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.

Associations between CWP and most comorbidities are mediated by unmeasured genetic and family environmental factors in the general population. The extent of mediation via familial factors is likely to be disorder specific.

Objective. To estimate the relative importance of genetic and environmental factors in chronic widespread pain, and to assess whether there are sex differences in the type or magnitude of these influences.Methods. Data were collected from a national sample of twins >42 years of age, all of whom were participants in the Swedish Twin Registry. The presence of chronic widespread pain was assessed via computerassisted telephone interviews, which were conducted between 1998 and 2002, using the American College of Rheumatology criteria for fibromyalgia. No clinical examinations were performed. In preliminary analyses, probandwise concordance rates and tetrachoric correlations were calculated. Structural equation modeling was then performed to estimate additive genetic, shared environmental, and nonshared environmental sources of variability in susceptibility for the development of chronic widespread pain.Results. Of 61,355 eligible twins, 44,897 individuals (73.2%) responded to the interview. Both members of 15,950 pairs responded to the items regarding pain symptoms; of these pairs, 4,170 were monozygotic, 5,881 were same-sex dizygotic, and 5,755 were opposite-sex dizygotic. The prevalence of chronic widespread pain was 4.1%, and the ratio of women to men was 3.3 to 1. Probandwise concordance rates and tetrachoric correlations suggested modest genetic influences for both women and men. Genetic and shared environmental influences explained approximately half of the total variance, with no indication of sex differences in either the type or magnitude of these influences.Conclusion. Individual differences in the likelihood of developing chronic widespread pain reflect modest genetic influences. There are no significant sex differences in the type or expression of the genes responsible for chronic widespread pain or in the magnitude of the relative importance of these influences on chronic widespread pain.Fibromyalgia is a chronic disorder that is characterized by widespread pain and tenderness at specific body locations. The prevalence of fibromyalgia is relatively high (estimates of the prevalence in the general population range from 0.66% to 3.3%), and the difference in prevalence between men and women is consistent and striking (1). The etiology of fibromyalgia (or its cardinal symptom, chronic widespread pain), including the relative importance of genetic factors, is poorly understood.In a few studies, familial aggregation of fibromyalgia was observed (2-4). First-degree relatives of probands with fibromyalgia have an 8.5-fold elevated risk of the disorder, compared with first-degree relatives of probands with rheumatoid arthritis (2). None of these studies could disentangle genetic and shared family environmental sources of variation in liability. No studies have demonstrated familial risk of chronic widespread pain in adults. When twin studies are sufficiently large, they are well suited to quantify the relative importance of these influences.The present study was based on the Swedish Twin Registry, which is the l...

Elevated premorbid stress is a significant risk factor for chronic fatigue-like illness, the effect of which may be buffered by genetic influences. Emotional instability assessed 25 years earlier is associated with chronic fatigue through genetic mechanisms contributing to both personality style and expression of the disorder. These findings suggest plausible mechanisms for chronic fatiguing illness.