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 Petrill | J 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 | | |||||
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
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] 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. 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. 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] 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] 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. 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. 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] 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 The peroxisome proliferator activated receptor (PPAR) 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. 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. 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. 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] 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. 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] 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] 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. 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. 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] 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 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. 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. 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] 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. 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.
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] 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. 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] 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. 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] 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. 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. 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. 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. 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. 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. 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] 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 ( The extent to which specific facets of antisocial personality pathology, family environment and alcohol misuse
share a common genetic and environmental aetiology was estimated. Participants were 347 adult monozygotic twin
pairs (209 sister & 138 brother pairs) and 346 dizygotic twin pairs (170 sister, 82 brother, & 94 sister-brother pairs).
All twin pairs completed self-report measures of alcohol misuse and personality pathology contained in the
Dimensional Assessment of Personality Pathology (Livesley, W.J. & Jackson, D.N.,in press, Manual for the
Dimensional Assessment of Personality Problems-Basic Questionnaire. Port Huron, MI, Sigma)and family
environment (Family Environment Scale: Moos, R.H. & Moos, B.S.,1986, Manual: Family Environment Scale, Palo
Alto, Consulting Psychologists Press). Bivariate genetic correlations between the scales identified a number of the
specific aspects of antisocial personality, such as recklessness, impulsivity, and interpersonal hostility that shared a
common genetic basis with alcohol misuse. Other characteristics typical of antisocial personality, such as
hypervigilance, suspiciousness, dominance, and attention seeking had negligible associations with alcohol misuse.
Simultaneous analysis of family environmental variables showed that the genetic influences underlying antisocial
personality also influence alcohol misuse both directly and through its influence on the family environment. The
results also confirmed the lack of relationship between alcohol misuse and personality variables unrelated to
antisocial characteristics (e.g., neuroticism) at the phenotypic and genetic levels. Recent research has noted that height is related to an individual's success as a leader. Taken in combination with
the identification of leadership style as a heritable characteristic, this raises the question of whether the heritability
of certain styles of leadership is linked to the heritability of height. 250 pairs of adult twins (150 monozygotic and
100 dizygotic) completed the Multifactor Leadership Questionnaire, a measure that can be factor-analyzed to give
two dimensions of leadership style: transformational and transactional leadership. Transformational leadership relies
more heavily on physical charisma, while transactional leadership tends to tap skills and characteristics that are
learned. Regression analyses on factor scores from these factors reveal that both height (BETA=.142, t=2.195,
p<.05) and weight (BETA=-.115, t=-2.136, p<.05) are significant predictors of transformational, but not
transactional, leadership. Results are discussed with reference to the effects of including height and weight as
variables in univariate heritability analyses. [Poster] Acquired tolerance is part of the diagnostic picture for alcohol dependence and is a possible marker of
biological vulnerability for alcoholism. As such, it has been the focus of a great deal of research into the etiology of
alcoholism. Recently, there has been interest in determining whether individuals are able to self-report specific
differences in their responses to alcohol over time, whether their reports of acquired tolerance are heritable, and
whether reported tolerance predicts outcome, such as future drinking and future drinking problems. In a genetically
informative sample of twins and siblings (N=900), we investigated individuals' retrospective self-report of
sensitivity to alcohol at different drinking periods (experimental, early, heaviest, current) by asking how many
drinks they needed to consume to achieve specific bodily sensations (e.g. to feel drowsy, stumble, etc.). We then
used these self-reported changes in sensitivity to estimate individual differences in acquired tolerance. Individuals
reported the expected pattern of needing to consume a higher number of drinks to achieve sensations associated
with higher levels of intoxication. Individuals also report the expected change in sensitivity to alcohol over time,
reporting decreased sensitivity to alcohol with increasing drinking experience (acquired tolerance). Adults who
have passed their heaviest drinking period report that they need fewer drinks to achieve the same effects as in their
heaviest drinking period. Test-retest reliability of the sensitivity and tolerance composite variables was substantial.
There were moderate correlations between reported sensitivity and tolerance to alcohol and reported alcohol
problems, suggesting possible predictive utility. Behavior genetic analyses revealed that there is substantial
familiality for self-reported sensitivity and tolerance to alcohol. There was clear evidence of genetic influences on
sensitivity and less consistent evidence for genetic influences on acquired tolerance. We examined the relationships between early T-maze behavior, growth, sociality and stress responsiveness in
broiler chickens. The latencies to traverse a T-maze and thereby reestablish visual contact with their companions
were measured in individually tested, 2 or 3-day-old chicks. They were then assigned to high (HP) or low (LP)
performance categories if their latencies were below 40 or above 90 s, respectively. In Experiment 1, body weight at
3 days of age was unaffected by category or sex but male and female HP chicks were significantly heavier at 15 and
49 days (in laboratory and commercial conditions, respectively) than LP birds. In Experiment 2, we found no
differences between the home-cage behaviors (e.g. walking, pecking) of LP and HP chicks. Neither were there
differences between their latencies to emerge from a sheltered area into an exposed, potentially frightening one nor
in their tonic immobility fear reactions to brief manual restraint. On the other hand, HP chicks stayed closer together
in the home cage and spent longer at that end of a runway nearest a goal box containing other chicks. Experiment 3
showed that circulating corticosterone (C) concentrations were similar in undisturbed LP and HP chicks, that
exposure to a stressor (partial water immersion) markedly increased plasma C levels, and that this elevation was
more pronounced in LP than HP chicks. Collectively, our findings suggest that rapid escape from a T-maze was
positively associated with subsequent growth, that contrasting T-maze performance did not reflect differences in
underlying activity levels or fearfulness, that individual variation in sociality was probably influential, and that LP
chicks were more sensitive to stressful stimulation. Given its simplicity, rapidity and non-invasiveness, the T-maze
test might represent a particularly useful and commercially important selection criterion for future breeding
programmes. Genetic selection for certain production related characteristics has undoubtedly compromised the well-being of
poultry. However, there is growing awareness that selective breeding could be used to improve well-being as well as
productivity. This talk focuses on fear and distress. Intense or prolonged fear and chronic elevation of circulating
corticosterone levels can cause major problems, including injury, pain and reduced egg production, growth rate and
product quality. Our studies of Japanese quail that have been genetically selected for short (STI) or long (LTI) tonic
immobility (TI) fear reactions, for reduced (low stress, LS) or exaggerated (high stress, HS) adrenocortical
responses to mechanical restraint, and for low (LBW) or high (HBW) body weight are yielding valuable insights.
Divergence was rapid and marked in all the selection programmes. The manipulation of narrow stimulus-specific
responses would have little practical value. However, we showed that fear-related behavior (silence, immobility or
withdrawal) was less pronounced in STI and LS quail than in LTI and HS ones in a variety of test situations
including manual restraint, mechanical immobilization, an approaching human, and exposure to novel objects and
places. Adrenocortical responses to a range of known stressors were also markedly lower in LS than HS birds.
Similar divergence was observed in STI and LTI quail though only when a mild stressor was used. Selection for LS
or STI also decreased stress-induced reductions in productivity and product quality, respectively. Finally, fear and
adrenocortical activation were much less pronounced in HBW quail than their smaller (LBW) counterparts. Thus,
selection for one fear behavior, one physiological reaction, or one production trait affected the birds' reactions to
diverse stressful stimuli. The similarities suggest that these independent programmes had influenced the same
underlying characteristic, perhaps fearfulness. This apparently common genetic link provides a platform for future
studies. The sleep-disturbing effect of caffeine is well-known, with suggestions being made that coffee could be used to
induce symptoms mimicking those of insomnia in order to promote further understanding of that disorder. In a
questionnaire mailed to 3808 pairs of adult twins, 10% of respondents indicated that drinking coffee in the evening
"always" or "usually" prevented them from getting to sleep, with a further 20% mentioning that this was
"sometimes" the case. Even among those who stated that drinking coffee in the evening never prevented them from
getting to sleep, coffee consumption was significantly higher among men and women who reported waking due to
nervous tension and worries, and among women who woke spontaneously. Twin correlations for coffee-related
insomnia were substantially greater for monozygotic twins than dizygotic twins, indicating that approximately 43%
of phenotypic variance is attributable to genetic influences. Genetic and environmental influences on coffee-related
insomnia were found to be largely distinct from those affecting general sleep quality and sleep disturbance related to
anxiety, depression and neuroticism. Individual differences in both reading and mathematics performance appear to be due to many of
the same genetic influences (J. J. Gillis, J. C. DeFries, and D. W. Fulker, 1992, Acta Geneticae
Medicae et Gemellologiae 41, 287-300). In order to explore further the etiology of the
observed relationship between reading and math performance, data from samples of same-sex twin pairs
tested in the Colorado Learning Disabilities Research Center were analyzed using structural equation
modelling techniques. Bivariate phenotypic and genetic twin models were fitted to data from 526
twin pairs selected for reading deficits (290 identical and 236 same-sex fraternal) and 355 control
pairs (220 identical and 135 same-sex fraternal). Subtests of the Peabody Individual Achievement
Test (PIAT; Reading Recognition, Reading Comprehension, and Spelling) were used as measures of
reading performance, and scores from the Wechsler Intelligence Scale for Children-Revised (WISC-R)
or Wechsler Adult Intelligence Scale-Revised (WAIS-R) Arithmetic subtest, the Wide Range Achievement
Test Arithmetic subtest, and the PIAT Math subtest were used as indices for mathematics performance.
The results of these confirmatory factor analyses indicate that genetic and environmental
covariances between reading and math latent factors do not differ significantly for twin pairs in
the proband and control groups. Moreover, the resulting estimates of heritability for reading
performance were 0.81 for the proband sample and 0.69 for the control sample, while heritability for
math performance was 0.88 and 0.67, in the proband and control groups, respectively. Finally,
whereas genetic influences were found to account for 83% of the covariation between the reading and
math factors in the proband group and 58% in the control group, shared environmental influences
neither contributed significantly to the relationship between the two latent factors nor accounted
for significant independent variation in the reading and math variables. There exists evidence that responses to apparently similar environmental pressures may be differentially
influenced by genotype (e.g., C.E. Cutrona et al., 1994, Comprehensive Psychiatry,, 35,171-179).
