenger, Goyer and Major (1979). A very high and significant negative correlation (r = -0.78) was found between aggressiveness and the serotonin metabolite. Brown, Ebert, Goyer, Jimerson, Klein, Bunney and Goodwin (1982) also found that the Buss-Durkee measure of Hostility and the Psychopathic Deviate scale of the MMP I correlated negatively with 5-HIAA in a group with borderline disorders and some psychotic symptomatology. In both studies by Brown and his colleagues, the Ss with antisocial, and impulsive type of personality disorders had higher aggression and lower 5-HIAA levels than more passive types of personality disorder. Low levels of the serotonin metabolites are also associated with violent acts of murder or suicide attempts (Asberg, Bertilsson and Martensson, 1984; Lidberg, Tuck, Asberg, Scalia-Tomba and Bertisson, 1985; Van Praag, 1984, 1986; Van Praag and Plutchik, 1984). Lower levels of serotonin itself were found in the hypothalamus of nonschizophrenic suicide victims as opposed to the brains of controls who died of natural causes (Korpi, Kleinman, Goodman, Phillips, DeLisi, Linnoila and Wyatt, 1986). An increase in numbers of serotonin receptors, a sign of decreased serotonin activity, was found in the frontal cortices of

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violent suicide victims compared with controls who died from trauma or cardiac arrest. Van Praag (1984) showed that the suicide attempters with low serotonin levels had prior histories of aggressive and hostile behavior and constituted a special type of depressive in which both extrapunitive and intropunitive tendencies were combined. Soubrik (1986) has summarized the animal literature which shows that serotonin depletion by a specific drug increases predatory and shock-induced aggression in rats. File, Hyde and MacLeod (1979) found that chemical lesioning of the serotonergic system facilities social contact and sexual behavior as well as aggression in rats. Soubriks integration of the animal and human data suggests to him that serotonin normally inhibits behavior in conflict situations which have been associated with punishment or where there is the expectation of punishment. Reduction of serotonin reduces conflict and makes the organism more prone to act impulsively. According to some theories this release of inhibition would occur because serotonin is a critical neurotransmitter mediating fear (Gray, 1982). However, serotonin system lesioning does not produce a fearless animal, but actually one that is prone to exaggerated startle responses and fearfulness in novel situations (Ellison, 1977). Extrapolating from the animal studies to human personality dimensions, extremely low serotonin may be related to a combination of high P and N (rather than one of high P and low N), recalling that this is the factor quadrant in which we (Zuckerman et al., 1988) found human traits of aggression, anger and hostility.
Norepinephrine (NE)

NE is often measured by its metabolite MHPG in CSF, plasma or urine, although NE itself may be measured from any of these sources. CSF NE and MHPG are fairly reliable over periods of l-6 months (Linnoila, Ninan, Scheinin, Waters, Chane, Bartko and Van Kammen, 1983). Ballenger et al. (1983) found a negative relationship between sensation seeking and CSF NE; plasma MHPG correlated positively and significantly with questionnaire measures of hostility and sexual experience (number of sex partners), and negatively with trait measures of anxiety and neuroticism. Brown et al. (1979) found a positive relationship between CSF MHPG and ratings of aggression in men but most studies which have found a negative relationship between aggression and the serotonin metabolite have not found any relationship of aggression to CSF MHPG (Brown et al., 1982). CSF NE tends to be extremely elevated in states of mania and somewhat elevated in states of depression (Post, Jimerson, Ballenger, Lake, Uhde and Goodwin, 1984). In contrast, urinary MHPG is high in manic states and low in depressed states (Schildkraut, Orsulak, Schatzberg and Rosenbaum, 1984). A lack of regulation is seen in bipolar disorders with shifts from underactivity to overactivity in the NE system. Interestingly, the shift from low or normal to high activity seems to precede the changes in a clinical state.
Epinephrine (Epi) or adrenaline

