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Comparative Study
, 39 (3), 497-505

A Population-Based Twin Study of Functional Somatic Syndromes

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Comparative Study

A Population-Based Twin Study of Functional Somatic Syndromes

K Kato et al. Psychol Med.

Abstract

Background: The mechanisms underlying the co-occurrence of the functional somatic syndromes are largely unknown. No empirical study has explicitly examined how genetic and environmental factors influence the co-morbidity of these syndromes. We aimed to examine how the co-morbidity of functional somatic syndromes is influenced by genetic and environmental factors that are in common to the syndromes.

Method: A total of 31318 twins in the Swedish Twin Registry aged 41-64 years underwent screening interviews via a computer-assisted telephone system from 1998 to 2002. Four functional somatic syndromes (chronic widespread pain, chronic fatigue, irritable bowel syndrome, and recurrent headache) and two psychiatric disorders (major depression and generalized anxiety disorder) were assessed using structured questions based on standard criteria for each illness in a blinded manner.

Results: Multivariate twin analyses revealed that a common pathway model with two latent traits that were shared by the six illnesses fit best to the women's data. One of the two latent traits loaded heavily on the psychiatric disorders, whereas the other trait loaded on all four of the functional somatic syndromes, particularly chronic widespread pain, but not on the psychiatric disorders. All illnesses except the psychiatric disorders were also affected by genetic influences that were specific to each.

Conclusions: The co-occurrence of functional somatic syndromes in women can be best explained by affective and sensory components in common to all these syndromes, as well as by unique influences specific to each of them. The findings clearly suggest a complex view of the multifactorial pathogenesis of these illnesses.

Figures

Figure 1
Figure 1
Examples of models for underlying structures of comorbidities (multivariate AE models). A: additive genetic factors; E: nonshared environmental factors. L: latent factor. Factors with a subscript “u” are unique to each syndrome. For simplicity, only one twin of a pair is shown and shared environmental factors are excluded.
Figure 1
Figure 1
Examples of models for underlying structures of comorbidities (multivariate AE models). A: additive genetic factors; E: nonshared environmental factors. L: latent factor. Factors with a subscript “u” are unique to each syndrome. For simplicity, only one twin of a pair is shown and shared environmental factors are excluded.
Figure 1
Figure 1
Examples of models for underlying structures of comorbidities (multivariate AE models). A: additive genetic factors; E: nonshared environmental factors. L: latent factor. Factors with a subscript “u” are unique to each syndrome. For simplicity, only one twin of a pair is shown and shared environmental factors are excluded.
Figure 1
Figure 1
Examples of models for underlying structures of comorbidities (multivariate AE models). A: additive genetic factors; E: nonshared environmental factors. L: latent factor. Factors with a subscript “u” are unique to each syndrome. For simplicity, only one twin of a pair is shown and shared environmental factors are excluded.
Figure 2
Figure 2
Best-fit (2-factor common pathway) model with age-adjusted, standardized parameter estimates for the 6 illnesses in women aged 41–64. A: additive genetic factors; E: nonshared environmental factors. Factors with a subscript “u” are unique to each illness. L1, L2: latent factors. MD: major depression. GAD: generalized anxiety disorder. IBS: irritable bowel syndrome. CF: chronic impairing fatigue. CWP: chronic widespread pain. The total variances of L1 and L2 as well as each variable were fixed at 1. Non-significant paths were dropped from the model. For simplicity, only one twin of a pair is shown.

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