BEHAVIOR GENETICS ASSOCIATION
29th ANNUAL MEETING
VANCOUVER, BC, CANADA
July 1999

The purpose of the Behavior Genetics Association is to promote scientific study of the interrelationship of genetic mechanisms and behavior, both human and animal; to encourage and aid the education and training of research workers in the field of behavior genetics; and to aid in the dissemination and interpretation to the general public of knowledge concerning the interrelationship of genetics and behavior, and its implications for health and human development and education.

For additional information about the Behavior Genetics Association, please contact Dr. Hermine Maes BGA Secretary, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Box 980003, Richmond VA 23298

EXECUTIVE COMMITTEE 1998-1999 1999-2000
President
President-Elect
Past President
Secretary
Treasurer
Member-at-Large
Member-at-Large
Member-at-Large
Norman Henderson
Richard Rose
Nicholas Martin
Hermine Maes
Matt McGue
Nancy Pedersen
Deborah Finkel
Irwin Waldman
Richard Rose
John Hewitt
Norman Henderson
Hermine Maes
Pamela Madden
Deborah Finkel
Irwin Waldman
Jennifer Harris

MEETING INFORMATION

The 29th Annual Meeting of the Behavior Genetics Association will be held at the Coast Plaza Suite Hotel at Stanley Park in Vancouver, British Columbia, Canada. The conference begins with an executive meeting on Saturday, July 3. Paper, poster and plenary sessions will be held throughout the day on July 4, 5, and 6. The opening reception is scheduled to begin at 6:00 PM on July 4. The banquet will be held on July 6 starting at 6:30 PM. A joint session of BGA and 9th biennial meeting of International Society for Study of Individual Differences (ISSID) will be held on the morning of July 7. This half-day session will be composed of symposia and paper presentations of mutual interest to and presented by members of both societies. The ISSID meeting itself runs from July 5 to 9 at the Coast Plaza Hotel.

Vancouver is situated on the coast of British Columbia, nestled between the Rocky and Coast mountain ranges and the Pacific Ocean, and is a popular resort and tourist destination. Vancouver has consistently been named one of the best cities to live in North America and is known for the natural beauty of its environs. The Coast Plaza Hotel is located next to the warm beaches of English Bay harbor (a two minute walk from the hotel) and Stanley Park consisting of five square miles of old growth forest in the heart of downtown Vancouver. Mountain hiking or sailing excursions are no more than an hour away from the hotel. Nearby attractions include Vancouver Island and Victoria a few hours away by ferry. The climate in July is warm and sunny, average temperature being 26C.

Local Host: Dr. Kerry L. Jang
Department of Psychiatry
University of British Columbia
2255 Wesbrook Mall Tel: (604) 822-7895
Vancouver B.C. Fax: (604) 822-7756
Canada, V6T 2A1 Email: kjang@unixg.ubc.ca

Year Presidents Dobzhansky Awardees Thompson Awardees Local Hosts
1971 R Osborne/B Ginsburg - Storrs CT
1972 Th. Dobzhansky GE McClearn - Boulder CO
1973 John L. Fuller WS Pollitzer - Chapel Hill NC
1974 Gerald E. McClearn S Scarr - Minneapolis MN
1975 J. P. Scott J Bruell - Austin TX
1976 Irving I. Gottesman JC DeFries - Boulder CO
1977 W. R. Thompson Steven Vandenberg Nancy Galvin R Wilson - Louisville KY
1978 Lee Ehrman Elliott Slater Gregory Carey T Klein - Davis CA
1979 V. Elving Anderson Ernst Caspari Marla Sokolowski C Lynch - Middletown CT
1980 John C. Loehlin Benson Ginsburg RD Bock - Chicago IL
1981 Norman D. Henderson Sheldon Reed Michael Pogue-Geile L Erhman - Purchase NY
Rose/Guttman/Guttman - Jerusalem
1982 John C. DeFries Gardner Lindzey Paul Sharp D Nash - Ft Collins CO
1983 David W. Fulker Peter Broadhurst Michael Neale D Fulker - London
1984 Steven G. Vandenberg Leonard Heston Christine Michard & George Vogler R Rose - Bloomington IN
1985 Sandra Scarr Nikki Erlenmeyer-Kimling Dorret Boomsma & Lucinda Miner G McClearn - State College PA
1986 Ronald S. W ilson Raymond Cattell David Harder G Ashton/R Johnson - Honolulu HI
1987 Peter A. Parsons J L Fuller & J P Scott J. S. de Belle L Heston - Minneapolis
1988 Leonard L. Heston Lee Erhman Joanne Meyer S Kerbusch - Nijmegen, Netherl.
1989 Robert Plomin Gerald McClearn Susan Parlour S Scarr - Charlottesville VA
1990 Carol B. Lynch Irving Gottesman Lon Cardon & Philip Welbergen P Roubertoux - Aussois, France
1991 Lindon J. Eaves John Loehlin Abel Bult & Lawrence Rodriguez G Vogler - St Louis MO
1992 David A. Blizard John DeFries Deborah Finkel J Wilson - Boulder CO
1993 Thomas J. Bouchard, Jr.Peter Parsons Hermine Maes N Martin - Sydney, Australia
1994 Glayde Whitney Aubrey Manning Frans Sluyter A Fernandez-Teruel/RM Escorihuela/A Tobena - Barcelona
1995 James Wilson David Fulker Soo HyunRhee & Stephen PetrillJ Meyer/L Eaves -Richmond
1996 Nicholas Martin Stephanie Schmitz G McClearn/G Vogler/D Blizard/B Jones - Pittsburgh PA
1997 Nicholas Martin Ronald Johnson Martine Thomis Tony Vernon -Toronto, Canada
1998 Norm Henderson Stephen Maxson Javier Gayán & Alexander Weiss N Pedersen - Stockholm, Sweden

BEHAVIOR GENETICS ASSOCIATION
29th ANNUAL MEETING
Vancouver, BC, Canada
July 4-7, 1999
Saturday July 3
4:00 - 5:00
EXECUTIVE COMMITTEE MEETING Bayside Room
SUNDAY JULY 4
Sunday July 4
8:15 - 10:15
PAPER SESSION I Barclay/Gilford Rooms
Genes and Behavioral Disorders
Chair: Dorret Boomsma
8:15 Genetics of Depression in a Selected Sample of Twins and Siblings
Dorret I. Boomsma, Mireille van den Berg, Conor V. Dolan, A.L. Beem, P.Eline Slagboom, Judith R. Koopmans, and Eco J.C. de Geus
8:30 The GENESiS Study: Measures of Depression and Anxiety in a Community Based Sample of 5,000 Sib-Pairs
A. Sterne, Pak C. Sham, Shaun Purcell, and Robert Plomin
8:45 The Association between Antisocial Behavior and Pathological Gambling
Wendy S. Slutske, Seth A. Eisen, Hong Xian, William R. True, Michael J. Lyons, Jack Goldberg, and Ming T. Tsuang
9:00 Genetic and Environmental Influences on Behavioral Disinhibition
Susan E. Young, Michael C. Stallings, and John K. Hewitt
9:15 Albino Gene Effects on Fear-Related Behaviors of Male and Female Mice
Norman D. Henderson, M. Bohl, C. Cykowski, and John C. DeFries
9:30 The Genetic Aetiology of Somatic Distress
Nathan Gillespie, Katherine M. Kirk, Andrew C. Heath, Ian Hickie, and Nicholas G. Martin
10:15 - 10:45 Coffee
10:45 - 12:00 PLENARY LECTURE Barclay/Gilford Rooms
Fine fly Dining: A Role for cGMP-Dependent Protein Kinase in Natural Behavioural Variation
Marla Sokolowski, University of Toronto
12:00 - 1:00 Lunch
Sunday July 4
1:00 - 3:30
SYMPOSIUM I Barclay/Gilford Rooms
Confusing IQ Curves
Organized by Helmuth Nyborg
Sponsored by BGA and ISSID
Introductory Remarks
Helmuth Nyborg
IQ Gains and Fluid g: A Research Design to Discover Causes
James R. Flynn
The Secular Rise in Intelligence: Many Gains, Many Causes
Ulric Neisser
Secular and Non-Secular Change in Intelligence
Nathan Brody
Secular Changes in Longitudinal IQ: Individual and Group Differences
Helmuth Nyborg
Implications of the Secular Rise in IQ for Convergence of Black and White IQ Scores
Charles Murray
Arthur R. Jensen
Discussant
3:30 - 4:00 Coffee
Sunday July 4
4:00 - 5:30
PAPER SESSION II Barclay Room
QTLs and TDTs
Chair: John K. Hewitt
4:00 Selecting Maximally Informative Sibships for QTL Linkage Analysis
Stacey S. Cherny, Pak C. Sham, Shaun Purcell, and John K. Hewitt
4:15 Selecting Maximally Informative Sibships for QTL Association Analysis
Shaun Purcell, Stacey S. Cherny, Pak C. Sham
4:30 Power of QTL Linkage and Association Analysis
Pak C. Sham, Stacey S. Cherny, and John K. Hewitt
4:45 Testing Linkage and Linkage Disequilibrium with Quantitative Trait Loci in Nuclear Families: A DF Regression Model and Variance Component Extensions
Lon Cardon, G.R. Abecasis, and W.O.C. Cookson
5:00 Genotype x Environment Factors in Transmission Disequilibrium Tests
Lindon J. Eaves, and Patrick F. Sullivan
Sunday July 4
4:00 - 5:30
PAPER SESSION III Gilford Room
Marriage, Parenting, and Personality
Chair: Jenae M. Neiderhiser
4:00 Genetic Effects in Parental Bonding
Paul Lichtenstein, David Reiss, Marianne Cederblad, Olle Elthammer, Jenae M. Neiderhiser, Kjell Hansson, and Nancy L. Pedersen
4:15 The Association between Mothering and Marital Relationships: Is it all in the Genes?
Jenae M. Neiderhiser, Erica Spotts, Paul Lichtenstein, Nancy L. Pedersen, Kjell Hansson, Marianne Cederblad, Olle Elthammer, and David Reiss
4:30 Exploring the genetic and environmental structure of the Tridimensional Personality Questionnaire
Michael C. Stallings, John K. Hewitt, Scott M. Hofer, Andrew Heath, and Lindon J. Eaves
6:00 - 7:30 WELCOME RECEPTION 35TH FLOOR
MONDAY JULY 5
Monday July 5
8:15 - 10:15
SYMPOSIUM II Barclay/Gilford Rooms
QTL Mapping: Exploring the Genetic Basis of Variation in Brains and Behaviors
Organized by Pierre Roubertoux and R W. Williams
Phenotypic QTL Introgression: Analysis of the Midbrain Dopamine System
Csaba Vadasz and Laszlo Zaborszky
Identification of QTLs for Saline and Ethanol-Induced Locomotor Responses
R Hitzeman, J. Demarest, J. Koyner, L. Cipp, B. Hitzeman, and J. McCaughran
Mapping QTLs that Modify the Architecture of the Mouse Brain: A Prelude to Behavioral Analysis
R.W. Williams
Co-Detection of Quantitative Trait Loci (QTL) for Cerebellar Patterns of Foliation (cpf) and Hindlimb Coordination in Mice
I. Le Roy, F. Pérez-Diaz, M. Navet, and Pierre L. Roubertoux
QTL mapping: A Tool to Found Behavioral Neurogenetics
Pierre L. Roubertoux, and I. Le Roy
A QTL for Light-Phase Slow-Wave Sleep in Influenza-Infected CXB Recombinant Inbred Mice
L.A. Toth, and R.W. Williams
10:15 - 10:45 Coffee
Monday July 5
10:45 - 12:00
PAPER SESSION IV Barclay Room
Assumptions, Methods and Moderators
Chair: Rick Viken
10:45 The Equal Environments Assumption and Similarity of Mother Reports of Emotional and Behavioral Problems among Female Adolescent Twins
Nikole J. Cronk, Wendy S. Slutske, Pamela A.F. Madden, Kathleen K. Bucholz, and Andrew C. Heath [T]
11:00 An Easy Method of Linking Databases to Internet White Pages for Systematic Tracking and Identification of Research Participants
Michael B. Miller, and Marc Kayson
11:15 Estimating Genetic and Cultural Transmission with Genetically Informative Data from both Parental and Offspring Generations
Richard J. Viken, Richard J. Rose, Jaakko Kaprio, and Markku Koskenvuo
11:30 The P300 Event-Related Brain Potential in Neuropsychiatric Disorders: A Moderator of Genetic Risk
Andrey P. Anokhin, J.W. Rohrbaugh, Alexandre A. Todorov, and A.B. Vedeniapin
11:45 Peroxisome Proliferator-Activated Receptor PPAR (gamma) as a DZ Twinning Gene in Man
Andreas Busjahn, H. Knoblauch, H.D. Faulhaber, M. Rosenthal, R. Uhlmann, H. Schuster, and F.C. Luft
Monday July 5
10:45 - 12:00
PAPER SESSION V Gilford Room
Substance Use and Misuse
Chair: Nick Martin
10:45 Antisocial Personality, Family Environment, and Alcohol Misuse
Kerry L. Jang, W. John Livesley, and Phillip A. Vernon
11:00 Longitudinal Analysis of Genetic and Environmental Influences on Drinking Across Late Adolescence
Danielle M. Dick, Richard J. Rose, Richard J. Viken, and Jaakko Kaprio [T]
11:15 Genetic and Environmental Influences on Self-Reported Sensitivity and Tolerance to Alcohol
Jennifer K. Johnson, Richard J. Viken, and Richard J. Rose [T]
11:30 Association of Monoamine Oxidase (MAO) with Smoking, Alcohol Dependence and other Measures of Psychopathology and Personality
Nicholas G. Martin, John B. Whitfield, Donna Pang, Katherine M. Kirk, and Andrew Heath
11:45 Vulnerability to Substance Abuse
Marvin Zuckerman
12:00 - 1:30 Lunch
Monday July 5
1:30 - 3:30
SYMPOSIUM III Barclay Room
Behavior Genetic Studies in Non-Human Primates
Organized by Alexander Weiss
Heritability of Hand Preference in Chimpanzees (pan troglodytes): Evidence from a PartialInterspecies Cross-Fostering Study
William Hopkins
Heritability of Some Common Measures of Cognitive and Reflex Development in Infant Pigtailed Macque Monkeys
James C. Ha
Can We Breed a Happier Ape? The Heritability of Subjective Well-Being in Zoo Chimpanzees
Alexander Weiss
Genetic Linkage Mapping in Primates as a Tool in Behavior Genetics
Jeffrey Rogers
Impaired CNS Serotonin Functioning, Excessive Alcohol Intake and Aggression: A Nonhuman Primate Model of Genetic and Environmental Influences
J.Dee Higley and Allyson Bennett
Norm Henderson
Discussant
Monday July 5
1:30 - 3:30
SYMPOSIUM IV Gilford Room
The Boundaries between Normality and Psychopathology: Behavior Genetic Approaches
Organized by Kathryn S. Lemery and Irwin D. Waldman
Early Motor-Cognitive Development: A Study of 5-Month-Old Twins
Daniel Pérusse, Richard E. Tremblay, Michel Boivin, and B. Boulerice
Exploring the Etiology of the Relationship Between Temperament and Behavior Problems with Temperamentally Extreme Twins
Kathryn S. Lemery, Amber Gahagan, and H. Hill Goldsmith [T]
The Aetiology of Anxiety Symptoms in Pre-School Children: Temperament or Psychopathology?
Thalia Eley, and the Twins' Early Development Study (TEDS)
Are Genetic and Environmental Influences on ADHD the same throughout the Range of Symptoms as at the Disordered Extreme?
Irwin D. Waldman, Soo Hyan Rhee, David A Hay, and Florence Levy
Structural Equation Modeling Approaches to Identifying Normal vs Abnormal Variation
Michael C. Neale, Discussant
3:30 - 4:00 Coffee
4:00 - 6:00 POSTER SESSION Conference Foyer
TUESDAY JULY 6
Tuesday July 6
8:15 - 10:00
PAPER SESSION VI Barclay Room
Behavior Disorders in Childhood and Adolescence
Chair: David C. Rowe
8:15 Genetic Contributions to Personality Disorders in Childhood
Frederick L. Coolidge, Linda L. Thede, and Kerry L. Jang
8:30 Sibling Influences on Adolescent Antisocial Behavior
Kristen C. Jacobson, and D.C. Rowe [T]
8:45 Etiology of Sex Differences in Inattention and Hyperactivity/Impulsivity
Soo Hyun Rhee, and Irwin D. Waldman
9:00 Genetic Influences on Childhood Disruptive Disorder Symptoms Estimated through Measured and Latent Genetic Variables in Full Siblings
David C. Rowe, and Irwin D. Waldman
9:15 Links between Temperament and Behavior Problems: Why do the Results Depend on the Sample?
Stephanie Schmitz, and Kimberly J. Saudino
9:30 Examining the Heritability of Stuttering in Australian Twins: Descriptive and Epidemiological Analyses
Susan Felsenfeld, G. Zhu, D. Statham, and Nicholas Martin
Tuesday July 6
8:15 - 10:00
PAPER SESSION VII Gilford Room
Cognitive Performance, Intellectual Resemblance and T-Maze Behavior
Chair: Nancy Segal
8:15 Association Between apoE Genotype, apoE Levels, and Cognitive Performance
Danielle Posthuma, G. Caroline M. Van Baal, Eco J.C. de Geus, Harold Snieder, and Dorret I. Boomsma [T]
8:30 Is There an Association between 'Normal' Cognitive Functioning and Tri-Nucleotide Repeat Expansion at Loci Involved in Neurogenerative Disorders?
Margie Wright, Glen Smith, Gina Geffen, Laurie Geffen, and Nick Martin
8:45 Performance on Raven's Matrices by African and White University Students in South Africa (with a possible note on African g and the Flynn Effect)
J. Philippe Rushton
9:00 Intellectual Resemblance of Same-Age Unrelated Siblings: New Findings
Nancy L. Segal
9:15 T-Maze Behavior, Growth, Sociability and Stress in Unselected Broiler Chickens: Strategic Implications
Bryan Jones, and Raul H. Marin
10:00 - 10:30 Coffee
Tuesday July 6
10:30 -12:30
SYMPOSIUM V Barclay Room
The Relationship between Mental and Physical Health
Organized by Jennifer R. Harris
What is self-rated health about after all? Genetic and Environmental Contributions to the Associations between Subjective Well-Being, Health Symptoms, Health Behaviours, and Self-Rated Health
Espen Røysamb, Jennifer R. Harris, and Kristian Tambs
Individual and Family Factors Associated with Medical Nonadherence
Marianne Z. Wamboldt, John Hewitt, and Frederick S. Wamboldt
Depression and Autonomic Nervous System Activity in Dizygotic Twins and their Siblings
Mireille van den Berg, Eco JC de Geus, Dorret I. Boomsma, and Hans Elich [T]
Genetic and Environmental Factors for Body Mass Index and Depression in the Virginia 30,000
Hermine H. Maes, Michael C. Neale, Lindon J. Eaves
Cardiovascular Reactivity to Psychological Stress: A Twin Study
Michael F. Pogue-Geile, S.B. Manuck, T. Kamarck, and T. Debski
Jennifer R. Harris
Discussant
Tuesday July 6
10:30 -12:30
SYMPOSIUM VI Gilford Room
Genes and Vice
Organized by Andrew Heath
Genetic and Environmental Influences on Behavior Disorder Symptom Count in Adolescent Females
Tara L. McLaughlin, Kathleen K. Bucholz, Pamela A.F. Madden, Wendy S. Slutske, and Andrew C. Heath
Heritability of Stages of Cigarette Smoking in Australian Adult Twins
Pamela A.F. Madden, Kathleen K. Bucholz, Andrew C. Heath, and Nicholas G. Martin
Coffee-Related Sleep Disturbance: A Study of Australian Twins
Katherine M. Kirk, Andrew C. Heath, and Nicholas G. Martin
Genetic and Environmental Associations between Childhood Conduct Problems and Adolescent Marijuana Use
Julia D. Grant, Kathleen K. Bucholz, Wendy S. Slutske, Tara L. McLaughlin, Pamela A.F. Madden, and Andrew C. Heath
Genetic and Environmental Effects on Suicidality: Findings from USA Veteran Era Twin (VET) Registry
Qiang Fu, Andrew C. Heath, Kathleen K. Bucholz, Seth A. Eisen, Jack Goldberg, Michael J. Lyons, and William R. True
Andrew Heath
Discussant
12:30 - 2:00 Lunch
Tuesday July 6
2:00 - 4:00
SYMPOSIUM VII Barclay Room
The Mammalian Y Chromosome, Sex Differences and Behavior: Recent Advances
Organized by Stephen C. Maxson
Attack Behavior in Mice: Implication of the Sts Gene Mapped on the Pairing Region of the X-Y Chromosomes
Pierre L. Roubertoux, I. Le Roy, S. Mortaud, and S. Tordjman
Spatial Ability of XY Sex-Reversed Female Mice
V.H. Denenberg, and A.J. Stavnezer
Non-Hormonal Mechanisms of Brain Sexual Differentiation
A.P. Arnold
Role of the Y Chromosome in Alcohol Dependence and Related Personality Traits: A Cladistic Analysis with Eight-Locus Haplotypes in Finnish Males
D. Goldman, R.A. Kittles, A.W. Bergen, M. Eggert, M. Virkkunen, and J. Long
Tuesday July 6
2:00 - 4:00
PAPER SESSION VIII Gilford Room
Cognitive and Reading Performance and Athletic Ability
Chair: Deborah Finkel
2:00 Odor and Cognitive Functioning: A Twin Study
Deborah Finkel, Nancy L. Pedersen, and Maria Larsson
2:15 Reading and Mathematics Performance in Twin Pairs with and without Reading Difficulties
Valerie S. Knopik, and John C. DeFries [T]
2:30 The Use of Biometric Genetic Data to Evaluate the Structural, Kinematic, and Dynamic Theory of Fluid and Crystallized Intelligence
John J. McArdle, and John L. Horn
4:00 - 5:00 BUSINESS MEETING Barclay/Gilford Rooms
6:30 BANQUET Denman/Nelson Rooms
PRESIDENTIAL ADDRESS: 2.5 Cheers for Behavior Genetics
Norm Henderson
WEDNESDAY JULY 7
Wednesday July 7 JOINT HALF-DAY MEETING OF BGA AND ISSID Comox/Denman Rooms
Organized by Richard J. Rose
8:15 - 9:45 Studying Personality the Hard Way: By other than Self-Report
INVITED ADDRESS
Multi-Modal Measurement of Personality: First Results from the German Observational Study of Adult Twins
Rainer Riemann, University of Bielefeld
Discussants
Nathan Brody
Paul Costa
Richard J. Rose
9:45 - 10:15 Coffee
10:15 - 11:30 The Elusive Nature of Nurture
INVITED ADDRESS
Will the Real Nonshared Environment Please Stand Up?
Eric Turkheimer, University of Virginia
Discussants
Thomas J. Bouchard
Michael C. Neale
11:30 - 12:30 ROUNTABLE DISCUSSION
2:00 - 4:00 EXECUTIVE COMMITTEE MEETING Bayside Room

Monday July 5
4:00 - 6:00
POSTER SESSION Conference Foyer
1 Comparison of the genetic structures between TCI and NEO
Juko Ando, and Yutaka Ono
2 Serotonin transporter gene variation and early rearing environment interact to affect CSF-HIAA concentrations, aggressive behavior, and alcohol consumption in rhesus monkeys
Allyson J. Bennett, Klaus-Peter Lesch, Armin Heils, Jeff Long, Joseph P. Lorenz, Susan E. Shoaf, Maribeth Champoux, Steven J. Suomi, and J. Dee Higley
3 Using diazepam to reduce anxiety in mouse strains derived from lines selected for low activity in an Open Field
Michelle L. Bohl, C. Cykowski, B. Bowers, and N. Henderson
4 An examination of the heritability common to attitude and achievement
S. Alexandra Burt, Lisa N. Legrand, Matthew K. McGue, and William G. Iacono [T]
5 Peroxisome Proliferator Activated Receptor PPAR gene locus is related to body mass index and lipid values in normal subjects
Andreas Busjahn
6 The association between the serotonin transporter gene, neuroticism and temperament levels
Elizabeth Celi, F. Judd, G. Morahan, I. Schweitzer, H. Jackson, A. Cockram, A. Komiti, C. Hordern, K. Wainwright, G. Murray, M. Kyrios, and B. Singh
7 Substance experimentation in adopted adolescents in the Colorado Adoption Project: Uncommon environmental effects?
Robin P. Corley, and S. A. Rhea
8 Etiology of the relationship between reading performance and rapid automatic naming: A twin study
Chayna J. Davis, Valerie S. Knopik, Sally J. Wadsworth, and John C. DeFries [T]
9 A behavioral genetic analysis of children's traits
Filip De Fruyt, and Ivan Mervielde
10 A genome screen for sexual orientation: Progress report
Michael G. DuPree, Leo A. Sirota, and Dean H. Hamer
11 Contribution of age, genes, and environment to the relationship between perceptual speed and cognitive ability
Deborah Finkel, and Nancy L. Pedersen
12 A study of maternal sensitivity in 5-month-old twins
Nadine Forget-Dubois, Marie-Claude Martel, Daniel Pérusse, George Tarabulsy, Michel Boivin, and Richard E. Tremblay
13 Behavioral genetic analysis of individual differences in printed word recognition, phonological and orthographic coding, phoneme awareness and IQ
Javier Gayán, and R. K. Olson
14 Effects of birth weight discordance on cognitive ability: A longitudinal infant twin study
E.R. Goldberg, Andrew M. Johnson, and Philip A. Vernon
15 Is malevolence or proteanism heritable in chimpanzees (Pan troglodytes)?
Cathleen B. Hunt, Alexander Weiss, and J.E. King
16 Fear, well-being and productivity in poultry: Potential benefits of genetic selection
Bryon Jones
17 Standing tall: The effect of height on heritability estimates of leadership style
Andrew M. Johnson, Philip A. Vernon, and Kerry L. Jang [T]
18 Early Adolescent Substance Use: A Search for Gene-Environment Interactions and an Understanding of the Contributions of Personality
Lisa N. Legrand, Matt McGue, and William G. Iacono [T]
19 Life events and depressed mood in the Virginia Twin Study of Adolescent Behavioral Development
Jeff M. Lessem, John K. Hewitt, Lindon J. Eaves, Judy L. Silberg, Michael Rutter, Emily Simonoff [T]
20 Telepathy in twins
Paul Lichtenstein, and M. Reiss Baker
21 Number of CAG repeats in the androgen receptor gene and psychological femininity
John C. Loehlin, Amanda Spurdle, and Nicholas G. Martin
22 Thinking about drinking: Genetic and environmental influences on alcohol expectancies
Kari A. Merrill, Richard J. Viken, Jaakko Kaprio, and Richard J. Rose [T]
23 Genetic and environmental influence on parenting in Japanese population
Naoko Onodal, Yutaka Ono, and Juko Ando
24 Lack of effect of intra-pair contact and aspirations to be similar on twin similarity for personality, marital adjustment, and parenting
Nancy L. Pedersen, Erica L. Spotts, Marianne Cederblad, Paul Lichtenstein, Kjell Hansson, Jenae M. Neiderhiser, Olle Elthammar, and David Reiss
25 Adding non-twin siblings to increase power
Danielle Posthuma, and Dorret I. Boomsma [T]
26 A twin study of the sources of comorbidity between alcoholism and major depression
Carol A. Prescott, Steven H. Aggen, and Kenneth S. Kendler
27 The Genetic Influence on Primary Athletic Ability and Athletic Ability's Relationship with Intelligence
Joanne Ruthsatz, Rolando D. Tiu, Lee A. Thompson, and D.K. Detterman
28 Novelty-seeking and harm-avoidance: A molecular-genetic test of Cloninger's dopamine and serotonin hypotheses
Gerard Saucier, Paul F. Collins, David E. Comings, Nancy Gonzalez, Donn Muhleman, and James P. MacMurray
29 Genetic and environmental influences on marital relationships
Erica L. Spotts, Jenae M. Neiderhiser, Paul Lichtenstein, Nancy Pedersen, Kjell Hansson, Marianne Cederblad, Olle Elthammer, and David Reiss [T]
30 Differences in heritability across levels of father's occupation
Lee A.Thompson, Rolando D. Tiu, and D.K. Detterman
31 An exploration of the genetic and environmental etiology of heart rate in childhood
Carol Van Hulle, and John K. Hewitt
32 Antisociality, substance dependence, and the DRD5 gene
M. Vanyukov, Howard B. Moss, Barry B. Kaplan, and Ralph E. Tarter
33 Univariate genetic analyses of factors underlying the Coloured Raven Matrices
Philip A. Vernon, Paula Meunier, Andrew M. Johnson, and Kerry L. Jang
34 Manifestations of Tourette Syndrome in a single pedigree
Spice Joy Vice, and Donald J. Nash
35 Etiology of the stability of reading performance from 7 to 12 years of age in the Colorado Adoption Project
Sally J. Wadsworth, Robert Plomin, and John C. DeFries
36 Fetal MHC odortypes play a functional role in regulating social interactions
Kunio Yamazaki, M. Curran, and G.K. Beauchamp

