To assess longitudinal changes in genetic and environmental influences on Type D personality and its subcomponents negative affectivity (NA) and social inhibition (SI) over a 9-year period. Most personality constructs have good retest reliability over long periods, with stability attributed to genes, and changes to environmental factors. Type D personality is stable across an 18-month period and is influenced by genetic factors. However, there is no knowledge on long-term stability, and the contributions of genes and environment to that stability.
Type D personality was determined from survey data collected in 1991 (n = 3235; mean age = 17.3 years), 1997 (n = 3133; mean age = 25.3 years), and 2000 (n = 4456; mean age = 29.6 years) in a population sample of healthy twins. Multivariate structural equation modeling was employed.
Type D heritability ranged from 50% in 1997 to 34% in 2000, with the same genetic factor affecting Type D at all time points. Heritability of SI ranged from 49% (1991) to 42% (2000), with the same genetic factor influencing SI at all times. Heritability estimates for NA ranged from 45% (1991) to 40% (2000), with one genetic factor influencing NA at all times, and one genetic factor influencing NA at the second and third occasions. Different environmental factors acted on Type D, NA, and SI at each of the three measurement occasions.
Type D personality and both subcomponents are stable over time, which is largely due to genetic factors. Different unique environmental factors influence the Type D components at different occasions.
A = additive genetic variance; C = common or shared environmental variance; D = dominance genetic variance; DZ = dizygotic; E = unique or nonshared environmental variance; GWAS = genome-wide association study; MZ = monozygotic; NA = negative affectivity; SI = social inhibition; SNP = single nucleotide polymorphism.
From the CoRPS-Center of Research on Psychology in Somatic Diseases (N.K., J.D.), Tilburg University, Tilburg, Netherlands; and the Department of Biological Psychology (D.I.B., E.J.C.d.G., G.W.), VU University Amsterdam, Amsterdam, Netherlands.
Address correspondence and reprint requests to Nina Kupper, PhD, CoRPS-Center of Research on Psychology in Somatic Diseases, Department of Medical Psychology and Neuropsychology, Tilburg University, Warandelaan 2, 5037 AB Tilburg, Netherlands. E-mail: email@example.com
This work was supported, in part, by Grant NWO 985–10-002 (D.I.B.) and VICI Grant NWO 453–04-004 (J.D.) from the Netherlands Organization for Scientific Research, The Hague, Netherlands.
Received for publication November 18, 2009; revision received August 19, 2010.