Olweus (1986) found negative correlations between urinary Epi and peer ratings of unprovoked physical aggression in Swedish adolescent school boys. However, Epi also correlated negatively with extraversion and positively with an anxiety trait scale. Rated aggression correlated positively with extraversion but not with anxiety. Similar relationships were found for urinary NE but they were less consistent and significant than those for Epi. In another study a group of highly aggressive bullies had lower Epi levels than normal groups of boys. Magnusson (1985) found that there were negative correlations between urinary Epi and aggressiveness and motor restlessness in normal 13 yr old boys. Both behavioral variables and Epi excretion at age 13 predicted adult criminality in the same group at ages 18-25 and Epi correlated negatively with number of registered criminal offenses (chronicity or recidivism). The data suggested that motor restlessness was the more significant behavioral variable both in relation to Epi and prediction of adult criminality. Adrenergic reactivity also seems to be low in more psychopathic adults (Lidberg, Levander, Schalling and Lidberg, 1978). Men awaiting trial in Sweden were classified into high and low psychopathic groups on the basis of Goughs Delinquency (De) scale (an earlier version of the Socialization scale). Epi and NE levels were measured prior to their trial and on the actual day

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of their trial. Low De prisoners showed increases in both E and NE on the day of the trial, but high De Ss showed little change in the catecholamines suggesting a deficient stress response.
Dopamine

In correlational studies of the dopamine metabolite HVA obtained from CSF the pattern of relationships is similar to those found for the serotonin metabolite 5-HIAA, only somewhat weaker (Schalling ef al., 1984). This is not unexpected since the two metabolites in CSF have been found to correlate very highly for reasons unknown. CSF HVA shows a high retest reliability (Linnoila et al., 1983) so unreliability is not the source of its general failure to correlate highly with psychological variables. Since drug abusers who use stimulants tend to be even higher sensation seekers than those who use depressants (Carrol and Zuckerman, 1977), and since the major effect of stimulants like amphetamine and cocaine seems to be on dopaminergic systems, the administration of stimulants to Ss furnishes an experimental approach to this system. The occurrence of paranoid psychotic episodes in chronic amphetamine and cocaine addicts has been noted for some time. Violent, senseless murders are often committed by chronic stimulant drug abusers. Paranoid, hostile psychotic reactions have been produced in volunteers by increased doses of amphetamine, although the initial effects are usually pleasant for the Ss (Griffith, Cavanaugh, Held and Oates, 1972). While the immediate implication of such studies and clinical data suggest that high levels of dopamine activity might be involved in the P-ImpUSS dimension, Ellison (1979) has suggested that high levels of amphetamine may actually damage the dopamine systems making the receptors supersensitive to the low levels of dopamine produced in the neurons. Another way of increasing dopamine activity is to administer the dopamine precursor L-DOPA. L-DOPA has been used in treatment of neurological and psychiatric patients with a frequent complication of precipitation or worsening of a psychotic disorder. Given to bipolar depressed patients, L-DOPA frequently throws the patient into the manic phase of the disorder (Murphy, 1977). Given to patients suffering from long-term Parkinsonism conditions, L-DOPA often changes the patient from the torpor and unresponsiveness of the neurological condition into a manicy, restless, excited, psychotic condition after a brief sojourn in a euphoric, sociable, optimal state (Sacks, 1983). However, Sacks notes the effects are individual depending in part on the patients personality before he developed the Parkinsonism disease.
Cortisol

The release of the hormone cortisol from the adrenal cortex during psychological stress is the end result of a stress pathway originating in the higher brain centers, mediated through the hypothalamus which secretes corticotropin-releasing factor (CRF). CRF causes the anterior pituitary to release adrenocorticotropic hormone (ACTH) and ACTH is carried to the adrenal cortex where it results in the release of corticosteroid hormones, including cortisol. Although Trhskman, Tybring, Asberg, Berthisson, Lanlto and Schafiing (1980) reported a substantial correlation between urinary and CSF cortisol, Ballenger et al. (1983) found no significant correlations among CSF, plasma and urinary cortisol. Among the normal volunteers in the Ballenger et al. (1983) study, CSF cortisol correlated negatively with 3 markers for the P dimension: the EPQ P scale, the SSS Disinhibition scale, and a report of the number of heterosexual partners given in response to a sex experience inventory. CSF cortisol also correlated negatively with the MMPI Ego Strength scale and positively with anxiety state on the morning of the lumbar puncture. Plasma cortisol showed tendencies in the same direction as CSF cortisol on sensation seeking, but in addition correlated negatively with the MMPI Hypomania and Depression and EPQ Neuroticism scales and positively with the Ego Strength scale. Urinary cortisol showed only one significant correlation: a positive one with Depression on the MAACL trait form. Urinary-free cortisol is high in both bipolar and unipolar depressed states and low in manic states (Rubinow, Post, Gold, Ballenger and Wolff, 1984). Depressed patients also have high cortisol levels in CSF (Traskman et al., 1980). Studies of individual bipolar patients have shown that cortisol is high in their depressed phase and low in the manic phase. The dexamethasone suppression test (DST), developed by Carroll, Feinberg, Gneden, Tarika, Albala, Haskett, James, Kronful, Lohr, Steines, de Vigna and Young (1981), is based on the normal suppression of cortisol