BEHAVIOR GENETICS ASSOCIATION
29th ANNUAL MEETING
Vancouver, BC, Canada July 4-7, 1999
Program Overview

SUNDAY JULY 4

8:15 - 10:15 PAPER SESSION I Barclay/Gilford Rooms
Genes and Behavioral Disorders
10:45 - 12:00 PLENARY LECTURE Barclay/Gilford Rooms
Fine fly Dining: A Role for cGMP-Dependent Protein Kinase in Natural Behavioural Variation
1:00 - 3:30 SYMPOSIUM I Barclay/Gilford Rooms
Confusing IQ Curves
4:00 - 5:30 PAPER SESSION II Barclay Room
QTLs and TDTs
PAPER SESSION III Gilford Room
Marriage, Parenting, and Personality
6:00 - 7:30 WELCOME RECEPTION 35TH FLOOR

MONDAY JULY 5

8:15 - 10:15 SYMPOSIUM II Barclay/Gilford Rooms
QTL Mapping: Exploring the Genetic Basis of Variation in Brains and Behaviors
10:45 - 12:00 PAPER SESSION IV Barclay Room
Assumptions, Methods and Moderators
PAPER SESSION V Gilford Room
Substance Use and Misuse
1:30 - 3:30 SYMPOSIUM III Barclay Room
Behavior Genetic Studies in Non-Human Primates
SYMPOSIUM IV Gilford Room
Boundaries between Normality and Psychopathology: Behavior Genetic Approaches
4:00 - 6:00 POSTER SESSION Conference Foyer

TUESDAY JULY 6

8:15 - 10:00 PAPER SESSION VI Barclay Room
Behavior Disorders in Childhood and Adolescence
PAPER SESSION VII Gilford Room
Cognitive Performance, Intellectual Resemblance and T-Maze Behavior
10:30 -12:30 SYMPOSIUM V Barclay Room
The Relationship between Mental and Physical Health
SYMPOSIUM VI Gilford Room
Genes and Vice
2:00 - 4:00 SYMPOSIUM VII Barclay Room
The Mammalian Y Chromosome, Sex Differences and Behavior: Recent Advances
PAPER SESSION VIII Gilford Room
Cognitive and Reading Performance
4:00 - 5:00 BUSINESS MEETING Barclay/Gilford Rooms
6:30 BANQUET Denman/Nelson Rooms

WEDNESDAY JULY 7

8:15 - 12:30 JOINT HALF-DAY MEETING OF BGA AND ISSID Comox/Denman Rooms
Studying Personality the Hard Way: By other than Self-Report
The Elusive Nature of Nurture
2:00 - 4:00 EXECUTIVE COMMITTEE MEETING Bayside Room

ABSTRACTS for BGA '99 in alphabetical order


Juko Ando1, and Yutaka Ono2
Comparison of the genetic structures between TCI and NEO3
1 Faculty of Letters, Keio University, Mita, Tokyo 180-8345 2 School of Medicine, Keio University, Shinanomachi, Tokyo 160-8582 3 Supported by Grant-For-Aid of Scientific Research
Address:2-15-45, Mita, Minato-ku, Tokyo 108-8345, Japan Tel 81+3+3453+4511 /Fax 81+3+3798+7480 /Email juko@media.or.jp

Two comprehensive personality inventories, NEO-PI-R(P.T.Costa, & R.R.McCrae,1985) and TCI (Temperament and Character Inventory; C.R. Cloninger, D.M. Svrakic., & T.R. Przybeck, 1993; N. Kijima, et al.,1996) were carried out for 257 pairs of the Japanese twins from 15 to 27 years old (118 MZf, 40 MZf, 48 DZf, 19 DZm, and 32 DZo). All of the Big Five factors measured by NEO-PI-R showed substantial additive genetic influences (33 - 56 % ) with no nonadditive genetic and shared environmental contribution. (Among seven factors by TCI, all but one (self-transcendence which showed no genetic contribution) showed additive genetic influences. Contrary to Cloninger's theory, two character dimensions, self-directedness and cooperativeness, which are claimed to be environmental, had more genetic variances (42 and 43 %) than four temperament dimensions ( 17 - 36 % ) which are claimed to be genetic. Multivariate genetic analyses indicated that the Big Five factors are not genetically independent whereas three temperament dimensions, novelty seeking, harm avoidance, and reward dependence are genetically independent. It also showed that the genetic component of persistence is completely derived from novelty seeking and harm avoidance, and that genetic components of self-directedness and cooperativeness are partially mediated by those of harm avoidance, and reward dependence. [Poster]


Andrei P.Anokhin1, J.W.Rohrbaugh1, A.A.Todorov1, and A.B.Vedeniapin1.
The P300 event-related brain potential in neuropsychiatric disorders: a moderator of genetic risk?
1 Washington University School of Medicine, St.Louis, MO 63108
Address: A.P.Anokhin, Dept. of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, St.Louis, MO 63108

Reduced P300 amplitude has been implicated as a phenotypic marker of genetic risk for substance use disorders and neuropsychiatric diseases. However, the mechanism through which P300 contributes to risk is unclear, given the non-specificity of P300 as a marker of risk and a lack of clear evidence for its neural substrates. We propose a model of predisposition that includes (a) disease-specific liability factors, (b) relatively independent non-specific factor(s) that modulate the expression of this liability. Psychophysiological and clinical studies, as well as personality correlates of P300 suggest that low P300 amplitude may indicate a deficit in inhibitory self-regulation of behavior, a non-specific factor that can facilitate the expression of liability for a variety of disorders. Conversely, higher self-regulation ability indicated by larger P300 amplitude can operate as a protective factor by suppressing the manifestation of disease symptoms. We illustrate this model using our analysis of smoking as a prototypical form of substance abuse (based on data from Collaborative Study on the Genetics of Alcoholism (COGA). P300 is reduced in current, but not in ex-smokers (P<0.001), and larger P300 is associated with higher probability for ever-smokers to quit (P<0.01), polysubstance abusers have lowest P300. Finally, we have recently shown that P300 may moderate a relationship between smoking and the dopamine D2 receptor gene polymorphism (DRD2), a controversial candidate gene for addictive behaviors (A.P. Anokhin, A.A. Todorov, P.A.F. Madden, J.D. Grant, and A.C. Heath, 1999,Genet. Epidemiol., in print). In individuals with lower P300 amplitudes, there is a significant association between A1 allele and smoking (p < 0.01). On the other hand, this association is not observed in individuals with higher P300 amplitudes. In conclusion, we suggest that P300 may be an important moderator variable which is useful to consider in genetic association studies of addiction and neuropsychiatric disorders.


Arthur P. Arnold1,2
Non-hormonal mechanisms of brain sexual differentiation
1 Departments of Physiological Science and Neurobiology, Laboratory of Neuroendocrinology of the Brain Research Institute, UCLA, Los Angeles CA 90095-1527 2Supported by NIH grants DC00217 and MH59268
Address: Department of Physiological Science UCLA PO Box 951527 Los Angeles CA 90095-1527 USA phone 310-825-2169 fax 310-825-8081 email arnold@ucla.edu

Sexual differentiation of the brain is classically attributed to the action of gonadal steroid hormones. In mammals, males secrete testosterone during fetal and neonatal life, which acts by itself, or after conversion to estradiol, to induce masculine patterns of neural development. In the relative absence of androgen, feminine patterns of neural development occur. These sex differences in brain development are manifested in sex differences in adult behavior. Despite the wealth of evidence supporting the dominant role of gonadal steroids as inducers of sexually dimorphic neural development, several recent studies suggest that not all sex differences in development are attributable to the effects of sex steroids. We have studied sexual differentiation of the zebra finch brain. Male but not female zebra finches sing a courtship song, and males have a much larger neural circuit for song. Although estrogen treatment of female finches at hatching causes some masculinization of neural development, it has not been possible to prevent masculine patterns of neural development in males using various manipulations of the levels of gonadal hormones. Moreover, it has been possible to create genetic females that possess large amounts of testicular tissue that secretes androgen. These females retain feminine plumage and a feminine neural song system. Thus, it appears that testicular secretions are not by themselves sufficient to masculinize neural development. An alternative to hormonally induced sexual differentiation is "direct genetic" induction of sexual differentiation, in which a non-hormonal gene product, expressed in brain of one sex, triggers sex-specific patterns of neural development. The best model for direct genetic induction of sexual differentiation is the induction of masculine differentiation of the mammalian gonadal ridge by the Y chromosome gene Sry. Future studies will address sex chromosomal gene effects on neural development. A.P. Arnold (1997) J. Neurobiology 33:572-584.


Allyson J. Bennett1, Klaus-Peter Lesch2, Armin Heils2, Jeff Long1, Joseph P. Lorenz1, Susan E. Shoaf1, Maribeth Champoux3, Steven J. Suomi3, and J. Dee Higley1
Serotonin transporter gene variation and early rearing environment interact to affect CSF 5-HIAA concentrations, aggressive behavior, and alcohol consumption in rhesus monkeys
1National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892 2Department of Psychiatry, University of Würzburg, Würzburg, Germany 97080 3National Institute of Child Health and Human Development, Bethesda, MD 20892
Address: Laboratory of Clinical Studies, NIAAA, NIHAC, P.O. Box 529, Building 112, Poolesville, MD 20837. Tel (301) 496-9550. Fax (301) 496-0630. Email: allysonb@exchange.nih.gov

A polymorphism in the serotonin (5-HT) transporter gene regulatory region has been associated with measures of human 5-HT transporter (5-HTT) expression (G.L. Hanna, et al., 1998, Neuropsychopharm., 18 102-111) and with 5-HT-mediated behaviors (K.P. Lesch, et al., Science, 274 1527-1531). We examined the effect of an analogous length variation of the gene's regulatory region (rh5-HTTLPR) and early rearing history on central 5-HT functioning, as measured by cerebrospinal fluid 5-hydroxyindoleacetic acid (CSF 5-HIAA), competitive aggressive behavior and alcohol consumption. There was a significant genotype by rearing interaction on CSF 5-HIAA concentrations (n=132). Parentally deprived, peer-reared monkeys exhibited differences in CSF 5-HIAA concentrations that were dependent upon genotype. Peer-reared monkeys with the short rh5-HTTLPR allele exhibited lower CSF 5-HIAA than either their homozygous long allele counterparts or mother-reared monkeys. Peer-reared homozygotes had higher CSF 5-HIAA than any other group. CSF 5-HIAA concentrations for mother-reared monkeys were not differentiated by genotype. A gene/environment interaction was also suggested by a marginally significant interaction effect for alcohol consumption (n=115). Monkeys reared in absence of adult conspecifics consumed significantly more alcohol than monkeys reared by their mothers. The effect of peer-rearing on alcohol consumption was exacerbated in monkeys with the short allele, whereas mother-reared monkeys with the short allele consumed less alcohol than their peer-reared counterparts, although the effect did not quite reach statistical significance. Mother-reared monkeys were more likely than peer-reared monkeys to engage in competitive aggression and, in both rearing conditions, monkeys with the short allele exhibited significantly more aggressive behaviors than their counterparts with the homozygous long allele (n=100). This study provides evidence of an environment-dependent association between variation in the 5-regulatory region of the 5-HT transporter gene and CSF 5-HIAA concentrations and suggests a similar effect in voluntary alcohol consumption, as well as genotype and rearing group differences in competitive aggression. [Poster]


Michelle L. Bohl1, C. Cykowski1, B. Bowers1, Norm Henderson2
Using diazepam to reduce anxiety in mouse strains derived from lines selected for low activity in an Open Field3
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309 2 Department of Psychology, Oberlin College, Oberlin, OH 44074 3 Supported by NIMH Grant MH-53480
Address: Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309 Phone: (303) 735-0077 Fax: (303) 492-8063 e-mail: bohlm@Colorado.edu

DeFries, Gervais, and Thomas, 1978, Behavior Genetics, 8, 3-13, used two replicate sets of F3 mice derived from BALB/cJ X C57BL/6J cross to select for High- or Low open field (OF) activity. Following 30 generations of bi-directional selection the lines were inbred using brother-sister mating. Mice from the two replicate strains selected for high OF activity have exhibited behaviors associated with low anxiety in a variety of test situations. Conversely, the low active OF strains exhibit behaviors associated with high anxiety. The goal of the experiment was to attempt to reduce the difference in anxiety level between the high and low strains by administering diazepam to the two high anxiety strains. Mice from both replicates were administered either 0.5 or 1.0 mg/kg diazepam or cyclodextrin vehicle. Half of each group were tested sequentially in an open field, elevated square maze, light/dark box and an elevated plus maze and the remaining half in the reverse test order. Diazepam reduced the anxiety of both replicate strains in all but the open field. On all tests however, the two low active OF strains showed considerably more anxiety than the two high active OF strains administered only the vehicle. The magnitude of the genetic differences in the many measures of anxiety were always substantially greater than the changes brought about by the diazepam. An attempt was also made to further lower anxiety levels in the two low anxiety strains. This was unsuccessful at all doses attempted. At the highest dose used (4.0 mg/kg), the low anxiety strains exhibited sedation effects and a general decrease in activity, even in low-threatening environments. [Poster]


Dorret I. Boomsma1, Mireille van den Berg1, Conor V. Dolan2, AL Beem1, P. Eline Slagboom3, Judith R. Koopmans1, and Eco J.C. de Geus1
Genetics of depression in a selected sample of twins and siblings4
1Vrije Universiteit, Dept of Biological Psychology 2Universiteit van Amsterdam, Dept of Developmental Psychology 3TNO/PG, Gaubius Laboratory, Leiden 4Supported by NWO grant 904-61-090
Address: De Boelelaan 1111, 1081 HV Amsterdam, The Netherlands Phone 31-20-4448787, Fax 31-20-4448832, Email: dorret@psy.vu.nl

In a longitudinal study of Dutch twins, their parents and siblings we collected questionnaire data on depression, anxiety and correlated personality traits. Data were collected by mailed surveys in 1991, 1993, 1995 and 1997. Over 13,300 subjects from 3381 families were included in the study. A total of 532 families participated on all 4 occasions. The number of families that participated on three, two and one occasion is 855, 833 and 1161, respectively. Genetic analyses of anxiety, depression and neuroticism showed individual differences in these traits to be heritable. Genetic factors accounted for roughly 50% of the variance at each measurement occasion and for most of the stability in these traits. Based on these data, families were selected for the localization of QTLs involved in anxiety and depression. A family was selected if at least 2 siblings (or DZ twins) scored extreme on a multivariate anxiety/depression/neuroticism criterion. Both discordant (high-low) and concordant (high-high and low-low) pairs were included. Once a family was selected, all family members (parents and offspring) who had at least once returned a questionnaire booklet were asked to provide a DNA sample. All offspring were asked for a telephone interview, during which they received part of the computerized version of the WHO-Composite International Diagnostic Interview (CIDI-Auto). CIDI interview data were obtained from 1251 offspring. These data were used to obtain DSM-IV (single or recurrent) depression status. There is a clear relationship between extreme scores on the neuroticism, anxiety and depression questionnaires and DSM-IV diagnoses. Correlations between CIDI scores of family members for DSM-IV depression are higher in MZ twins than in DZ twins and siblings and suggest genetic influences.


Nathan Brody1
Secular and non-secular change in Intelligence
1 Department of Psychology, Wesleyan University, Middletown, USA
Address: nbrody@mail.wesleyan.edu

This paper reviews research on spontaneous changes in intelligence over the life-span and as a result of planned interventions. This research is reviewed as a basis for establishing what changes and what remains constant. These findings are related to research on secular changes in intelligence. Evidence is presented that indicates that secular and non-secular changes are partially congruent and that the latter may help to understand the former. In particular, educational interventions are likely to influence changes in fluid intelligence. These findings indicate that educational changes have contributed to secular increases in intelligence. Changes in intelligence (whether secular or non-secular) are considered from a behavioral genetic perspective. The paper also discusses evidence for the construct validity of tests of intelligence and considers whether or not changes in intelligence change or compromise the predictive validity of test scores.


S. Alexandra Burt1, Lisa N. Legrand1, Matthew K. McGue1, and William G. Iacono1
An examination of the heritability common to attitude and achievement2
1 Department of Psychology, University of Minnesota, Minneapolis, MN 55455 2 Supported in part by NIH Grants DA05147, AA09367, and AA00175
Address: Department of Psychology, Elliott Hall University of Minnesota 75 East River Road Minneapolis, MN 55455-0344 (612) 874-8821 burt0105@tc.umn.edu

Recent studies have found that heritability accounts for a moderate to large amount of the variance in scholastic achievement, (S. A. Petrill & L. A. Thompson, 1993, Personality and Individual Differences 16, 631-640). However, other studies have determined that attitude towards school has an effect on scholastic achievement, (V B. Hinsz & R. E. Ployhart, 1998, Journal of Applied Social Psychology 28, 1051-1066). This study seeks to better understand this relationship between attitude towards school and scholastic achievement. Specifically, to what extent is it a consequence of common genetic or shared environmental factors? Using 11 and 17 year-old male and female cohorts from the Minnesota Twin Family Study (DZ=926 and MZ=1706), we assessed IQ, attitude towards school, and school achievement. Preliminary findings partially replicated earlier studies, (L. Eaves, et al., 1997, Behavior Genetics 27, 121-124.), of genetic influence on attitude, (rmz=.42, rdz=.35 for 17 year-olds; rmz=.39, rdz=.16 for 11 year-olds). Correlations for scholastic achievement suggest genetic influence, as well (rmz=.63, rdz=.30 for 17 year-olds; rmz=.51, rdz=.35 for 11 year-olds). Moreover, for both attitudes and scholastic achievement, twin correlations also suggest shared environmental influence, albeit moderated by age. In order to explore the relationship between attitude, ability, and achievement, results from a multivariate genetic analysis will be presented. [Poster]


Andreas Busjahn1, H.Knoblauch2, H.-D.Faulhaber1, M.Rosenthal1, R.Uhlmann1, H.Schuster1, F.C.Luft1, and B.Müller-Myhsok3
Peroxisome Proliferator-Activated Receptor PPAR as a DZ Twinning Gene in Man.
1Franz Volhard Clinic and Max Delbrück Center 2Department of Medical Genetics, Medical Faculty of the Charite, Humboldt University of Berlin 3Bernhard Nocht Institute for Tropical Medicine, University of Hamburg, Germany
Address: busjahn@fvk-berlin.de

Weinberg suggested that dizygotic (DZ) twinning is transmitted through the female line. Mormon records support a recessive mode of inheritance. Data from Finland support a role for natural selection. Increased DZ twinning in fragile X has implicated CCG repeats. The Booroola fecundity gene is responsible for multiple ovulation in sheep. However, the genetic mechanisms for DZ twinning in man remain a mystery. About 40% of spontaneous DZ twin pregnancies result in singleton births, a phenomenon termed "vanishing twins". We tested the hypothesis that PPAR is a "human DZ twinning" gene and present three lines of evidence. We studied 100 pairs of MZ twins, 64 sets of DZ twins, and 40 parental couples. First, a linkage analysis gave a maximum multipoint MLB-LOD of 3.09, right on D3S3608. The mean sharing among DZ sibs where DNA from both parents was available for study on D3S3608 was 0.72. Second, we used a biallelic polymorphism (C->T) in exon 6 of PPAR and found that the T allele was remarkably lower (P<0.0006) in frequency in MZ twins (0.09) than in DZ twins (0.23). Third, the biallelic polymorphism was not in Hardy-Weinberg equilibrium in the population of DZ twins (P<0.0005) with a sizeable over-representation of homozygotes. This over-representation was not present in the MZ twins or in the parents of DZ twins, where Hardy-Weinberg proportions were maintained. PPAR is a transcription factor involved in adipocyte differentiation, insulin-related effects, lipid metabolism, body mass index, and appears pivotal to the growth process. We suggest that intra-uterine selection based on genetic variation in PPAR may be responsible for the deviation from Hardy-Weinberg equilibrium.


Andreas Busjahn1, H.Knoblauch2, H.-D.Faulhaber1, M.Rosenthal1, R.Uhlmann1, H.Schuster1, F.C.Luft1, and B.Müller-Myhsok3
Peroxisome proliferator activated receptor PPAR gene locus is related to body mass index and lipid values in normal subjects
1Franz Volhard Clinic and Max Delbrück Center 2Department of Medical Genetics, Medical Faculty of the Charite, Humboldt University of Berlin 3Bernhard Nocht Institute for Tropical Medicine, University of Hamburg, Germany
Address: busjahn@fvk-berlin.de

The peroxisome proliferator activated receptor (PPAR) is a transcription factor involved in adipocyte differentiation, insulin-related effects, lipid metabolism, body mass index, and appears pivotal to the growth process. The PPAR gene has been implicated in morbid obesity and is important to lipid and carbohydrate metabolism. However, the relevance of gene variations in normal subjects is not defined. We recruited monozygotic (MZ) and dizygotic (DZ) normal twin subjects to test the hypothesis that the PPAR gene is important to body mass index and lipid concentrations in normal subjects. Both linkage and association strategies were employed in the same DZ twin subjects. The PPAR gene locus was linked (p<0.01) to high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL) and body mass index (BMI) as quantitative traits. A biallelic variant in the PPAR gene was associated with the HDL and BMI (p<0.05). We also looked for linkage between the same variables and the retinoic X receptor gene locus. This locus was linked to total and LDL cholesterol as well as triglycerides. We conclude that the PPAR gene is highly relevant to lipid metabolism and body mass index, not only in the morbidly obese, but in normal subjects as well. The same appears to be true for its binding partner. Sequencing these genes in the twin subjects would serve to identify gene variations contributing to BMI and lipid concentrations in normal subjects.


Lon R. Cardon1, G.R. Abecasis1, and W.O.C. Cookson1
Testing linkage and linkage disequilibrium with quantitative trait loci in nuclear families: A DF regression model and variance components extensions
Address: Wellcome Trust Centre for Human Genetics, University of Oxford, Windmill Road, Oxford OX3 7BN United Kingdom Tel: +44 01865 740 002 Fax: +44 01865 742 193 Email: lon@well.ox.ac.uk

Fulker et al. (D. W. Fulker, S. S. Cherny, P. C. Sham and J. K. Hewitt, 1999, Am J Hum Genet. 64, 259-267) recently described a combined test of association and linkage in sib-pair families using the variance components framework. This model has considerable advantages over existing methods for fine-mapping quantitative trait loci (QTLs), including a direct test of population substructure vs. linkage disequilibrium and the absence of model dependence on parental genotypes. We describe extensions of this approach to the DF regression model and to sibships of any size using variance components. Analytical expectations for the regression coefficients are described, allowing direct interpretation of the parameter estimates. Parental data are not required in the extensions, although such data do give additional power to test QTL-marker allele association and to determine whether any such association is attributable to linkage disequilibrium or population admixture. The relationship between power and family structure, explored using simulation studies, indicates that when parental genotypes are available, power is largely independent of the number of offspring in each family. Power is reduced in the absence of parental genotypes, but the loss in power is negligible when four or more offspring per family are genotyped. When multiple siblings are available, the total number of genotypes required to achieve comparable power is smaller when parents are not genotyped. These results are discussed in the context of sampling designs and genotyping strategies for fine-mapping quantitative trait loci.


Stacey S. Cherny1,2, Pak C. Sham2, Shaun Purcell2, and John K. Hewitt1
Selecting maximally informative sibships for QTL linkage analysis3
1Institute for Behavior Genetics, University of Colorado, Boulder, CO 80309-0447 2Social, Genetic and Development Psychiatry Research Centre, Institute of Psychiatry, DeCrespigny Park, Camberwell, London SE5 8AF, United Kingdom 3Supported in part by EY-12562 and a Programme Project grant from the Medical Research Council of Great Britain
Address: Institute for Behavioral Genetics Campus Box 447 University of Colorado Boulder, CO 80309-0447 Phone: +1 303 492 0835 FAX: +1 303 492 8063 Email: Stacey.Cherny@Colorado.EDU WWW: http://ibgwww.colorado.edu/~cherny/

Much work has been done in the area of increasing power of linkage studies by use of selective sampling. It is generally known that maximally discordant sib pairs are most informative, although affected pairs can be more informative still in the presence of a rare recessive. However little work has been done in the area of construction of an optimal sample, once the sample size for genotyping has been determined. For example, clearly even under a simple additive model, the most extremely affected pairs will be more informative than all most but the most extremely discordant pairs. When conducting a large scale study where all sibships have been phenotyped and the next task is to select the potentially most informative sibships or members of a sibship for genotyping, a method for rank ordering all the sibships in a study by their potential informativeness for linkage would be most desirable. This will describe such a method and its implementation in a freely-distributed Fortran program.


Frederick L. Coolidge1, Linda L. Thede1, and Kerry L. Jang1
Genetic Contributions to Personality Disorders in Childhood
1 Psychology Department, University of Colorado at Colorado Springs, CO 80933-7150
Address: Psychology Department, P. O. Box 7150, University of Colorado, Colorado Springs, CO 80933-7150. Telephone: 719/262-4146; fax: 719/262-4166; e-mail: fcoolidg@mail.uccs.edu

Evidence for a genetic basis of normal and abnormal personality traits has gathered increasing attention in recent years. Much of this research has been confined to adults, particularly with respect to abnormal personality traits. The present study examined heritability of personality disorders in childhood and early adolescence. Personality disorders are chronic and pervasive maladaptive behaviors that cause significant disruption in social and occupational functioning. There is evidence that many personality disorders begin in adolescence or even earlier, but the lack of evidence of a genetic basis of personality disorders in childhood, in part, may be due to the lack of assessment measures. The present study assessed the heritability of 12 personality disorders in 82 monozygotic (MZ) twins and 68 dizygotic (DZ) twins between the ages of 5 and 14 years old. The Coolidge Personality and Neuropsychological Inventory (CPNI; F. L. Coolidge, 1998, CPNI ManualAuthor, Colorado Springs), a DSM-IV criteria based, standardized, 200-item, parent-as-respondent questionnaire was given to the parents of the 150 twins. The CPNI has been normed on 329 children ages 5-17, the median scale reliability of the 12 personality disorder scales is .67, and validity studies support its use in a variety of clinical settings. Heritability estimates were determined by using Holzinger's H statistic (L. J. Eaves, H. J. Eysenck, & N. G. Martin, 1989, Genes, Culture and PersonalityAcademic Press, San Diego). It was found that the median heritability for the 12 personality disorder scales was 51%, ranging from 27% for the passive aggressive personality disorder scale to 68% for the conduct disorder scale. Six of the 12 personality disorder scales had significantly greater MZ correlations than DZ correlations (borderline, conduct, dependent, histrionic, paranoid, and schizotypal personality disorders). It was concluded that personality disorders appear to have a strong genetic component measurable in childhood, and the sizes of the heritability coefficients appear to be similar to those found in most adult studies.


