What might be the biological mechanism underpinning our observed relationship? One possible explanation may be due to the long-term neuroendocrine dysfunction beginning in the early life of some individuals.
The CWP [Chronic widespread pain] is known to be characterized by sensitization of central pain pathways, with lowered pain threshold and increased levels of psychological distress. The hypothalamicpituitaryadrenal (HPA) axis, the primary neuroendocrine stress response system, has been demonstrated to be associated with childhood behaviour [29].
Similarly, altered HPA axis function has been reported to be associated with CWP [30]. Interestingly, a recent study has also demonstrated a role of HPA pathway genes in the susceptibility of developing musculoskeletal pain [31].
Together with previous findings, we hypothesize that a long-term HPA axis dysfunction, as a potential mediator, may be the mechanism linking childhood behaviour problems and CWP in adulthood, in particular, among individuals with persistent (chronic) behaviour problems in childhood. But future molecular/genetic studies are required to clarify this.
The observed association with childhood behaviour, however, is not specific to CWP. Adolescents with behavioural and conduct disorders have been found to be associated with a variety of other somatic functioning disorders in adult life in addition to the association with CWP which we reported here.
These include poor long-term psychiatric outcomes in adult life [13, 32], such as depression and anxiety [3339], suicidal behaviour [33, 35], substance abuse and being treated for psychiatric illness [32], particularly in this population [40].
Childhood behaviour problems may lead to the above proposed common pathway of a long chain of mutable events and CWP may be one of the outcomes of such a pathway.