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release by dexamethasone. In patients with the endogenous melancholic type of depression there is usually a failure of the drug in suppressing cortisol release which, according to early reports, rarely occurs in other types of patients including those with dysphoric depressions. Plasma cortisol elevations are a common reaction after major operations such as open-heart surgery (Naber and Bullinger, 1985) but they subside in all but those with major depressive episodes following surgery. Virkkunen (1985) measured urinary cortisol in habitually violent offenders. A group who combined antisocial personality disorder with habitually violent tendencies had lower cortisol than other groups without either or both of these two qualities. Cortisol in the brain, like serotonin, may have a behaviorally inhibitory effect while urinary cortisol may be more reflective of current stress and depression. Low levels of brain cortisol may put one at risk for impulsive and antisocial behavior.
Factor analysis of psychological traits and neurochemical variables

Most studies compare one neurochemical variable with a single psychological variable. Since many of these factors tend to interact biologically, a factor analysis of a broad group of neurochemical variables along with psychological variables might be enlightening in the search for common psychobiological dimensions. A factor analysis (Zuckerman, Ballenger and Post, 1984) was done of most of the relevant variables in the Ballenger et al. (1983) study with the results shown in Fig. 8. This figure shows a plot of two of the three factors rotated. Factor I along the vertical dimension is clearly identifiable as the P-ImpUSS factor with loadings from sensation seeking, the MMPI Hypomania, and the EPQ P scales. Factor II is identifiable as the N dimension with the EPQ N scale at the negative pole. At the negative pole of the P factor are CSF cortisol and norepinephrine with the highest loadings, followed by plasma DBH, serum cortisol and plasma amine oxidase with lesser loadings. Plasma and urinary MHPG define the positive pole of neuroticism. The association of cortisol and NE at the negative pole of the P factor is consistent with studies showing that adrenergic stimulation in the CNS increases ACTH and thereby increases plasma corticosteroid levels (Pepper and Krieger, 1984).
Gonadal hormones

Eysenck proposed that the hormone testosterone may be a major part of the biological basis of the P dimension because of marked sex differences on the P scale as well as the behavioral traits
P
l l

0.7 0.6

Sensation

seeking-* Disinhibition Hypomonia Psychoticism .

Sensation seeking-general

Ur-MHPG

.
0.1 0 -0.1

CSF- calcium
l

Ego strength

t .

Extroversion . Ur-cLtiso1

-0.2 -0.3
-0.4 -0.5

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Plasma DBH* .- Serum cortisol . Plasma amlne oxidase

-0.6
-0.7 I -0.6 I I

CSF-cork01

. CSF-norepinephrine

-0.6

-0.4

-0.2

0.2

0.4

0.6

0.6

Fig. 8. Factor plot of P-ImpUSS vs Neuroticism dimensions based on psychological and biochemical variables. From Zuckerman, Ballenger and Post (1984). Reprinted by permission.

408

MARVIN ZUCKERMAN lI
social deviancy 0.e

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Fig. 9. Factor plot of P-ImpUSS (Social Deviancy) and E-Sociability (Stable Extraversion vs Neurotic Introversion) dimensions based on psychological and gonadal hormone variables. From Daitzman and Zuckerman (1980). Reprinted with permission.