Robin P. Corley1, and S. A. Rhea1
Substance experimentation in adopted adolescents in the Colorado Adoption Project: Uncommon environmental effects?2
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309-0447. 2 Supported by NICHD grant HD-10333, NIMH grant MH-43899, and NIDA grants DA-05131 and DA-11015
Address: IBG, Campus Box 447,University of Colorado, Boulder, Boulder, CO 80309-0447. Phone: 303-492-5189, FAX #: 303-492-8063, E-mail: corley@colorado.edu

As part of an ongoing study of adolescent substance experimentation in subjects participating in the Colorado Adoption Project, we examined self-reported use of nicotine, alcohol, marijuana, and other drugs for 199 adopted adolescents, and 212 non-adopted adolescents, obtained when the subjects were age 16 years. Adopted subjects were more likely, though not always significantly more likely, to have experimented with each individual substance, as well as with multiple substances, with odds ratios ranging from 1.20 for ever tried marijuana to 1.87 for ever tried other drugs. Both genetic and sociocultural factors may help explain these differences. We examine the predictive power for experimentation within the adoptee sample of several different measures including the personality domains of harm-avoidance and novelty-seeking, major life-events such as divorce, a known positive history for substance use in biological parents, and measures specific to adoptive families adapted from the Search Institute's national study of adoptive families (A.R. Sharma, M.K. McGue, and P.L. Benson, 1996, Children and Youth Services Review, 18, 83-100). [Poster]


Nikole J. Cronk1, Wendy S. Slutske1, Pamela A. F. Madden2, Kathleen K. Bucholz2, and Andrew C. Heath2
The equal environments assumption and similarity of mother reports of emotional and behavioral problems among female adolescent twins3
1Department of Psychology, University of Missouri-Columbia, Columbia, MO 65211 2Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63108 3 Supported by NIH grants AA09022, AA00264, AA07728, and DA00272
Address: Department of Psychology, University of Missouri, 210 McAlester Hall, Columbia, MO 65211 phone: (573) 882-4043 fax: (573) 882-7710 email: nikole@taxa.psyc.missouri.edu

Critics of the twin study method often assert that the greater similarity of monozygotic (MZ) compared to dizygotic (DZ) twins is caused by the relatively greater degree of experiences shared by MZ versus DZ twins, rather than by the greater degree of genetic resemblance of MZ versus DZ twins. We assessed the influence of environmental similarity on MZ and DZ twin resemblance for mother-reported emotional and behavioral problems in a sample of 1,948 female adolescent twin pairs. Twins were identified from state of Missouri birth records and the measures of environmental similarity (perceptions of twin zygosity, having the same friends, being in the same classes, and dressing alike) and emotional and behavioral problems (symptoms of separation anxiety disorder, attention-deficit hyperactivity disorder, oppositional-defiant disorder, and conduct disorder) were obtained via structured telephone interviews with the twins' biological mothers. There were significant differences between MZ and DZ twin correlations for all of the symptom scales prior to accounting for environmental similarity. After controlling for environmental similarity, there were still significant differences between MZ and DZ twin correlations for nearly every combination of symptom scale and environmental similarity measure. In most cases, within-zygosity comparisons of twins differing in greater and lesser degrees of environmental similarity yielded non-significant differences, although there were a few consistent effects of environmental similarity on twin resemblance. Overall, this study supports the conclusion that genetic similarity is the predominant factor leading to greater MZ than DZ similarity in twin studies of mother-reported emotional and behavioral problems.


Chayna J. Davis1, Valerie S. Knopik1, Sally J. Wadsworth1, and John C. DeFries1
Etiology of the relationship between reading performance and rapid automatic naming: A twin study2
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309 2Supported by grant HD-27802 from NICHD, and grant MH-16880 from NIMH
Address: Chayna J. Davis Institute for Behavioral Genetics Campus Box 447 Boulder, Colorado 80309 Phone: 303-492-2817 Fax: 303-492-8063 E-mail: davisc@colorado.edu

Scarborough (1998, Annals of Dyslexia 48, 115-136) recently found that early literacy scores were the best predictor of later reading performance in a normally achieving sample, but prediction was significantly improved by including rapid naming tasks in a reading-disabled sample. In the present study, the relationship between reading performance and rapid automatic naming (RAN) was examined by fitting structural equation models to data from 679 twin pairs (291 monozygotic and 388 dizygotic) in which at least one member of the pair was reading-disabled (RD) and from 439 control twin pairs (218 monozygotic and 221 dizygotic) tested in the Colorado Learning Disabilities Research Center. The measures included the reading recognition, reading comprehension and spelling subtests (READ) of the Peabody Individual Achievement Test, as well as 4 subtests (numbers, colors, pictures, and letters) of the RAN paradigm. Results from a bivariate phenotypic model with two hypothesized latent factors, READ and RAN, indicated that the correlation between reading and RAN performance for the reading-disabled sample (.58) was significantly different from that of the control sample (.29). When this model was partitioned to include estimates of genetic, shared environmental and non-shared environmental influences, resulting heritability estimates did not differ significantly for the RD and control samples for either READ (h2 = .86 and .71, respectively) or RAN (h2 = .72 and .64, respectively). However, the genetic correlation between the READ and RAN latent factors could not be equated for the two groups (rg = .66 for probands and .32 for controls). Thus, the etiology of the relationship between reading performance and RAN may differ for reading-disabled and normally-achieving readers. Moreover, these results support previous findings that the best predictors of reading skills may differ for samples of children with normal reading levels and those with reading difficulties (Scarborough, 1998).[Poster]


Filip De Fruyt1, and Ivan Mervielde1
A behavioral genetic analysis of children's traits
1 Department of Psychology, University of Ghent, Belgium
Address: H. Dunantlaan 2, B-9000, Gent, Belgium

A behavioral genetic analysis of children's traits. The construction and cross-validation of the Hierarchical Personality Inventory for Children (HiPIC) will be described and data will be reported from a Flemish twin study in which the HiPIC was used to describe individual differences among children aged 6 to 12. The HiPIC is a 144-item inventory assessing 5 broad personality domains and 18 more specific personality facets. The facets are empirically constructed and closely cover individual differences denoted in parental free descriptions of childhood personality. 284 parents of mono- (MZ) and dizygotic (DZ) twins aged 6 to 12 provided independent ratings of their twins using the HiPIC. The fit of different models to represent the trait variance, including models to examine contrast effects, were investigated, showing substantial additive genetic effects and a relatively small contribution of the shared environment. The results are in line with previous behavioural genetic studies with children using temperament inventories and extend the findings obtained for adults using hierarchical conceptualisations of the Five-Factor Model to children. [Poster]


V.H Denenberg, and A.J. Stavnezer
Spatial Ability of XY Sex-reversed Female Mice

Perinatal gonadal hormones significantly affect sex differences in rodents for both reproductive and non-reproductive behaviors. However, the influence of the sex chromosomes has been largely ignored. To assess the influence of the non-pairing region of the Y chromosome, C57BL/6J male and female mice and mice from theC57BL/6JEi-YPOS consomic strain were given behavioral tests known to distinguish males from females. The C57BL/JEi-YPOS strain contains sex-reversed XY -females which, when compared to their XX-female siblings, allow assessment of the influence of the Y chromosome in a female phenotype. XX females and XY-females did not differ on open-field activity, the Lasley maze, or active avoidance learning, but the XY -females were significantly better than the XX-females on the Morris hidden platform spatial maze. These findings suggest that normal males may have two functional mechanisms (hormonal and genetic) to ensure visuospatial superiority.


Danielle M. Dick1, Richard J. Rose1, Richard J. Viken1, and Jaakko Kaprio2
Longitudinal analyses of genetic and environmental influences on drinking across late adolescence3
1Indiana University, Department of Psychology, Bloomington, IN 47405 2University of Helsinki, Department of Public Health, Helsinki, Finland, 00014 3Supported by NIAAA grants AA-09203 and AA-07611, and the Academy of Finland
Address: ddick@indiana.edu, 812-855-4101 (ph), 812-855-4691 (fax)

Late adolescence is a critical time period for the development of patterns of alcohol use and abuse, underscoring the importance of research among adolescent populations. Using three waves of data collected at ages 16, 17, and 18.5 from FinnTwin16, we analyzed longitudinal change in the influence of genetic and environmental factors on self-reported drinking frequency. Complete drinking data were provided at all three time points by 1,570 pairs of same-sex Finnish twins, ascertained through Finland's Central Population Register: 296 male MZ pairs, 389 male DZ pairs, 480 female MZ pairs, and 405 female DZ pairs. Trivariate analyses were conducted using the statistical package Mx (Neale, M., 1997, Mx: Statistical modeling, Box 126 MCV, Richmond, VA 23298: Department of Psychiatry, 4th Edition). At the baseline assessment at age 16, genetic factors accounted for approximately 20% of the variance in drinking frequency, and common environmental factors accounted for 60%, with the remaining variance attributed to unique environmental factors and error. The influence of genetic factors increased substantially from age 16 to age 17 and remained relatively stable thereafter. No new genetic effects were evident at age 17; however, new genetic effects were apparent at age 18. The influence of common environment decreased progressively over the study period, while the influence of unique environmental effects increased. The model in which parameter estimates for males and females were constrained to be equal provided a parsimonious and adequate fit to the data. Differences in longitudinal influences on drinking among twins differing in socioregional background and family history will be explored in further analyses.


Michael G. DuPree1,2, Leo A. Sirota1, Dean H. Hamer1
A Genome Screen for Sexual Orientation: Progress Report3
1Laboratory of Biochemistry, National Cancer Institute, The National Institutes of Health, Bethesda, MD 20892 2Department of Anthropology, The Pennsylvania State University, University Park, PA 16802
Address: Laboratory of Biochemistry, Section on Gene Structure and Regulation, National Cancer Institute, National Institutes of Health, Bldg 37: 4A-13, Bethesda, MD 20892, (301)496-1747, dupreem@pop.nci.nih.gov

Despite twin evidence that male and female homosexuality have a heritable component(J.M. Bailey, D.S. Benishay, 1993, Am.J.Psychiatry 150(2), 272-277.; J.M. Bailey, A.P. Bell, 1993, Behavior Genetics 23, 313-322.; F.L. Whitman, M. Diamond, J. Martin, 1993, Archives of Sexual Behavior 22,187-206.), nothing is known about the underlying molecular genetic factors in the development of sexual orientation. The finding of X chromosome linkage for male homosexuality (D.H. Hamer, S. Hu, V.L Magnuson, N. Hu, A.M. Pattatucci, 1993, Science 261(5119), 321-327.; S. Hu, A.M. Pattatucci, C. Patterson, L. Li, D.W. Fulker, S.S. Cherny, L. Kruglyak, D.H. Hamer, 1995, Nature Genetics 11(3), 248-256.) does not fully explain the occurrence of the behavior and there have been few investigations into the possible contributions of loci on other chromosomes (J.P. Macke, N. Hu, S. Hu, M. Bailey, V.L. King, T. Brown, D. Hamer, J. Nathans, 1993, Am. J.Hum.Genet 53, 844-852.). Using a battery of 400 markers, we are conducting a genome screen of a sample of nearly 500 individuals consisting of 135 sib-pairs and 10 sib-trios concordant for homosexuality and any heterosexual family members available for genotyping. We report on our progress midway through the research, discussing findings to date as well as our statistical methods. [Poster]


Lindon J. Eaves1, and Patrick F. Sullivan1
Genotype x Environment Interaction in Transmission Disequilibrium Tests2
1 Virginia Institute for Psychiatric & Behavioral Genetics, Department of Human Genetics and Psychiatry, Virginia Commonwealth University2 Supported by NIH grants MH45268
Address: VIPBG, MCV/VCU, P.O. Box 980003, Richmond VA 23298-0003. 804/828-8155 (phone); 804/828-8801(fax); eaves@hsc.vcu.edu; http://www.vipbg.vcu.edu/vipbg/

Transmission disequilibrium tests (TDTs) provide an approach to the detection of associations between alleles at marker loci and risk to complex disorders. The logistic regression approach to TDTs proposed by Sham and Curtis (1995) is generalized to provide separate tests of the main effects of marker loci on genetic risk and genotype x environment interaction (GxE) arising because alleles differ in their sensitivity to specified environmental covariates. The same model may be used to detect the effects of genomic imprinting on the expression of susceptibility loci. In the presence of GxE, highly significant genetic effects may be present that will not produce marked twin or sibling resemblance and not yield significant associations in conventional TDTs. However, simulation studies show how the logistic regression model can be used to detect the main effects of marker alleles and their interaction with covariates on continuous and dichotomous outcomes in offspring-parent trios, pairs of siblings and their parents, and monozygotic twins pairs and their parents. TDT tests with MZ twin pairs permit the detection of alleles whose primary effects on the phenotype are mediated through the control of sensitivity to latent features of the within-family environment. It is shown the genotype-environment correlations, caused by the environmental effects of parental alleles on offspring phenotypes can produce spurious marker-phenotype association in population studies that do not bias the outcome of TDTs


Thalia Eley1, and the Twins' Early Development Study (TEDS)
The Aetiology of Anxiety Symptoms in Pre-school Children: Temperament or Psychopathology?
1 Social, Genetic, & Developmental Psychiatry Research Centre, Institute of Psychiatry, London
Address: Social, Genetic, & Developmental Psychiatry Research Centre, Institute of Psychiatry, 111 Denmark Hill, London, UK SE5 8AF Phone: +44 171 919 3890 Fax: +44 171 919 3866 Email: T.Eley@iop.bpmf.ac.uk

This study examines the aetiology of anxious temperament and psychopathology in both the normal and abnormal range in order to assess whether these two aspects of anxiety are better considered together or apart. The sample included over 3000 pairs of twins, recruited from the entire birth cohort of twin pairs born in England and Wales in 1994. Anxiety symptoms were assessed using the pre-school version of the Behar scale, which includes three items assessing emotional temperament, and 3 items assessing anxiety and depression psychopathology. Highly different patterns of response were revealed for these two types of items, with roughly normally distributed answers on the temperament items as compared to highly skewed responses for the psychopathology items. Two sub-scales were created: emotional temperament and anxiety psychopathology. The emotional temperament scale showed a pattern of very low DZ correlations relative to MZ, indicating substantial non-additive genetic variance. In fact, the model of best fit included significant non-additive genetic (d2 = .52) and non-shared environmental (e2 = .48) influences. Shared environment was non-significant. For extreme group membership (highest 8%) the same pattern resulted, d2 = .35 and e2 = .65. In contrast, DZ twin correlations on the anxiety psychopathology scale were at least half as great as MZ correlations indicating both additive genetic and shared environment contributions. This was also confirmed using model-fitting in which additive genetic (a2 = .52), shared environment (c2 = .10), and non-shared environment (e2 = .39) parameters were all significant contributors to the variance. For the extreme group (top 8%) the same pattern was found, a2 = .40, c2 = .13, and e2 = .47. In summary, emotional temperament and anxious psychopathology have very different aetiologies, yet both scales appear influenced by similar factors both in the normal and abnormal range. Bivariate genetic analyses will also be presented.


Susan Felsenfeld1, G. Zhu2, D. Statham2, and N. Martin2
Examining the heritability of stuttering in Australian twins: Descriptive and epidemiological analyses
1 Department of Speech-Language Pathology, Duquesne University, Pittsburgh, PA 15282 2 Queensland Institute of Medical Research, Brisbane, QLD 4029, Australia 3 Supported by NIH Grant RO1 DC03776-01
Address: Susan Felsenfeld, Ph.D. Department of Speech-Language Pathology 600 Forbes Avenue Duquesne University Pittsburgh, PA 15282-2231 Phone: 412-396-4205 Fax: 412-396-4196 Email: felsenfeld@duq.edu

The occurrence of stuttering has been found to be at least moderately heritable in the small number of twin and family studies of this disorder completed to date (N. Ambrose, E. Yairi, & N. Cox, 1993, Journal of Speech and Hearing Research 36, 701-706; G. Andrews, A. Morris-Yates, P. Howie, & N. Martin, 1991, Archives of General Psychiatry 48, 1034-1035; P. Howie, 1981, Journal of Speech and Hearing Disorders 24, 317-321; K. Kidd, 1984, in R.F. Curlee and W.H. Perkins, eds., Nature and Treatment of Stuttering: New Directions, Boston: Allyn and Bacon). The present study adds significantly to these findings by assessing directly a large sample of stuttering twins drawn from the Australian Twin Registry. From a database of 6,717 subjects in two age cohorts who responded to a questionnaire item about stuttering, 407 subjects who indicated a positive stuttering history were identified. These positive cases, their cotwin, and a small age-matched control sample were subsequently interviewed by telephone to confirm the diagnosis and to provide descriptive information (N=589 completed interviews). In the present study, selected descriptive findings (i.e., symptom frequencies, age of onset, recovery status, relapse history, frequency of comorbid speech problems) for the confirmed affected cases will be reported. In addition, probandwise concordance values for confirmed cases will be presented, and discordant twin pairs will be examined to identify for future study possible nongenetic risk factors for this disorder.


Deborah Finkel1, and Nancy L. Pedersen2
Contribution of age, genes, and environment to the relationship between perceptual speed and cognitive ability3
1 Division of Social Sciences, Indiana University Southeast, New Albany, IN 47150. 2 Genetic Epidemiology, Karolinska Institute, Stockholm S-171 77 and Department of Psychology, University of Southern California, Los Angeles, CA. 3 Supported by American-Scandinavian Foundation fellowship and NIA grant AG15211 awarded to Dr. Finkel. SATSA is supported by NIA (AG04563, AG10175), The MacArthur Foundation Research Network on Successful Aging, and the Swedish Council for Social Research (97:0147:1B)
Address: Division of Social Sciences, Indiana University Southeast, 4201 Grant Line Road, New Albany, IN 47150, phone: 812-941-2668, fax: 812-941-2591, e-mail:dfinkel@ius.edu

The aim of the present analysis was to examine genetic influences on cognitive ability in adulthood in the context of the relationship between perceptual speed and cognitive aging. Quantitative genetic analysis of data from the Swedish Adoption/Twin Study of Aging allowed for estimation of the contribution of age, genetic, and environmental effects to the variance in a latent cognitive factor and to the covariance between the cognitive factor and perceptual speed. The sample included 302 pairs of monozygotic and dizygotic twins, both reared together and reared apart, ranging in age from 40 to 84 years. Analysis of components of total variance in the cognitive factor indicated that 90% of the age-related variance in the cognitive factor was shared with perceptual speed, and 70% of the genetic variance in the cognitive factor was shared with perceptual speed. The correlation between the speed and cognitive factors was primarily genetically mediated. [Poster]


Deborah Finkel1, Nancy L. Pedersen2, and Maria Larsson3
Odor perception and its relationship with cognitive functioning: A twin study4
1 Division of Social Sciences, Indiana University Southeast, New Albany, IN 47150. 2 Division of Genetic Epidemiology, Karolinska Institute, Stockholm S-171 77 and Department of Psychology, University of Southern California, Los Angeles, CA. 3 Department of Clinical Neuroscience and Family Medicine, Division of Geriatric Medicine, Karolinska Institute, and Department of Psychology, Uppsala University, Sweden 4 Supported in part by NIA grant AG15211 awarded to Dr. Finkel. SATSA is supported by NIA (AG04563, AG10175), The MacArthur Foundation Research Network on Successful Aging, and the Swedish Council for Social Research (97:0147:1B)
Address: Division of Social Sciences, Indiana University Southeast, 4201 Grant Line Road, New Albany, IN 47150, phone: 812-941-2668, fax: 812-941-2591, e-mail:dfinkel@ius.edu

Results from the National Geographic study of odor perception demonstrated marked individual differences and age differences in the sense of smell (R.J. Russell, B.J. Cummings, B.F. Proffitt, C.J. Wysocki, A.N. Gilbert, and C.W. Cottman, 1993, J. Gero., 48, P49-P53.). Twin studies have reported significant heritabilities for odor thresholds for some, but not all, odors (N.L. Segal, T.D. Topolski, S.M. Wilson, K.W. Brown, and L. Araki, 1995, Phys. and Beh., 57, 605-609.). The purpose of the present analysis was to incorporate data from both reared apart and reared together twins in a behavior genetic investigation of odor perception. A sample of 37 MZA pairs, 62 MZT pairs, 87 DZA pairs, and 77 DZT pairs from SATSA, age 40 to 84 years, completed the National Geographic smell survey. Measures included odor detection, odor identification, and qualitative measures of odor strength for 6 different odorants. Responses were corrected for the effects of sex, age, and smoking (packyears). Univariate analysis indicated heritabilities ranging from .40 for the detection of mercaptans (natural gas) to .60 for the detection of galaxolide (musk). Heritability of perceived odor strength was .36, with the remaining variance attributable to nonshared environmental influences. Signicant correlations between percent correct odor identification and cognitive measures such as Analogies and Synonyms were predominantly genetically mediated. The results suggest a possible identification mechanism that may be common both to odor identification and more verbal measures of identification.


James R. Flynn1
IQ gains and fluid g: a research design to discover causes
1 Political Studies, University of Otago, Dunedin, New Zealand
Address: email jim.flynn@stonebow.otago.ac.nz

It has long been known that IQ gains are greatest on tests of fluid g. An analysis of differential gains on WISC subtests adds confirmation. The magnitude of gains on various subtests is correlated with the the fluid-g loading of the subtests. Ravens is used as an index of a subtest's fluid-g loading. In so far as fluid g plays a role in the theory of intelligence, the fact that IQ gains are unaccompanied by the real-world effects normally associated with g poses theoretical problems. These are exacerbated, not solved, by the relatively low gains in crystallized g. The pattern of gains suggests a research model for determining causes. Gains are highest on Ravens, Block Design, and Verbal Similarities; they are lowest on Arithmetic, General Information, and Vocabulary. Therefore, if contemporary samples were divided into two groups who are matched on the low-gain tests, but diverge by about one SD on the high-gain tests, we might simulate two generations separated by 'time'. The problems and promise of this design are discussed. The author speculates that the proximate cause of gains is a new motivational disposition to take certain kinds of problems seriously. This hypothesis could be tested by an attitude survey. The ultimate causes suggested in the literature, ranging from breast feeding and number of siblings to more progressive schooling and parenting, could be tested by perceived correlations, or lack of such, with the score patterns that separate the two groups.


Nadine Forget-Dubois1, Marie-Claude Martel2, Daniel Pérusse1, George Tarabulsy2, Michel Boivin3, and Richard E. Tremblay4
A study of maternal sensitivity in 5-month-old twins5
1Department of Anthropology, University of Montreal/Centre de recherche Fernand-Seguin, L.-H. Lafontaine Hospital, Montreal, Quebec, Canada 2Department of Psychology, University of Quebec at Trois-Rivieres, Trois-Rivieres, Quebec, Canada 3School of Psychology, Laval University, Quebec, Quebec, Canada 4 Department of Psychology, University of Montreal, Montreal, Quebec, Canada 5Supported by grants to D. Pérusse from the Medical Research Council of Canada, the National Health Research and Development Program/Health Canada, The Social Sciences and Humanities Research Council of Canada, the Fond de la recherche en sante du Quebec and the Quebec Ministry of Health and Social Services. Nadine Forget-Dubois is supported by a fellowship from the Fonds pour la formation de chercheurs et l'aide a la recherche/Fond de la recherche en santé du Quebec
Address: Centre de recherche Fernand-Seguin, 7331 Hochelaga, Montreal, Canada, H1N 3V2. E-mail: forgetdubois@sympatico.ca. Phone: (514) 251-4015. Fax: (514) 251-2617

Maternal sensitivity is associated with various aspects of socioaffective and cognitive development (e.g. Ainsworth et al., 1978, Patterns of attachment: A psychological study of the strange situation. Hillsdale, NJ: Erlbaum, Lewis, M.D., 1993, Developmental Psychology 29, 1036-1045, etc.). Bell and Harper (1977, Child effects on adult, Hillsdale, NJ: Erlbaum) proposed that individual characteristics of children could influence parental behavior. The present research examines the variation in maternal sensitivity according to zygosity in a sample of 100 same-sex, five month-old twins and their mothers. Maternal sensitivity was assessed independently for each dyad (mother-twin 1, mother-twin 2) using the Maternal Behavior Q-Sort (Pederson et al., 1990, Child Development 61, 1974-1983). Assessment was performed from videotapes of free interactions occurring during a laboratory visit, between experimental situations. Each visit lasted between 4 and 5 hours; observation time for each twin ranges between 0,60 and 1,92 hours. We found higher intra-class correlations of maternal sensitivity scores in MZ than in DZ twins for both sexes. Heritability estimates for maternal sensitivity reached 50%. These results show that (1) maternal sensitivity varies according to infant's characteristics and (2) that variation in these latent characteristics are under genetic influence. Considering that maternal sensitivity may act as a variable of the infant's environment, these results suggest the potential for genotype-environment correlations in child development. [Poster]


Qiang Fu1, Andrew C. Heath 1, Kathleen K. Bucholz 1, Seth A. Eisen1, Jack Goldberg2, Michael J. Lyons3, and William R. True 4
Genetic and Environmental Effects on Suicidality: Findings from USA Vietnam Era Twin (VET) Registry5
1Washington University School of Medicine, St. Louis, MO 63108 2University of Illinois, Chicago School of Public Health and the Cooperative Studies Program Coordinating Center, VAMC, Hines, IL 3Harvard Medical School, Department of Psychiatry at the Brockton/West Roxbury VAMC and Department of Psychology, Boston University 4St. Louis University School of Public Health, St. Louis, MO 6308 5Supported by AA11822 AA10339, DA04604, LIP No. 41-065, MH37685, MH31302
Address: Washington University, 40 N. Kingshighway Blvd., Suite 2, St. Louis, MO 63108

Suicidal behavior has been found to occur more often among people experiencing psychiatric disorders and traumatic life events and also aggregates in families. However, general population studies examining genetic and environmental contributions to suicid al behavior are rare. Recent data from 5,995 twins from the community yielded heritability extimates for suicidal behavior of 45% (33-51%) (D.J. Statham, A.C. Heath, P.A.F. Madden, K.K. Bucholz, L. Bierut, S.H. Dinwiddie, W.S. Slutske, M.P. Dunne & N.G. Martin, 19 98, Psychol Med 28, 839-855). The present study explores genetic and environmental contributions to suicidality based on a national representative sample of same sex U.S. male twins from the VET registry. We studied 3,372 complete twin pairs who were interviewed by telephone in 1992 with a computer version of the DIS-III-R. Lifetime prevalence of suicidal thoughts and attempts was 16.1% and 2.4%, respectively. Adjusting for demographic variables and combat exposure, respondents with suicidal thoughts were more likely to qualify for lifetime DSM-III-R diagnosis on alcohol (OR=1.36, 95%CI=1.13, 1.64), drugs (OR=1.79, 95%CI=1.15, 2.76), and both substances (OR=2.07, 95%CI=1.55, 2.75), Antisocial Personality Disorder (OR=1.74, 95%CI=1.18, 2.55), Major Depressive Episode (OR=6.61, 95%CI=5.32, 8.20), Panic Disorder (OR=1.96, 95%CI=1.12, 3.34), and to report a family history of depression (OR=1.75, 95%CI=1.46, 2.10). Those with suicide attempts were more likely to meet criteria for Major Depressive Episode (OR=4.54, 95%CI=2.95, 7.00), nicotine dependence (OR=1.99, 95%CI=1.22, 3.26), to have a cotwin with depression (OR=1.83, 95%CI=1.18, 2.84), and to report family history of alcohol abuse (OR=1.84, 95%CI=1.20, 2.83). Multiple logistic regression ana lyses revealed genetic influence on suicide thoughts and a familial effect on suicide attempts. A series of models were assessed using model-fitting procedure with MX. Although none of these models fit the data well, the most improved model yielded heritability estimates for suicidal thoughts and attempts of 47% and 40%, respectively (X2=6.19, d.f.=1, p<.02). Our results suggest that both genetic and environmental effects influence on suicidality.


