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 personalit