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Genetic and environmental influences on expression of recurrent headache as a function of the reporting age in twins.
Author(s) -
Svensson DA,
Larsson B,
Waldenlind E,
Pedersen NL
Publication year - 2003
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1046/j.1526-4610.2003.03085_5.x
Subject(s) - twin study , demography , migraine , analysis of variance , medicine , environmental effect , young adult , age groups , pediatrics , heritability , biology , genetics , ecology , sociology , environmental impact assessment
Twin Res. 2002;5:277‐286. To explore age‐related mechanisms in the expression of recurrent headache, we evaluated whether genetic and environmental influences are a function of the reporting age using questionnaire information that was gathered in 1973 for 15‐ to 47‐year‐old Swedish twins (n = 12,606 twin pairs). Liability to mixed headache (mild migraine and tension‐type headache) was explained by non‐additive genetic influences (49%) in men aged from 15 to 30 years and additive genetic plus shared environmental influences (28%) in men aged from 31 to 47 years. In women, the explained proportion of variance, which was mainly due to additive genetic effects, ranged from 61% in adolescent twins to 12% in twins aged from 41 to 47 years, whereas individual specific environmental variance was significantly lower in twins aged from 15 to 20 years than in twins aged from 21 to 30 years. Liability to migrainous headache (more severe migraine) was explained by non‐additive genetic influences in men, 32% in young men and 45% in old men, while total phenotypic variance was significantly lower in young men than in old men. In women, the explained proportion of variance ranged from 91% in the youngest age group to 37% in the oldest age group, with major contributions from non‐additive effects in young and old women (15‐20 years and 41‐47 years, respectively) and additive genetic effects in intermediate age groups (21‐40 years). While total variance showed a positive age trend, genetic variance tended to be stable across age groups, whereas individual specific environmental variance was significantly lower in adolescent women as compared to older women. Comment: Does this mean that most of the genetic contribution to headache in women is likely to occur during adolescence, which would be in agreement with the peak incidence? Some clinical interpretation would be helpful here. DSM