Javier Gayán1 and R. K. Olson1
Behavioral Genetic Analysis of Individual Differences in Printed Word Recognition, Phonological and Orthographic Coding, Phoneme Awareness and IQ2
1Institute for Behavioral Genetics and Department of Psychology, University of Colorado, Boulder, CO 80309-0447 2Supported by NICHD Grants HD-11681 and HD-27802, and RO1 HD-22223
Address: Javier Gayán Institute for Behavioral Genetics University of Colorado Boulder, CO 80309-0447 Phone: 303 492 2817 Fax: 303 492 8063 Email: javier.gayan@colorado.edu

Data from two samples of identical and fraternal twins were used to assess genetic and environmental influences on individual differences in error-free latent traits for printed word recognition, phonological decoding, orthographic coding, phoneme awareness, and IQ. One group of twins (239 pairs) had been selected with at least one member of each pair having some school history for reading problems. A second group (158 pairs) included twins with no school history for reading problems. In both groups, a series of behavioral-genetic analyses revealed genetic influences common to all latent traits and IQ, separate shared genetic influences for phonological awareness and the reading constructs, and independent genetic influences on orthographic coding. Common environment influences on IQ and each of the latent traits were small, not statistically significant, and could be dropped from the models assuming additive genetic influence. However, models assuming non-additive genetic influences provided an equally good fit to the data. Thus, the possible operation of non-additive genetic effects may have tended to obscure some common environment influences on individual differences under the additive genetic models. There were significant but generally small unique environment influences, some common and some specific to different constructs or groups of constructs. The overall pattern for the level of genetic and environmental influences was similar in both twin samples, although there was some suggestion that the balance of additive and non-additive genetic influences may be different. [Poster]


Nathan Gillespie1, Katherine M. Kirk1, Andrew C. Heath 2, Ian Hickie3, and Nicholas G. Martin1
The genetic aetiology of somatic distress
1 Queensland Institute of Medical Research, Brisbane, Australia 2 Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri. 3 School of Psychiatry, University of New South Wales; the Academic Department of Psychiatry, St George Hospital and Community Health Service; Sydney, Australia. This work was supported by NIH grants AA04535, AA07728, and AA10249 and NHMRC (Australia) grants 941177, and 971232. We thank the twins, who were drawn from the Australian NH&MRC Twin Registry for their cooperation.
Address: Queensland Institute of Medical Research Post Office, Royal Brisbane Hospital Brisbane QLD 4029 Telephone: (61) 7 3362 0228 Fax: (61) 7 3362 0101 E-mail: nathanG@qimr.edu.au

Measures of anxiety, depression, phobic anxiety, somatic distress and sleep difficulty were administered in a self-report questionnaire format to a community-based sample of 3468 Australian twins aged between 18 to 28 years. Factor analysis using an oblique rotation produced four interpretable factors: depression; phobic anxiety with panic features; somatic distress; and sleep disturbance. These factors were subject to genetic analysis. Univariate analysis revealed that best fitting model for the self-report symptoms of depression, phobic anxiety, and somatic distress, for male and female twins alike, was best explained by additive genetic and specific environmental effects (AE). Multivariate analysis showed that 38% of the genetic effects in somatic distress were due to specific gene action unrelated to either depression or phobic anxiety. In addition, 56% of the environmental factors that influence somatic distress were due to specific/non-shared environmental effects unrelated to either depression or phobic anxiety. The current results lend additional support to findings that somatic symptoms demonstrate aetiologically distinct pathways (genetic and environmental) from those of anxiety and depression.


E. R. Goldberg1, A. M. Johnson1, and P. A. Vernon1
Effects of birth weight discordance on cognitive ability: A longitudinal infant twin study
1 Department of Psychology, The University of Western Ontario
Address: Department of Psychology Social Science Centre The University of Western Ontario, London, Ontario, N6A 5C2 Tel: 519-661-4050 Fax: 519-661-3961 Email: erg@julian.uwo.ca

A consistent finding for small, premature children has been demonstrated in regards to cognitive ability such that prognosis tends to worsen as birth weight and gestational length decrease. As cognitive abilities are highly heritable, studies looking at multiple birth children who are discordant for birth weight provide an opportunity to assess the effect of low birth weight on cognitive ability, while holding genetic factors and gestational length constant. A sample of infant twin pairs who had birth weights more than 15% discordant received a broad range of cognitive tests at 12 intervals between the ages of 3 months and 6 years. Cognitive ability scores across these 12 assessments were compared using a series of t-tests to determine the effect of birth-weight differences and, specifically, to see if heavier twins demonstrated cognitive advantages over smaller twins. A longitudinal twin design represents a unique opportunity to follow the effect of low birth weight on of cognitive abilities across development, while controlling for other factors. Furthermore, the present study includes a much broader range of cognitive measures than previous studies including standard psychometric measures of intelligence and language development, as well as computer-based measures of working memory capacity and information-processing speed. [Poster]


D. Goldman1, R.A. Kittles1, A.W. Bergen1, M. Eggert1, M. Virkkunen1, and J. Long1
Role of the Y chromosome in alcohol dependence and related personality traits: a cladistic analysis with eight-locus haplotypes in Finnish males
1 Lab of Neurogenetics, NIAAA
Address: Lab of Neurogenetics, NIAAA, Park Bldg Room 451, 12420 Parklawn Drive, Rockville MD 20852, Tel 301 443 0059, Fax 301 443 8579, Email dgneuro@box-d.nih.go

The extent to which genes found on the Y chromosome influence behavioral differences between males is unknown. We used haplotype analysis to evaluate the role of Y chromosome genetic variation in alcohol dependence and TPQ personality traits. Haplotypes of 359 psychiatrically interviewed Finnish males were determined using alleles at seven microsatellite loci as well as the nucleotide substitution in the DYZ3 alphoid satellite locus. An unrooted phylogeny of the 102 observed haplotypes was constructed using parsimony with a single step mutation model. Using the algorithm of Templeton, associations of these haplotypes to behavior were tested in a nested design starting at the terminal [0 step] ends of the Y cladogram and then defining progressively larger groupings of Y haplotypes[1 step connected, 2 step connected, etc]. Significant association with alcohol dependence was found for three Y haplotype clades, with significance levels of p=0.002, p=0.02 and p=0.01 for those clades. However, there were no associations to three personality traits: harm avoidance, reward dependence and novelty seeking, which have proposed to mediate vulnerability to alcoholism. These results, obtained with a fully objective association design, indicate that a gene located on the Y chromosome may contain a functional variant influencing behavior, and more specifically, vulnerability to alcoholism.


Julia D. Grant1, Kathleen K. Bucholz1, Wendy S. Slutske2, Tara L. McLaughlin1, Pamela A.F. Madden1, and Andrew C. Heath1
Genetic and environmental associations between childhood conduct problems and adolescent marijuana use3
1Department of Psychiatry, Washington University School of Medicine, 40 N. Kingshighway, Suite 1, St. Louis, MO 2University of Missouri, Columbia, MO. 3 Supported by AA09022, AA07728, DA07261, DA00272
Address: Department of Psychiatry, Washington University School of Medicine, 40 N. Kingshighway, Suite 1, St. Louis, MO 63108 Phone: (314) 286-2299 FAX: (314) 286-2213 Email: julie@matlock.wustl.edu

Previous research has indicated that conduct problems in childhood are associated with increased substance use during adolescence (e.g., S. Miller-Johnson, J.E. Lochman, J.D. Coie, R. Terry, & C. Hyman, 1998, J. Abnorm. Child Psychol., 26, 221-232). However, the extent to which genetic and environmental influences on these measures overlap has not been investigated. In the present analyses we examined the relationship between self-reported conduct problems and self- reported marijuana use in a sample of adolescent female twins. Data from 916 twin pairs (MZ=530, DZ=386; mean age at follow-up=16.95 years) who participated in both the initial telephone diagnostic interview and the one-year brief follow-up assessment of the Missouri Adolescent Female Twin Study were analyzed. Conduct problems were measured on a continuous scale (M=3.43; range=0-40). Marijuana use was analyzed on a 3 point scale: never tried marijuana (N=1321), tried marijuana once (N=121), used marijuana multiple times (N=390). Mean age of first marijuana use was 15.68 years. Correlational analyses indicated familiality for both measures: Pearson correlations for conduct problems were MZ=.75, DZ=.48; polychoric correlations for marijuana use were MZ=.82, DZ=.63. A bivariate Cholesky model was tested using Mx. Additive genetic and shared environmental influences were significant for both measures. For conduct problems, additive genetic influences accounted for 49% of the variance, shared environmental influences accounted for 26% of the variance, and nonshared environmental influences accounted for 25% of the variance. For marijuana use, additive genetic, shared environmental, and nonshared environmental influences accounted for 36%, 46%, and 18% of the variance respectively. The genetic correlation between the measures was .52 and the shared environmental correlation was .82.


James C. Ha1
Heritability of some common measures of cognitive and reflex development in infant pigtailed macque monkeys
1 Regional Primate Research Center and Psychology Department, University of Washington
Address: Regional Primate Center, University of Washington, Box 357330, Seattle WA 98195-7330 phone 206-543-2420 fax 206-685-8606 email jcha@u.washington.edu

The University of Washington's Infant Primate Research Laboratory has maintained an infant primate nursery since 1972, and has developed a battery of assessments for infant primate development, modified from those used to monitor child development. The nursery animals are part of a pedigreed breeding colony of pigtailed macaque monkeys. The pedigree now contains 11,000+ animals, and provides an invaluable tool for quantitative genetic analysis of the phenotype data maintained in our large computer records system, including the infant primate development measures. I will present the results of a series of variance-component analyses of heritability on several data sets, including birthweight (a strong predictor of later psychological delays), reflex development tests (e.g. sucking, grasping, visual orientation, clasping: h2 = 0.0 to 0.64), and object permanence development tests (h2 = 0.0 to 0.40). Future plans will also be described.


Norman D. Henderson1, M. Bohl2, C. Cykowski2 and J. C. DeFries2
Albino gene effects on fear-related behaviors of male and female mice 3
1 Department of Psychology, Oberlin College, Oberlin, OH 44074 2 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309 3 Supported by NIMH Grant MH-53480 and by an Oberlin College Research Status Award to first author
Address: Department of Psychology, Oberlin College, Oberlin, OH 44074 Phone: (303)517-2486 FAX: (440)775-8356 e-mail: fhenders@oberlin.edu

Although DeFries, Hegmann and Weir (1966, Science, 154, 1577-1579) found that albino mice from segregating F2-F4 generations had lower activity and higher defecation scores than pigmented mice in a brightly lighted open field, Flint et al. (1995, Science, 269, 1432-1435) were unable to localize a QTL for these measures at or near the albino locus. We assessed coat color and sex differences in fear-related behaviors in 577 F2 mice derived from strains originally selected for high and low open-field activity prior to inbreeding (DeFries, Gervais, and Thomas, 1978, Behavior Genetics, 8, 3-13). All animals were tested in a battery consisting of an open field, a light-dark box, a mirror chamber, an elevated plus maze and an elevated square maze. These tests vary substantially in environmental conditions and each generates several putative measures of fear or anxiety in mice and rats. As expected, significant coat color differences were found for several open field behaviors. Albino mice had significantly less total activity and spent less time in the center of the brightly lit field, and defecated significantly more than pigmented animals. In addition, however, albino mice spent less time and exhibited less locomotor activity and less scanning over the open arms of the plus and square mazes, which are both tested under low illumination. In contrast, albino mice were slightly more active in the enclosed arms of both the plus and square mazes as well as in the light-dark box and mirror chamber box. In all cases albino effects were highly significant but too small to account for the magnitude of the behavioral differences observed between the High- and Low-selected parent strains. Estimates of h2 due to segregation at the albino locus ranged from .02 to .06 for activity- and time-based measures of fear/anxiety and .01 or less for defecation measures. Although female mice were significantly less active and had lower defecation and urination scores than males in most tests, no significant Sex by Albino interactions were observed.


J. Dee Higley1, and Allyson Bennett 1
Impaired CNS Serotonin Functioning, Excessive Alcohol Intake, and Aggression: A Nonhuman Primate Model of Genetic and Environmental Influences
1 Laboratory of Clinical Studies - Primate Unit, NIH Animal Center, NIAAA, Poolesville, MD 20837
Address: Address NIH Animal Center, PO Box 529, Building 112, Poolesville, MD 20837, Telephone 301-496-9550; FAX 301-496-0630, email- higleyd@exchange.nih.gov

Studies show that rhesus macaques with low CNS serotonin functioning, as measured by low concentrations of cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA), are impulsive, consume alcohol excessively, are socially ostracized, and exhibit high levels of aggression (Higley et al., 1998, Annals of the New York Academy of Sciences, 836, 39-56). One of the most replicated studies in our laboratory is that interindividual differences in CSF 5-HIAA concentrations are trait-like, showing stability across time and situations. We will present data showing that maternal and paternal genetic influences play major roles beginning early in life in producing low CSF 5-HIAA concentrations. Such differences are further exacerbated by early deleterious rearing experiences, particularly parental deprivation. We have recently analyzed molecular genetic data to investigate the relationship between serotonin transporter (5-HTT) genotypes, CSF 5-HIAA concentrations, and alcohol-related aggression. Our results show that monkeys with the short (s) allele 5-HTT variant have low CSF 5-HIAA concentrations, consume alcohol in excess, and are particularly aggressive when intoxicated. However, the phenotypic expression of this s variant is environmentally-dependent, with the s variant affecting CSF 5-HIAA concentrations and alcohol consumption only in subjects reared by age-mates, without adult influence.


R. Hitzemann1, K. Demarest1, J. Koyner1, L. Cipp1, B. Hitzemann1, and J. McCaughran1
Identification of QTLs for Saline and Ethanol-Induced Locomotor Responses 2
1 Departments of Psychiatry and Neurobiology, SUNY at Stony Brook, Stony Brook, NY 11794-8101 and Research and Psychiatry Services, VAMC, Northport, NY 11768 2Supported in part by MH-51372, AA-11043 and the Department of Veterans Affairs
Address: Robert Hitzemann, Ph.D., Department of Psychiatry, SUNY at Stony Brook, Stony Brook, NY 11794-8101; Tel. (516) 444-2903; E-mail: rhitzemann@mail.psychiatry.sunysb.edu

We have phenotyped 25 strains of the BXD recombinant inbred (RI) series (N = 13/strain) and 1825 C57BL/6J x DBA/2J F2 intercross animals for the saline and the ethanol (1.5 g/kg) induced (difference score) responses. Data were collected as the distance traveled, under normal laboratory lighting, in four 5 min blocks beginning immediately after drug administration. The RI data confirm that both the saline and ethanol responses have a high split halves reliability (> 0.8) and significant heritability (0.38 and 0.32, respectively). There was no significant correlation between the saline and ethanol responses (p > 0.2); however, there was a significant correlation between the ethanol response and both chlordiazepoxide-induced activity (r = 0.60, p < 0.01) and acute ethanol-withdrawal (r = 0.58, p < 0.01). Analysis of the RI strain means revealed significant (p < 0.01) saline QTLs on chromosomes 1, 3, 5, 10, 13, and 18 and significant ethanol QTLs on chromosomes 2, 4, 6, and 9. Between 300 and 600 of the F2 animals were phenotyped in a pseudo-random fashion for microsatellite markers spaced at approximately 20 cM across the genome. QTLs exceeding the LOD threshold of 4.3 were found on chromosomes 1 (saline) and chromosomes 2 (ethanol), complimenting the RI data. Numerous suggestive QTLs (LOD 2.5 to 3.5) were also detected for both phenotypes; these QTLs largely exhibited dominant allele effects. Heterogeneous stock (HS) mice (8-way cross, G24) (N = 200) were used for fine mapping. A chromosome 1 saline QTL was mapped to 57 +/- 1.5 cM (EUCIB panel) and accounted for 11% of the phenotypic variance; a chromosome 2 ethanol QTL mapped to 56 +/- 2 cM and accounted for 8% of the phenotypic variance. The saline QTL compliments previous work (Flint et al. 1995; Gershenfeld et al. 1997) demonstrating open-field activity QTLs on chromosome 1. The ethanol QTL is in the same general region of chromosome 2 where QTLs have been identified for seizure sensitivity (Frankel et al. 1995) and acute ethanol withdrawal (Buck et al. 1997). Using a variety of behavioral genetic techniques, we have identified the central nucleus of the amygdala (CeA) as a locus for the variation in ethanol response (e.g. Hitzemann and Hitzemann, 1997). Congenic strains (under construction) will be used to determine what are the relationships among ethanol response, chromosome 2 QTL(s) and the CeA.


Cathleen B. Hunt1, Alexander Weiss1, J. E. King1
Is malevolence or proteanism heritable in Chimpanzees (Pan troglodytes)?2
1 Department of Psychology, The University of Arizona, Tucson, AZ 85721. 2 Supported by ChimpanZoo and the Jane Goodall Institute
Address: Cathleen B. Hunt, Department of Psychology, The University of Arizona, Tucson, AZ 85721. (520) 319-1087 huntc@u.arizona.edu

Recent research shows that two chimpanzee personality traits, dominance and dependability, are heritable (A. Weiss and J.E. King, 1998, BGA Meeting, Stockholm). However, further examination of the dependability factor indicates that it may be composed of two sub-factors, malevolence and proteanism. Four item descriptors of dependability: jealous, defiant, aggressive and irritable, describe a malevolent personality dimension. Three other items that describe dependability: erratic, (un)predictable, and disorganized, capture what is meant by "proteanism." Some evolutionary theorists suggest that disorganized and unpredictable (protean) behavior can be adaptive in primate courtship and competition and that different levels of proteanism may be maintained in a population by means of frequency dependent selection (G.F. Miller, 1997, in A. Whiten and R.W. Byrne, eds., Machiavellian Intelligence II, Cambridge University Press, Cambridge, UK). If this is true, then proteanism should be heritable. As expected, principal factor analysis with promax rotation of the nine dependability items found two correlated factors, malevolence and proteanism. We created factor scores by unit-weighting items that loaded on the factor at .57 or greater. Two items, impulsive and reckless, did not meet this criteria and were removed from final analyses. The Symmetric Differences Squared (SDS) method was used to estimate genetic, shared zoo, and non-shared environmental variance components of malevolent and protean traits among 145 zoo chimpanzees (L.W. Grimes and W.R. Harvey, 1980, Journal of Animal Science, 50, 634-644). Non-shared environmental effects accounted for almost all of the variance in malevolence. As hypothesized, proteanism was highly heritable with negligible shared zoo effects. These results indicate that malevolent characteristics in chimpanzees are primarily defined by their unique experiences with their zoo environment and conspecifics. The heritability of proteanism supports Miller's assertion that varying levels of unpredictability can be adaptive and may be maintained by frequency dependent selection in primate populations. [Poster]


Kristen C. Jacobson1, and D.C. Rowe1
Sibling influences on adolescent antisocial behavior
1Department of Family Studies, University of Arizona, Tucson, Arizona 85721
Address: P.O. Box 210033; The University if Arizona; Tucson, AZ 85705. Phone: (520) 621-7127. Fax: (520) 621-3401. Email: kjacobso@u.arizona.edu

The present study investigated whether the amount of time siblings spend together moderated the heritability of adolescent antisocial behavior. Data are from the Sibling Pairs sample of the National Longitudinal Study of Adolescent Health (Add Health). Only same-sex siblings less than 2 years apart in age were used in these analyses. The average age of siblings was 16. Adolescent self-reports of antisocial behavior were divided into two scales: aggression (4 items) and non-violent delinquency (11 items). The time together variable was created by averaging sibling reports of how much time they spent with one another and how much time they spent with the same group of friends. Standard regression analyses indicated that time together moderated sibling similarity for delinquency, but not aggression. Siblings who spent more time together were more alike in delinquent behavior. Based on results from DeFries-Fulker regressions (J.C. DeFries, and D.W. Fulker, 1985, Behav. Genet.15, 467-473), the heritability of aggression was .20, and the heritability of delinquency was .18. Shared environmental influences accounted for 18% of the variation in aggression, and 24% of the variation in delinquency. An augmented DeFries-Fulker model indicated that time together moderated the heritability of delinquency, but not aggression. Time together did not moderate the shared environmental influence on either aggression or delinquency. Follow-up analyses using Mx revealed that the heritability of delinquent behavior was .34 among adolescents who spent more time together; genetic influences did not account for any of the variation in delinquency among siblings who spent less time together. This model fit the data well (2 = 29.8, df = 24, p > .10). Shared environmental influences in both groups were estimated at .21. Equating the parameters across the two groups resulted in a significantly poorer fit (2 = 17.5, df = 3, p < .001).


Kerry L. Jang1, W. John Livesley1, and Philip A. Vernon2
Antisocial Personality, Family Environment, and Alcohol Misuse
1Department of Psychiatry, University of british Columbia, Vancouver, Canada 2Department of Psychology, University of Western Ontario, London, Canada
Address: Dr. Kerry L. Jang Department of Psychiatry University of British Columbia 2255 Wesbrook Mall Vancouver, BC Canada. V6T 2A1 Voice: (604) 822-7895 Fax: (604) 822-7756 e-mail: kjang@unixg.ubc.ca

The extent to which specific facets of antisocial personality pathology, family environment and alcohol misuse share a common genetic and environmental aetiology was estimated. Participants were 347 adult monozygotic twin pairs (209 sister & 138 brother pairs) and 346 dizygotic twin pairs (170 sister, 82 brother, & 94 sister-brother pairs). All twin pairs completed self-report measures of alcohol misuse and personality pathology contained in the Dimensional Assessment of Personality Pathology (Livesley, W.J. & Jackson, D.N.,in press, Manual for the Dimensional Assessment of Personality Problems-Basic Questionnaire. Port Huron, MI, Sigma)and family environment (Family Environment Scale: Moos, R.H. & Moos, B.S.,1986, Manual: Family Environment Scale, Palo Alto, Consulting Psychologists Press). Bivariate genetic correlations between the scales identified a number of the specific aspects of antisocial personality, such as recklessness, impulsivity, and interpersonal hostility that shared a common genetic basis with alcohol misuse. Other characteristics typical of antisocial personality, such as hypervigilance, suspiciousness, dominance, and attention seeking had negligible associations with alcohol misuse. Simultaneous analysis of family environmental variables showed that the genetic influences underlying antisocial personality also influence alcohol misuse both directly and through its influence on the family environment. The results also confirmed the lack of relationship between alcohol misuse and personality variables unrelated to antisocial characteristics (e.g., neuroticism) at the phenotypic and genetic levels.


A.M. Johnson1, P.A. Vernon1, and K.L. Jang2
Standing tall: The effect of height on heritability estimates of leadership style
1Department of Psychology, University of Western Ontario 2Department of Psychiatry, University of British Columbia
Address: Department of Psychology Social Science Centre The University of Western Ontario, London, Ontario, N6A 5C2 Tel: 519-680-5997 Fax: 519-661-3961 Email: ajohnson@julian.uwo.ca

Recent research has noted that height is related to an individual's success as a leader. Taken in combination with the identification of leadership style as a heritable characteristic, this raises the question of whether the heritability of certain styles of leadership is linked to the heritability of height. 250 pairs of adult twins (150 monozygotic and 100 dizygotic) completed the Multifactor Leadership Questionnaire, a measure that can be factor-analyzed to give two dimensions of leadership style: transformational and transactional leadership. Transformational leadership relies more heavily on physical charisma, while transactional leadership tends to tap skills and characteristics that are learned. Regression analyses on factor scores from these factors reveal that both height (BETA=.142, t=2.195, p<.05) and weight (BETA=-.115, t=-2.136, p<.05) are significant predictors of transformational, but not transactional, leadership. Results are discussed with reference to the effects of including height and weight as variables in univariate heritability analyses. [Poster]


Jennifer K. Johnson1, Richard J. Viken1, and Richard J. Rose1
Genetic and environmental influences on self-reported sensitivity and tolerance to alcohol2
1Indiana University, Department of Psychology, Bloomington, IN 47405 2Supported by NIAAA grant AA-07611
Address: jennjohn@indiana.edu, 812-855-4101 (ph), 812-855-4691 (fax)

Acquired tolerance is part of the diagnostic picture for alcohol dependence and is a possible marker of biological vulnerability for alcoholism. As such, it has been the focus of a great deal of research into the etiology of alcoholism. Recently, there has been interest in determining whether individuals are able to self-report specific differences in their responses to alcohol over time, whether their reports of acquired tolerance are heritable, and whether reported tolerance predicts outcome, such as future drinking and future drinking problems. In a genetically informative sample of twins and siblings (N=900), we investigated individuals' retrospective self-report of sensitivity to alcohol at different drinking periods (experimental, early, heaviest, current) by asking how many drinks they needed to consume to achieve specific bodily sensations (e.g. to feel drowsy, stumble, etc.). We then used these self-reported changes in sensitivity to estimate individual differences in acquired tolerance. Individuals reported the expected pattern of needing to consume a higher number of drinks to achieve sensations associated with higher levels of intoxication. Individuals also report the expected change in sensitivity to alcohol over time, reporting decreased sensitivity to alcohol with increasing drinking experience (acquired tolerance). Adults who have passed their heaviest drinking period report that they need fewer drinks to achieve the same effects as in their heaviest drinking period. Test-retest reliability of the sensitivity and tolerance composite variables was substantial. There were moderate correlations between reported sensitivity and tolerance to alcohol and reported alcohol problems, suggesting possible predictive utility. Behavior genetic analyses revealed that there is substantial familiality for self-reported sensitivity and tolerance to alcohol. There was clear evidence of genetic influences on sensitivity and less consistent evidence for genetic influences on acquired tolerance.


R. Bryan Jones1, Raul H. Marin2
T-maze behavior, growth, sociality and stress in unselected broiler chickens: strategic implications3
1Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, Scotland 2CRILAR (CONICET), Mendoza y Entre Rios, 5301 Anillaco, La Rioja, Argentina 3Supported by CONICET, University of Cordoba, British Council / CONICOR, and the Biotechnology and Biological Sciences Research Council, UK
Address: Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, Scotland Phone: ++ 44 131 527 4466; Fax: ++ 44 131 440 0434; E-mail: Bryan.Jones@BBSRC.AC.UK

We examined the relationships between early T-maze behavior, growth, sociality and stress responsiveness in broiler chickens. The latencies to traverse a T-maze and thereby reestablish visual contact with their companions were measured in individually tested, 2 or 3-day-old chicks. They were then assigned to high (HP) or low (LP) performance categories if their latencies were below 40 or above 90 s, respectively. In Experiment 1, body weight at 3 days of age was unaffected by category or sex but male and female HP chicks were significantly heavier at 15 and 49 days (in laboratory and commercial conditions, respectively) than LP birds. In Experiment 2, we found no differences between the home-cage behaviors (e.g. walking, pecking) of LP and HP chicks. Neither were there differences between their latencies to emerge from a sheltered area into an exposed, potentially frightening one nor in their tonic immobility fear reactions to brief manual restraint. On the other hand, HP chicks stayed closer together in the home cage and spent longer at that end of a runway nearest a goal box containing other chicks. Experiment 3 showed that circulating corticosterone (C) concentrations were similar in undisturbed LP and HP chicks, that exposure to a stressor (partial water immersion) markedly increased plasma C levels, and that this elevation was more pronounced in LP than HP chicks. Collectively, our findings suggest that rapid escape from a T-maze was positively associated with subsequent growth, that contrasting T-maze performance did not reflect differences in underlying activity levels or fearfulness, that individual variation in sociality was probably influential, and that LP chicks were more sensitive to stressful stimulation. Given its simplicity, rapidity and non-invasiveness, the T-maze test might represent a particularly useful and commercially important selection criterion for future breeding programmes.