Such gene-environment interactions are intriguing and may help explain how the shared family environment can be
largely without etiological significance for most psychopathologies. This study seeks to expand upon the very
modestly sized literature investigating gene by environment interactions in the prediction of substance abuse. Using
the youngest male cohort of the Minnesota Twin Family Study, genetic risk was estimated from the presence or
absence of parental substance abuse/dependency. To index environmental risk, strength of affiliation with various
social groups likely to either encourage or discourage substance abuse was assessed at age 11. Individuals were
designated high, medium, or low on each of the two dimensions. Both inferred genetic risk and assessed
environmental risk independently predicted the number of substances tried by age 14 (p < .005; N =
591). A gene-environment interaction was suggested but failed to reach significance (p = .060). When the
analyses were replicated with a dispositional risk (externalizing assessed at age 11) in place of the inferred genetic
risk, the environmental variable no longer significantly predicted substance use (p =.093) and no interaction
emerged (p = .157). Externalizing, however, was significantly related to subsequent substance use
(p < .001). Externalizing is also strongly related to our measures of environmental risk (r = .60), and
further analyses will include partialing out its contribution to the genetic and environmental risk variables in their
prediction of substance use. Behavioral genetic modeling will further elucidate the genesis of the relationships
between these measures of genetic risk, environmental risk, externalization, and early initiation into substance use.
[Poster] From detailed temperament questionnaires, we identified subgroups of 3-7 year old twins with extreme
temperaments from the Wisconsin Twin Panel. Our battery included sufficient item content to screen for three
at-risk groups: externalizing (subdivided into motor excess problems, disinhibition problems, and
oppositional-defiant issues), attentional problems, and internalizing. Internal consistency was high for these scales
(.80s). We formed a composite from mother and father report, and selected individuals with composite scores
greater than 1 sd above the mean (approximately 100 individuals in each group). Families in which at least one
twin was extreme in temperament were recontacted when the twins were 5-8 years old, and detailed parent report
temperament (Rothbart's Children's Behavior Questionnaire) and behavioral problem (i.e., Offord's Ontario Child
Health Scale-Revised) measures were completed by mothers and fathers. We first examined intraclass correlations
on our extreme group screening items for the full sample (N = 120 MZ pairs; 182 DZ pairs). All three screening
scales, Internalizing (MZ = .64; DZ = .17), Externalizing (MZ = .71; DZ = .03), and Attention Problems (MZ = .47;
DZ = .11) portrayed prominent genetic influences. We fit DF regression models to these data to determine whether
or not our extremes have the same etiology as the normal range. For all three extreme groups, the difference
between the extreme group mean and the unselected mean was heritable, with identical cotwins being more similar
to their extreme cotwins than fraternal cotwins. Similar analyses will be reported using the Offord scales.
Additionally, multivariate genetic model fitting will be used to decompose the phenotypic association between
temperament and behavior problems. The NZB/BlNJ and C57BL/6JBy inbred strains exhibit large differences in simple sequences length
polymorphisms (SSLPs), cerebellar patterns of foliation (CPF), and hind limb coordination. Quantitative trait loci
(QTLs) modulating variation in these traits were mapped using a panel of 260 F2 male and female mice. Sixty-five
SSLPs spaced an average of 20 cM apart were genotyped. Variation in the intraculminate fissure was found to be
associated wtih three QTLs: Cpfi1 on Chr 1, Cpfi2 on Chr 4 (corresponding to the previously
mapped Cfp1), and Cpfi3 on Chr 19. One of these QTLs, Cpfu1(Chr 1), is responsible for
variation in the uvula fissure. Four QTLs were implicated in variation in the declive fissure; namely, Cpfd1
(Chr 1) Cpfd2 (Chr 5), Cpfd3 (Chr 9), and Cpfd4 (Chr 13). The Cfp2 and
Cfp3 loci do not contribute to CPF variation between the parental strains. The abnormal coordination of the
hind limbs (measured with the scarved bar generously provided by Hans-Peter Lipp) is correlated with five QTLs.
Cpfd1 and Cpfu1 and one QTL that contributes to 17% of the variance in motor coordination are
located on the same region of the telomeric part of Chr 1. This result suggests a functional link between variation in
both the uvula and declive fissures with coordination of the hind limbs. Extensive analyses have been performed relating life events and depressed mood in the Virginia Twin Study of
Adolescent Behavioral Development. With self and parental reports on both life events and depressed mood
available at multiple time points, analyses have been done to examine the discrepancy between parents' and
children's responses and the genetic and environmental relationship between life events and depressed mood across
time. Phenotypic results generally agree with the adolescent life event and depression literature, in that on average
girls report more life events and a higher level of depressed mood than boys. Discrepancies in life event reporting
appear to be "mistakes" on the self report, because most disagreements are due to a child endorsing (or not
endorsing) an event contrary to the reports by the rest of the family. The variance of depressed mood and life
events can be broken down into additive genetic and environmental factors. The effect of life events on mood does
not appear to endure over a 1-2 year period of time, but the effect of depressed mood does endure over time.
[Poster] In psychological theories, the importance of an adult's remembered bonding with parents is often underscored
and assumed to be an important influence on psychopathology. Behavior genetic research has shown that
remembered childhood environments are in part genetically influenced - especially the types of relationships that
tap into the warmth dimension. It is often hypothesized, but not yet shown empirically, that heritable stable
characteristics (like personality) in the children influence parental bonding behavior. As part of larger study on
family processes and maternal adjustment in 326 pairs of female twins age 33-55 we have evaluated remembered
childhood experiences with the Parental Bonding Instrument (PBI), as well as a number of stable characteristics in
the adult twins. Genetic influences accounted for 32% of the variation in the twins' reports of the PBI subscale
Warmth regarding their mothers. Shared and nonshared environmental influences were also significant and
contribute with approximately 1/3 of the variance each. For the other maternal subscales - Protectiveness and
Authoritarian- only shared and nonshared environmental effects were evident. There were no indications of genetic
influences for any of the subscales regarding the twins' fathers. Stepwise regression analyses revealed that four
stable characteristics - Positivity, Indirect aggression, Suspiciousness, and Humor - explained most of the variance
in the maternal Warmth subscale. The highest correlation (r=.22) was with Positivity and this scale also shared the
largest part of genetic variance with Warmth. Multivariate genetic analyses showed that the four variables together
explained about half of the genetic variance in Warmth. Thus, remembered maternal (but not paternal) warmth
seems to be elicited partly by stable characteristics. The popular press is filled with reports of telepathic and other types of extrasensory experiences between
monozygotic twins. To our knowledge there are no empirical studies on whether twins themselves feel any type of
extrasensory experiences. As a part of larger study on family processes and maternal adjustment we have asked 652
female twins age 33-55 how often they experience telepathic contact with each other. Several stable individual
characteristics, such as personality, were also measured. Forty percent of the MZ twins responded that they have
telepathic experiences to some or to a high degree as compared to 12% of the DZ twins. There was no difference in
twin similarity (polychoric correlation) between MZ (.47) and DZ (.46). The only stable characteristics that were
correlated with telepathy were two personality scales from the Temperament and Character Inventory (TCI). The
scales are Persistence (r=.11; p<.01) measuring perseverance despite frustration and Self-transcendence (r=.17;
p<.00001) measuring acceptance, identification, or spiritual union with nature and its source. Heritability and twin
similarity for those scales were the same regardless whether the twins experienced telepathy or not, and regardless
of whether they were concordant for telepathy or not. There are two interpretations of the higher degree of telepathy
among the MZ twins; 1) MZ twins more often have a telepathic contact; 2) MZ twins are more similar than DZ
twins, and greater similarity for, e.g., personality makes them more able to guess what their co-twin will do in a
certain situation. We are more prone to believe in the latter interpretation even though case studies most often
suggest that the former is most important. [Poster] For a study on uterine cancer risk, one member of each of 300 adult Australian female monozygotic twin pairs
had been genotyped for the X-linked androgen receptor gene and scored for the number of repeats of the triplet
CAG. (A low number of CAG repeats has been associated with greater risk of prostate cancer in males and more
effective transcription of androgens.) These twins were part of a large twin study in which short versions of
Eysenck's and Cloninger's personality questionnaires had been used. For the present study, three separate measures
of masculinity-femininity were constructed from the items of these questionnaires, using item and factor analysis.
Two of the three measures--admitting to fears and worries and a willingness to break rules--were not significantly
correlated with CAG repeats among the genotyped females. The third measure, reserved versus confiding in others,
showed a modest relationship with CAG repeats: fewer repeats went with scores in the reserved (i.e., masculine)
direction on this scale. [Poster] Evidence from twin studies suggests that genetic influences play an important role in all stages of cigarette use,
including experimentation, regular smoking, nicotine dependence, and persistence in smoking. Important
relationships have been found between lifetime depression and a history of cigarette smoking. In follow-up data
from female twins (obtained in the U.S.) (Kendler, et al., Arch Gen Psychiatry 50:36-43, 1993) a
strong genetic correlation was found between average lifetime cigarette consumption and one-year prevalence of
major depression. The purpose of this study is to determine the extent to which genetic influence on risk of major
depressive disorder might mediate some of the genetic influence on smoking risks in Australian women compared
with men. Telephone interview data on measures of DSM-IV nicotine dependence and the use of cigarettes were
obtained from over 2,000 adult Australian twins, 20-34 years of age. Consistent with other studies, we found
evidence for additive genetic influences on risks for major depression (34%, 95% CI: 17-44%), cigarette
experimentation (65%, 95% CI: 56- 72%), regular smoking (66%, 95% CI: 48-83%), and DSM-IV nicotine
dependence (62%, 95% CI: 54-70%), Fagerstrom nicotine dependence (74%, 95% CI: 66-81%), and smoking
persistence (65%, 95% CI: 56-72%) in both men and women. In logistic regression analyses, except for
experimentation in men, we found history of DSM-IV major depression to be a significant predictor of all stages of
cigarette use (OR range: 1.55-2.40). When variables coding for zygosity and zygosity x cotwin's smoking were
included with a measure of respondent's major depression in the regression equation, the cotwin smoking variables
remained significant predictors, implying that genetic factors that increase risk for the initiation and the maintenance
of smoking in women and in men cannot be entirely explained by factors responsible for major depression. Associations between platelet monoamine oxidase (MAO) activity and susceptibility to psychiatric conditions
such as alcohol dependence, other drug use, conduct disorder and depression have been reported. However, MAO
activity has been shown to be inhibited by some component of cigarette smoke, and prevalence of smoking is higher
in many of the conditions in which MAO has been implicated. We have measured platelet MAO in 1551
individuals recruited from the Australian NHMRC Twin Registry, for whom information on alcohol use and
dependence, smoking, conduct disorder, depression, attempted suicide, panic disorder, social phobia and several
personality scales was available. Current smoking reduced platelet MAO activity in a significant and dose-related
manner, with no evidence of lower MAO in ex-smokers or non-smoking subjects with co-twins who smoked.
