title: Genetic and environmental contributions to hay fever among young adult twins.
abstract: BACKGROUND
  The susceptibility to develop hay fever is putatively the result both of genetic and environmental causes. We estimated the significance and magnitude of genetic and environmental contributions to hay fever among young adult twins.
  
  
  METHODS
  From the birth cohorts 1953-82 of The Danish Twin Registry 11,750 twin pairs were identified through a nationwide questionnaire survey. Subjects were regarded hay fever cases when responding affirmatively to the question 'Do you have, or have you ever had hay fever?' Latent factor models of genetic and environmental effects were fitted to the observed data using maximum likelihood methods.
  
  
  RESULTS
  The overall cumulative prevalence of hay fever was 12.6%. Identical twins were significantly more likely to be concordant for hay fever than were fraternal twins (P<0.001). Additive genetic effects accounted for 71% and non-shared environmental effects accounted for 29% of the individual susceptibility to hay fever. The same genes contributed to the susceptibility to hay fever both in males and in females. In families with asthma, the susceptibility to develop hay fever was, in addition to genes, to a great extent ascribable to family environment, whereas the aetiology of 'sporadic' hay fever was mainly genetic.
  
  
  CONCLUSIONS
  The susceptibility to develop hay fever is attributable to major genetic influences. However, effects of family environment and upbringing are also of importance in families where asthma is present. These results indicate that different sub-forms of hay fever may have different aetiologies.
authors.affiliation: Department of Respiratory Medicine, Bispebjerg Hospital, DK-2400 Copenhagen NV, and The Danish Twin Registry, University of Southern Denmark, Odense, Denmark. sft@city.dk
authors.forename: Simon Francis
authors.initials: SF
authors.lastname: Thomsen
authors.forename: Charlotte Suppli
authors.initials: CS
authors.lastname: Ulrik
authors.forename: Kirsten Ohm
authors.initials: KO
authors.lastname: Kyvik
authors.forename: Jacob
authors.initials: J
authors.lastname: von Bornemann Hjelmborg
authors.forename: Lars Rauff
authors.initials: LR
authors.lastname: Skadhauge
authors.forename: Ida
authors.initials: I
authors.lastname: Steffensen
authors.forename: Vibeke
authors.initials: V
authors.lastname: Backer
mesh_terms: D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000150:complications / Q000453:epidemiology / Q000235:genetics; D002648:Child; D003718:Denmark / Q000453:epidemiology; D004200:Diseases in Twins / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics; D004781:Environmental Exposure / Q000009:adverse effects; D005192:Family Health; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D008297:Male; D011159:Population Surveillance / Q000379:methods; D015995:Prevalence; D006255:Rhinitis, Allergic, Seasonal / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics; D017678:Sex Distribution; D014429:Twins, Dizygotic / Q000235:genetics; D014430:Twins, Monozygotic / Q000235:genetics