R. Bryan Jones1
Fear, well-being and productivity in poultry: potential benefits of genetic selection 2
1Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, Scotland 2Supported by the Biotechnology and Biological Sciences Research Council, UK. The following also contributed to this study: J.M. Faure and A.D. Mills (France), D.G. Satterlee and H.L. Marks (USA)
Address: Roslin Institute, Roslin, Midlothian EH25 9PS, Scotland Phone: ++ 44 131 527 4466; Fax ++ 44 131 440 0434; E-mail: Bryan.Jones@BBSRC.AC.UK

Genetic selection for certain production related characteristics has undoubtedly compromised the well-being of poultry. However, there is growing awareness that selective breeding could be used to improve well-being as well as productivity. This talk focuses on fear and distress. Intense or prolonged fear and chronic elevation of circulating corticosterone levels can cause major problems, including injury, pain and reduced egg production, growth rate and product quality. Our studies of Japanese quail that have been genetically selected for short (STI) or long (LTI) tonic immobility (TI) fear reactions, for reduced (low stress, LS) or exaggerated (high stress, HS) adrenocortical responses to mechanical restraint, and for low (LBW) or high (HBW) body weight are yielding valuable insights. Divergence was rapid and marked in all the selection programmes. The manipulation of narrow stimulus-specific responses would have little practical value. However, we showed that fear-related behavior (silence, immobility or withdrawal) was less pronounced in STI and LS quail than in LTI and HS ones in a variety of test situations including manual restraint, mechanical immobilization, an approaching human, and exposure to novel objects and places. Adrenocortical responses to a range of known stressors were also markedly lower in LS than HS birds. Similar divergence was observed in STI and LTI quail though only when a mild stressor was used. Selection for LS or STI also decreased stress-induced reductions in productivity and product quality, respectively. Finally, fear and adrenocortical activation were much less pronounced in HBW quail than their smaller (LBW) counterparts. Thus, selection for one fear behavior, one physiological reaction, or one production trait affected the birds' reactions to diverse stressful stimuli. The similarities suggest that these independent programmes had influenced the same underlying characteristic, perhaps fearfulness. This apparently common genetic link provides a platform for future studies.


Katherine M. Kirk 1, Andrew C. Heath 2 and Nicholas G. Martin 1
Coffee-related sleep disturbance: a study of Australian twins
1 Queensland Institute of Medical Research, Brisbane Australia 2 Department of Psychiatry, Washington University School of Medicine, St Louis USA
Address: Queensland Institute of Medical Research, Post Office, Royal Brisbane Hospital, Brisbane QLD 4029 Australia Telephone: +61 7 3362 0272 Facsimile: +61 7 3362 0101 E-mail: kathE@qimr.edu.au

The sleep-disturbing effect of caffeine is well-known, with suggestions being made that coffee could be used to induce symptoms mimicking those of insomnia in order to promote further understanding of that disorder. In a questionnaire mailed to 3808 pairs of adult twins, 10% of respondents indicated that drinking coffee in the evening "always" or "usually" prevented them from getting to sleep, with a further 20% mentioning that this was "sometimes" the case. Even among those who stated that drinking coffee in the evening never prevented them from getting to sleep, coffee consumption was significantly higher among men and women who reported waking due to nervous tension and worries, and among women who woke spontaneously. Twin correlations for coffee-related insomnia were substantially greater for monozygotic twins than dizygotic twins, indicating that approximately 43% of phenotypic variance is attributable to genetic influences. Genetic and environmental influences on coffee-related insomnia were found to be largely distinct from those affecting general sleep quality and sleep disturbance related to anxiety, depression and neuroticism.


Valerie S. Knopik 1, and John C. DeFries 1
Reading and Mathematics Performance in Twin Pairs With and Without Reading Difficulties 2
1 Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309 2 Supported in part by NICHD grant HD-27802, HD-11681, and NIMH grant MH-16880
Address: Valerie S. Knopik Institute for Behavioral Genetics Campus Box 447 University of Colorado Boulder, CO 80309 Telephone: 303/492-7362 FAX: 303/492-8063 E-Mail: Valerie.Knopik@Colorado.EDU

Individual differences in both reading and mathematics performance appear to be due to many of the same genetic influences (J. J. Gillis, J. C. DeFries, and D. W. Fulker, 1992, Acta Geneticae Medicae et Gemellologiae 41, 287-300). In order to explore further the etiology of the observed relationship between reading and math performance, data from samples of same-sex twin pairs tested in the Colorado Learning Disabilities Research Center were analyzed using structural equation modelling techniques. Bivariate phenotypic and genetic twin models were fitted to data from 526 twin pairs selected for reading deficits (290 identical and 236 same-sex fraternal) and 355 control pairs (220 identical and 135 same-sex fraternal). Subtests of the Peabody Individual Achievement Test (PIAT; Reading Recognition, Reading Comprehension, and Spelling) were used as measures of reading performance, and scores from the Wechsler Intelligence Scale for Children-Revised (WISC-R) or Wechsler Adult Intelligence Scale-Revised (WAIS-R) Arithmetic subtest, the Wide Range Achievement Test Arithmetic subtest, and the PIAT Math subtest were used as indices for mathematics performance. The results of these confirmatory factor analyses indicate that genetic and environmental covariances between reading and math latent factors do not differ significantly for twin pairs in the proband and control groups. Moreover, the resulting estimates of heritability for reading performance were 0.81 for the proband sample and 0.69 for the control sample, while heritability for math performance was 0.88 and 0.67, in the proband and control groups, respectively. Finally, whereas genetic influences were found to account for 83% of the covariation between the reading and math factors in the proband group and 58% in the control group, shared environmental influences neither contributed significantly to the relationship between the two latent factors nor accounted for significant independent variation in the reading and math variables.


Lisa N. Legrand1, Matt McGue1, and William G. Iacono1
Early Adolescent Substance Use: A Search for Gene-Environment Interactions and an Understanding of the Contributions of Personality 2
1 University of Minnesota, Minneapolis, Minnesota 55455 2 Supported in part by NIH Grants MH17069, DA05147, and AA09367
Address: Department of Pyschology, University of Minnesota, 75 East River Road, Minneapolis, Minnesota 55455. E-mail: llegrand@tfs.psych.umn.edu

There exists evidence that responses to apparently similar environmental pressures may be differentially influenced by genotype (e.g., C.E. Cutrona et al., 1994, Comprehensive Psychiatry,, 35,171-179). Such gene-environment interactions are intriguing and may help explain how the shared family environment can be largely without etiological significance for most psychopathologies. This study seeks to expand upon the very modestly sized literature investigating gene by environment interactions in the prediction of substance abuse. Using the youngest male cohort of the Minnesota Twin Family Study, genetic risk was estimated from the presence or absence of parental substance abuse/dependency. To index environmental risk, strength of affiliation with various social groups likely to either encourage or discourage substance abuse was assessed at age 11. Individuals were designated high, medium, or low on each of the two dimensions. Both inferred genetic risk and assessed environmental risk independently predicted the number of substances tried by age 14 (p < .005; N = 591). A gene-environment interaction was suggested but failed to reach significance (p = .060). When the analyses were replicated with a dispositional risk (externalizing assessed at age 11) in place of the inferred genetic risk, the environmental variable no longer significantly predicted substance use (p =.093) and no interaction emerged (p = .157). Externalizing, however, was significantly related to subsequent substance use (p < .001). Externalizing is also strongly related to our measures of environmental risk (r = .60), and further analyses will include partialing out its contribution to the genetic and environmental risk variables in their prediction of substance use. Behavioral genetic modeling will further elucidate the genesis of the relationships between these measures of genetic risk, environmental risk, externalization, and early initiation into substance use. [Poster]


Kathryn S. Lemery1, Amber Gahagan1, and H. Hill Goldsmith1
Exploring the etiology of the relationship between temperament and behavior problems with temperamentally extreme twins
1 University of Wisconsin-Madison
Address: Wisconsin Twin Project, 1202 West Johnson Street, Madison, WI 53706. phone: (608) 265-4946 fax: (608) 265-3649 email: klemery@students.wisc.edu

From detailed temperament questionnaires, we identified subgroups of 3-7 year old twins with extreme temperaments from the Wisconsin Twin Panel. Our battery included sufficient item content to screen for three at-risk groups: externalizing (subdivided into motor excess problems, disinhibition problems, and oppositional-defiant issues), attentional problems, and internalizing. Internal consistency was high for these scales (.80s). We formed a composite from mother and father report, and selected individuals with composite scores greater than 1 sd above the mean (approximately 100 individuals in each group). Families in which at least one twin was extreme in temperament were recontacted when the twins were 5-8 years old, and detailed parent report temperament (Rothbart's Children's Behavior Questionnaire) and behavioral problem (i.e., Offord's Ontario Child Health Scale-Revised) measures were completed by mothers and fathers. We first examined intraclass correlations on our extreme group screening items for the full sample (N = 120 MZ pairs; 182 DZ pairs). All three screening scales, Internalizing (MZ = .64; DZ = .17), Externalizing (MZ = .71; DZ = .03), and Attention Problems (MZ = .47; DZ = .11) portrayed prominent genetic influences. We fit DF regression models to these data to determine whether or not our extremes have the same etiology as the normal range. For all three extreme groups, the difference between the extreme group mean and the unselected mean was heritable, with identical cotwins being more similar to their extreme cotwins than fraternal cotwins. Similar analyses will be reported using the Offord scales. Additionally, multivariate genetic model fitting will be used to decompose the phenotypic association between temperament and behavior problems.


I. Le Roy1, F. Pérez-Diaz1, M. Navet1, and P. L. Roubertoux1
Co-detection of quantitative trait loci for cerebellar patterns of foliation and hind limb coordination in mice2
1 UPR CNRS 9074, Génétique, Neurogénétique, Comportement, Institut de Transgénose, Institut de Transgénose, 3 B rue de la Ferollerie; 45071, Orléans Cedex 02, France 2 Supported by CNRS (UPR 9074), Ministry for Research and Technology, Région Centre and Préfecture de la Région Centre, Fondation pour la Recherche Médicale. UPR 9074 is affiliated with INSERM and University of Orléans.
Address: Isabelle Le Roy, University of Orleans, Institut de Transgenose, CNRS 3 b rue de la Ferollerie 45071 Orleans cedex 02, France. Phone: 33 2 38 25 79 70, Fax: 33 2 38 25 79 79, e-mail: leroy@cnrs-orleans.fr

The NZB/BlNJ and C57BL/6JBy inbred strains exhibit large differences in simple sequences length polymorphisms (SSLPs), cerebellar patterns of foliation (CPF), and hind limb coordination. Quantitative trait loci (QTLs) modulating variation in these traits were mapped using a panel of 260 F2 male and female mice. Sixty-five SSLPs spaced an average of 20 cM apart were genotyped. Variation in the intraculminate fissure was found to be associated wtih three QTLs: Cpfi1 on Chr 1, Cpfi2 on Chr 4 (corresponding to the previously mapped Cfp1), and Cpfi3 on Chr 19. One of these QTLs, Cpfu1(Chr 1), is responsible for variation in the uvula fissure. Four QTLs were implicated in variation in the declive fissure; namely, Cpfd1 (Chr 1) Cpfd2 (Chr 5), Cpfd3 (Chr 9), and Cpfd4 (Chr 13). The Cfp2 and Cfp3 loci do not contribute to CPF variation between the parental strains. The abnormal coordination of the hind limbs (measured with the scarved bar generously provided by Hans-Peter Lipp) is correlated with five QTLs. Cpfd1 and Cpfu1 and one QTL that contributes to 17% of the variance in motor coordination are located on the same region of the telomeric part of Chr 1. This result suggests a functional link between variation in both the uvula and declive fissures with coordination of the hind limbs.


J. M. Lessem1, J. K. Hewitt1, L. J. Eaves2, J. L. Silberg2, M. Rutter3, E. Simonoff3
Life Events and Depressed Mood in the Virginia Twin Study of Adolescent Behavioral Development4
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309-0447. 2Department of Human Genetics, Medical College of Virginia, Richmond, VA 23298 3MRC Child Psychiatry Unit, Institute of Psychiatry, University of London, London, UK 4Supported by PHS Grant MH45268
Address: University of Colorado Campus Box 447 Boulder, CO 80309-0447 303-492-2843 303-492-8063 (fax) Jeff.Lessem+BGA@Colorado.EDU http://ibgwww.Colorado.EDU/~lessem

Extensive analyses have been performed relating life events and depressed mood in the Virginia Twin Study of Adolescent Behavioral Development. With self and parental reports on both life events and depressed mood available at multiple time points, analyses have been done to examine the discrepancy between parents' and children's responses and the genetic and environmental relationship between life events and depressed mood across time. Phenotypic results generally agree with the adolescent life event and depression literature, in that on average girls report more life events and a higher level of depressed mood than boys. Discrepancies in life event reporting appear to be "mistakes" on the self report, because most disagreements are due to a child endorsing (or not endorsing) an event contrary to the reports by the rest of the family. The variance of depressed mood and life events can be broken down into additive genetic and environmental factors. The effect of life events on mood does not appear to endure over a 1-2 year period of time, but the effect of depressed mood does endure over time. [Poster]


Paul Lichtenstein1, D. Reiss2, M. Cederblad 3, O. Elthammer3, J.M. Neiderhiser2, K. Hansson3, and N.L. Pedersen1,4
Genetic effects in parental bonding5
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden 2Center for Family Research, The George Washington University, Washington, D.C. 3Department Child and Adolescent Psychiatry, Lund University, Lund, Sweden 4Department of Psychology, University of Southern California 5Supported by NIMH grant MH-54610
Address: Box 218, SE-171 77 Stockholm. Email: paul.lichtenstein@imm.ki.se, Phone +46 8 728 7424, Fax: + 46 8 304 571

In psychological theories, the importance of an adult's remembered bonding with parents is often underscored and assumed to be an important influence on psychopathology. Behavior genetic research has shown that remembered childhood environments are in part genetically influenced - especially the types of relationships that tap into the warmth dimension. It is often hypothesized, but not yet shown empirically, that heritable stable characteristics (like personality) in the children influence parental bonding behavior. As part of larger study on family processes and maternal adjustment in 326 pairs of female twins age 33-55 we have evaluated remembered childhood experiences with the Parental Bonding Instrument (PBI), as well as a number of stable characteristics in the adult twins. Genetic influences accounted for 32% of the variation in the twins' reports of the PBI subscale Warmth regarding their mothers. Shared and nonshared environmental influences were also significant and contribute with approximately 1/3 of the variance each. For the other maternal subscales - Protectiveness and Authoritarian- only shared and nonshared environmental effects were evident. There were no indications of genetic influences for any of the subscales regarding the twins' fathers. Stepwise regression analyses revealed that four stable characteristics - Positivity, Indirect aggression, Suspiciousness, and Humor - explained most of the variance in the maternal Warmth subscale. The highest correlation (r=.22) was with Positivity and this scale also shared the largest part of genetic variance with Warmth. Multivariate genetic analyses showed that the four variables together explained about half of the genetic variance in Warmth. Thus, remembered maternal (but not paternal) warmth seems to be elicited partly by stable characteristics.


Paul Lichtenstein1, and M. Reiss Baker2
Telepathy in twins
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden 2 Bess and Paul Sigel Hebrew Academy, Bloomfield, Connecticut
Address: Box 218, SE-171 77 Stockholm. Email: paul.lichtenstein@imm.ki.se, Phone +46 8 728 7424, Fax: + 46 8 304 571

The popular press is filled with reports of telepathic and other types of extrasensory experiences between monozygotic twins. To our knowledge there are no empirical studies on whether twins themselves feel any type of extrasensory experiences. As a part of larger study on family processes and maternal adjustment we have asked 652 female twins age 33-55 how often they experience telepathic contact with each other. Several stable individual characteristics, such as personality, were also measured. Forty percent of the MZ twins responded that they have telepathic experiences to some or to a high degree as compared to 12% of the DZ twins. There was no difference in twin similarity (polychoric correlation) between MZ (.47) and DZ (.46). The only stable characteristics that were correlated with telepathy were two personality scales from the Temperament and Character Inventory (TCI). The scales are Persistence (r=.11; p<.01) measuring perseverance despite frustration and Self-transcendence (r=.17; p<.00001) measuring acceptance, identification, or spiritual union with nature and its source. Heritability and twin similarity for those scales were the same regardless whether the twins experienced telepathy or not, and regardless of whether they were concordant for telepathy or not. There are two interpretations of the higher degree of telepathy among the MZ twins; 1) MZ twins more often have a telepathic contact; 2) MZ twins are more similar than DZ twins, and greater similarity for, e.g., personality makes them more able to guess what their co-twin will do in a certain situation. We are more prone to believe in the latter interpretation even though case studies most often suggest that the former is most important. [Poster]


John C. Loehlin1, Amanda Spurdle2, Nicholas G. Martin2
Number of CAG repeats in the androgen receptor gene and psychological femininity
1 Department of Psychology, University of Texas, Austin, TX 78712 2 Queensland Institute of Medical Research, Brisbane 4029, Australia
Address: John C. Loehlin, Department of Psychology, University of Texas, Austin, TX 78712; e-mail loehlin@psy.utexas.edu; telephone (512) 475-4008; fax (512) 471-6175

For a study on uterine cancer risk, one member of each of 300 adult Australian female monozygotic twin pairs had been genotyped for the X-linked androgen receptor gene and scored for the number of repeats of the triplet CAG. (A low number of CAG repeats has been associated with greater risk of prostate cancer in males and more effective transcription of androgens.) These twins were part of a large twin study in which short versions of Eysenck's and Cloninger's personality questionnaires had been used. For the present study, three separate measures of masculinity-femininity were constructed from the items of these questionnaires, using item and factor analysis. Two of the three measures--admitting to fears and worries and a willingness to break rules--were not significantly correlated with CAG repeats among the genotyped females. The third measure, reserved versus confiding in others, showed a modest relationship with CAG repeats: fewer repeats went with scores in the reserved (i.e., masculine) direction on this scale. [Poster]


Pamela A.F. Madden 1, K.K. Bucholz1, A.C. Heath1, and N.G. Martin2
Heritability of Stages of Cigarette Smoking in Australian Adult Twins3
1Washington University School of Medicine, St. Louis, MO, 63110 2Queensland Institute of Medical Research, Brisbane, Australia 3Supported by NIH grants AA10249, AA07728 and DA00272
Address: 40 N. Kingshighway, Suite #2, St. Louis, MO 63108; Phone: (314) 286-2286; Fax: (314) 286-2213; E-Mail: pam@matlock.wustl.edu

Evidence from twin studies suggests that genetic influences play an important role in all stages of cigarette use, including experimentation, regular smoking, nicotine dependence, and persistence in smoking. Important relationships have been found between lifetime depression and a history of cigarette smoking. In follow-up data from female twins (obtained in the U.S.) (Kendler, et al., Arch Gen Psychiatry 50:36-43, 1993) a strong genetic correlation was found between average lifetime cigarette consumption and one-year prevalence of major depression. The purpose of this study is to determine the extent to which genetic influence on risk of major depressive disorder might mediate some of the genetic influence on smoking risks in Australian women compared with men. Telephone interview data on measures of DSM-IV nicotine dependence and the use of cigarettes were obtained from over 2,000 adult Australian twins, 20-34 years of age. Consistent with other studies, we found evidence for additive genetic influences on risks for major depression (34%, 95% CI: 17-44%), cigarette experimentation (65%, 95% CI: 56- 72%), regular smoking (66%, 95% CI: 48-83%), and DSM-IV nicotine dependence (62%, 95% CI: 54-70%), Fagerstrom nicotine dependence (74%, 95% CI: 66-81%), and smoking persistence (65%, 95% CI: 56-72%) in both men and women. In logistic regression analyses, except for experimentation in men, we found history of DSM-IV major depression to be a significant predictor of all stages of cigarette use (OR range: 1.55-2.40). When variables coding for zygosity and zygosity x cotwin's smoking were included with a measure of respondent's major depression in the regression equation, the cotwin smoking variables remained significant predictors, implying that genetic factors that increase risk for the initiation and the maintenance of smoking in women and in men cannot be entirely explained by factors responsible for major depression.


Nicholas G. Martin 1, John B. Whitfield 2, Dona Pang 2 Katherine M. Kirk 1, and Andrew C. Heath 3
Association of monoamine oxidase (MAO) with smoking, alcohol dependence and other measures of psychopathology and personality 4
1 Queensland Institute of Medical Research, Brisbane Australia 2 Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Sydney Australia 3 Department of Psychiatry, Washington University School of Medicine, St Louis USA 4 Supported in part by a grant from the National Institute for Alcohol Abuse and Alcoholism, AA07535
Address: Queensland Institute of Medical Research, Post Office, Royal Brisbane Hospital, Brisbane QLD 4029 Australia Telephone: +61 7 3362 0278 Facsimile: +61 7 3362 0101 E-mail: nickM@qimr.edu.au

Associations between platelet monoamine oxidase (MAO) activity and susceptibility to psychiatric conditions such as alcohol dependence, other drug use, conduct disorder and depression have been reported. However, MAO activity has been shown to be inhibited by some component of cigarette smoke, and prevalence of smoking is higher in many of the conditions in which MAO has been implicated. We have measured platelet MAO in 1551 individuals recruited from the Australian NHMRC Twin Registry, for whom information on alcohol use and dependence, smoking, conduct disorder, depression, attempted suicide, panic disorder, social phobia and several personality scales was available. Current smoking reduced platelet MAO activity in a significant and dose-related manner, with no evidence of lower MAO in ex-smokers or non-smoking subjects with co-twins who smoked. Alcohol use and lifetime DSM-IIIR alcohol dependence history were not associated with MAO activity when smoking was taken into account, while depression, panic disorder, social phobia and attempted suicide were no significantly associated with platelet MAO activity either before or after correcting for smoking effects. Of the personality scales, only Neuroticism from the Eysenck Personality Questionnaire was significantly correlated with MAO, with a stronger correlation observed after correction for smoking status. Results of structural equation modelling of the relationship between MAO, Neuroticism and smoking will be presented.


John J. McArdle1, and John L. Horn2
The use of biometric genetic data to evaluate the structural, kinematic, and dynamic hypotheses of the theory of "fluid and crystallized intelligence"
1 Department of Psychology, University of Virginia, Charlottesville, VA 22903 2 Department of Psychology, University of Southern California, Los Angeles, CA 96275 1 Supported by NIA grant AG-07137
Address: Psychology, University of Virginia, Charlottesville, VA 22903. 804/924-0656(phone); 804/982-4766(fax); jjm@virginia.edu; http://kiptron.psyc.virginia.edu/jack_mcardle/

The theory of fluid and crystalized intelligence (Cattell, 1941; Cattell & Horn, 1984; Horn & Cattell, 1966; Horn, 1991) grew out of three major predictions about the complex nature of human cognitive abilities. The first predictions were "structural": a single general factor (i.e., Spearman's "g") will not account for the patterns of individual differences seen among multiple abilities; at least two broad factors (Gf and Gc) are required for resonable level of fit to observations. A second set of predictions of Gf-Gc theory were "kinematic": over the life-span there is anexpected rise of gc and an expected rise through childhood into young adulthood of Gf and consequent fall throughout adulthood. A third set of predictions were "dynamic": the "investment" of Gf, coupled with other lower order factors in the context of educationally relevant settings, was thought to lead to individual differences in the development of Gc. Aspects of these predictions have been repeatedly examined and found to provide support for the theory (cf. Horn & Cattell, 1967; Horn & Donaldson, 1980; McArdle & Prescott,1992; Horn, 1994; Schaie & Baltes, 1996; McArdle, Prescott, Hamagami & Horn, 1998). This paper presents a review on the use of behavioral genetic information to evaluate the construct validity of these structural, kinematic, and dynamic predictions. Multivariate structural equation models based on biometric data are then illustrated to evaluate the generative hypotheses of gf/gc theory.


Tara L. McLaughlin1, Kathy K. Bucholz1, Pamela A.F.Madden1, Wendy S. Slutske2, and Andrew C. Heath1
Genetic and environmental influences on behavioral disorder symptom count in adolescent females3
1Department of Psychiatry, Washington University School of Medicine, St.Louis, MO 63108 2Department of Psychology, University of Missouri, Columbia 3Supported by AA09022, AA07728, DA07261, DA00272
Address: 40 N.Kingshighway, Suite 1, Box 8134 St.Louis, MO 63108, USA. Phone:(314) 286-2270. FAX: (314) 286-2213. e-mail:tara@matlock.wustl.edu

The Missouri Adolescent Female Twin Study (MOAFTS) is focused on the exploration of behavioral and psychiatric correlates of substance dependence in girls and young women. Telephone interview data from over 2,600 female adolescent twins (770 MZ pairs and 562 DZ pairs) and their parents participating in MOAFTS were utilized in the present report. We sought to explore how genetic and environmental factors influence behavioral disorders in girls, as measured through a composite variable reflecting total symptom count of conduct problems (obtained through child self report), attentional deficits, hyperactivity and oppositional defiant behaviors (obtained through parental report). Twin pair correlations for this composite measure suggested that shared environmental factors as well as genetic factors influence the occurrence of behavioral problems in girls (r= .82 for MZ pairs, r= .50 for DZ pairs). Subsequent genetic model fitting suggested that about 61% of the variance in this measure could be attributed to additive genetic effects while shared and unique environmental effects accounted for approximately 20% and 19% of the variance respectively. These results are thus consistent with those of other twin studies (e.g., Slutske et al., 1997,J. Abnorm. Psychol.106, 266-279)in which substantial genetic influences on behavioral problems in females have been demonstrated.


