Genetic Epidemiology, Translational Neurogenomics, Psychiatric Genetics and Statistical Genetics Laboratories investigate the pattern of disease in families, particularly identical and non-identical twins, to assess the relative importance of genes and environment in a variety of important health problems.
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PMID
11665341
TITLE
A twin study of the etiology of prolonged fatigue and immune activation.
ABSTRACT
Risk factors to prolonged fatigue syndromes (PFS) are controversial. Pre-morbid and/or current psychiatric disturbance, and/or disturbed cell-mediated immunity (CMI), have been proposed as etiologic factors. Self-report measures of fatigue and psychologic distress and three in vitro measures of CMI were collected from 124 twin pairs. Crosstwin-crosstrait correlations were estimated for the complete monozygotic (MZ; 79 pairs) and dizygotic (DZ; 45 pairs) twin groups. Multivariate genetic and environmental models were fitted to explore the patterns of covariation between etiologic factors. For fatigue, the MZ correlation was more than double the DZ correlation (0.49 versus 0.16) indicating strong genetic control of familial aggregation. By contrast, for in vitro immune activation measures MZ and DZ correlations were similar (0.49-0.69 versus 0.42-0.53) indicating the etiologic role of shared environments. As small univariate associations were noted between prolonged fatigue and the in vitro immune measures (r = -0.07 to -0.12), multivariate models were fitted. Relevant etiologic factors included: a common genetic factor accounting for 48% of the variance in fatigue which also accounted for 4%, 6% and 8% reductions in immune activation; specific genetic factors for each of the in vitro immune measures; a shared environment factor influencing the three immune activation measures; and, most interestingly, unique environmental influences which increased fatigue but also increased markers of immune activation. PFS that are associated with in vitro measures of immune activation are most likely to be the consequence of current environmental rather than genetic factors. Such environmental factors could include physical agents such as infection and/or psychologic stress.
DATE PUBLISHED
2001 Apr
HISTORY
PUBSTATUS PUBSTATUSDATE
pubmed 2001/10/23 10:00
medline 2002/01/05 10:01
entrez 2001/10/23 10:00
AUTHORS
NAME COLLECTIVENAME LASTNAME FORENAME INITIALS AFFILIATION AFFILIATIONINFO
Hickie IB Hickie I B IB School of Psychiatry, University of New South Wales, Sydney, Australia. i.hickie@unsw.edu.au
Bansal AS Bansal A S AS
Kirk KM Kirk K M KM
Lloyd AR Lloyd A R AR
Martin NG Martin N G NG
INVESTIGATORS
JOURNAL
VOLUME: 4
ISSUE: 2
TITLE: Twin research : the official journal of the International Society for Twin Studies
ISOABBREVIATION: Twin Res
YEAR: 2001
MONTH: Apr
DAY:
MEDLINEDATE:
SEASON:
CITEDMEDIUM: Print
ISSN: 1369-0523
ISSNTYPE: Print
MEDLINE JOURNAL
MEDLINETA: Twin Res
COUNTRY: Australia
ISSNLINKING: 1369-0523
NLMUNIQUEID: 9815819
PUBLICATION TYPE
PUBLICATIONTYPE TEXT
Journal Article
Twin Study
COMMENTS AND CORRECTIONS
GRANTS
GENERAL NOTE
KEYWORDS
MESH HEADINGS
DESCRIPTORNAME QUALIFIERNAME
Age Factors
Analysis of Variance
Diseases in Twins genetics
Environment genetics
Fatigue Syndrome, Chronic immunology
Female immunology
Humans immunology
Immunity, Cellular immunology
Male immunology
Risk Factors immunology
Sex Factors immunology
Stress, Psychological complications
Time Factors complications
SUPPLEMENTARY MESH
GENE SYMBOLS
CHEMICALS
OTHER ID's