associated with P such as aggressiveness. A similar line of reasoning suggested that we look at the relationship of gonadal hormones to sensation seeking as well as other traits and life experience reports in the area of sexuality. Two studies (Daitzman and Zuckerman, 1980; Daitzman, Zuckerman, Sammelwitz and Ganjam, 1978) showed positive relationships between plasma levels of androgens (testosterone) and estrogens (178 estradiol and estrone) and the disinhibition scale from the SSS in male college students. A factor analysis of the psychological trait variables (shown in Fig. 9) and the four hormone variables revealed two primary factors defined primarily by the trait scales. The first (1) factor was defined at the positive pole by scales for sociability and self esteem as well as the E scale from the EPI; at the negative pole were MMPI scales of social introversion, depression and psychasthenia, usually defining the N dimension. This dimension runs from stable extraversion to neurotic introversion. Testosterone loaded on the positive or stable extraverted side of the dimension. The second factor was defined at the positive pole by MMPI scales for schizophrenia, psychopathic deviate, hypomania, and F (general deviancy of responses). It also included permissive attitudes toward both heterosexuality and homosexuality, and homosexual experience. At the other pole were socialization, tolerance, need for control and achievement. Clearly this is a P dimension. Estradiol loaded positively on this dimension. Estrone and progesterone did not show significant loadings on either dimension. Olweus (1986) found that plasma testosterone in Swedish school boys (15-17 yr old) correlated positively with scales measuring aggression, although item analyses revealed that the relationship was limited to items assessing provoked aggression and not to those measuring unprovoked aggression or to peer ratings of the latter type of aggression. Testosterone also correlated with lack of frustration tolerance. Although testosterone was not related directly to unprovoked aggression or to antisocial behavior it could affect these through its relationship to frustration tolerance which was more highly related to these types of behavior.

Personality in the third dimension

409

Schalling (1983) studied incarcerated male delinquents. Plasma testosterone correlated positively with self-reported verbal aggression against adults and aggression in general, extraversion, sociability (but not impulsivity), monotony avoidance (sensation seeking), and a preference for physical sports. There was no significant correlation of testosterone with the P or N scales of the EPQ. Self and staff ratings suggested that the high testosterone boys were high rank individuals in the group and not likely to be the target of aggression from others. This is in line with the finding of Ehrenkranz, Bliss and Sheard (1974) that male prisoners who were socially dominant had high testosterone levels compared to the general group of non-aggressive or non-dominant prisoners. They also found that the group of prisoners whose past crimes and current prison behavior justified the label of chronically aggressive had higher testosterone levels than all other groups except the socially dominant group. Similarly, Rada, Laws and Kellner (1976) found that while rapists in general did not differ from normals, those who were rated as being the most violent in the commission of the rape had higher testosterone levels than less violent rapists. The S with the highest testosterone level was the only one who had murdered his victim. The general findings suggest that testosterone in normal males in primarily related to sociability. sensation seeking, heterosexual experience, provoked aggressiveness and lack of frustration tolerance. In populations of delinquents or adult criminals testosterone is related to social dominance and sensation seeking, but is also related to extreme levels of unprovoked physical aggression. This would explain why the relationship between aggression and testosterone is not found in normal populations where such extreme manifestations of aggression are less common.

HERITABILITY OF P-ImpUSS AND BIOLOGICAL CORRELATES

ITS

We do not inherit personality or behavioral traits as such. What we do inherit are differences in enzymes which control the formation of neuronal systems and their physiological characteristics. To the extent that variations in such inherent biological characteristics determine personality, we would expect that their heritability would be even higher than that for psychological traits. However, some of the biological factors may have less trait characteristics, i.e. be less stable, and therefore heritability may seem low because of the many environmental influences at the time of assessment. Causal attributions for these state variables may be more dubious than those for more stable biological factors, although a highly reactive biological system may assume trait characteristics only under stressful conditions.
Twin studies

Table 2 shows the results from four twin studies of the P scale itself or related variables and factors. Correlations between identical or monozygotic (MZ) twins range from 0.40 to 0.60 and those for fraternal twins range from 0.04 to 0.33. Heritabilities, calculated using the Jinks and Fulker (1970) or similar ANOVA methods, range from 39 to 58% with a median of 51%. These heritabilities may be in part a function of the reliability of the measures, which may explain the lower h* for the P scale which is the least reliable measure. Correcting for the reliabilities would probably raise the typical heritability estimates to about 60%. The Tellegen Lykken, Bouchard, Wilcox and Segal (1988) results are based on twins reared together. For a smaller sample of identical twins reared apart from birth until maturity the correlation was exactly the same, 0.52. The results are similar for other personality traits in this study indicating a lack of shared family rearing influences, a result which is appearing with monotonous regularity in the biometric behavior genetics literature. Twin studies of most of the biological correlates of the factors in the P-ImpUSS dimension are included in Table 3 and compared with the median values for the four studies of the psychological trait dimension from Table 2. Since most of these studies are based on small ns, median values are used where at least several studies have been done. These combine studies using different substrates for MAO and different sources of DBH (serum, plasma, CSF), but these factors do not introduce much variation in results and the correlations between MAO values using different substrates are generally over 0.9. Heritabilities here are calculated directly from the correlations