Kari A. Merrill1, Richard J. Viken1, Jaakko Kaprio2, and Richard J. Rose1
Thinking about drinking: Genetic and environmental influences on alcohol expectancies
1 Department of Psychology, Indiana University 2 National Public Health Institute, Finland
Address: Department of Psychology Indiana University 1101 E. 10th St. Bloomington, IN 47405-7007 Phone (812) 855-2311 Fax (812) 855-4691 e-mail kamerril@indiana.edu

We examined genetic and environmental influences on alcohol-related expectancies, measured by the Effects of Drinking Alcohol scale (EDA; Leigh, B.C., 1987, J. Stud. Alc.48(5), 467-475), in a sample of over 2,300 pairs of Finnish twins, including 778 MZ, 790 DZ, and 810 OSDZ pairs. Path modeling of twin covariances on the EDA subscales, derived from factor analysis of all individual twins, showed moderate contributions of additive genetic and unique environmental influences. Sex limitation models were also tested, revealing sex-related differences in the relative contributions of genes and environment on several of the subscales. Because expectancies consistently have been shown to correlate highly with drinking behavior, bivariate analyses were performed to estimate the contribution of environmental and genetic effects to the phenotypic covariance. [Poster]


Michael B. Miller1, and Marc Kayson1
An easy method of linking databases to internet white pages for systematic tracking and identification of research participants
1Department of Psychology, University of Missouri, Columbia, MO
Address: Michael B. Miller, Department of Psychology, 210 McAlester Hall, University of Missouri, Columbia, MO 65211 e-mail: mbmiller@taxa.psyc.missouri.edu web: http://taxa.psyc.missouri.edu/~mbmiller/

Locating people has become much easier in recent years with the advent of the internet. Freely available "white pages" databases allow users to search for individuals with listed telephone numbers in the United States, Canada, Austria, Belgium, Germany, Italy, Luxembourg, Spain and the United Kingdom (and perhaps other countries). The better on-line white pages allow users to search by name, address or telephone number, and the search can be limited to a city, metropolitan area, state or entire country. These resources can be extremely helpful when attempting to locate twins from vital records data, or when attempting to recontact participants in a longitudinal study. We have developed an simple approach using Microsoft Access and Microsoft Word that allows us to automate the search process. Data on subjects are stored in a Microsoft Access database. Information from the database can be inserted into an HTML (web) document using the Microsoft Word mail merge function. The web document allows users to submit a query to the white pages for information about an individual simply by clicking on a hypertext link. Links can be added to query about the phone number, address, or the name of a subject's family member. This approach saves a lot of time and reduces data-entry errors. The address and telephone information taken from the white pages can be pasted electronically into other programs for further processing. The whole procedure is very simple and does not require extensive knowledge of computers. The web document does not have to be stored on a web server because it can be accessed as a local file. Microsoft programs do not have to be used either. For example, one could use UNIX awk to translate a tab-delimited text file to a web document.


Charles Murray1
Implications of the secular rise in IQ for convergence of black and white IQ scores
1 American Enterprise Institute, Washington, DC, USA
Address: American Enterprise Institute, 1150 17th Street NW, Washington, DC 20036, USA. Phone 301.834.7425 Fax 301.834.9421 Email chasmurray@earthlink.net

The secular and international rise in IQ has been widely interpreted as evidence that black and white IQ scores may be expected to converge over time. The present study first examines the logic behind this position, then explores the consistency of that logic with data from the National Longitudinal Study of Youth (NLSY), a large national sample that has been followed since 1979. Elaborating Jensen's procedure (A.R. Jensen, 1973, Educability and Group Differences, Methuen), the analyses focus on sibling pairs and mother-offspring pairs within the NLSY. For the sibling analysis, a sample of blacks and whites are matched on IQ and on parental education, occupation, and income. For the mother-offspring analysis, a sample of black and white mothers are matched on IQ and their own education and family income. Parallel analyses of the IQs of the comparison siblings and of the offspring are conducted. Despite equivalent means and variance on IQ and the socioeconomic variables in the black and white reference samples, the IQs of the comparison siblings and of the offspring regressed to means with a black/white difference of 16.9 IQ points (sibling sample) and 21.6 IQ points (mother-offspring sample). Alternative possibilities for reconciling these findings with the secular rise in IQ are discussed.


Jenae M. Neiderhiser1, Erica Spotts1, Paul Lichtenstein2, Nancy Pedersen2,4, Kjell Hansson3, Marianne Cederblad3, Olle Elthammer 3, and David Reiss1
The association between mothering and marital relationships: is it all in the genes?5
1Center for Family Research, George Washington University, Washington, DC 20037 2Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden 3 Department of Child & Youth Psychiatry, Lund University, Lund, Sweden 4 University of Southern California 5Supported by grant R01MH54610 from the National Institute of Mental Health
Address: 2300 Eye St., N.W., Room 613 Ross Hall. Email: cfrjmn@gwumc.edu, Phone 202.994.2212, Fax: 202.994.4812

Family systems research has long focused on relationships within the family within the context of the family as a whole. One of the most compelling findings in behavioral genetic research has been the importance of genetic factors on measures typically conceptualized as environmental (e.g. parenting). The majority of research in this area has employed child-based designs, although the few studies that have employed a parent-based design have also found evidence of genetic influences (S.H. Losoya, S. Callor, D.C. Rowe, & H.H. Goldsmith, 1997, Developmental Psychology 33, 1012-1023). To date, there have been no studies that have examined genetic influences on marital relationships, although genetic influences on divorce have been found (M. McGue & D.T. Lykken, 1992, Psychological Science 3, 368-373). It is likely that genetic influences on parenting will overlap with any genetic influences on the marital relationship that are found. The present report employs a sample 326 pairs of twin mothers of adolescents from Sweden (148 MZ, 174 DZ). Results indicate that there are genetic influences on mother-child and marital relationships (heritability ranges from 26% to 62% for marital positivity and negativity and from 18% to 32% for maternal positivity and negativity). There is also evidence of modest phenotypic correlation between mother's relationships with her child and her spouse. Cross-twin correlations suggest that this relationship can be explained in part by overlapping genetic influences on the association between mother's positivity towards her child and towards her spouse. Additional analyses will be conducted to further examine these associations across raters and constructs.


Ulric Neisser1
The secular rise in intelligence: Many gains, many causes
1 Cornell University
Address: Department of Psychology, Cornell University, Ithaca NY 14853 (un13@cornell.edu) 607 255 6355

It seems likely that many aspects of modernization have contributed to the Flynn rise. School is the most obvious candidate: the amount of time people spend in school has been growing right along with IQ, and we have clear evidence that schooling raises scores even on tests of fluid intelligence. Increases in non-school forms of environmental complexity (such as visual displays and digital devices) have probably developed a corresponding set of mental skills as well. It would not be surprising to find that improvements in health and nutrition have played a role, along with the growing public interest in intellectual aspects of infant and child development. Whatever their causes, these gains are not artifacts. They manifest themselves in domains other than testing itself: the extraordinary technological progress visible everywhere around us is perhaps the most obvious of those manifestations. Other evidence comes from recent demonstrations of increases of chess-playing skill at early ages and (surprisingly!) in the complexity of political discourse. Overall, the scope and patterning of the Flynn gains presents major challenges to contemporary theories of intelligence.


Helmuth Nyborg1
Secular changes in longitudinal IQ: Individual and group differences
1 PNE Research Center, Institute of Psychology, University of Aarhus, Denmark
Address: PNE Research Center, Institute of Psychology, Asylvej 4, DK-8240 Risskov, Denmark. Phone 45* 8942 4900, Fax 45* 8942 4901, email helmuth@psy.au.dk

Most information on the secular Flynn IQ rise derives from intergenerational comparisons. The present study examined whether a similar secular rise is seen in a repeated-measures analysis of longitudinal IQ data. Army General Technical (GT) intelligence was measured first at about age 19 in a large sample of fairly representative American armed forces veterans and again when they were in their late thirties. Individual variations over time in full GT IQ, in verbal reasoning and in arithmetic reasoning IQ changes were monitored and related to middle-age level of education, personality, and psychopathology. The full GT IQ score rose on average 0,27 IQ points/year for the total sample, but the amount of gain or loss related to young IQ level. Low, medium and moderately high ability individuals thus tended to gain and high ability individuals (i.e. young GT IQ > 1,5 SD) to lose, and the more so the higher the IQ. We thus face the paradox that a typical high IQ loser is one with a long formal education, a large income, benign personality traits, and few symptoms of psychopathology, whereas the typical low IQ gainer spends significantly fewer years in school, earn less, obtain higher Psychoticism, Neuroticism, and Extraversion scores, and score high on MMPI-II and DSM-III scales for psychopathology and substance abuse. Race differences in overall IQ gain were noted, too.


Naoko Onoda11, Y. Ono2, and J. Ando3
Genetic and environmental influence on parenting in Japanese population
1Department of Medical Science, Keio University Graduate School, Tokyo 2 Department of Psychiatry and Neuroscience, Keio University of Medicine, Tokyo 3 Department of Education, Faculty of Letters, Keio University, Tokyo
Address: 35 Shinanomachi Sinjuku-ku Tokyo, 160-8582 tel.03-3353-1211(2453) fax.03-5379-0187 e-mail address naoko-o@mc.med.keio.ac.jp

This study investigates the genetic and environmental influences on parenting experiences children received. PBI(Parental Bonding Instrument)was carried out for 213 twin pairs (38 MZm, 101 MZf, 16 DZm, 30 DZf, 28 DZo twin pairs) from 15 to 27 years old. They were required to recall their parenting experiences they had received from each of their parents in their childhood. Two dimensions of parental behavior, care and overprotection were subjected to model fitting. As for the father's care score, the best fitting model was CE model(the variance was due to common environmental factor and specific environmental factor). For the female subjects, however, ACE model couldn't be rejected with the heritability of 28%. Father's overprotection reported by male was explained best by AE model with 75% of the additive genetic variance and 25% specific environmental factor. Father's overprotection reported by female was explained best by CE model with 53% common environment and 47% specific environment. For the mother's care score, the best fitting model was AE with heritability of 64% and 56% by male subjects and female subjects respectively. Mother's overprotection showed 57% common environment with no genetic influence for both sex. Genetic factor of the elicitation of mother's care was verified in Japanese population.


N.L. Pedersen 1,2, E.L. Spotts 3, M. Cederblad 4, P. Lichtenstein 1, K. Hansson 4, J.M. Neiderhiser 3, O. Elthammar 4, and D. Reiss 3
Lack of effect of intra-pair contact and aspirations to be similar on twin similarity for personality, marital adjustment, and parenting 5
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden, 2Department of Psychology, University of Southern California, Los Angeles, 3Center for Family Research, The George Washington University, Washington, D.C. 4Department of Child and Adolescent Psychiatry, Lund University, Lund, Sweden, 5Supported by NIMH grant MH-54610
Address: Box 281, SE-171 77 Stockholm. Email: Nancy.Pedersen@imm.ki.se, Phone +46 8 728 7418, Fax: + 46 8 30 45 71

The equal environments assumption has been repeatedly tested for a wide range of phenotypes. Neither presumed zygosity nor parental attempts to make similar have been demonstrated to affect twin similarity for measures of personality or cognition. Aspirations to be similar are seldom evaluated as a source or as a potential outcome of similarity for personality. In the Twin Moms study of maternal adjustment in the context of familial processes, we are particularly interested in measures of personality, parenting, and marital relationships. We have developed 3 scales describing contact and aspirations to be similar: behavioral contact, aspirations to be similar, confiding in sister. For all three measures, MZ pairs (N=144) reported slightly, but significantly more contact than DZ pairs (N=171). Intraclass correlations for reported contact and confiding in sister were high (.81 and .80 for contact, .75 and .62 for confiding in MZ and DZ pairs, respectively). Intraclass correlations for aspirations to be similar were .38 and .35. Intrapair similarity for personality, marital adjustment, and parenting was not associated with either level of or intrapair similarity for any of the three contact measures. Thus, aspirations to be similar and contact with/confiding in twin partner do not influence heritability estimates of personality, parenting or marital adjustment. [Poster]


Daniel Pérusse1, R E. Tremblay1, M. Boivin2, and B. Boulerice1
Early motor-cognitive development: A study of 5-month-old twins3
1 Research Unit on Children's Psycho-Social Maladjustment, University of Montreal, Montreal, Canada. 2 Research Unit on Children's Psycho-Social Maladjustment, Laval University, Quebec City, Canada. 3 Supported by grants to the first author from the Medical Research Council of Canada, the National Health Research and Development Program/Health Canada, the Social Sciences and Humanities Research Council of Canada, the Fonds de la recherche en sante du Quebec, and the Quebec Ministry of Health and Social Services
Address: Fernand-Seguin Research Center, University of Montreal, 7331 Hochelaga, Montreal, Canada, H1N 3V2, Tel. (514) 251-4015 ext. 2352, Fax: (514) 251-2617, email: Daniel.Perusse@umontreal.ca

Infants develop a variety of sensory, motor, and cognitive skills that gradually enable them to adapt to their environment. Early developmental delays have been found to be important predictors of later learning difficulties, school problems, and other aspects of psychosocial maladjustment. In the present study, the genetic-environmental contributions to early development were examined in a population-based sample of infant twins. Subjects were recruited by contacting all mothers having given birth to twins in the Greater Montreal Area between 1 April, 1995 and 31 December, 1998. Zygosity was determined by physical similarity assessment and validated with DNA analysis. Development was measured when the twins were 5 months old (corrected for gestational age) through mother interview employing a scale used in the Canadian National Longitudinal Survey of Children. Twelve items (e.g., "Has he/she ever sat for 10 minutes without any support at all?"; "Has he/she ever said good-bye without help from another person?") were retained for the scale by item analysis (alpha = .74). Genetic analysis was performed on the aggregate score using hierarchical multilevel random effect modeling. Strong intraclass correlations were found for both MZ and DZ pairs. This resemblance was entirely due to shared environmental factors which accounted for 75% of the variance, with heritability = 0. Reporting bias (mothers answering similarly for both twins) appears unlikely since interviews were conducted separately for each twin and the scale was strongly related to a laboratory assessment of motor-cognitive skills in a subsample of subjects. These findings suggest that infant motor-cognitive development is influenced by familial environmental factors and that developmental delays may result from exposure within families to risks that still need to be identified.


Michael F. Pogue-Geile1,2, S.B. Manuck,1,2 T. Kamarck,1,2 & T. Debski1
Cardiovascular reactivity to psychological stress: A twin study3
1 Department of Psychology, University of Pittsburgh, Pittsburgh, PA 2 Department of Psychiatry, University of Pittsburgh 3 Supported in part by NIH HL40962
Address: Department of Psychology 4015 O'Hara St. University of Pittsburgh Pittsburgh, PA, 15260, USA tel: 412.624.8818 fax: 412.624.5407 mfpg@pop.pitt.edu

Evidence increasingly suggests that individual differences in cardiovascular reactivity to psychological stressors during young adulthood may be predictive of later risk for clinical cardiovascular disease. However, despite this clinical importance, relatively little is known concerning the genetic and environmental causes of variation in cardiovascular reactivity to stress. Therefore, as part of the University of Pittsburgh Twin Study, 160 MZ and 80 same-sex DZ (zygosity based on DNA fingerprinting), young adult (18-28 years old), normotensive twin pairs from the community were evaluated in a protocol measuring cardiovascular reactivity to five laboratory stressors (Mental Arithmetic, Stroop Test, Mirror Tracing, Video Game, and Cold Pressor). Heart rate, diastolic and systolic blood pressure, as well as indexes from impedance cardiography were measured at baseline and during task performance. Multivariate genetic analyses were performed in order to address the following questions: 1) are there genetic influences on cardiovascular reactivity to stress that are independent of those influencing baseline cardiovascular function, 2) what is the factor structure of these genetic influences across multiple measures of cardiovascular reactivity, and 3) what is the factor structure of these genetic influences across the five laboratory stressors? Based on this final sample, analyses indicate that in general novel genetic influences (independent of those influencing baseline cardiovascular function) are important in determining individual differences in cardiovascular reactivity to psychological stressors. The structure of these genetic influences suggests the existence of a common genetic factor across both the multiple cardiovascular measures and across the different psychological stressors. These results support the generality of the construct of cardiovascular reactivity to laboratory psychological stress.


Clare Porac11
Variation in human hand preference patterns: Effects of age and pressures to switch side2
1 Department of Psychology, University of Victoria, Victoria, BC V8W 3P5 Canada 2 Supported by grants from the Natural Sciences and Engineering Research Council and the University of Victoria Centre on Aging, the David and Dorothy Lam Endowment
Address: P.O. Box 3050, Department of Psychology, University of Victoria, Victoria, BC V8W 3P5 Canada, Phone: (250) 721-7537, Fax: (250) 721-8929

Recent genetic theories of human hand preference have emphasized the role of environmental factors as contributory to the variation seen in this set of common behaviors; the environmental factors are proposed to be biological (T.A. Markow, 1992, Genetica, 87, 87-94; R.A. Yeo, S.W. Gangestad, and W.F.Daniel, 1993, Psychobiol., 21, 161-168) or cultural (K.N. Laland, J. Kumm, J.D. Van Horn, and M.W. Feldman, 1995, Behav. Genet., 25, 433-446) in origin. Data from three separate studies of right- and left-handers of different ages (I.B. Perelle and L. Ehrman, 1994, Behav. Genet., 24, 217-228; C. Porac, I.C. Friesen, M.P. Barnes, and V. Gruppuso, 1998, Develop. Neuropsychol., 14, 157-172; C. Porac, unpublished) are presented and analyzed in order to show how age-related variations in hand preference patterns interact with participants reported histories of hand preference switch attempts. This age/switch history interaction promotes not only variation in the degree to which left hand preference is apparent at different ages, but also the degree to which individual hand preference items display sidedness consistency or inconsistency. The data reveal that the writing hand is the most frequently switched behavior and, in individuals over the age of 75 years, the writing hand is a poor predictor of left hand preference. Although both young (<30 years) and older (>65 years) report pressures to switch hand preference, the disassociation between writing and other preference behaviors is most apparent in older adult groups. In addition to switch history, the data also reveal the possibility of a more subtle developmental shift toward the right side when young adult groups are compared to older adults; however, the effect of switch history remains the strongest variable in determining age differences across the age span of older and oldest-old adults (65 to 100 years).


Danielle Posthuma 1, G.Caroline M. van Baal1, Eco J.C. de Geus1, Harold Snieder2, Dorret I. Boomsma1
Association between apoE genotype, apoE-levels and cognitive performance
1 Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands 2 Twin Research and Genetic Epidemiology, St. Thomas Hospital, London, UK
Address: D. Posthuma Vrije Universiteit Department of Biological Psychology De Boelelaan 1111 1081 HV Amsterdam The Netherlands Phone: +31 20 4448814 Fax: +31 20 4448832 e-mail: danielle@psy.vu.nl

ApoE genotype is a risk factor for cognitive decline in old age. It has been associated with the risk of developing Alzheimer's disease and with deterioration of memory function. One of the theories explaining the association between the apoE genotype and cognitive decline, focuses on the effect of the apoE-genotype on apoE levels in blood. ApoE bloodlevels affect the binding of beta amyloid and may increase deposits of beta amyloid which eventually turn into plaques characteristic for cognitive decline in Alzheimer's disease. Variance in apoE bloodlevels is for 16% explained by the apoE-genotype. In roughly 100 families, consisting of twins and their siblings (aged 20-35), the apoE locus was genotyped and apoE blood levels were measured. Cognitive ability was assessed with the Wechsler Adult Intelligence Scale (WAIS-3R, Dutch revised version). We found a negative association between apoE levels in plasma and full scale IQ and performance IQ. We also found an association between the apoE genotype and WAIS subtests similarities and digit-symbol free recall. The same analyses will be done for roughly 150 families consisting of twins and their siblings aged 35 - 65 years.


Danielle Posthuma 1, and Dorret I. Boomsma1
Adding non-twin siblings to increase power
1 Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands
Address: D. Posthuma Vrije Universiteit Department of Biological Psychology De Boelelaan 1111 1081 HV Amsterdam The Netherlands Phone: +31 20 4448814 Fax: +31 20 4448832 e-mail: danielle@psy.vu.nl

The power to detect an effect varies with sample size, effect size and study design. The power of the classical twin study may be increased by extending the familysize by adding non-twin siblings. We conducted a power analysis in Mx to determine whether adding one or two non-twin siblings to the classical twin design would increase the power to detect genetic and common environmental influences. We compared three possible designs, namely families consisting of only an MZ or DZ twin pair, families with MZ or DZ twins and one non-twin sibling, and families with MZ or DZ twins and two non-twin siblings. Total sample size and MZ/DZ ratio were held constant. We found that adding one non-twin sibling caused an increase in the power to detect heritability, but that adding two non-twin siblings nullified this effect. For the power to detect common environmental factors a large effect of adding one non-twin sibling was found. Adding two non-twin siblings had an additional small increase on top of the effect of adding one non-twin sibling. [Poster]


Carol A. Prescott1, Steven H. Aggen1, and Kenneth S. Kendler1
A twin study of the sources of comorbidity between alcoholism and major depression2
1 Virginia Institute for Psychiatric & Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond VA 23298 2 Supported by NIH grants R01-MH/AA-49492, R01-AA/DA-09095, and K01-AA-00236
Address: VIPBG, MCV/VCU, P.O. Box 980126, Richmond VA 23298-0126. 804/828-5968(phone); 804/828-1471(fax); cprescott@gems.vcu.edu; http://www.vipbg.vcu.edu/vipbg/

Alcoholism and depression frequently co-occur, but the basis of this comorbidity remains uncertain. This association is further complicated by sex differences in the prevalences and timing of these disorders. One explanation is that major depression and alcoholism represent alternative manifestations of the same underlying vulnerability, and there are sex-specific factors which influence clinical presentation. Alternatively, this clinical heterogeneity may reflect separate etiologies for depression and alcoholism. We address these issues using data from a recent study of 8,700 adult twins identified from a population-based twin registry and assessed for lifetime major depression (MD) and alcohol abuse or dependence (AAD) by structured psychiatric interview. For both males and females, individuals with one disorder were at significantly increased risk for the other (OR=2.5, 95% CI=2.1-2.9). Risk of AAD was increased among both identical and fraternal same-sex cotwins of individuals with MD. However, when the analyses were restricted to primary alcoholism (excluding comorbid cases where MD preceded AAD), this association was attenuated. Structural modeling analyses of the twin-pair correlations suggest that the comorbidity of alcoholism and depression is due primarily to individual-specific environmental factors and that the disorders are not sex-specific manifestations of common genetic vulnerability. [Poster]


Shaun Purcell1, Stacey S. Cherny2, and Pak C. Sham1
Selecting maximally informative sibships for QTL association analysis
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, SE5 8AF, United Kingdom 2Institute for Behavior Genetics, University of Colorado, Boulder, CO 80309-0447 1,2Supported in part by a Programme Project grant from the Medical Research Council of Great Britain
Address: Social, Genetic & Developmental Psychiatry Research Centre, 111 Denmark Hill, London SE5 8AF. Tel: +44 (0) 171 740 5267 Fax: +44 (0) 171 919 3866 e-mail: s.purcell@iop.kcl.ac.uk

Fulker et al (1999) have proposed a partitioning of association to between-sibships and within-sibship components, and shown that a test based on the within-sibship variance is robust to population stratification. As in QTL linkage analysis, the efficiency of an association design may be improved by selecting phenotypically extreme sibships. We have developed a method of measuring the informativeness of sibships for QTL association analysis, in terms of the expected contributions of the sibship to the likelihood ratio chi-squared tests for between-sibships and within-sibship association. These expected contributions are calculated conditional on the measured trait values of the siblings, under a biometrical genetic model where QTL effects are parameterized by allele frequencies and genotypic means, and which allows for residual sibling correlations. This presentation will describe the method and its implementation in a freely-distributed computer program. Refs. Fulker DW, Cherny SS, Sham PC, Hewitt JK (1999) Combined linkage and association sib-pair analysis for quantitative traits. American Journal of Human Genetics, 64, 259-267


Soo Hyun Rhee1, and Irwin D. Waldman1
Etiology of sex differences in inattention and hyperactivity/impulsivity2
1Department of Psychology, Emory University, Atlanta, GA 30322 2Supported by NIMH National Research Service Award 1 F31 MH11772-01
Address: Department of Psychology, Emory University, Atlanta, GA 30322. Phone: (573) 442-3890. Fax: (404) 727-0372. e-mail: srhee01@emory.edu

Attention-deficit/hyperactivity disorder (ADHD) is more common in boys than girls, with sex ratios ranging from 3:1 to 8:1. Researchers have suggested two competing explanations for this sex difference in prevalence: the polygenic multiple threshold (PMT) model (e.g., Kashani, Chapel, Ellis, & Shekim, 1979, Journal of Operational Psychiatry 10, 145-148), which suggests a sex difference in the threshold for the liability needed to express the disorder, and the constitutional variability (CV) model (e.g., James & Taylor, 1990, Journal of Child Psychology and Psychiatry 31, 437-446), which suggests a sex difference in the causal factors. Studies testing the assumptions of these models report conflicting results, with some studies (e.g., Faraone et al., 1995, Journal of Abnormal Psychology 104, 334-345) finding support for the PMT model and some studies (e.g., Silverthorn, Frick, Kuper, & Ott, 1996, Journal of Clinical Child Psychology 25, 52-59) finding evidence against the PMT model. One possible reason for the variability in findings may be the heterogeneity in the constructs being examined. Given this possibility and the evidence that there are two separate dimensions of ADHD (inattention and hyperactivity-impulsivity), the assumptions of the two models were tested for inattention and hyperactivity-impulsivity separately in the present study. Participants were Georgia Twin Registry members (N = 56 to 375) who met the symptom list criteria for the diagnosis of one or more types of DSM-IV ADHD and their DZ co-twins and co-siblings. We found evidence for the PMT model and evidence against the CV model for all three types of ADHD: the predominantly inattentive type, the predominantly hyperactive-impulsive type, and the combined type. These results suggest that boys are more likely to be diagnosed with any type of ADHD than girls because girls have a higher threshold for the liability needed to express the disorder of ADHD.


Jeffrey Rogers1
Genetic linkage mapping in primates as a tool in behavior genetics
1 Dept. of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas
Address: Dept. of Genetics, Southwest Foundation, P.O. Box 760549, San Antonio, TX 78245-0549 phone 210-258-9532 fax 210-670-3316 email jrogers@darwin.sfbr.org

Nonhuman primates play a major role in studies of behavioral genetics. However, research has been limited to testing candidate genes. The mapping and identification of previously unknown genes that influence variation in primate behavior and/or neurobiology has not been possible because genetic linkage maps for primates have not been available. We have developed a 10 centiMorgan genetic linkage map of the baboon (Papio hamadryas) genome. This genetic map includes more than 350 highly polymorphic microsatellite loci that were originally cloned from and mapped in the human genome. The baboon map now makes it possible to use genome-wide linkage screening in large pedigrees to identify chromsomal segments within baboons that contain genes which influence any phenotype of interest. The baboon linkage map has been successfully used to locate several genes that influence bone metabolism. These analyses used data from 700 pedigreed baboons genotyped for the panel of 350 microsatellites. Other complex traits have also showed significant linkage results. We are beginning studies in which the same methods and microsatellite loci are being used to investigate behavioral phenotypes in baboons, including measures of temperament and of monoamine metabolites. We are also extending this research strategy (i.e. genetic analysis of large pedigreed colonies) to other nonhuman primate species.


Pierre L. Roubertoux1, I. Le Roy1, S. Mortaud1, and S. Tordjman1
Attack behavior in mice: Implication of the Sts gene mapped on the pairing region of the X-Y chromosomes
1 UPR CNRS 9074, Génétique, Neurogénétique, Comportement, Institut de Transgénose, Institut de Transgénose, 3 B rue de la Ferollerie; 45071, Orléans Cedex 02, France. Supported by CNRS (UPR 9074), Ministry for Research and Technology, Région Centre and Préfecture de la Région Centre. UPR 9074 is affiliated with INSERM and University of Orléans
Address: Phone: 33 2 38 25 79 70, Fax: 33 2 38 25 79 79, E-mail: rouber@cnrs-orleans.fr

The sexual dimorphism of aggression has led to a search for its Y- chromosomal correlates. We have previously confirmed that initiation of attack behavior against a conspecific male is Y- dependent in two strains of laboratory mice (NZB and C57BL/6J). We have provided evidence that the nonpairing region of the Y is not involved in this behavior whereas the pairing region of the Y co-segregates with attack behavior, in these strains. In addition, the genetic correlates of attack behavior are not expressed when borne on the homologous pairing region on the X chromosome but only when carried on the Y chromosome. Only one functional gene (coding for steroid sulfatase or STS) is mapped on this region as of yet, suggesting that it could be a candidate for attack behavior. We estimated the genetic correlation between the concentration of STS protein in the liver and initiation of attack behavior. We have employed also mice in which gene invalidation induced attack behavior. Pharmacological modulations of STS or of its metabolites modifies the frequencies of attack in these male mice, confirming the implication of STS in aggression. Recent investigations have demonstrated the involvement of STS in neurosteroid biochemical pathways, and several lines of evidence indicate that neurosteroids interact with neurotransmitters. These conclusions and our present results support the hypothesis that sulfatation of steroids may be the prime mover of a complex network, including genes shown to be implicated in aggression by mutagenesis.