Alcohol use and lifetime DSM-IIIR alcohol dependence history were not associated with MAO activity when
smoking was taken into account, while depression, panic disorder, social phobia and attempted suicide were no
significantly associated with platelet MAO activity either before or after correcting for smoking effects. Of the
personality scales, only Neuroticism from the Eysenck Personality Questionnaire was significantly correlated with
MAO, with a stronger correlation observed after correction for smoking status. Results of structural equation
modelling of the relationship between MAO, Neuroticism and smoking will be presented. The theory of fluid and crystalized intelligence (Cattell, 1941; Cattell & Horn, 1984; Horn & Cattell, 1966;
Horn, 1991) grew out of three major predictions about the complex nature of human cognitive abilities. The first
predictions were "structural": a single general factor (i.e., Spearman's "g") will not account for the patterns of
individual differences seen among multiple abilities; at least two broad factors (Gf and Gc) are required for
resonable level of fit to observations. A second set of predictions of Gf-Gc theory were "kinematic": over the
life-span there is anexpected rise of gc and an expected rise through childhood into young adulthood of Gf and
consequent fall throughout adulthood. A third set of predictions were "dynamic": the "investment" of Gf, coupled
with other lower order factors in the context of educationally relevant settings, was thought to lead to individual
differences in the development of Gc. Aspects of these predictions have been repeatedly examined and found to
provide support for the theory (cf. Horn & Cattell, 1967; Horn & Donaldson, 1980; McArdle & Prescott,1992;
Horn, 1994; Schaie & Baltes, 1996; McArdle, Prescott, Hamagami & Horn, 1998). This paper presents a review on
the use of behavioral genetic information to evaluate the construct validity of these structural, kinematic, and
dynamic predictions. Multivariate structural equation models based on biometric data are then illustrated to evaluate
the generative hypotheses of gf/gc theory. The Missouri Adolescent Female Twin Study (MOAFTS) is focused on the exploration of behavioral and
psychiatric correlates of substance dependence in girls and young women. Telephone interview data from over
2,600 female adolescent twins (770 MZ pairs and 562 DZ pairs) and their parents participating in MOAFTS were
utilized in the present report. We sought to explore how genetic and environmental factors influence behavioral
disorders in girls, as measured through a composite variable reflecting total symptom count of conduct problems
(obtained through child self report), attentional deficits, hyperactivity and oppositional defiant behaviors (obtained
through parental report). Twin pair correlations for this composite measure suggested that shared environmental
factors as well as genetic factors influence the occurrence of behavioral problems in girls (r= .82 for MZ pairs, r=
.50 for DZ pairs). Subsequent genetic model fitting suggested that about 61% of the variance in this measure could
be attributed to additive genetic effects while shared and unique environmental effects accounted for approximately
20% and 19% of the variance respectively. These results are thus consistent with those of other twin studies (e.g.,
Slutske et al., 1997,J. Abnorm. Psychol.106, 266-279)in which substantial genetic
influences on behavioral problems in females have been demonstrated. We examined genetic and environmental influences on alcohol-related expectancies, measured by the Effects of
Drinking Alcohol scale (EDA; Leigh, B.C., 1987, J. Stud. Alc.48(5), 467-475), in a sample of over
2,300 pairs of Finnish twins, including 778 MZ, 790 DZ, and 810 OSDZ pairs. Path modeling of twin covariances
on the EDA subscales, derived from factor analysis of all individual twins, showed moderate contributions of
additive genetic and unique environmental influences. Sex limitation models were also tested, revealing sex-related
differences in the relative contributions of genes and environment on several of the subscales. Because expectancies
consistently have been shown to correlate highly with drinking behavior, bivariate analyses were performed to
estimate the contribution of environmental and genetic effects to the phenotypic covariance. [Poster] Locating people has become much easier in recent years with the advent of the internet. Freely available "white
pages" databases allow users to search for individuals with listed telephone numbers in the United States, Canada,
Austria, Belgium, Germany, Italy, Luxembourg, Spain and the United Kingdom (and perhaps other countries). The
better on-line white pages allow users to search by name, address or telephone number, and the search can be
limited to a city, metropolitan area, state or entire country. These resources can be extremely helpful when
attempting to locate twins from vital records data, or when attempting to recontact participants in a longitudinal
study. We have developed an simple approach using Microsoft Access and Microsoft Word that allows us to
automate the search process. Data on subjects are stored in a Microsoft Access database. Information from the
database can be inserted into an HTML (web) document using the Microsoft Word mail merge function. The web
document allows users to submit a query to the white pages for information about an individual simply by clicking
on a hypertext link. Links can be added to query about the phone number, address, or the name of a subject's family
member. This approach saves a lot of time and reduces data-entry errors. The address and telephone information
taken from the white pages can be pasted electronically into other programs for further processing. The whole
procedure is very simple and does not require extensive knowledge of computers. The web document does not have
to be stored on a web server because it can be accessed as a local file. Microsoft programs do not have to be used
either. For example, one could use UNIX awk to translate a tab-delimited text file to a web document. The secular and international rise in IQ has been widely interpreted as evidence that black and white IQ scores
may be expected to converge over time. The present study first examines the logic behind this position, then
explores the consistency of that logic with data from the National Longitudinal Study of Youth (NLSY), a large
national sample that has been followed since 1979. Elaborating Jensen's procedure (A.R. Jensen, 1973,
Educability and Group Differences, Methuen), the analyses focus on sibling pairs and mother-offspring
pairs within the NLSY. For the sibling analysis, a sample of blacks and whites are matched on IQ and on parental
education, occupation, and income. For the mother-offspring analysis, a sample of black and white mothers are
matched on IQ and their own education and family income. Parallel analyses of the IQs of the comparison siblings
and of the offspring are conducted. Despite equivalent means and variance on IQ and the socioeconomic variables
in the black and white reference samples, the IQs of the comparison siblings and of the offspring regressed to means
with a black/white difference of 16.9 IQ points (sibling sample) and 21.6 IQ points (mother-offspring sample).
Alternative possibilities for reconciling these findings with the secular rise in IQ are discussed. Family systems research has long focused on relationships within the family within the context of the family as
a whole. One of the most compelling findings in behavioral genetic research has been the importance of genetic
factors on measures typically conceptualized as environmental (e.g. parenting). The majority of research in this area
has employed child-based designs, although the few studies that have employed a parent-based design have also
found evidence of genetic influences (S.H. Losoya, S. Callor, D.C. Rowe, & H.H. Goldsmith, 1997,
Developmental Psychology 33, 1012-1023). To date, there have been no studies that have
examined genetic influences on marital relationships, although genetic influences on divorce have been found (M.
McGue & D.T. Lykken, 1992, Psychological Science 3, 368-373). It is likely that genetic
influences on parenting will overlap with any genetic influences on the marital relationship that are found. The
present report employs a sample 326 pairs of twin mothers of adolescents from Sweden (148 MZ, 174 DZ). Results
indicate that there are genetic influences on mother-child and marital relationships (heritability ranges from 26% to
62% for marital positivity and negativity and from 18% to 32% for maternal positivity and negativity). There is also
evidence of modest phenotypic correlation between mother's relationships with her child and her spouse. Cross-twin
correlations suggest that this relationship can be explained in part by overlapping genetic influences on the
association between mother's positivity towards her child and towards her spouse. Additional analyses will be
conducted to further examine these associations across raters and constructs. It seems likely that many aspects of modernization have contributed to the Flynn rise. School is the most
obvious candidate: the amount of time people spend in school has been growing right along with IQ, and we have
clear evidence that schooling raises scores even on tests of fluid intelligence. Increases in non-school forms of
environmental complexity (such as visual displays and digital devices) have probably developed a corresponding set
of mental skills as well. It would not be surprising to find that improvements in health and nutrition have played a
role, along with the growing public interest in intellectual aspects of infant and child development. Whatever their
causes, these gains are not artifacts. They manifest themselves in domains other than testing itself: the extraordinary
technological progress visible everywhere around us is perhaps the most obvious of those manifestations. Other
evidence comes from recent demonstrations of increases of chess-playing skill at early ages and (surprisingly!) in
the complexity of political discourse. Overall, the scope and patterning of the Flynn gains presents major challenges
to contemporary theories of intelligence. Most information on the secular Flynn IQ rise derives from intergenerational comparisons. The present study
examined whether a similar secular rise is seen in a repeated-measures analysis of longitudinal IQ data. Army
General Technical (GT) intelligence was measured first at about age 19 in a large sample of fairly representative
American armed forces veterans and again when they were in their late thirties. Individual variations over time in
full GT IQ, in verbal reasoning and in arithmetic reasoning IQ changes were monitored and related to middle-age
level of education, personality, and psychopathology. The full GT IQ score rose on average 0,27 IQ points/year for
the total sample, but the amount of gain or loss related to young IQ level. Low, medium and moderately high ability
individuals thus tended to gain and high ability individuals (i.e. young GT IQ > 1,5 SD) to lose, and the more so the
higher the IQ. We thus face the paradox that a typical high IQ loser is one with a long formal education, a large
income, benign personality traits, and few symptoms of psychopathology, whereas the typical low IQ gainer spends
significantly fewer years in school, earn less, obtain higher Psychoticism, Neuroticism, and Extraversion scores, and
score high on MMPI-II and DSM-III scales for psychopathology and substance abuse. Race differences in overall
IQ gain were noted, too. This study investigates the genetic and environmental influences on parenting experiences children received.