410

MARVIN

ZUCKER.~N

Table 2. Twin correlations

and heritabilities

of P tyDe scales

Eaves and Evsenck (1977): P scale Rushton. Fuikers. Neale.Nias and Eysenck (1986)t: Altruism Empathy Nuturance Aggressiveness Tellcgen er al. (1988): Constraint factor Fulker, Eysenck and Zuckcrman (1980): Sensation seeking scale Medians. 7 measures

0.53 0.54 0.49 0.40 0.52 0.60 0.52

0.25 0.20 0.14 0.04 0.33 0.21 0.21

0.5 I 0.51 0.43 0.39 0.56 0.58 0.51

l Jinks and Fulker (1970) Biometric genetical method. tThese 4 scales in the study correlated significantly with Eysencks P scale and with each other although the correlations were generally low (Rushton. personal communication, 1987).

Table 3. Comparisons

of psychological

and biological

trait heritabilities Twin rs MZ DZ 0.21 0.09 0.50 0.45 0.56 0.65 0.44 0.52 0.32 0.50 h?. 0.51 0.71 0.38 0.86 0.76 0.60 0.64 0.12 0.42 0.80

Psychological trait P-ImpUSS scales: 4 studies (from Table 2) Psychophysiological EP augmenting, slope: I studyt Hormonal Plasma testosterone: I study: Enzymes Platelet MAO: 4 studies@ Serum, plasma, CSF DBH: 3 studies COMT (red blood cells): I study I Monoamine metabolites (Oxenstierna er al., 1986) Norepinephrine CSF MHPG Dopamine CSF HVA Serotonin CSF 5-HIAA 5 samples** Height

0.52 0.71 0.69 0.88 0.94 0.95 0.76 0.58 0.53 0.90

Falconer method: 2 x (MZr - DZr); when h2 is higher than MZr. MZr is used instead since h2 should not exceed MZr. tBuchsbaum (1974). :Tumer er al. (1986). Murphy (1973). Nits, Robinson, Lamborn and Lampert (1973). Oxenstiema er al. (1986). Winter. Herschel. Proppmg. Fried1 and Vogel (1978). *Oxenstiema t-f al. (1986). Ross, Wetterberg and Myrhed (1973). Winter CI al. (1978). /I Winter et 01. (1978).

using the Falconer (1981) method since the samples are too small for more sophisticated methods and the authors themselves have not attempted to use them. The Buchsbaum (1974) study of the heritability of EP augmenting found a substantial 0.71 correlation for identical twins but a near zero correlation for fraternal twins. This is not what one would expect for simple polygenetic inheritance where the correlation for fraternal twins should be about half of that found for identical twins. A trait which depends on a complex configuration of genes rather than an additive effect (epistasis, see Lykken, 1982) would produce similarity in identical twins but little similarity in fraternal twins or siblings. Turners study (Turner, Ford, West and Meckle, 1986) of plasma testosterone showed a high correlation for identical twins but the heritability (38%) is relatively low because of the relatively high correlation for fraternal twins. This could indicate either an influence of common family variance or a sampling error. The studies of the enzymes involved in biosynthesis or breakdown of monoamines, MAO, DBH, and COMT, show the highest identical twin correlations and heritabilities of all of these variables. Perfect heritability of an additive, polygenetical trait would give a correlation of 1.0 for identical and 0.5 for fraternal twins, since identicals share all of their genes in common while fratemals share half of their genes. The enzyme correlations approach these figures for complete heritability although the actual h values range from 60 (COMT) to 86% (MAO). It must be remembered that unreliability of the assessment method accounts for some of the remaining variance (maybe l&20%). For the sake of comparison, the calculations for measures of body height from 5 samples in large scale studies are listed: these yield a median MZ correlation of 0.9 for identicals and 0.5 for fratemals with a calculated heritability of 80%. The results are similar to those for enzymes. All of the data on the neurotransmitter metabolites comes from one recent study (Oxenstiema, Edman, Iselius, Oreland, Ross and Sedvall, 1986). Of the three CSF metabolites, only the NE

Personality in the third dimension

311

metabolite MHPG shows a heritability (68%) comparable to those found for enzymes. CSF 5-HIAA shows a relatively low heritability of 42% and HVA shows practically no heritability, but evidence of within family similarity.
Heritability of criminality and antisocial personality