Pierre L. Roubertoux1, and Isabelle Le Roy1
QTL mapping: A fundamental tool in behavioral neurogenetics 2
1 UPR CNRS 9074, Génétique, Neurogénétique, Comportement, Institut de Transgénose, Institut de Transgénose, 3 B rue de la Ferollerie; 45071, Orléans Cedex 02, France 2 Supported by CNRS (UPR 9074), Ministry for Research and Technology, Région Centre and Préfecture de la Région Centre, Fondation pour la Recherche Médicale. UPR 9074 is affiliated with INSERM and University of Orléans
Address: Pierre L. Roubertoux University of Orleans Director UPR 9074 CNRS Genetique, Neurogenetique, Comportement Institut de Transgenose CNRS 3 b rue de la Ferollerie 45071 Orleans cedex 02, France Phone: 33 2 38 25 79 70, Fax: 33 2 38 25 79 79, E-mail: rouber@cnrs-orleans.fr

QTL mapping was initiated forty years ago but its introduction in behavioral neurobiology is still comparatively new. Several studies have employed recombinant inbred strains, backcrosses, and intercrosses to analyze a wide range of behaviors (drug-related behaviors, handedness, sensory, and motor development, pup care, etc.). With the advent of advanced intercrosses, congenic, recombinant congenic, and consomic lines, QTL analysis is now entering a second generation. The utility and power of QTL analysis depends, however, on the reliability of the methods, an issue that is still in dispute. Here we demonstrate that a large number of QTLs that we have previously mapped in the neurobehavioral field have been successfully replicated. Our findings suggest that concern regarding Type I error (the probability of detecting false QTLs) has been somewhat overstated. We anticipate that two properties of QTL analysis will lead to a better understanding of the relations between structure and function. (1) The identification of strong candidate genes for QTL associated with a behavioral trait will in some instances provide partial validation of mapping results and will often lead to the formulation of testable hypothesis regarding the genetic basis of behavioral variation. This is illustrated by our work on maternal behavior in mice in which we have shown that a key olfactory receptor gene maps within the confidence interval defined by a QTL associated with pup retrieval performance. (2) Defining a list of plausible candidate genes for a QTL--what we refer to as QTL-gene coidentification--also provides an opportunity to explore possible aberrant behavior when the expression of candidates is altered. This is exemplified by our studies of aggression and handedness. QTL mapping is simply the initial step in a complex process that culminates in gene inactivation or overexpression. The potential of this approach will be demonstrated in the context of QTLs that modulate patterns of cerebellar foliation and that are implicated in abnormal coordination. A final characteristic of QTL map studies is that it becomes possibility to exploit the homologous synteny between mouse and human to probe the complex genetics of human behavioral disorders.


David C. Rowe 1, and Irwin B. Waldman 2
Genetic Influences on Childhood Disruptive Disorder Symptoms Estimated Through Measured and Latent Genetic Variables in Full Siblings
1 Graduate Program in Genetics and Family Studies, University of Arizona, Tucson, AZ 85721. 2 Department of Psychology, Emory University, 532 North Kilgo Circle, Atlanta, Georgia 30322
Address: School of Family and Consumer Resources, 1110 E. South Campus Dr., University of Arizona, Tucson, AZ 85721. dcr091@ag.arizona.edu.

Genotyping for measured genetic markers permits a combination of quantitative trait loci (QTL) and genetic factors in behavioral genetic models. This modeling approach is illustrated using data on disruptive behavior disorder symptoms in children and adolescents in 50 sibling pairs. The sample contains both probands referred for psychiatric disorder and their siblings (34 pairs) and controls and their siblings (16 pairs). The 100 individuals were genotyped for repeat polymorphisms in the dopamine transporter (DAT1) and in the dopamine D4 receptor (DRD4) genes. For the dopamine transporter locus, low and high risk genotypes were scored as follows: LL=0, LR=1, and RR=2, where L is a low risk allele and R is a high risk allele. For the DRD4 locus, the rare RR homozygote was combined with the heterozygote (LL=0, LR=1, RR=1). The dependent variables were three disruptive behavior disorder symptom count traits; i.e, hyperactive-impulsive symptoms, inattentive symptoms, and oppositional-defiant symptoms. Each trait was regressed on age and on family status (clinic referred = 1, control = 0) and residuals from this regression were used in a biometric model. The biometric model assumed no shared environmental influences, consistent with results from previous behavior genetic analyses. It allowed for measurement error on each trait and for four factors: a genetic factor uncorrelated with the QTLs, a DRD4 QTL factor, a DAT1 QTL factor, and a nonshared environmental factor. The full model yielded an excellent fit (chi2 = 27.64, df = 39, p = .913, AIC = -50.36). The change in chi square from dropping the DRD4 QTL was statistically significant (chi2 = 10.36, df = 3, p < .05). The loss of fit for the DAT1 QTL was marginally significant (chi2 = 7.60, df = 3, p < .10). The DRD4 QTL factor loaded most strongly on inattentive symptoms, whereas the DAT1 QTL factor loaded most heavily on hyperactive-impulsive symptoms. Of the variation in the three symptom traits, the DRD4 QTL explained (on average) 3.6%, whereas the DAT1 QTL explained (on average) 5%.


Espen Røysamb1, Jennifer R. Harris1, and Kristian Tambs1
What is self-rated health about after all? Genetic and environmental contributions to the associations between subjective well-being, health symptoms, health behaviours and self-rated health
1 National Institute of Public Health, Oslo, Norway
Address: National Institute of Public Health, P.O.Box 4404 Torshov, 0403 Oslo, Norway. Phone: +47 22 04 25 69. Fax: +47 22 04 23 51. Email: espen.roysamb@psykologi.uio.no

Self-rated health (SRH) is a component of health that is associated with, but not completely defined by, psychological and physical well-being. Although the factors comprising self-rated health are not totally understood, there is evidence for age differences in the predictors of SRH. This study analyzes two aspects of SRH in a sample of young adult twins. First, how do genes and environments mediate the relationships between between SRH and subjective well-being (SWB), health symptoms (HS) and health behaviors (HB)? Next, how important are genes and environments for variance in SRH that is not associated with SWB, HS and HB? Analyses were based on a Norwegian sample of 5864 twins, 18-23 years of age. Self-rated health correlates 0.41 with subjective well-being, -0.26 with health symptoms, and 0.24 with health behaviors. Regression procedures indicated a unique and significant effect of SWB, HS and HB for predicting SRH. Preliminary results suggest that genes are important mediators of the relationships with self-rated health, but that the patterns of mediation vary between SRH and the physical versus psychological measures of health. Final results, based on model fitting approaches that incorporate sex differences, will be presented.


J. Philippe Rushton1
Performance on Raven's Matrices by African and White University Students in South Africa(with a possible note on African g and the Flynn Effect)
1Department of Psychology, University of Western Ontario, London, Ontario, Canada N6A 5C2
Address: Department of Psychology, University of Western Ontario, London, Ontario, Canada N6A 5C2. Phone: 519-661-3685; Fax: 519-850-2302; email: rushton@julian.uwo.ca

Untimed Raven's Standard Progressive Matrices (SPM) were administered to 309 17- to 23- year-old students at two leading South African universities (173 Africans, 136 Whites; 205 women, 104 men). African students solved an average of 44 of the 60 problems whereas White students solved an average of 54 of the problems (p<0.001). By the standards of the 1993 U.S. normative sample, the African university students scored at the 14th percentile with an IQ equivalent of 84 and the White university students scored at the 61st percentile with an IQ equivalent of 105. A small sex difference favoring males was found in both the African and the White samples. These results confirm earlier reports of these race and sex differences. Two additional studies will be mentioned to shed light on possible causes. African 13- to 15-year olds given the Wechsler Intelligence Scale for Children-Revised (WISC-R) showed the most pronounced differences from the U.S. standardization sample on the gfactor. A principal components analysis by J. P. Rushton (1999, Person. and Indiv. Diffs.26,381-389) found that whereas five sets of IQ gain scores over time on the WISC-R and WISC-III do cluster (the Flynn Effect), suggesting they are a reliable phenomenon, these are independent of the cluster of (U.S.) Black-White differences, inbreeding depression scores (calculated on the WISC-R from Japan), and gfactor loadings.


Joanne Ruthsatz1, R.D. Tiu1, L.A. Thompson1, and D.K. Detterman1
The genetic influence on primary athletic ability and athletic ability's relationship with intelligence
1Case Western Reserve University
Address: Joanne Ruthsatz Department of Psychology Case Western Reserve University Cleveland, Ohio 44106 (216)368-6670 jxr@po.cwru.edu

The present study investigated the heritability of athletic ability using the twin design. At the same time, athletic ability was correlated with the WISC-R intelligence test. Previously unused data from the Western Reserve Twin Project (WRTP) were analyzed (Thompson, Detterman, & Plomin, 1991; Thompson, Detterman, & Plomin, 1993). The original sample consisted of 135 same-sex fraternal twin (DZ) and 148 identical (MZ) twins. Significant heritability was found for two of the four measures of athletic ability. Intelligence was significantly correlated with athletic ability. The etiology of the covariance between intelligence and athletic ability will be discussed.


Gerard Saucier1, Paul F. Collins1, David E. Comings2, Nancy Gonzalez2, Donn Muhleman2, and James P. MacMurray3
Novelty-Seeking and Harm-Avoidance: A Molecular-Genetic Test of Cloninger's Dopamine and Serotonin Hypotheses4
1Department of Psychology, University of Oregon, Eugene, OR 97403 2Department of Medical Genetics, City of Hope Medical Center, Duarte, CA 91010 3Department of Psychiatry, Loma Linda University School of Medicine, Loma Linda, CA 92357 4Supported by NIDA grant R01-DA08417 and TRRDP grant 4RT-0110
Address: Gerard Saucier, Department of Psychology, 1227 University of Oregon, Eugene OR 97403-1227, tel. 541-346-4927, fax 541-346-4911, email gsaucier@oregon.uoregon.edu

Cloninger (1987,Archives of General Psychiatry 44,573-588) proposed that Novelty-Seeking (NS) -- variation in aspects of activation or initiation of behavior including tendencies toward impulsivity and extravagance -- is discriminantly related to variation in dopaminergic function. In turn, Harm-Avoidance (HA) -- variation in aspects of inhibition of behaviors including shyness and rapid fatigability -- was proposed to be discriminantly related to variation in serotonergic function. We tested Cloninger's set of proposed convergent and discriminant relations in a sample of college-student volunteers (age 23 to 49) who were administered the Temperament and Character Inventory (TCI) scales for NS and HA. Variation related to age, sex, and ethnicity was partialed from the dependent variables. Participants (N 196 to 243) were genotyped for a set of polymorphisms at dopamine (DA) genes (including DRD2 TaqI A, D4DR exon III, DA transporter) and at serotonin (5HT) genes (including 5HT 2A and 2C receptors, and 5HT transporter). In analyses (ANOVA followed by Bonferroni and Tukey HSD tests where applicable), global NS and HA were less related to genetic variation than were specific subcomponent scales like NS3 (extravagance), HA3 (shyness with strangers), and HA4 (fatigability/asthenia). There were statistically significant associations of DA genes with certain subcomponents of both NS and HA, and of 5HT genes with certain subcompoments of both NS and HA -- but effect sizes were fairly small. Overall, results were partially supportive of Cloninger's proposed convergent relations, but not supportive of the proposed discriminant relations. Pertinent issues related to statistical power, strengths and limitations of candidate-gene association studies, level of measurement, and accurate discernment of penetrance functions are discussed. [Poster]


Stephanie Schmitz1, and Kimberly J. Saudino2
Links between temperament and behavior problems -- why do the results depend on the sample?3
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309-0447 2 Psychology Department, Boston University, Boston, MA 02215 3Supported by NIH grants HD 18426 and MH 43899 and a grant from the John D. and Catherine T. MacArthur Foundation
Address: Institute for Behavioral Genetics, University of Colorado, Campus box 447, CO 80309-0447 telephone: (303) 492-0835 fax: (303) 492-8063 email: schmitzs@colorado.edu

Twin, adoption, and genetically non-informative studies show phenotypic associations between temperament rated at prior age points and later aspects of problem behavior. These associations are moderate, usually in the .20 to .30 range. Genetically informative samples can help to elucidate the genetic and environmental mediation of these correlations which are particularly consistent for the emotionality and, to a lesser degree, for the shyness aspect of temperament. However, while twin studies pointed mainly towards a genetic influence, with MZ cross-correlations being much higher than those for DZs (Schmitz et al., in press, International Journal of Behavioral Development), the currently used sample of matched adopted and non-adopted children differed in two ways. For one, only the emotionality aspect of temperament was predictive of later problem behavior, and two, the cross-correlations for natural siblings were higher than those for DZs (.15 to .39 for non-adopted siblings vs. .20 to .34 for MZs and .03 to .20 for DZs), indicating possibly shared environmental mediation. Since previous studies pointed to the influence of contrasting effects on parental ratings of temperament (Saudino et al., 1997, Behavior Genetics, 27(6), 604), these approaches will be incorporated into modeling the relationship between temperament and problem behavior. Additionally, the equality of the shared environment for twins and adopted children will be tested, since the twins are rated at the same time while sibling ratings are three years apart, on average. A combination of twin and adoption data will likely show more unbiased results


Nancy L. Segal1
Intellectual resemblance of same-age unrelated siblings: New findings2
1Psychology Department, California State University, Fullerton, California 92834 2Supported by the National Science Foundation (SBR-9712875) and a faculty research award from California State University, Fullerton
Address: Psychology Department, California State University, Fullerton, California 92834. 714-278-2142, 714-278-4843, nsegal@fullerton.edu

A study of same-age unrelated siblings (UST-SA) has been ongoing at California State University, Fullerton since 1983. An early report from this project, based on 21 pairs, indicated an IQ correlation of .17, a verbal IQ correlation of -.01 and a performance IQ correlation of .29. Additional data have now been collected for 84 pairs, who range in age from 4 - 54 years. New analyses will be reported for the larger sample, e.g., IQ correlations for the full sample, IQ correlations for adopted-adopted vs. adopted-biological pairs, and correlations between intellectual resemblance and pair characteristics such as mean age, age difference, sex (same/different), rearing status (one vs both adopted) and school placement (same/different classes). Implications of the findings for theories of intellectual development and for the rearing and educating of children and adolescents will be discussed. Future plans for this ongoing study will be described.


Pak C. Sham1, Stacey S. Cherny2, and John K. Hewitt2
Power of QTL linkage and association analysis
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, SE5 8AF, United Kingdom 2Institute for Behavior Genetics, University of Colorado, Boulder, CO 80309-0447 Supported in part by a Programme Project grant from the Medical Research Council of Great Britain
Address: Pak Sham SGDP Research Centre Institute of Psyciatry De Crespigny Park London SE5 8AF Phone: +44 171 919 3534 Email: p.sham@iop.kcl.ac.uk

Linkage and association analyses are complementary methods for QTL mapping. Fulker et al (1999) proposed a method of combined QTL linkage and association analysis of unselected sib-pairs under a variance components model. We have derived approximate expressions for the expected non-centrality parameters (per sib-pair) for the linkage and association tests. For an additive QTL of small effect size, the non-centrality parameter for linkage is approximately equal to the product of the square of the QTL heritability and the variance of the estimated proportion of alleles IBD. The non-centrality parameter for the robust test of association based on within-pair differences is approximately half the QTL heritability times the degree of linkage disequilibrium between the QTL and marker, as measured by the squared correlation between the two loci. Necessary sample sizes for linkage become prohibitively large as QTL heritability decreases, being of the order of several milllion sib-pairs when QTL heritability is 1%. In contrast, even at this low level of QTL heritability, the necessary sample sizes for association are feasible when linkage disequilibrium is strong, being of the order of several thousand sib-pairs. However, there are ways of improving the performance of both tests, including more accurate and repeated measures, multiple phenotypes, as well as larger and selected sibships. Refs. Fulker DW, Cherny SS, Sham PC, Hewitt JK (1999) Combined linkage and association sib-pair analysis for quantitative traits. American Journal of Human Genetics, 64, 259-267


Wendy S. Slutske1, Seth A. Eisen2,3, Hong Xian2,3, William R.True2,4, Michael J. Lyons5,6, Jack Goldberg7,8, and Ming T. Tsuang6
The association between antisocial behavior and pathological gambling9
1 Department of Psychology, University of Missouri, Columbia, MO 65211 2 Research Service, St. Louis Department of Veterans Affairs Medical Center, St. Louis, MO, 63106 3 Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, 63110 4 School of Public Health, St. Louis University, St. Louis, MO, 63108. 5 Department of Psychology, Boston University, Boston, MA, 02215 6 Department of Psychiatry, Harvard Medical School and Harvard Institute of Psychiatric Epidemiology and Genetics, Boston, MA, 02115 7 Department of Epidemiology , University of Illinois School of Public Health, Chicago, IL, 60612 8 Department of Veterans Affairs, Health Services Research and Development Service, Hines, IL, 60141 9 Supported by the Department of Veterans Affairs Health Services Research and Development Service (CSP #992), NIH grants DA04604, AA00264, AA10339, AA11822, and the Great Lakes Veterans Affairs Health Services Research and Development Program (LIP 41-065)
Address: Department of Psychology, University of Missouri, 210 McAlester Hall, Columbia, MO 65211 phone: (573) 882-4043 fax: (573) 882-7710 email: wendy@martha.psyc.missouri.edu

Antisocial behavior (ASB) frequently occurs among individuals who have problems with pathological gambling (PG), and it has often been assumed that ASB is mainly a result of the PG. We examined the extent to which ASB and PG share a common familial vulnerability, and the extent to which childhood ASB (that most likely preceded PG) and adult ASB (that could have occurred prior to, concurrently with, or subsequent to PG) might be differentially associated with PG. Subjects were 1,874 MZ and 1,498 DZ adult male twin pairs (mean age 44.6 years, range 34-55) from the Vietnam Era Twin Registry. Measures of childhood ASB, adult ASB, and a history of PG were assessed by structured psychiatric telephone interview. As expected, we found that a diagnosis of antisocial personality disorder (ASPD) was significantly associated with a lifetime history of PG (r = 0.32, odds ratio = 3.9). Both childhood ASB (r = 0.26, odds ratio = 2.7) and adult ASB (r = 0.33, odds ratio = 3.4) were significantly associated with PG. Seventy-four percent of the association between ASPD and PG was familial, and all of this was accounted for by common genetic risk factors. The overlap between childhood ASB and PG (81%) and adult ASB and PG (69%) was also predominantly accounted for by common familial risk factors. Most of the common familial risk for childhood ASB and PG (64%) and adult ASB and PG (100%) was accounted for by common genetic risk factors. Because PG shared familial risk factors with earlier-occurring ASB as well as later-occurring ASB, it is unlikely that the association between ASB and PG is completely due to the causal influence of PG on ASB, at least among men. The results of this study suggest that the co-occurrence of ASB and PG is predominantly due to their sharing a common familial vulnerability.


Erica L. Spotts1, Jenae M. Neiderhiser1, Paul Lichtenstein2, Nancy Pedersen23, Kjell Hansson4, Marianne Cederblad4, Olle Elthammer4, and David Reiss1
Genetic and Environmental Influences on Marital Relationships5
1Center for Family Research, The George Washington University, Washington, DC 20037 2Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden 3University of Southern California 4Department of Child and Youth Psychiatry, Lund University, Lund, Sweden 5Supported by grant RO1MH54610 from the National Institute of Mental Health MAIL:2300 I St. NW Room 613 Ross Hall, Washington, DC 20037 Email:elspotts@gwu.edu. Phone 202.994.2404. Fax: 202.994.4812

Previous research has examined the role of genetic and environmental influences on various family subsystems and the overlap thereof (D. Reiss, J. M. Neiderhiser, E. M. Hetherington, and R. Plomin, in press, The Relationship Code: Detecting Links Between Genetic and Social Influences on Psychological Development). The subsystem that has yet to be explored is the marital relationship. Save for a study finding genetic influences on divorce (McGue & Lykken, 1992, Psychological Science, 3, 368-373), characteristics of the marital relationship have been ignored, primarily because most research in this area focuses on child's genes, not the parents'. It would be expected that the marital subsystem would follow the trend of other family subsystems and be influenced primarily by genetic factors. The current report employed a sample of 326 pairs of Swedish twin mothers (MZ = 148; DZ = 174; unknown = 4) and their families. Marital positivity and negativity wer! e evaluated with self-report measures and observer ratings. Intraclass correlations indicate that genetic and nonshared environmental influences are primarily responsible for observational ratings of mother's positive and negative behavior toward her husband (positive: MZ=.28, DZ=-.03; negative: MZ=.43, DZ=-..01). Self-report measures and the genetic and environmental influences on husband's behavior toward his wife will also be considered. These results warrant further attention, not only because this is the first report of genetic and environmental influences on the marital subsystem, but also because the pattern of influences is similar to that of the parent-child subsystems. [Poster]


Michael C. Stallings1, J. K. Hewitt1, S. M. Hofer2, A. C. Heath3, and L. J. Eaves4
Exploring the genetic and environmental structure of the Tridimensional Personality Questionnaire5
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309 2 Center for Dev. & Health Genetics, Pennsylvania State University, University Park, PA 16802 3 Department of Psychiatry, Washington University, St. Louis, MO 63110 4 Department of Human Genetics, Medical College of Virginia, Richmond, VA 23298 5 Supported by NIH Grants AA-08672 and DA-11015
Address: Michael C. Stallings, Ph.D. Institute for Behavioral Genetics Campus Box 447 University of Colorado Boulder, CO 80309-0447 Ph (303) 492-2826 Fa (303) 492-8063 Michael.Stallings@Colorado.Edu

The Tridimensional Personality Questionnaire (TPQ) was developed to assess three higher-order personality dimensions proposed by Cloninger (C. R. Cloninger, 1986, Psychiatric Developments 3, 167-226): Novelty Seeking (NS), Harm Avoidance (HA), and Reward Dependence (RD). These dimensions are hypothesized to be associated with genetically independent neurobiological systems in the brain (behavioral activation, behavioral inhibition, and behavioral maintenance, respectively). Each of the higher-order TPQ dimensions consists of four primary subscales (Exploratory Excitability, Impulsivity, Extravagance and Disorderliness for NS; Anticipatory Worry, Fear of Uncertainty, Shyness with Strangers and Fatigability for HA; Sentimentality, Persistence, Attachment and Dependence for RD). In this study we tested the hypothesized genetic structure of the 12 TPQ subscales in a sample of 889 adult female twin pairs (599 MZ, 290 DZ) from the AARP Twin Sample. Both phenotypic and biometrical analyses suggested greater complexity of the TPQ than hypothesized by Cloninger. With the exception of Fatigability (HA4), the primary subscales for NS and HA showed moderate heritabilities (.25 to .43), however, each assessed substantial unique genetic variance (e.g., genetic correlations among the subscales ranged from .40 to .69). Heritablities for the RD subscales were relatively low (.11 to .31) and common enviromental influences were significant for Sentimentality and Dependence.


A. Sterne1, Pak C. Sham1, Shaun Purcell1, and Robert Plomin1
The GENESiS Study : Measures of depression and anxiety in a community based sample of 5,000 sib-pairs
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, SE5 8AF, United Kingdom Supported in part by a Programme Project grant from the Medical Research Council of Great Britain
Address: Abram Sterne The GENESiS Study SGDP Research Centre Institute of Psyciatry De Crespigny Park London SE5 8AF Phone: +44 171 919 3837 Email: a.sterne@iop.kcl.ac.uk

The GENESiS study (Genetic-Environmental Nature of Emotional States in Siblings) is aiming to recruit more than 25,000 people in a community-based sample across the United Kingdom via a postal survey. The questionnaire has various measures of depression and anxiety including the GHQ, EPQ-N, as well as measures of life events and social issues. We have now recruited more than 5,000 sibling pairs and are able to conduct a sibling analysis of depression and anxiety. The sibling data can be interpreted to provide upper-limit estimates of heritability of depression/anxiety and the genetic correlations between depression and anxiety. This questionnaire stage of the GENESiS study will be presented in greater detail. The initial sib-pair findings for the GHQ and EPQ-N will be discussed in the context of selecting sib-pairs for the QTL mapping stage of the GENESiS Study.


Lee A. Thompson1, Rolando D. Tiu, 1, and D.K. Detterman, 1
Differences in heritability across levels of father's occupation2
1Department of Psychology, Case Western Reserve University, Cleveland, OH 44106-7123 2We thank the twins and their families who so graciously participated in the Western Reserve Twin Project.
Address: Lee A. Thompson, Department of Psychology Case Western Reserve University Cleveland, OH 44106-7123 U.S.A. 216-369-6477 216-368-4891 (F) lat@po.cwru.edu

In a previous report on the Western Reserve Twin Project (L. A. Thompson, D. K. Detterman, and R. Plomin, 1993, Behav. Genet. 23, 331-336), individual differences for a composite ability/achievement score showed significantly greater influence of shared family environment at the low end of the IQ distribution. Identifying specific aspects of the environment that influence individual differences at the low end of the IQ distribution but not the high end remains an unanswered question. In the current report we apply the DF regression approach to general cognitive ability scores across the continuum of father's occupation. Results suggest that heritability is significantly higher at the high end of the occupation continuum and shared family environment becomes increasingly more salient at the low end. These finding appear to be a result of the increased similarity of dizygotic twins at the low end of the occupation continuum. Implications of these findings will be discussed. [Poster]


L.A. Toth1 and R.W. Williams2
A QTL for Light-Phase Slow-Wave Sleep in Influenza-Infected CXB Recombinant Inbred Mice3
1Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105 2Department of Anatomy and Neurobiology, University of Tennessee, Memphis, TN, 38163 3Supported in part by NS-26429, NS-35485, CA-21765, and ALSAC.
Address: Dr. Linda A. Toth Animal Resource Center St. Jude Children's Research Hospital 332 N. Lauderdale Memphis, TN 38105 phone: 901-495-3385 fax: 901-495-3112 email: linda.toth@stjude.org

Influenza-infected C57BL/6J mice spend increased amounts of time in slow-wave sleep (SWS) during the dark phase of the circadian cycle as compared to healthy mice. In contrast, infected BALB/cByJ mice show normal or reduced time in SWS, particularly during the light phase. To identify genetic loci with linkage to these traits, we measured sleep in 13 CXB recombinant inbred (RI) strains derived from a cross between C57BL/6ByJ and BALB/cByJ mice. The probability density distribution of light-phase SWS in influenza-infected CXB RI mice showed two modes. One mode corresponded roughly to that of the C57BL/6 parental strain, whereas the other was intermediate between parental modes. This pattern is consistent with the presence of a low number of major effect quantitative trait loci (QTLs). Linkage analysis revealed a 10–12 cM interval on chromosome 6 between D6Mit74 and D6Mit188 that contains a QTL which influences the SWS response to influenza infection during the light phase. We have provisionally named this QTL Srilp1 (sleep response to influenza, light phase 1). The point-wise LRS score associated with this locus was 14.6 (nominal p value = 0.0001). Permutation analysis was used to establish genome-wide statistical thresholds for assessment of linkage. Simple interval mapping indicated that a peak LOD of 3.6 occurred 1 cM proximal to D6Mit316 (genome-wide p < 0.05). Confidence intervals (CI) delineating the locus extend from approximately 26 to 29 cM (one LOD, or 50% CI), and from approximately 21 to 31 cM (two LOD, or 95% CI). Genes that are located within these intervals and that could theoretically influence sleep phenotypes include Ghrhr (growth hormone releasing hormone receptor; 26 cM), Crhr2 (corticotropin releasing hormone receptor 2; 28 cM), and Cd8a (an epitope on cytotoxic T lymphocytes; 30 cM).