PBI(Parental Bonding Instrument)was carried out for 213 twin pairs (38 MZm, 101 MZf, 16 DZm, 30 DZf, 28 DZo
twin pairs) from 15 to 27 years old. They were required to recall their parenting experiences they had received from
each of their parents in their childhood. Two dimensions of parental behavior, care and overprotection were
subjected to model fitting. As for the father's care score, the best fitting model was CE model(the variance was due
to common environmental factor and specific environmental factor). For the female subjects, however, ACE model
couldn't be rejected with the heritability of 28%. Father's overprotection reported by male was explained best by AE
model with 75% of the additive genetic variance and 25% specific environmental factor. Father's overprotection
reported by female was explained best by CE model with 53% common environment and 47% specific
environment. For the mother's care score, the best fitting model was AE with heritability of 64% and 56% by male
subjects and female subjects respectively. Mother's overprotection showed 57% common environment with no
genetic influence for both sex. Genetic factor of the elicitation of mother's care was verified in Japanese
population. The equal environments assumption has been repeatedly tested for a wide range of phenotypes. Neither
presumed zygosity nor parental attempts to make similar have been demonstrated to affect twin similarity for
measures of personality or cognition. Aspirations to be similar are seldom evaluated as a source or as a potential
outcome of similarity for personality. In the Twin Moms study of maternal adjustment in the context of familial
processes, we are particularly interested in measures of personality, parenting, and marital relationships. We have
developed 3 scales describing contact and aspirations to be similar: behavioral contact, aspirations to be similar,
confiding in sister. For all three measures, MZ pairs (N=144) reported slightly, but significantly more contact than
DZ pairs (N=171). Intraclass correlations for reported contact and confiding in sister were high (.81 and .80 for
contact, .75 and .62 for confiding in MZ and DZ pairs, respectively). Intraclass correlations for aspirations to be
similar were .38 and .35. Intrapair similarity for personality, marital adjustment, and parenting was not
associated with either level of or intrapair similarity for any of the three contact measures. Thus, aspirations to be
similar and contact with/confiding in twin partner do not influence heritability estimates of personality, parenting or
marital adjustment. [Poster] Infants develop a variety of sensory, motor, and cognitive skills that gradually enable them to adapt to their
environment. Early developmental delays have been found to be important predictors of later learning difficulties,
school problems, and other aspects of psychosocial maladjustment. In the present study, the genetic-environmental
contributions to early development were examined in a population-based sample of infant twins. Subjects were
recruited by contacting all mothers having given birth to twins in the Greater Montreal Area between 1 April, 1995
and 31 December, 1998. Zygosity was determined by physical similarity assessment and validated with DNA
analysis. Development was measured when the twins were 5 months old (corrected for gestational age) through
mother interview employing a scale used in the Canadian National Longitudinal Survey of Children. Twelve items
(e.g., "Has he/she ever sat for 10 minutes without any support at all?"; "Has he/she ever said good-bye without help
from another person?") were retained for the scale by item analysis (alpha = .74). Genetic analysis was performed
on the aggregate score using hierarchical multilevel random effect modeling. Strong intraclass correlations were
found for both MZ and DZ pairs. This resemblance was entirely due to shared environmental factors which
accounted for 75% of the variance, with heritability = 0. Reporting bias (mothers answering similarly for both
twins) appears unlikely since interviews were conducted separately for each twin and the scale was strongly related
to a laboratory assessment of motor-cognitive skills in a subsample of subjects. These findings suggest that infant
motor-cognitive development is influenced by familial environmental factors and that developmental delays may
result from exposure within families to risks that still need to be identified. Evidence increasingly suggests that individual differences in cardiovascular reactivity to psychological stressors
during young adulthood may be predictive of later risk for clinical cardiovascular disease. However, despite this
clinical importance, relatively little is known concerning the genetic and environmental causes of variation in
cardiovascular reactivity to stress. Therefore, as part of the University of Pittsburgh Twin Study, 160 MZ and 80
same-sex DZ (zygosity based on DNA fingerprinting), young adult (18-28 years old), normotensive twin pairs from
the community were evaluated in a protocol measuring cardiovascular reactivity to five laboratory stressors (Mental
Arithmetic, Stroop Test, Mirror Tracing, Video Game, and Cold Pressor). Heart rate, diastolic and systolic blood
pressure, as well as indexes from impedance cardiography were measured at baseline and during task performance.
Multivariate genetic analyses were performed in order to address the following questions: 1) are there genetic
influences on cardiovascular reactivity to stress that are independent of those influencing baseline cardiovascular
function, 2) what is the factor structure of these genetic influences across multiple measures of cardiovascular
reactivity, and 3) what is the factor structure of these genetic influences across the five laboratory stressors? Based
on this final sample, analyses indicate that in general novel genetic influences (independent of those influencing
baseline cardiovascular function) are important in determining individual differences in cardiovascular reactivity to
psychological stressors. The structure of these genetic influences suggests the existence of a common genetic factor
across both the multiple cardiovascular measures and across the different psychological stressors. These results
support the generality of the construct of cardiovascular reactivity to laboratory psychological stress.
Recent genetic theories of human hand preference have emphasized the role of environmental factors as
contributory to the variation seen in this set of common behaviors; the environmental factors are proposed to be
biological (T.A. Markow, 1992, Genetica, 87, 87-94; R.A. Yeo, S.W. Gangestad, and W.F.Daniel, 1993,
Psychobiol., 21, 161-168) or cultural (K.N. Laland, J. Kumm, J.D. Van Horn, and M.W. Feldman, 1995, Behav.
Genet., 25, 433-446) in origin. Data from three separate studies of right- and left-handers of different ages (I.B.
Perelle and L. Ehrman, 1994, Behav. Genet., 24, 217-228; C. Porac, I.C. Friesen, M.P. Barnes, and V. Gruppuso,
1998, Develop. Neuropsychol., 14, 157-172; C. Porac, unpublished) are presented and analyzed in order to show
how age-related variations in hand preference patterns interact with participants reported histories of hand
preference switch attempts. This age/switch history interaction promotes not only variation in the degree to which
left hand preference is apparent at different ages, but also the degree to which individual hand preference items
display sidedness consistency or inconsistency. The data reveal that the writing hand is the most frequently switched
behavior and, in individuals over the age of 75 years, the writing hand is a poor predictor of left hand preference.
Although both young (<30 years) and older (>65 years) report pressures to switch hand preference, the
disassociation between writing and other preference behaviors is most apparent in older adult groups. In addition to
switch history, the data also reveal the possibility of a more subtle developmental shift toward the right side when
young adult groups are compared to older adults; however, the effect of switch history remains the strongest
variable in determining age differences across the age span of older and oldest-old adults (65 to 100 years). ApoE genotype is a risk factor for cognitive decline in old age. It has been associated with the risk of
developing Alzheimer's disease and with deterioration of memory function. One of the theories explaining the
association between the apoE genotype and cognitive decline, focuses on the effect of the apoE-genotype on apoE
levels in blood. ApoE bloodlevels affect the binding of beta amyloid and may increase deposits of beta amyloid
which eventually turn into plaques characteristic for cognitive decline in Alzheimer's disease. Variance in apoE
bloodlevels is for 16% explained by the apoE-genotype. In roughly 100 families, consisting of twins and their
siblings (aged 20-35), the apoE locus was genotyped and apoE blood levels were measured. Cognitive ability was
assessed with the Wechsler Adult Intelligence Scale (WAIS-3R, Dutch revised version). We found a negative
association between apoE levels in plasma and full scale IQ and performance IQ. We also found an association
between the apoE genotype and WAIS subtests similarities and digit-symbol free recall. The same
analyses will be done for roughly 150 families consisting of twins and their siblings aged 35 - 65 years. The power to detect an effect varies with sample size, effect size and study design. The power of the classical
twin study may be increased by extending the familysize by adding non-twin siblings. We conducted a power
analysis in Mx to determine whether adding one or two non-twin siblings to the classical twin design would increase
the power to detect genetic and common environmental influences. We compared three possible designs, namely
families consisting of only an MZ or DZ twin pair, families with MZ or DZ twins and one non-twin sibling, and
families with MZ or DZ twins and two non-twin siblings. Total sample size and MZ/DZ ratio were held constant.
We found that adding one non-twin sibling caused an increase in the power to detect heritability, but that adding
two non-twin siblings nullified this effect. For the power to detect common environmental factors a large effect of
adding one non-twin sibling was found. Adding two non-twin siblings had an additional small increase on top of the
effect of adding one non-twin sibling. [Poster] Alcoholism and depression frequently co-occur, but the basis of this comorbidity remains uncertain. This
association is further complicated by sex differences in the prevalences and timing of these disorders. One
explanation is that major depression and alcoholism represent alternative manifestations of the same underlying
vulnerability, and there are sex-specific factors which influence clinical presentation. Alternatively, this clinical
heterogeneity may reflect separate etiologies for depression and alcoholism. We address these issues using data
from a recent study of 8,700 adult twins identified from a population-based twin registry and assessed for lifetime
major depression (MD) and alcohol abuse or dependence (AAD) by structured psychiatric interview. For both
males and females, individuals with one disorder were at significantly increased risk for the other (OR=2.5, 95%
CI=2.1-2.9). Risk of AAD was increased among both identical and fraternal same-sex cotwins of individuals with
MD. However, when the analyses were restricted to primary alcoholism (excluding comorbid cases where MD
preceded AAD), this association was attenuated. Structural modeling analyses of the twin-pair correlations suggest
that the comorbidity of alcoholism and depression is due primarily to individual-specific environmental factors and
that the disorders are not sex-specific manifestations of common genetic vulnerability. [Poster] Fulker et al (1999) have proposed a partitioning of association to between-sibships and within-sibship
components, and shown that a test based on the within-sibship variance is robust to population stratification. As in
QTL linkage analysis, the efficiency of an association design may be improved by selecting phenotypically extreme
sibships. We have developed a method of measuring the informativeness of sibships for QTL association analysis,
in terms of the expected contributions of the sibship to the likelihood ratio chi-squared tests for between-sibships
and within-sibship association. These expected contributions are calculated conditional on the measured trait values
of the siblings, under a biometrical genetic model where QTL effects are parameterized by allele frequencies and
genotypic means, and which allows for residual sibling correlations. This presentation will describe the method and
its implementation in a freely-distributed computer program. Refs. Fulker DW, Cherny SS, Sham PC,
Hewitt JK (1999) Combined linkage and association sib-pair analysis for quantitative traits. American Journal of
Human Genetics, 64, 259-267 Attention-deficit/hyperactivity disorder (ADHD) is more common in boys than girls, with sex ratios ranging
from 3:1 to 8:1. Researchers have suggested two competing explanations for this sex difference in prevalence: the
polygenic multiple threshold (PMT) model (e.g., Kashani, Chapel, Ellis, & Shekim, 1979, Journal of