If we accept criminality per se as a behavioral sign of a P-ImpUSS personality, then the adoptive studies of criminality are relevant to the issue of the inheritance of this personality dimension. The best data on this comes from the adoption studies of Mednick, Moffit, Gabrielli and Hutchings (1986) conducted in Denmark where criminal (court convictions) and adoption records are virtually complete on a stable population. The incidence of convictions for criminal offenses in adoptees was compared to the conviction records of both biological and adoptive parents. This comparison is equivalent to the cross-fostering studies done with animals and allows an estimate of the relative influence of genetics and environment in the parental influence on criminality. The results showed a significant relationship of criminality in the biological parents to criminality in the adopted-away sons, but no relationship was found between criminality in the adopted sons and their adopting parents (who provided the familial environment). The interaction effect between biological and adoptive parents was not significant. Furthermore, there was a significant linear relationship between chronicity (number of convictions) in the biological parents and the percentages of male adoptees with convictions. The sons of more chronic offenders were more likely to have criminal records. Recidivism in the adoptees also increased as a function of recidivism in the biological parents. Siblings with a common biological criminal father raised apart in different families had a 31% concordance rate for criminality compared to a rate of only 8.5% for biologically unrelated children raised together in adoptive homes. Criminality in male adoptees varied inversely with socioeconomic status in both biological and adoptive parent homes suggesting that regardless of genetic background the benefits of higher social class can lower probabilities of criminal behavior. Mednick et al. do not speculate on what this influence of social class might be. It has been suggested that environment may provide more outlets for sensation seeking tendencies, one component of the P dimension, that are not antisocial (Farley, 1973). Another important influence may be the higher prevalence of role models for criminality in the peer groups outside of the home in the lower socioeconomic class. Crowe (1975) obtained similar results to those of the Danish study using an American sample. However, Crowes proband sample consisted of male and female children born to female offenders with prison records and adopted up to 18 months after birth (mean age at adoption = 4 months). Controls were adoptees matched for age, sex, race and socioeconomic status of adoptive homes. Nineteen per cent of the probands and 5% of controls were arrested for crimes as adults and 19% of the probands and 3% of the controls were convicted. Blind diagnoses of a subsample with complete records and interviews showed that 55% of the probands and none of the controls were diagnosed as antisocial personalities. Although Crowes study was not of the same scale as the Danish study, both studies lead to the conclusion that genetic influences play a much larger role in criminality than was previously suspected. However, neither study attempted to explore the influence of the social environment outside of the family. Considering the fact that shared family influences seem to exert little role in most personality traits, including those of the P type, the emphasis on the family atmosphere as a major cause of antisocial tendencies may be misplaced and we must look outside of the family for the important environmental influences on criminal behavior. Crowes data also suggest that a more careful separation of antisocial personalities from the general population of delinquents will show an even stronger genetic influence within the subsample. The relationship of chronic criminal behavior of parents and sons in the Mednick et al. study suggests a similar conclusion since such recidivistic offenders are more likely to be antisocial personalities. This underlines the importance of developing good measures of the P tendency for prognostic purposes. SUMMARY Four questions were posed at the beginning of this article. Is there a coherent P dimension of personality and if so what are its characteristics? The answer from factor analysis is: yes there is