Csaba Vadasz1, and Laszlo Zaborszky1
Phenotypic QTL introgression: Analysis of the midbrain dopamine system
1 Laboratory of Neurobehavior Genetics, The Nathan S. Kline Institute for Psychiatric Research, New York University Medical Center, Orangeburg, NY 10962 and Center for Molecular and Behavioral Neuroscience, 197 University Avenue, Rutgers University, Newark, NJ 07102
Address: Csaba Vadasz, Laboratory of Neurobehavior Genetics, The Nathan S. Kline Institute for Psychiatric Research, New York University Medical Center, Orangeburg, NY 10962 Tel. (914)398-5536, E-mail: vadasz@nki.rfmh.org

Current behavior genetic studies need to shed light on the genetic architecture of complex traits by identifying the involved QTLs, and on the functions and interactions of the involved genes by studying their expression, and by determining the rules of phenotypic compensation and plasticity during development. Towards these goals, we explored the method of phenotypic QTL introgression for creating animal models and tools for QTL mapping. We developed >100 quasi-congenic Recombinant QTL Introgression (RQI) strains by repeated backcrosses and concomitant bidirectional selection in replicate lines for the extreme phenotypic expression of mesencephalic tyrosine hydroxylase activity (TH/MES; C. Vadasz et al., 1998, Neurochem. Res. 23, 1337-1354.). Each of the quasi-congenic RQI strains shares about 95% of its genome with its C57BL/6By background strain, and carries introgressed chromosome segments from BALB/cJ (high TH/MES) or CXBI (low TH/MES) strains. Based on data obtained by testing the b4i5 series of the RQI strains, the results suggested that (1) a virtually complete transfer of QTLs was possible by phenotypic introgression; (2) in a small set of RQI strains provisional locations of QTLs for TH/MES could be assigned to chromosomes 1, 4, and 18; and (3) an inverse relationship was found between TH/MES and the number of midbrain (substantia nigra and ventral tegmentum) dopamine neurons in a study using C57BL/6By, CXBI, and B6.Cb4i5-Alpha6 strains by unbiased stereological methods.


Mireille van den Berg1, Eco JC de Geus1, Hans Elich1, and Dorret I Boomsma1
Depression and autonomic nervous system activity in dizygotic twins and their siblings
1 Vrije Universiteit, Dept of Biological Psychology
Address: De Boelelaan 1111, 1081 HV Amsterdam, The Netherlands Phone 31-20-4448809, Fax 31-20-4448832, Email m.van.den.berg@psy.vu.nl

Depression is associated with hyperactivity of the HPA (hypothalamic-pituitary-adrenocortical) axis and low cardiac parasympathetic tone, possibly coupled to hyperactivity of the sympathetic-medullary axis. In this study an association between autonomic reactivity and depression is examined in a genetic design. The population exists of 894 selected (young) adults from 424 families that are registered with the Netherlands Twin Register. They have completed 1 to 4 personality questionnaires in the period 1991-1998. The selected individuals form sibpairs that are extreme concordant or discordant on depression and are selected for the purpose of QTL-analysis. Autonomic nervous system activity was measured by means of 24-hour ambulatory recording of hearth rate (HR), blood presure (BP), respiratory sinus arrythmia (RSA) and pre-ejection period (PEP). Changes in PEP and RSA index changes in cardiac sympathetic and parasympathetic tone, respectively. In addition to cardiovascular monitoring, 6 samples of salivary cortisol were taken at 9 am, 11 am, 3 pm, 8 pm, 11 pm and directly after waking. Results will be presented that show which of the cardiovascular and ANS parameters best discriminate depressive and non-depressive subjects during which part of the day. The relationship between depression and these parameters will then be explored from a genetic perspective in a bivariate model that decomposes the covariance of ANS parameters and depression into a genetic and a non-genetic part.


Carol Van Hulle 1, and John K. Hewitt1
An exploration of the genetic and environmental etiology of heart rate in childhood 2
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309-0447 2 Supported by a grant from the John D. and Catherine T. MacArthur Foundation
Address: Institute for Behavioral Genetics, University of Colorado, C.B. 447 Boulder, CO 80309-0447 Phone:(303) 492-1475 Fax: (303) 492-8063 vanhulle@colorado.edu

Heart rate was recorded on 224 MZ and 179 DZ same sex twin pairs participating in the Longitudinal Twin Study (MALTS) at ages 14, 20, 24, 36 months and 7 years. Heart rate was monitored in the lab at all ages. At ages 14 months through 36 months, baseline heart rate was obtained by monitoring heart rate prior to a set of cognitive tasks. At age 7 years heart rate was recorded during a mood eliciting videotaped presentation. Baseline heart rate was calculated from heart rate monitored during neutral portions of the presentation. Mean heart rate is roughly equivalent for MZ and DZ twins at all time points. Mean heart rate at age 14 months is approximately 133 bpm and falls steadily to 80 bpm by age 7 years. However, heart rate is moderately correlated at all time points suggesting that individual differences in heart rate are relatively stable over this age range. In order to examine the genetic and environmental etiology of individual differences in heart rate, a Cholesky decomposition was fit to raw data. The genetic covariances suggest that genetic factors contribute substantially to the continuity in heart rate from ages 14 months to 7 years. Surprisingly, shared environment also appears to contribute to the continuity in heart rate from ages 24 months to 7 years. It is suspected that this may be due to gender differences in heart rate. As expected unique environmental factors contribute substantially to individual differences in heart rate at each time point but contribute almost nothing to the continuity of heart rate over time. The phenotypic correlations suggest a possible simplex pattern. To obtain a clearer picture of the relative roles of genetic and environmental factors the data will be fit to simplex and factor models. Also, factors underlying the unexpectedly large shared environmental effect, including possible gender differences and other family variables, will be explored in greater depth. [Poster]


M. Vanyukov1, Howard B. Moss1, Barry B. Kaplan2, and Ralph E. Tarter1
Antisociality, Substance Dependence, and the DRD5 Gene3
1University of Pittsburgh, Pittsburgh, PA 15213 2Division of Intramural Research, National Institute of Mental Health, Bethesda, MD 20892 3Supported by the National Institute on Drug Abuse (DA05605, DA08955, DA00308, and DA05952
Address: CEDAR, University of Pittsburgh, 3811 O'Hara Street, Pittsburgh, PA 15213. Phone: 412-383-2138, Fax: 412-624-1929, Email: mmv@pop.pitt.edu, URL: http://www.pitt.edu/~cedar

In a population-based study of adult European American males and females, we have previously shown an association of a microsatellite polymorphism at the DRD5 locus with the liability to substance dependence (SD) (M. M. Vanyukov, H. B. Moss, A. E. Gioio, H. B. Hughes, B. B. Kaplan, and R. E. Tarter, 1998, Behav. Genet. 28:75-82). A study conducted in the same sample showed the association of this polymorphism also with symptom counts for oppositional defiant disorder (ODD) in males and females and adult antisocial personality disorder (ASP) in females, and no association with conduct disorder symptom count. ODD mediated the genotype-ASP relationship in females. Neither ODD nor ASP significantly mediated the relationship between the genotype and the liability to substance dependence (SD). The data suggest involvement of the DRD5 locus in the variation and sexual dimorphism of SD liability and antisociality, as well as in the developmental continuity of antisociality. [Poster]


Philip A. Vernon1, Paula Meunier1, Andrew M. Johnson1, and Kerry L. Jang2
Univariate genetic analyses of factors underlying the Coloured Raven Matrices
1Department of Psychology, University of Western Ontario, London, Ontario, Canada 2Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada
Address: Tony Vernon, Department of Psychology, University of Western Ontario, London, Ontario, Canada N6A 5C2; phone: 519-661-3682; fax: 519-661-3961; email: vernon@julian.uwo.ca

Samples of 5 and 6-year-old MZ and DZ twins were administered the Coloured Raven Matrices. This test primarily measures a single factor (typically identified as Spearman's g, or general intelligence) but it has also been shown to tap at least 3 underlying factors or dimensions: Closure and Abstract Reasoning by Analogy, Pattern Completion through Identity and Closure, and Simple Pattern Completion (J.S. Carlson, and C.M. Jensen, 1980, Educ. and Psych. Meas.40,1111-1116). Although numerous studies have estimated the heritability of general intelligence and other cognitive abilities, no studies have yet performed univariate genetic analyses on the factors underlying the Raven. In the present study, the three factors identified above were separately derived from phi/phi max correlations and from tetrachoric correlations among the Coloured Raven Matrices items. Univariate genetic analyses revealed that all the factors (and total scores) had significant heritabilities (h2 ranging from .30 to .78), showed negligible shared environmental effects (c2 ranging from .02 to .08), and mostly showed a significant influence of nonshared environmental effects (e2 ranging from .20 to .62). The results are thus consistent with most previous behavior genetic studies investigating dimensions of mental ability, but extend these into dimensions underlying general intelligence that have not previously been investigated in a twin study. [Poster]


Spice Joy Vice1, and Donald J. Nash1
Manifestations of tourette syndrome in a single pedigree
1 Department of Biology, Colorado State University, Fort Collins, CO 80523
Address: Department of Biology, Colorado State University, Fort Collins, CO 80523 (Phone) 970-491-5481 (Fax) 970-491-0649 (e-mail) dnash@lamar.colostate.edu

Tourette syndrome (TS) is thought to be a single gene autosomal dominant disorder with incomplete penetrance and varied expressivity. The following study is based on a single family pedigree that was compiled starting from an individual with a severe case of TS. A family pedigree was constructed via a mail survey to all family members. The survey included TS as well as several other associated symptoms known to be related to TS. The range of phenotypic expression of symptoms in different individuals was quite varied. Three types of pedigrees were constructed according to the data. Each type classified symptoms in a different manner. The first was classified solely on the basis of an individual having TS or any related symptoms. The second was made based on the number of symptoms an individual possessed, and the third identified each symptom an individual exhibited. The data expressed in these three different ways are in concordance with the mode of inheritance being autosomal dominant. The results also lend support to TS being a single gene disorder. However, in the pedigree, TS appears to be have been passed down through both sides of the family of the proband and the data also suggest the possibility of some sort of semidominant effect of the gene so that homozygous dominant individuals exhibit more severe symptoms than do heterozygous individuals. [Poster]


Richard J. Viken1, Richard J. Rose1, Jaakko Kaprio2, Markku Kosenvuo3,and Kirsi Pietilaeinen2
Estimating genetic and cultural transmission with genetically informative data from both parental and offspring generations4
1Department of Psychology, Indiana University, Bloomington, IN 47405 2Department of Public Health, University of Helsinki, Finland, 00014 3 Department of Public Health, University of Turku, Finland, 20520 4Supported by NIAAA grant AA-08315 and the Academy of Finland
Address: Department of Psychology, Indiana University, Bloomington, IN 47405 viken@indiana.edu, 812-855-1697 (ph), 812-855-4691 (fax)

When data on twins are augmented by data from the parents of the twins, a variety of models can be fit to estimate genetic and environmental transmission from parents to offspring. In conventional twin-parent designs these models include a number of assumptions about the equality of heritabilities in the twin and parent generations, and about the stability of the genetic effects across time. With appropriate longitudinal twin samples in both generations, however, it is possible to include empirical estimates of these values rather than relying on assumptions. We combined twin-parent data in 2600 families drawn from the Finntwin16 study with longitudinal data from 1200 pairs of twins drawn from the Finnish Twin Cohort. Subjects from the Finnish Twin Cohort were matched in age to the parents of the Finntwin16 twins. We illustrate the use of such combined data sets by modeling genetic and environmental transmission for body mass index and alcohol consumption, two variables that show distinct patterns of genetic and environmental effects during adolescence.


Sally J. Wadsworth1, Robert Plomin2, and J. C. DeFries1
Etiology of the stability of reading performance from 7 to 12 years of age in the Colorado Adoption Project3
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO 2 Social, Genetic, & Developmental Psychiatry Research Centre, Institute of Psychiatry, London, UK 3 Supported by grants HD-10333 and HD-18426 from NICHD, and grant MH-43899 from NIMH
Address: Sally J. Wadsworth Institute for Behavioral Genetics Campus Box 447 Boulder, Colorado 80309 Phone: 303-492-6795 Fax: 303-492-8063 E-mail: wadswort@ibg.colorado.edu

The etiology of longitudinal stability of reading performance was assessed using data from adoptive (97 unrelated sibling pairs at age 7 and 90 pairs at age 12) and nonadoptive (106 related pairs at age 7 and 98 pairs at age 12) children tested in the Colorado Adoption Project. Results of longitudinal behavioral genetic analysis confirmed previous findings of moderate genetic influence on individual differences in reading performance at both 7 and 12 years of age (h2= .38 and .36, respectively), and a substantial age-to-age genetic correlation (rg=.98). Moreover, about 60% of the observed stability (r=.60) between the two ages was due to common genetic influences. Of particular interest, no new heritable or shared environmental variation emerged at age 12, suggesting that the same genetic and shared environmental influences were operating at both ages. In contrast, nonshared environmental influences were responsible for change, indicating the possible importance of such factors as instructional methods, teachers, peers, etc. for the development of individual differences in reading performance between 7 and 12 years of age. Because measures of reading performance are correlated with IQ, both phenotypically and genetically, and because IQ is relatively stable over time, the stability of reading performance may be mediated, at least in part, by IQ. Although results confirmed moderate phenotypic correlations between IQ at age 7 and reading performance at both ages (rp=.37 and .35 at ages 7 and 12, respectively), as well as substantial genetic correlations (rg=.65 and .49, respectively), only 22% of the phenotypic stability and 36% of the genetic stability of reading performance was due to influences shared with IQ. Therefore, although measures of reading performance at 7 and 12 years of age are correlated with general cognitive ability, the observed stability of reading performance is largely independent of IQ. [Poster]


Irwin D. Waldman1, Soo Hyun Rhee1, David A. Hay2, and Florence Levy3
Are genetic and environmental influences on ADHD the same throughout the range of symptoms as at the disordered extreme?
1Department of Psychology, 532 N. Kilgo Circle, Emory University, Atlanta, GA 30322. 2Department of Psychology, Curtin University, Perth, Western Australia, Australia. 3Department of Child and Adolescent Psychiatry, The Prince of Wales Children's Hospital, High Street, Randwick, NSW 2031, Australia
Address: mailing address - Department of Psychology, 532 N. Kilgo Circle, Emory University, Atlanta, GA 30322 phone - (404) 727-7430 fax - (404) 727-0372 e-mail - psyiw@emory.edu

A theme of considerable importance in the contemporary behavior genetic literature on psychopathology concerns whether genetic and environmental influences on a variety of traits and disorders are of the same magnitude throughout the range of the trait as at the disordered extreme. In this study we examined this issue for the symptoms and diagnosis of ADHD. Previous researchers have reported moderate to high heritability for ADHD, with genetic influences appearing to be of greater magnitude for the disordered extreme (e.g., the diagnosis) than for the full range of symptoms. We analyzed mothers' ratings of DSM-III-R ADHD symptoms from a population-based study of 2350 Australian twin pairs and 348 sibling pairs, aged 4 - 14. We used three different analytic methods to examine whether the genetic and environmental influences on ADHD are the same throughout the range of symptoms as at the disordered extreme. Results of a commonly-used method, DF extremes analysis, suggested that the heritability of ADHD did not differ statistically throughout the range of symptoms as compared with the disordered extreme, despite a substantial difference in the magnitude of genetic influences (h2 = .75 vs. hg2 = .91). In contrast, both moderated multiple regression and biometric model fitting analytic approaches detected differences in heritability throughout the range of symptoms as compared with the disordered extreme. These results suggest that inferences regarding differences in the magnitude of genetic influences for normal range variation as compared with the disordered extreme will differ across analytic methods, likely due to the statistical power of those methods. The meaning of the results of such analyses for the etiology and classification of psychopathology will be discussed.


Marianne Z. Wamboldt1, John Hewitt2, Frederick S. Wamboldt1
Individual and family factors associated with medical nonadherence 3
1National Jewish Medical and Research Center, Denver, CO 80220 2Institute for Behavioral Genetics, University fo Colorado, Boulder, CO 80309 3Supported by NIH grants 1RO1HL53391, 1 KO8MH01486, M01-RR00051and 2RO1 HL45157. We wish to thank Sandy McTaggart, Joan Bihun, Shannon O'Connor, Emily Millikan, Theresa O'Lonerghan and Kayte Fulton for help with this study.
Address: Pediatric Behavioral Helath, National Jewish, 1400 Jackson St., #K701, Denver, CO 80206. Phone: 303-398-1711. FAX: 303-270-2141. Email: wamboldtm@njc.org

Nonadherence to medical treatments is a very common phenomenon, in both clinical drug trials and in clinical care (Matsui, 1997, Pediatr Clin North Am44(1), 1-14). New electronic monitoring devices, which allow documentation of each date and time that patients take an oral or inhaled medication, have established that rates of adherence are approximately 50% across illnesses and age groups (Rand and Wise, 1994, Am J Resp Crit Care Med149 : S69-S76). Nonadherence with outpatient therapy is a causal factor in 25% of hospitalizations (Miller, 1997, Am J Med102(2A) : 43-9). In certain illnesses, e.g. asthma, nonadherence is a major risk for mortality. Despite the growing recognition of the scope of the problem, there are few effective interventions at this point in time (Giuffrida and Torgerson, 1997, BMJ315, 703-707). This talk will review the newer empirical data on rates of nonadherence, and discuss individual personality and family factors (Wamboldt, Wamboldt, et al., 1995, Journal of Psychosomatic Research39: 995-1005) associated with nonadherence to medical treatments. Preliminary data from an ongoing adolescent twin study on family factors associated with nonadherence and other health behaviors will be presented. The potential uses of behavioral genetic paradigms for understanding the etiology and course of health behaviors will be discussed.


Alexander Weiss1, J.E. King2, and R. M. Enns3
Can we breed a happier ape? The heritability of subjective well-being in zoo chimpanzees (Pan troglodytes)4
1Department of Psychology, University of Arizona, Tucson, AZ 85721. 2Department of Psychology, University of Arizona, Tucson, AZ 85721. 3Department of Animal Sciences, University of Arizona, Tucson, AZ 85721. 4Supported by ChimpanZoo and the Jane Goodall Institute
Address: Alexander Weiss, Department of Psychology, University of Arizona, Tucson, AZ 85721 520-881-2389 aweiss@u.arizona.edu

Recent research (A. Weiss and J.E. King, 1998, BGA Meeting, Stockholm) has shown that two of the six chimpanzee personality factors, dominance and dependability, are heritable. This research has also shown that shared zoo effects were negligible for all six factors. Recently, a four item subjective well-being (SWB) scale was developed for chimpanzees. Factor analysis revealed that this four-item scale could be represented by a single factor. A heritability study of human SWB (Tellgen et al., 1988, Journal of Personality and Social Psychology, 54(6), 1031-1039) showed high MZ twin correlations and low DZ twin correlations suggesting that SWB is an emergenic trait with an h2B approximately equal to .50. SWB in humans also has a small and non-significant shared environmental effects. We wanted to determine the heritability of SWB in chimpanzees. SWB ratings were taken on 138 zoo chimpanzees. Because of the complex family relationships in these chimpanzees, we used the Symmetric Differences Squared (SDS) to determine h2, z2, and e2. In SDS squared differences between the traits of each animal in all possible pairs are regressed onto 1-R and any environmental variable (L.W. Grimes and W.R. Harvey, 1980, Journal of Animal Science, 50, 4, 634-644). In our case, the latter term was whether the chimpanzees were in different zoos or the same zoo. We verified the heritability estimate obtained from SDS by also computing the heritability of SWB using Method R (Reverter, et al., 1994, Journal of Animal Science, 72, 2247-2253). Method R incorporates all relationships between animals in the calculations to solve for the variance components. We found that, unlike humans, additive genetic effects accounted for a borderline significant proportion of the variance in SWB. However, as with humans, our shared zoo effects accounted for a small, non-significant proportion of variance.


Robert W. Williams1
Mapping QTLs that modify the architecture of the mouse brain: a prelude to behavioral analyses2
1 Center for Neuroscience, Department of Anatomy and Neurobiology, University of Tenneessee, Memphis, TN 38163 2Supported by NIH Grant NS-35485. I thank Drs. R. C. Strom, Goumin Zhou, and Dan Goldowitz for their generous help.
Address: Dr. R. W. Williams, Department of Anatomy and Neurobiology, University of Tennessee, 855 Monroe Avenue, Memphis TN 38163. Phone (901) 448-7018, E-mail: RWILLIAM@nb.utmem.edu, web site: http://nervenet.org

We have mapped quantitative trait loci (QTLs) that modulate the size of the brain and the proliferation and survival of specific populations of neurons in the CNS of mice. One important goal of this work is to achieve a better understanding of neuronal substrates of behavioral variation. We have mapped (1) four QTLs responsible for variation in brain weight corrected for variation in body size; (2) three QTLs responsible for variation in cerebellar weight independent of brain weight, and (3) three QTLs responsible for variation in retinal ganglion cell number. Fixed brains and eyes of approximately 5,200 mice were dissected and weighed. The sample used for mapping includes the BXD, BXH, AXB, and BXA recombinant inbred (RI) strains, four F2 intercrosses, and a 10-generation advanced intercross between C57BL/6J and DBA/2J. Approximately half of the variance in brain weight is associated with factors such as age, body size, litter size, and parity. To minimize the influence of these and other extraneous sources of variation we computed multiple linear regression residuals for target variables. Residuals were then mapped using Map Manager QT. Permutation tests were performed to estimate genome-wide significance of linkage. The brain and all CNS subdivisions show significant variation among strains and progeny. For example, the weight of the olfactory bulbs ranges from 15 to 23 mg, and the cerebellum from 46 to 64 mg. Using the BXD RI strains, a major brain weight QTL was mapped to proximal Chr 11 near Egfr (genome-wide P<0.05). QTLs controlling brain weight were also mapped to Chrs 6, 7, and 14 using F2 intercrosses. QTLs with specific effects on the size of the cerebellum have been mapped to Chrs 2, 7, 8, and 19, and three QTLs controlling retinal ganglion cell number have been mapped to Chrs 1, 11, and 16.


Margie Wright 1, Glen Smith 2, Gina Geffen 2, Laurie Geffen 3, and Nick Martin 1
Is there an association between 'normal' cognitive functioning and tri-nucleotide repeat expansion at loci involved in neurodegenerative disorders?
1 Queensland Institute of Medical Research, Brisbane, Australia 2 School of Psychology, The University of Queensland, Brisbane, Australia 3 Department of Psychiatry, The University of Queensland, Brisbane, Australia
Address: Queensland Institute of Medical Research, Post Office, Royal Brisbane Hospital, Brisbane QLD 4029 Australia Telephone: +61 7 3362 0225 Facsimile: +61 7 3362 0101 E-mail: margieW@qimr.edu.au

Recent reports have shown neurodegenerative disorders to be associated with abnormal expansions of a CAG trinucleotide repeat allele at various autosomal loci. While normal chromosomes have 14 to 44 repeats, disease chromosomes may have 60 to 84 repeats. The number of CAG repeats on mutant chromosomes correlates with increasing severity of disease or decreasing age of onset of symptoms. Since we are interested in identifying the many quantitative trait loci (QTL) influencing brain functioning we examined the possibility that the number of CAG repeats in the normal size range at these loci are relevant to 'normal' neural functioning. We have used 150 pairs of adolescent (aged 16 years) twins and their parents to examine allele size at the MJD, SCA1 and DRPLA loci in heterozygous normal individuals. These are part of a large ongoing project using cognitive and physiological measures to investigate the genetic influences on cognition, and an extensive protocol of tests is employed to assess some of the key components of intellectual functioning. This study selected to examine full-scale psychometric IQ (FSIQ) and a measure of information processing (choice reaction time) and working memory (slow wave amplitude). CAG repeat size was determined on an ABI Genescan system following multiplex PCR amplification. Quantitative genetic analyses were performed to determine QTL effects of MJD, SCA1 and DRPLA on cognitive functioning. Analyses are in progress and will be discussed.


Kunio Yamazaki1, M. Curran,1, and G.K. Beauchamp1
Fetal MHC odortypes play a functional role in regulating social interactions 2
1 Monell Chemical Senses Center, Philadelphia, PA 19104. 2 Supported by NSF Grant 9728787
Address: 3500 Market Street Philadelphia PA 19104 Telephone: 215-898-3094 Fax: 215-898-2084 e-mail: yamazaki@monell.org

Odors that distinguish one individual from another member of the species and are determined by polymorphic genes and are called odortypes. Odortypes and their considerable societal significance have been intimately studied in mice and mainly with respect to the genes of the major histocompatibility complex (MHC). We have shown that the urine odor of the pregnant mouse is a combination of her own odors and that of her fetuses, and individuals can discriminate between identical females carrying fetuses differing in MHC types (G.K. Beauchamp et al.1994, Immunogenetics 39, 109-113). This study was designed as a first step in investigating the functional roles that fetal odortype might play in mouse behavior. We asked whether pregnant female mice given two-choice preference tests where the choices were 2 genetically identical pregnant females who carried 15-18 day old fetuses that differed only at MHC types would discriminate between the females . Indeed, preliminary results suggest that under some circumstances, test females showed differential preferences. This demonstrates for the first time that a specific set of genes expressed by fetuses alters the behavior of animals exposed to a pregnant female carrying those fetuses. [Poster]


Susan E. Young1, M. C. Stallings1, and J. K. Hewitt1
Genetic and environmental infuences on behavioral disinhibition 2
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309 2Supported by NIDA Center DA-11015, and the John D. and Catherine T. MacArthur Foundation
Address: Susan E. Young, Ph.D. Institute for Behavioral Genetics Campus Box 447 University of Colorado Boulder, CO 80309 (303)492-1235 (Phone) (303) 492-8063 (Fax) Susan.Young@Colorado.edu

Comorbidity among childhood disruptive behavioral disorders is commonly reported in both epidemiologic and clinical studies. These problems are also associated with early substance use and other markers of behavioral disinhibition. Previous twin research has suggested that much of the covariation between antisocial behavior and alcohol dependence is due to common genetic influences (Slutske et al., 1998, J. of Abnormal Psych., 107, 363-74.). Similar results have been reported for conduct problems and attention deficit-hyperactivity disorder (ADHD; Silberg et al., 1997, J. of Child and Adol. Psych., 37, 803-16). For the present study, a preliminary adolescent sample consisting of 77 MZ and 73 DZ twin pairs, recruited through the Colorado Twin Registry and the Longitudinal Twin Study were assessed using standardized psychiatric interviews and personality assessments. DSM-IV symptom counts for conduct disorder (CD) and ADHD, along with measures of substance experimentation, deviant behavior and novelty seeking were used as indices of a latent behavioral disinhibition trait. A principal components analysis of these variables show a strong common factor accounting for nearly 50% of the observed variance. Thus, a common pathway model which evaluates the genetic and environmental architecture of this latent factor was fit to the sex- and age-corrected data. Modeling fitting results suggested that both genetic and shared environmental influences make a significant contribution to the variation in behavioral disinhibition. Further, factor loadings on the five phenotypes could be equated without a significant reduction in model fit. Residual genetic variance was significant only for substance experimentation and novelty seeking. These results suggest that a variety of adolescent problem behaviors may share a common underlying familial risk.