Operational Psychiatry 10, 145-148), which suggests a sex difference in the threshold for the liability
needed to express the disorder, and the constitutional variability (CV) model (e.g., James & Taylor, 1990,
Journal of Child Psychology and Psychiatry 31, 437-446), which suggests a sex difference in the
causal factors. Studies testing the assumptions of these models report conflicting results, with some studies (e.g.,
Faraone et al., 1995, Journal of Abnormal Psychology 104, 334-345) finding support for the PMT
model and some studies (e.g., Silverthorn, Frick, Kuper, & Ott, 1996, Journal of Clinical Child Psychology
25, 52-59) finding evidence against the PMT model. One possible reason for the variability in findings
may be the heterogeneity in the constructs being examined. Given this possibility and the evidence that there are
two separate dimensions of ADHD (inattention and hyperactivity-impulsivity), the assumptions of the two models
were tested for inattention and hyperactivity-impulsivity separately in the present study. Participants were Georgia
Twin Registry members (N = 56 to 375) who met the symptom list criteria for the diagnosis of one or more types of
DSM-IV ADHD and their DZ co-twins and co-siblings. We found evidence for the PMT model and evidence
against the CV model for all three types of ADHD: the predominantly inattentive type, the predominantly
hyperactive-impulsive type, and the combined type. These results suggest that boys are more likely to be diagnosed
with any type of ADHD than girls because girls have a higher threshold for the liability needed to express the
disorder of ADHD. Nonhuman primates play a major role in studies of behavioral genetics. However, research has been limited to
testing candidate genes. The mapping and identification of previously unknown genes that influence variation in
primate behavior and/or neurobiology has not been possible because genetic linkage maps for primates have not
been available. We have developed a 10 centiMorgan genetic linkage map of the baboon (Papio hamadryas)
genome. This genetic map includes more than 350 highly polymorphic microsatellite loci that were originally
cloned from and mapped in the human genome. The baboon map now makes it possible to use genome-wide
linkage screening in large pedigrees to identify chromsomal segments within baboons that contain genes which
influence any phenotype of interest. The baboon linkage map has been successfully used to locate several genes
that influence bone metabolism. These analyses used data from 700 pedigreed baboons genotyped for the panel of
350 microsatellites. Other complex traits have also showed significant linkage results. We are beginning studies in
which the same methods and microsatellite loci are being used to investigate behavioral phenotypes in baboons,
including measures of temperament and of monoamine metabolites. We are also extending this research strategy
(i.e. genetic analysis of large pedigreed colonies) to other nonhuman primate species. The sexual dimorphism of aggression has led to a search for its Y- chromosomal correlates. We have previously
confirmed that initiation of attack behavior against a conspecific male is Y- dependent in two strains of laboratory
mice (NZB and C57BL/6J). We have provided evidence that the nonpairing region of the Y is not involved in this
behavior whereas the pairing region of the Y co-segregates with attack behavior, in these strains. In addition, the
genetic correlates of attack behavior are not expressed when borne on the homologous pairing region on the X
chromosome but only when carried on the Y chromosome. Only one functional gene (coding for steroid sulfatase or
STS) is mapped on this region as of yet, suggesting that it could be a candidate for attack behavior. We estimated
the genetic correlation between the concentration of STS protein in the liver and initiation of attack behavior. We
have employed also mice in which gene invalidation induced attack behavior. Pharmacological modulations of STS
or of its metabolites modifies the frequencies of attack in these male mice, confirming the implication of STS in
aggression. Recent investigations have demonstrated the involvement of STS in neurosteroid biochemical pathways,
and several lines of evidence indicate that neurosteroids interact with neurotransmitters. These conclusions and our
present results support the hypothesis that sulfatation of steroids may be the prime mover of a complex network,
including genes shown to be implicated in aggression by mutagenesis. QTL mapping was initiated forty years ago but its introduction in behavioral neurobiology is still
comparatively new. Several studies have employed recombinant inbred strains, backcrosses, and intercrosses to
analyze a wide range of behaviors (drug-related behaviors, handedness, sensory, and motor development, pup care,
etc.). With the advent of advanced intercrosses, congenic, recombinant congenic, and consomic lines, QTL analysis
is now entering a second generation. The utility and power of QTL analysis depends, however, on the reliability of
the methods, an issue that is still in dispute. Here we demonstrate that a large number of QTLs that we have
previously mapped in the neurobehavioral field have been successfully replicated. Our findings suggest that concern
regarding Type I error (the probability of detecting false QTLs) has been somewhat overstated. We anticipate that
two properties of QTL analysis will lead to a better understanding of the relations between structure and function.
(1) The identification of strong candidate genes for QTL associated with a behavioral trait will in some instances
provide partial validation of mapping results and will often lead to the formulation of testable hypothesis regarding
the genetic basis of behavioral variation. This is illustrated by our work on maternal behavior in mice in which we
have shown that a key olfactory receptor gene maps within the confidence interval defined by a QTL associated
with pup retrieval performance. (2) Defining a list of plausible candidate genes for a QTL--what we refer to as
QTL-gene coidentification--also provides an opportunity to explore possible aberrant behavior when the expression
of candidates is altered. This is exemplified by our studies of aggression and handedness. QTL mapping is simply
the initial step in a complex process that culminates in gene inactivation or overexpression. The potential of this
approach will be demonstrated in the context of QTLs that modulate patterns of cerebellar foliation and that are
implicated in abnormal coordination. A final characteristic of QTL map studies is that it becomes possibility to
exploit the homologous synteny between mouse and human to probe the complex genetics of human behavioral
disorders. Genotyping for measured genetic markers permits a combination of quantitative trait loci (QTL) and genetic
factors in behavioral genetic models. This modeling approach is illustrated using data on disruptive behavior
disorder symptoms in children and adolescents in 50 sibling pairs. The sample contains both probands referred for
psychiatric disorder and their siblings (34 pairs) and controls and their siblings (16 pairs). The 100 individuals were
genotyped for repeat polymorphisms in the dopamine transporter (DAT1) and in the dopamine D4 receptor (DRD4)
genes. For the dopamine transporter locus, low and high risk genotypes were scored as follows: LL=0, LR=1, and
RR=2, where L is a low risk allele and R is a high risk allele. For the DRD4 locus, the rare RR homozygote was
combined with the heterozygote (LL=0, LR=1, RR=1). The dependent variables were three disruptive behavior
disorder symptom count traits; i.e, hyperactive-impulsive symptoms, inattentive symptoms, and oppositional-defiant
symptoms. Each trait was regressed on age and on family status (clinic referred = 1, control = 0) and residuals from
this regression were used in a biometric model. The biometric model assumed no shared environmental influences,
consistent with results from previous behavior genetic analyses. It allowed for measurement error on each trait and
for four factors: a genetic factor uncorrelated with the QTLs, a DRD4 QTL factor, a DAT1 QTL factor, and a
nonshared environmental factor. The full model yielded an excellent fit (chi2 = 27.64, df = 39, p =
.913, AIC = -50.36). The change in chi square from dropping the DRD4 QTL was statistically significant
(chi2 = 10.36, df = 3, p < .05). The loss of fit for the DAT1 QTL was marginally significant
(chi2 = 7.60, df = 3, p < .10). The DRD4 QTL factor loaded most strongly on inattentive symptoms,
whereas the DAT1 QTL factor loaded most heavily on hyperactive-impulsive symptoms. Of the variation in the
three symptom traits, the DRD4 QTL explained (on average) 3.6%, whereas the DAT1 QTL explained (on average)
5%. Self-rated health (SRH) is a component of health that is associated with, but not completely defined by,
psychological and physical well-being. Although the factors comprising self-rated health are not totally understood,
there is evidence for age differences in the predictors of SRH. This study analyzes two aspects of SRH in a sample
of young adult twins. First, how do genes and environments mediate the relationships between between SRH and
subjective well-being (SWB), health symptoms (HS) and health behaviors (HB)? Next, how important are genes and
environments for variance in SRH that is not associated with SWB, HS and HB? Analyses were based on a
Norwegian sample of 5864 twins, 18-23 years of age. Self-rated health correlates 0.41 with subjective well-being,
-0.26 with health symptoms, and 0.24 with health behaviors. Regression procedures indicated a unique and
significant effect of SWB, HS and HB for predicting SRH. Preliminary results suggest that genes are important
mediators of the relationships with self-rated health, but that the patterns of mediation vary between SRH and the
physical versus psychological measures of health. Final results, based on model fitting approaches that incorporate
sex differences, will be presented. Untimed Raven's Standard Progressive Matrices (SPM) were administered to 309 17- to 23- year-old students at
two leading South African universities (173 Africans, 136 Whites; 205 women, 104 men). African students solved
an average of 44 of the 60 problems whereas White students solved an average of 54 of the problems (p<0.001). By
the standards of the 1993 U.S. normative sample, the African university students scored at the 14th percentile with
an IQ equivalent of 84 and the White university students scored at the 61st percentile with an IQ equivalent of 105.
A small sex difference favoring males was found in both the African and the White samples. These results confirm
earlier reports of these race and sex differences. Two additional studies will be mentioned to shed light on possible
causes. African 13- to 15-year olds given the Wechsler Intelligence Scale for Children-Revised (WISC-R) showed
the most pronounced differences from the U.S. standardization sample on the gfactor. A principal
components analysis by J. P. Rushton (1999, Person. and Indiv. Diffs.26,381-389) found that
whereas five sets of IQ gain scores over time on the WISC-R and WISC-III do cluster (the Flynn Effect), suggesting
they are a reliable phenomenon, these are independent of the cluster of (U.S.) Black-White differences, inbreeding
depression scores (calculated on the WISC-R from Japan), and gfactor loadings. The present study investigated the heritability of athletic ability using the twin design. At the same time, athletic
ability was correlated with the WISC-R intelligence test. Previously unused data from the Western Reserve Twin
Project (WRTP) were analyzed (Thompson, Detterman, & Plomin, 1991; Thompson, Detterman, & Plomin, 1993).
The original sample consisted of 135 same-sex fraternal twin (DZ) and 148 identical (MZ) twins. Significant
heritability was found for two of the four measures of athletic ability. Intelligence was significantly correlated with
athletic ability. The etiology of the covariance between intelligence and athletic ability will be discussed. Cloninger (1987,Archives of General Psychiatry 44,573-588) proposed that Novelty-Seeking
(NS) -- variation in aspects of activation or initiation of behavior including tendencies toward impulsivity and
extravagance -- is discriminantly related to variation in dopaminergic function. In turn, Harm-Avoidance (HA) --
variation in aspects of inhibition of behaviors including shyness and rapid fatigability -- was proposed to be
discriminantly related to variation in serotonergic function. We tested Cloninger's set of proposed convergent and
discriminant relations in a sample of college-student volunteers (age 23 to 49) who were administered the
Temperament and Character Inventory (TCI) scales for NS and HA. Variation related to age, sex, and ethnicity was
partialed from the dependent variables. Participants (N 196 to 243) were genotyped for a set of polymorphisms at
dopamine (DA) genes (including DRD2 TaqI A, D4DR exon III, DA transporter) and at serotonin (5HT) genes
(including 5HT 2A and 2C receptors, and 5HT transporter). In analyses (ANOVA followed by Bonferroni and
Tukey HSD tests where applicable), global NS and HA were less related to genetic variation than were specific
subcomponent scales like NS3 (extravagance), HA3 (shyness with strangers), and HA4 (fatigability/asthenia).