such a dimension clearly identifiable and similar in normal men and women. But P is more complex that the first two primary dimensions and includes impulsivity, lack of socialization and responsibility, aggression, a strong need for independence, and sensation seeking. I have labelled this dimension as P-ImpUSS for Zmpuhe (insocialized Sensation Seeking. The clinical extremes of this dimension are postulated to include antisocial personality disorder. bipolar affective disorder (manic phase), and hostile types of paranoid schizophrenia, but not other forms of schizophrenia characterized by withdrawal and sensation avoidance. The second question concerned the possible biological bases for the supertrait. While most of this evidence is correlational for humans it is buttressed by experimental studies with other species. Conditionability is a construct which Eysenck has used to bridge the gap between the arousal explanation for E and the phenomena of socialization. Since socialization seems to belong more properly to the P dimension in the new realignment of traits, one would expect conditionability to be more related to the P scale than the E scale. While one study has shown some main effects of P on eyelid conditioning, more consistent evidence is found for the trait of narrow impulsivity (fast decision time). Impulsives of this type are poor conditioners. The enzymes DBH and MAO are low in those high on one or more of the traits defining P. The first is involved in the synthesis of norepinephrine and the second is essential to the breakdown of NE and the other two monoamines as well. Both enzymes seem to serve a regulatory function and their scarcity has been associated with antisocial types of deviant behavior as well as the trait of sensation seeking. Low levels of NE in the CSF have also been associated with sensation seeking. Low levels of epinephrine in the urine have been related to aggressiveness and restlessness in young adolescent males and have been shown to be predictive of later adult criminality. Even among arrested delinquents low catecholamine reactivity to stress is apparent. Low levels of brain catecholamine activity have been postulated to be important biological determinants of sensation seeking behavior, even among normals (Zuckerman, 1984). Although the relationship of urinary catecholamine measurements to brain catecholamine activity is uncertain, the parallel findings for both types of measures are interesting. The neurotransmitter serotonin is involved in an antagonistic way to arousal produced by the catecholamines. Low levels of serotonin have been associated with the P scale directly in normals, and have been found in the plasma and brains of violent suicides and murderers. Animal studies suggests that the normal function of serotonin is a modulatory one involved in the inhibition of impulsive behavior which could lead to punishment. Cortisol is a peripheral hormone released from the adrenal cortex during stress. Found in the CSF it is also negatively related to traits of the P dimension, perhaps exerting some kind of negative feedback function on catecholamines. Gonadal hormones in males are positively related to sensation seeking, sexual behavior and social deviancy. However, testosterone seems to be more directly related to sociability, dominance and self-esteem in normal males and to unprovoked aggressivity in more antisocial males, while estradial in normal males is more directly related to social deviancy and tendencies toward psychopathology of the P variety. The third question concerned the heritability of personality in the third dimension and the biological traits related to it. Twin studies show that about 50% of the variance of P type traits is attributable to genetic influences. Some of the remainder represents the unreliability of the phenotype assessment methods and the rest represents non-shared environmental variance which probably originates outside of the family. The findings for P are quite similar to those for the other two major dimensions of personality, E and N. The reactions of cortical neurons to intense stimulation, or augmenting or reducing of the evoked potential, shows higher heritability than the P traits of sensation seeking and impulsiveness it is associated with. The enzymes involved in the biosynthesis and degradation of catecholamines, MAO, DBH and COMT, show close to complete determination by genetic factors. Not much data is available on heritability of neurotransmitters or their metabolites in humans so conclusions here must be more tentative. While the NE metabolite MHPG also shows high heritability, the CSF metabolites of dopamine (HVA) and serotonin (5-HIAA) do not show such evidence and therefore may represent the states of these systems that are responsive to immediate internal or environmental influences, rather than stable biological traits. The final question asked concerned the conceptualization of the interaction of the biological and

Personality in the third dimension

413

social determinants in forming the behavioral dispositions that define the trait at the phenomenal level. Since the discovery that shared family environments do not seem to play an important role in most personality traits, there has been a reconceptualization of the heredity-environment interaction. Specific family or peer influences seem of larger importance in the shaping of personality than shared family influences. The prevalent idea of the personality as the passive product of the family environment has been brought into question by behavioral genetic studies. It has been suggested that the individual selects friends, models and activities from the available environments and elicits reactions from the environment, in terms of his or her genetically determined temperament and needs (Plomin, 1986; Starr, Webber, Weinberg and Wittig, 1981). The adoption studies of criminality suggest the possibility that the broad P-ImpUSS trait is involved in chronic criminal behavior. It may be that environment alone is not sufficient to produce either the psychopathic or the highly socialized extremes of the trait, but given either extreme disposition, environment may play a role in either reinforcing, displacing, or even eventually moderating the tendency. Since the genetic influence can only act through creating differences in neurophysiology we must still understand how these physiological trait differences interact with environment. Eysencks proposal that the lack of conditionability poses difficulties in socialization is a cogent one, but is more applicable to the narrow impulsivity dimension than to broad E, N or even P dimensions. Work with psychopaths suggests that the difficulty in acquiring passive avoidance behavior, or restraining action when it may lead to punishment or loss of reward, may be intrinsically involved in their behavioral problem (Gray, 1982; Lykken and Katzenmeyer, 1968). Such a lack of restraint has been related to EP augmenting in cats (Saxton, Siegel and Lukas, 1987) and serotonin depletion in rats (Soubrii, 1986). The answer to the question of the biological substrate of the P dimension may lie in deficits in neuroregulating enzymes and neurotransmitters that play crucial roles in behavioral inhibition.

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