There were statistically significant associations of DA genes with certain subcomponents of both NS and HA, and of
5HT genes with certain subcompoments of both NS and HA -- but effect sizes were fairly small. Overall, results
were partially supportive of Cloninger's proposed convergent relations, but not supportive of the proposed
discriminant relations. Pertinent issues related to statistical power, strengths and limitations of candidate-gene
association studies, level of measurement, and accurate discernment of penetrance functions are discussed.
[Poster] Twin, adoption, and genetically non-informative studies show phenotypic associations between temperament
rated at prior age points and later aspects of problem behavior. These associations are moderate, usually in the .20 to
.30 range. Genetically informative samples can help to elucidate the genetic and environmental mediation of these
correlations which are particularly consistent for the emotionality and, to a lesser degree, for the shyness aspect of
temperament. However, while twin studies pointed mainly towards a genetic influence, with MZ cross-correlations
being much higher than those for DZs (Schmitz et al., in press, International Journal of Behavioral
Development), the currently used sample of matched adopted and non-adopted children differed in two ways.
For one, only the emotionality aspect of temperament was predictive of later problem behavior, and two, the
cross-correlations for natural siblings were higher than those for DZs (.15 to .39 for non-adopted siblings vs. .20 to
.34 for MZs and .03 to .20 for DZs), indicating possibly shared environmental mediation. Since previous studies
pointed to the influence of contrasting effects on parental ratings of temperament (Saudino et al., 1997, Behavior
Genetics, 27(6), 604), these approaches will be incorporated into modeling the relationship between temperament
and problem behavior. Additionally, the equality of the shared environment for twins and adopted children will be
tested, since the twins are rated at the same time while sibling ratings are three years apart, on average. A
combination of twin and adoption data will likely show more unbiased results A study of same-age unrelated siblings (UST-SA) has been ongoing at California State University, Fullerton
since 1983. An early report from this project, based on 21 pairs, indicated an IQ correlation of .17, a verbal IQ
correlation of -.01 and a performance IQ correlation of .29. Additional data have now been collected for 84 pairs,
who range in age from 4 - 54 years. New analyses will be reported for the larger sample, e.g., IQ correlations for the
full sample, IQ correlations for adopted-adopted vs. adopted-biological pairs, and correlations between intellectual
resemblance and pair characteristics such as mean age, age difference, sex (same/different), rearing status (one vs
both adopted) and school placement (same/different classes). Implications of the findings for theories of intellectual
development and for the rearing and educating of children and adolescents will be discussed. Future plans for this
ongoing study will be described. Linkage and association analyses are complementary methods for QTL mapping. Fulker et al (1999)
proposed a method of combined QTL linkage and association analysis of unselected sib-pairs under a variance
components model. We have derived approximate expressions for the expected non-centrality parameters (per
sib-pair) for the linkage and association tests. For an additive QTL of small effect size, the non-centrality parameter
for linkage is approximately equal to the product of the square of the QTL heritability and the variance of the
estimated proportion of alleles IBD. The non-centrality parameter for the robust test of association based on
within-pair differences is approximately half the QTL heritability times the degree of linkage disequilibrium
between the QTL and marker, as measured by the squared correlation between the two loci. Necessary sample sizes
for linkage become prohibitively large as QTL heritability decreases, being of the order of several milllion sib-pairs
when QTL heritability is 1%. In contrast, even at this low level of QTL heritability, the necessary sample sizes for
association are feasible when linkage disequilibrium is strong, being of the order of several thousand sib-pairs.
However, there are ways of improving the performance of both tests, including more accurate and repeated
measures, multiple phenotypes, as well as larger and selected sibships. Refs. Fulker DW, Cherny SS, Sham
PC, Hewitt JK (1999) Combined linkage and association sib-pair analysis for quantitative traits. American Journal
of Human Genetics, 64, 259-267 Antisocial behavior (ASB) frequently occurs among individuals who have problems with pathological gambling
(PG), and it has often been assumed that ASB is mainly a result of the PG. We examined the extent to which ASB
and PG share a common familial vulnerability, and the extent to which childhood ASB (that most likely preceded
PG) and adult ASB (that could have occurred prior to, concurrently with, or subsequent to PG) might be
differentially associated with PG. Subjects were 1,874 MZ and 1,498 DZ adult male twin pairs (mean age 44.6
years, range 34-55) from the Vietnam Era Twin Registry. Measures of childhood ASB, adult ASB, and a history of
PG were assessed by structured psychiatric telephone interview. As expected, we found that a diagnosis of
antisocial personality disorder (ASPD) was significantly associated with a lifetime history of PG (r = 0.32, odds
ratio = 3.9). Both childhood ASB (r = 0.26, odds ratio = 2.7) and adult ASB (r = 0.33, odds ratio = 3.4) were
significantly associated with PG. Seventy-four percent of the association between ASPD and PG was familial, and
all of this was accounted for by common genetic risk factors. The overlap between childhood ASB and PG (81%)
and adult ASB and PG (69%) was also predominantly accounted for by common familial risk factors. Most of the
common familial risk for childhood ASB and PG (64%) and adult ASB and PG (100%) was accounted for by
common genetic risk factors. Because PG shared familial risk factors with earlier-occurring ASB as well as
later-occurring ASB, it is unlikely that the association between ASB and PG is completely due to the causal
influence of PG on ASB, at least among men. The results of this study suggest that the co-occurrence of ASB and
PG is predominantly due to their sharing a common familial vulnerability.
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
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
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
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
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
Nathan Brody1
Secular and non-secular change in Intelligence
1 Department of Psychology, Wesleyan University, Middletown, USA
Address: nbrody@mail.wesleyan.edu
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
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
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
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
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/
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
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
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
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
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
V.H Denenberg, and A.J. Stavnezer
Spatial Ability of XY Sex-reversed Female Mice
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)
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
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/
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
A.M. Johnson1, P.A. Vernon1, and K.L. Jang2
Standing tall: The effect of height on heritability estimates of leadership style
1Department of Psychology, University of Western Ontario
2Department of Psychiatry, University of British Columbia
Address: Department of Psychology Social Science Centre The University of Western Ontario, London,
Ontario, N6A 5C2 Tel: 519-680-5997 Fax: 519-661-3961 Email: ajohnson@julian.uwo.ca
Jennifer K. Johnson1, Richard J. Viken1, and Richard J.
Rose1
Genetic and environmental influences on self-reported sensitivity and tolerance to
alcohol2
1Indiana University, Department of Psychology, Bloomington, IN 47405
2Supported by NIAAA grant AA-07611
Address: jennjohn@indiana.edu, 812-855-4101 (ph), 812-855-4691 (fax)
R. Bryan Jones1, Raul H. Marin2
T-maze behavior, growth, sociality and stress in unselected broiler chickens: strategic
implications3
1Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, Scotland
2CRILAR (CONICET), Mendoza y Entre Rios, 5301 Anillaco, La Rioja, Argentina
3Supported by CONICET, University of Cordoba, British Council / CONICOR, and the Biotechnology
and Biological Sciences Research Council, UK
Address: Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, Scotland Phone: ++ 44 131 527
4466; Fax: ++ 44 131 440 0434; E-mail: Bryan.Jones@BBSRC.AC.UK
R. Bryan Jones1
Fear, well-being and productivity in poultry: potential benefits of genetic selection
2
1Roslin Institute (Edinburgh), Roslin, Midlothian EH25 9PS, Scotland
2Supported by the Biotechnology and Biological Sciences Research Council, UK. The following also
contributed to this study: J.M. Faure and A.D. Mills (France), D.G. Satterlee and H.L. Marks (USA)
Address: Roslin Institute, Roslin, Midlothian EH25 9PS, Scotland Phone: ++ 44 131 527 4466; Fax
++ 44 131 440 0434; E-mail: Bryan.Jones@BBSRC.AC.UK
Katherine M. Kirk 1, Andrew C. Heath 2 and Nicholas G. Martin
1
Coffee-related sleep disturbance: a study of Australian twins
1 Queensland Institute of Medical Research, Brisbane Australia 2
Department of Psychiatry, Washington University School of Medicine, St Louis USA
Address: Queensland Institute of Medical Research, Post Office, Royal Brisbane Hospital, Brisbane
QLD 4029 Australia Telephone: +61 7 3362 0272 Facsimile: +61 7 3362 0101 E-mail: kathE@qimr.edu.au
Valerie S. Knopik 1, and John C. DeFries 1
Reading and Mathematics Performance in Twin Pairs With and Without Reading Difficulties
2
1 Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado
80309 2 Supported in part by NICHD grant HD-27802, HD-11681, and NIMH grant MH-16880
Address: Valerie S. Knopik Institute for Behavioral Genetics Campus Box 447 University of Colorado
Boulder, CO 80309 Telephone: 303/492-7362 FAX: 303/492-8063 E-Mail: Valerie.Knopik@Colorado.EDU
Lisa N. Legrand1, Matt McGue1, and William G.
Iacono1
Early Adolescent Substance Use: A Search for Gene-Environment Interactions and an Understanding
of the Contributions of Personality 2
1 University of Minnesota, Minneapolis, Minnesota 55455 2
Supported in part by NIH Grants MH17069, DA05147, and AA09367
Address: Department of Pyschology, University of Minnesota, 75 East River Road, Minneapolis,
Minnesota 55455. E-mail: llegrand@tfs.psych.umn.edu
Kathryn S. Lemery1, Amber Gahagan1, and H. Hill
Goldsmith1
Exploring the etiology of the relationship between temperament and behavior problems with
temperamentally extreme twins
1 University of Wisconsin-Madison
Address: Wisconsin Twin Project, 1202 West Johnson Street, Madison, WI 53706. phone: (608)
265-4946 fax: (608) 265-3649 email: klemery@students.wisc.edu
I. Le Roy1, F. Pérez-Diaz1, M. Navet1, and P.
L. Roubertoux1
Co-detection of quantitative trait loci for cerebellar patterns of foliation and hind limb coordination in
mice2
1 UPR CNRS 9074, Génétique, Neurogénétique,
Comportement, Institut de Transgénose, Institut de Transgénose, 3 B rue de la Ferollerie; 45071,
Orléans Cedex 02, France 2 Supported by CNRS (UPR 9074), Ministry for Research and
Technology, Région Centre and Préfecture de la Région Centre, Fondation pour la
Recherche Médicale. UPR 9074 is affiliated with INSERM and University of Orléans.
Address: Isabelle Le Roy, University of Orleans, Institut de Transgenose, CNRS 3 b rue de la Ferollerie
45071 Orleans cedex 02, France. Phone: 33 2 38 25 79 70, Fax: 33 2 38 25 79 79, e-mail: leroy@cnrs-orleans.fr
J. M. Lessem1, J. K. Hewitt1, L. J. Eaves2, J. L.
Silberg2, M. Rutter3, E. Simonoff3
Life Events and Depressed Mood in the Virginia Twin Study of Adolescent Behavioral
Development4
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO
80309-0447. 2Department of Human Genetics, Medical College of Virginia, Richmond, VA 23298
3MRC Child Psychiatry Unit, Institute of Psychiatry, University of London, London, UK
4Supported by PHS Grant MH45268
Address: University of Colorado Campus Box 447 Boulder, CO 80309-0447 303-492-2843
303-492-8063 (fax) Jeff.Lessem+BGA@Colorado.EDU http://ibgwww.Colorado.EDU/~lessem
Paul Lichtenstein1, D. Reiss2, M. Cederblad 3,
O. Elthammer3, J.M. Neiderhiser2, K. Hansson3, and N.L.
Pedersen1,4
Genetic effects in parental bonding5
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden
2Center for Family Research, The George Washington University, Washington, D.C.
3Department Child and Adolescent Psychiatry, Lund University, Lund, Sweden
4Department of Psychology, University of Southern California 5Supported by NIMH
grant MH-54610
Address: Box 218, SE-171 77 Stockholm. Email: paul.lichtenstein@imm.ki.se, Phone +46 8 728 7424,
Fax: + 46 8 304 571
Paul Lichtenstein1, and M. Reiss Baker2
Telepathy in twins
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden
2 Bess and Paul Sigel Hebrew Academy, Bloomfield, Connecticut
Address: Box 218, SE-171 77 Stockholm. Email: paul.lichtenstein@imm.ki.se, Phone +46 8 728 7424,
Fax: + 46 8 304 571
John C. Loehlin1, Amanda Spurdle2, Nicholas G.
Martin2
Number of CAG repeats in the androgen receptor gene and psychological femininity
1 Department of Psychology, University of Texas, Austin, TX 78712
2 Queensland Institute of Medical Research, Brisbane 4029, Australia
Address: John C. Loehlin, Department of Psychology, University of Texas, Austin, TX 78712; e-mail
loehlin@psy.utexas.edu; telephone (512) 475-4008; fax (512) 471-6175
Pamela A.F. Madden 1, K.K. Bucholz1, A.C.
Heath1, and N.G. Martin2
Heritability of Stages of Cigarette Smoking in Australian Adult Twins3
1Washington University School of Medicine, St. Louis, MO, 63110
2Queensland Institute of Medical Research, Brisbane, Australia 3Supported by NIH
grants AA10249, AA07728 and DA00272
Address: 40 N. Kingshighway, Suite #2, St. Louis, MO 63108; Phone: (314) 286-2286; Fax: (314)
286-2213; E-Mail: pam@matlock.wustl.edu
Nicholas G. Martin 1, John B. Whitfield 2, Dona Pang
2 Katherine M. Kirk 1, and Andrew C. Heath 3
Association of monoamine oxidase (MAO) with smoking, alcohol dependence and other measures of
psychopathology and personality 4
1 Queensland Institute of Medical Research, Brisbane Australia 2
Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Sydney Australia 3 Department of
Psychiatry, Washington University School of Medicine, St Louis USA 4 Supported in part by a grant
from the National Institute for Alcohol Abuse and Alcoholism, AA07535
Address: Queensland Institute of Medical Research, Post Office, Royal Brisbane Hospital, Brisbane
QLD 4029 Australia Telephone: +61 7 3362 0278 Facsimile: +61 7 3362 0101 E-mail: nickM@qimr.edu.au
John J. McArdle1, and John L. Horn2
The use of biometric genetic data to evaluate the structural, kinematic, and dynamic hypotheses of the
theory of "fluid and crystallized intelligence"
1 Department of Psychology, University of Virginia, Charlottesville, VA 22903
2 Department of Psychology, University of Southern California, Los Angeles, CA 96275
1 Supported by NIA grant AG-07137
Address: Psychology, University of Virginia, Charlottesville, VA 22903. 804/924-0656(phone);
804/982-4766(fax); jjm@virginia.edu; http://kiptron.psyc.virginia.edu/jack_mcardle/
Tara L. McLaughlin1, Kathy K. Bucholz1, Pamela
A.F.Madden1, Wendy S. Slutske2, and Andrew C. Heath1
Genetic and environmental influences on behavioral disorder symptom count in adolescent
females3
1Department of Psychiatry, Washington University School of Medicine, St.Louis,
MO 63108 2Department of Psychology, University of Missouri, Columbia 3Supported by
AA09022, AA07728, DA07261, DA00272
Address: 40 N.Kingshighway, Suite 1, Box 8134 St.Louis, MO 63108, USA. Phone:(314) 286-2270.
FAX: (314) 286-2213. e-mail:tara@matlock.wustl.edu
Kari A. Merrill1, Richard J. Viken1, Jaakko Kaprio2,
and Richard J. Rose1
Thinking about drinking: Genetic and environmental influences on alcohol expectancies
1 Department of Psychology, Indiana University 2 National Public
Health Institute, Finland
Address: Department of Psychology Indiana University 1101 E. 10th St. Bloomington, IN 47405-7007
Phone (812) 855-2311 Fax (812) 855-4691 e-mail kamerril@indiana.edu
Michael B. Miller1, and Marc Kayson1
An easy method of linking databases to internet white pages for systematic tracking and identification
of research participants
1Department of Psychology, University of Missouri, Columbia, MO
Address: Michael B. Miller, Department of Psychology, 210 McAlester Hall, University of Missouri,
Columbia, MO 65211 e-mail: mbmiller@taxa.psyc.missouri.edu web: http://taxa.psyc.missouri.edu/~mbmiller/
Charles Murray1
Implications of the secular rise in IQ for convergence of black and white IQ scores
1 American Enterprise Institute, Washington, DC, USA
Address: American Enterprise Institute, 1150 17th Street NW, Washington, DC 20036, USA. Phone
301.834.7425 Fax 301.834.9421 Email chasmurray@earthlink.net
Jenae M. Neiderhiser1, Erica Spotts1, Paul
Lichtenstein2, Nancy Pedersen2,4, Kjell Hansson3, Marianne
Cederblad3, Olle Elthammer 3, and David Reiss1
The association between mothering and marital relationships: is it all in the genes?5
1Center for Family Research, George Washington University, Washington, DC
20037 2Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden
3 Department of Child & Youth Psychiatry, Lund University, Lund, Sweden 4 University
of Southern California 5Supported by grant R01MH54610 from the National Institute of Mental
Health
Address: 2300 Eye St., N.W., Room 613 Ross Hall. Email: cfrjmn@gwumc.edu, Phone 202.994.2212,
Fax: 202.994.4812
Ulric Neisser1
The secular rise in intelligence: Many gains, many causes
1 Cornell University
Address: Department of Psychology, Cornell University, Ithaca NY 14853 (un13@cornell.edu) 607
255 6355
Helmuth Nyborg1
Secular changes in longitudinal IQ: Individual and group differences
1 PNE Research Center, Institute of Psychology, University of Aarhus, Denmark
Address: PNE Research Center, Institute of Psychology, Asylvej 4, DK-8240 Risskov, Denmark. Phone
45* 8942 4900, Fax 45* 8942 4901, email helmuth@psy.au.dk
Naoko Onoda11, Y. Ono2, and J. Ando3
Genetic and environmental influence on parenting in Japanese population
1Department of Medical Science, Keio University Graduate School, Tokyo
2 Department of Psychiatry and Neuroscience, Keio University of Medicine, Tokyo 3
Department of Education, Faculty of Letters, Keio University, Tokyo
Address: 35 Shinanomachi Sinjuku-ku Tokyo, 160-8582 tel.03-3353-1211(2453) fax.03-5379-0187
e-mail address naoko-o@mc.med.keio.ac.jp
N.L. Pedersen 1,2, E.L. Spotts 3, M. Cederblad 4,
P. Lichtenstein 1, K. Hansson 4, J.M. Neiderhiser 3, O. Elthammar
4, and D. Reiss 3
Lack of effect of intra-pair contact and aspirations to be similar on twin similarity for personality,
marital adjustment, and parenting 5
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden,
2Department of Psychology, University of Southern California, Los Angeles, 3Center for
Family Research, The George Washington University, Washington, D.C. 4Department of Child and
Adolescent Psychiatry, Lund University, Lund, Sweden, 5Supported by NIMH grant MH-54610
Address: Box 281, SE-171 77 Stockholm. Email: Nancy.Pedersen@imm.ki.se, Phone +46 8 728 7418,
Fax: + 46 8 30 45 71
Daniel Pérusse1, R E. Tremblay1, M.
Boivin2, and B. Boulerice1
Early motor-cognitive development: A study of 5-month-old twins3
1 Research Unit on Children's Psycho-Social Maladjustment, University of
Montreal, Montreal, Canada. 2 Research Unit on Children's Psycho-Social Maladjustment, Laval
University, Quebec City, Canada. 3 Supported by grants to the first author from the Medical Research
Council of Canada, the National Health Research and Development Program/Health Canada, the Social Sciences
and Humanities Research Council of Canada, the Fonds de la recherche en sante du Quebec, and the Quebec
Ministry of Health and Social Services
Address: Fernand-Seguin Research Center, University of Montreal, 7331 Hochelaga, Montreal,
Canada, H1N 3V2, Tel. (514) 251-4015 ext. 2352, Fax: (514) 251-2617, email: Daniel.Perusse@umontreal.ca
Michael F. Pogue-Geile1,2, S.B. Manuck,1,2 T.
Kamarck,1,2 & T. Debski1
Cardiovascular reactivity to psychological stress: A twin study3
1 Department of Psychology, University of Pittsburgh, Pittsburgh, PA
2 Department of Psychiatry, University of Pittsburgh 3 Supported in part by NIH
HL40962
Address: Department of Psychology 4015 O'Hara St. University of Pittsburgh Pittsburgh, PA, 15260,
USA tel: 412.624.8818 fax: 412.624.5407 mfpg@pop.pitt.edu
Clare Porac11
Variation in human hand preference patterns: Effects of age and pressures to switch
side2
1 Department of Psychology, University of Victoria, Victoria, BC V8W 3P5
Canada 2 Supported by grants from the Natural Sciences and Engineering Research Council and the
University of Victoria Centre on Aging, the David and Dorothy Lam Endowment
Address: P.O. Box 3050, Department of Psychology, University of Victoria, Victoria, BC V8W 3P5
Canada, Phone: (250) 721-7537, Fax: (250) 721-8929
Danielle Posthuma 1, G.Caroline M. van Baal1, Eco J.C. de
Geus1, Harold Snieder2, Dorret I. Boomsma1
Association between apoE genotype, apoE-levels and cognitive performance
1 Department of Biological Psychology, Vrije Universiteit, Amsterdam, The
Netherlands 2 Twin Research and Genetic Epidemiology, St. Thomas Hospital, London, UK
Address: D. Posthuma Vrije Universiteit Department of Biological Psychology De Boelelaan 1111
1081 HV Amsterdam The Netherlands Phone: +31 20 4448814 Fax: +31 20 4448832 e-mail: danielle@psy.vu.nl
Danielle Posthuma 1, and Dorret I. Boomsma1
Adding non-twin siblings to increase power
1 Department of Biological Psychology, Vrije Universiteit, Amsterdam, The
Netherlands
Address: D. Posthuma Vrije Universiteit Department of Biological Psychology De Boelelaan 1111
1081 HV Amsterdam The Netherlands Phone: +31 20 4448814 Fax: +31 20 4448832 e-mail: danielle@psy.vu.nl
Carol A. Prescott1, Steven H. Aggen1, and Kenneth S.
Kendler1
A twin study of the sources of comorbidity between alcoholism and major
depression2
1 Virginia Institute for Psychiatric & Behavioral Genetics, Department of
Psychiatry, Virginia Commonwealth University, Richmond VA 23298 2 Supported by NIH grants
R01-MH/AA-49492, R01-AA/DA-09095, and K01-AA-00236
Address: VIPBG, MCV/VCU, P.O. Box 980126, Richmond VA 23298-0126. 804/828-5968(phone);
804/828-1471(fax); cprescott@gems.vcu.edu; http://www.vipbg.vcu.edu/vipbg/
Shaun Purcell1, Stacey S. Cherny2, and Pak C.
Sham1
Selecting maximally informative sibships for QTL association analysis
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of
Psychiatry, De Crespigny Park, Denmark Hill, London, SE5 8AF, United Kingdom 2Institute for
Behavior Genetics, University of Colorado, Boulder, CO 80309-0447 1,2Supported in part by a
Programme Project grant from the Medical Research Council of Great Britain
Address: Social, Genetic & Developmental Psychiatry Research Centre, 111 Denmark Hill, London
SE5 8AF. Tel: +44 (0) 171 740 5267 Fax: +44 (0) 171 919 3866 e-mail: s.purcell@iop.kcl.ac.uk
Soo Hyun Rhee1, and Irwin D. Waldman1
Etiology of sex differences in inattention and hyperactivity/impulsivity2
1Department of Psychology, Emory University, Atlanta, GA 30322
2Supported by NIMH National Research Service Award 1 F31 MH11772-01
Address: Department of Psychology, Emory University, Atlanta, GA 30322. Phone: (573) 442-3890.
Fax: (404) 727-0372. e-mail: srhee01@emory.edu
Jeffrey Rogers1
Genetic linkage mapping in primates as a tool in behavior genetics
1 Dept. of Genetics, Southwest Foundation for Biomedical Research, San Antonio,
Texas
Address: Dept. of Genetics, Southwest Foundation, P.O. Box 760549, San Antonio, TX 78245-0549
phone 210-258-9532 fax 210-670-3316 email jrogers@darwin.sfbr.org
Pierre L. Roubertoux1, I. Le Roy1, S. Mortaud1,
and S. Tordjman1
Attack behavior in mice: Implication of the Sts gene mapped on the pairing region of the X-Y
chromosomes
1 UPR CNRS 9074, Génétique, Neurogénétique,
Comportement, Institut de Transgénose, Institut de Transgénose, 3 B rue de la Ferollerie; 45071,
Orléans Cedex 02, France. Supported by CNRS (UPR 9074), Ministry for Research and Technology,
Région Centre and Préfecture de la Région Centre. UPR 9074 is affiliated with INSERM
and University of Orléans
Address: Phone: 33 2 38 25 79 70, Fax: 33 2 38 25 79 79, E-mail: rouber@cnrs-orleans.fr
Pierre L. Roubertoux1, and Isabelle Le Roy1
QTL mapping: A fundamental tool in behavioral neurogenetics 2
1 UPR CNRS 9074, Génétique, Neurogénétique,
Comportement, Institut de Transgénose, Institut de Transgénose, 3 B rue de la Ferollerie; 45071,
Orléans Cedex 02, France 2 Supported by CNRS (UPR 9074), Ministry for Research and
Technology, Région Centre and Préfecture de la Région Centre, Fondation pour la
Recherche Médicale. UPR 9074 is affiliated with INSERM and University of Orléans
Address: Pierre L. Roubertoux University of Orleans Director UPR 9074 CNRS Genetique,
Neurogenetique, Comportement Institut de Transgenose CNRS 3 b rue de la Ferollerie 45071 Orleans cedex 02,
France Phone: 33 2 38 25 79 70, Fax: 33 2 38 25 79 79, E-mail: rouber@cnrs-orleans.fr
David C. Rowe 1, and Irwin B. Waldman 2
Genetic Influences on Childhood Disruptive Disorder Symptoms Estimated Through Measured and
Latent Genetic Variables in Full Siblings
1 Graduate Program in Genetics and Family Studies, University of Arizona,
Tucson, AZ 85721. 2 Department of Psychology, Emory University, 532 North Kilgo Circle, Atlanta,
Georgia 30322
Address: School of Family and Consumer Resources, 1110 E. South Campus Dr., University of
Arizona, Tucson, AZ 85721. dcr091@ag.arizona.edu.
Espen Røysamb1, Jennifer R. Harris1, and Kristian
Tambs1
What is self-rated health about after all? Genetic and environmental contributions to the associations
between subjective well-being, health symptoms, health behaviours and self-rated health
1 National Institute of Public Health, Oslo, Norway
Address: National Institute of Public Health, P.O.Box 4404 Torshov, 0403 Oslo, Norway. Phone: +47
22 04 25 69. Fax: +47 22 04 23 51. Email: espen.roysamb@psykologi.uio.no
J. Philippe Rushton1
Performance on Raven's Matrices by African and White University Students in South Africa(with a
possible note on African g and the Flynn Effect)
1Department of Psychology, University of Western Ontario, London, Ontario,
Canada N6A 5C2
Address: Department of Psychology, University of Western Ontario, London, Ontario, Canada N6A
5C2. Phone: 519-661-3685; Fax: 519-850-2302; email: rushton@julian.uwo.ca
Joanne Ruthsatz1, R.D. Tiu1, L.A. Thompson1, and
D.K. Detterman1
The genetic influence on primary athletic ability and athletic ability's relationship with
intelligence
1Case Western Reserve University
Address: Joanne Ruthsatz Department of Psychology Case Western Reserve University Cleveland,
Ohio 44106 (216)368-6670 jxr@po.cwru.edu
Gerard Saucier1, Paul F. Collins1, David E.
Comings2, Nancy Gonzalez2, Donn Muhleman2, and James P.
MacMurray3
Novelty-Seeking and Harm-Avoidance: A Molecular-Genetic Test of Cloninger's Dopamine and
Serotonin Hypotheses4
1Department of Psychology, University of Oregon, Eugene, OR 97403
2Department of Medical Genetics, City of Hope Medical Center, Duarte, CA 91010
3Department of Psychiatry, Loma Linda University School of Medicine, Loma Linda, CA 92357
4Supported by NIDA grant R01-DA08417 and TRRDP grant 4RT-0110
Address: Gerard Saucier, Department of Psychology, 1227 University of Oregon, Eugene OR
97403-1227, tel. 541-346-4927, fax 541-346-4911, email gsaucier@oregon.uoregon.edu
Stephanie Schmitz1, and Kimberly J. Saudino2
Links between temperament and behavior problems -- why do the results depend on the
sample?3
1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO
80309-0447 2 Psychology Department, Boston University, Boston, MA 02215
3Supported by NIH grants HD 18426 and MH 43899 and a grant from the John D. and Catherine T.
MacArthur Foundation
Address: Institute for Behavioral Genetics, University of Colorado, Campus box 447, CO 80309-0447
telephone: (303) 492-0835 fax: (303) 492-8063 email: schmitzs@colorado.edu
Nancy L. Segal1
Intellectual resemblance of same-age unrelated siblings: New findings2
1Psychology Department, California State University, Fullerton, California 92834
2Supported by the National Science Foundation (SBR-9712875) and a faculty research award from
California State University, Fullerton
Address: Psychology Department, California State University, Fullerton, California 92834.
714-278-2142, 714-278-4843, nsegal@fullerton.edu
Pak C. Sham1, Stacey S. Cherny2, and John K. Hewitt2
Power of QTL linkage and association analysis
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of
Psychiatry, De Crespigny Park, Denmark Hill, London, SE5 8AF, United Kingdom 2Institute for
Behavior Genetics, University of Colorado, Boulder, CO 80309-0447 Supported in part by a Programme Project
grant from the Medical Research Council of Great Britain
Address: Pak Sham SGDP Research Centre Institute of Psyciatry De Crespigny Park London SE5 8AF
Phone: +44 171 919 3534 Email: p.sham@iop.kcl.ac.uk
Wendy S. Slutske1, Seth A. Eisen2,3, Hong Xian2,3,
William R.True2,4, Michael J. Lyons5,6, Jack Goldberg7,8, and Ming T.
Tsuang6
The association between antisocial behavior and pathological gambling9
1 Department of Psychology, University of Missouri, Columbia, MO 65211
2 Research Service, St. Louis Department of Veterans Affairs Medical Center, St. Louis, MO, 63106
3 Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, 63110
4 School of Public Health, St. Louis University, St. Louis, MO, 63108. 5 Department of
Psychology, Boston University, Boston, MA, 02215 6 Department of Psychiatry, Harvard Medical
School and Harvard Institute of Psychiatric Epidemiology and Genetics, Boston, MA, 02115 7
Department of Epidemiology , University of Illinois School of Public Health, Chicago, IL, 60612 8
Department of Veterans Affairs, Health Services Research and Development Service, Hines, IL, 60141
9 Supported by the Department of Veterans Affairs Health Services Research and Development
Service (CSP #992), NIH grants DA04604, AA00264, AA10339, AA11822, and the Great Lakes Veterans Affairs
Health Services Research and Development Program (LIP 41-065)
Address: Department of Psychology, University of Missouri, 210 McAlester Hall, Columbia, MO
65211 phone: (573) 882-4043 fax: (573) 882-7710 email: wendy@martha.psyc.missouri.edu