Background Disrupted pain regulation has been proposed as a component in functional somatic disorders (FSD). The objective of this study was to examine a general population sample, encompassing three delimitations of FSD while assessing pain sensitivity and conditioning pain modulation (CPM). Methods Pressure pain thresholds (PPTs) at the tibialis and trapezius muscles were recorded at baseline. During cold pressor stimulation of the hand, the tibialis PPTs were re-assessed and the difference from baseline measures defined the CPM effect. Participants (n = 2,198, 53% females) were randomly selected from the adult Danish population. FSD was established by self-reported symptom questionnaires. Results With a few exceptions, only weak associations were seen between PPTs and CPM in cases with FSD (p > .1). A high PPT was associated with lower odds of having multi-organ bodily distress syndrome (ORPPT trapezius: 0.66, 95% CI: 0.49-0.88, p = .005), with the symptom profile characterized by all symptoms (ORPPT trapezius: 0.72, 95% CI: 0.58-0.90, p = .003 and ORPPT tibialis: 0.75, 95% CI: 0.62-0.91, p = .004), and with multiple chemical sensitivity (ORPPT trapezius: 0.81, 95% CI: 0.67-0.97, p = .022). High CPM was associated with high odds of having irritable bowel (ORCPM relative: 1.22, 95% CI: 1.04-1.43, p = .013 and ORCPM absolute = 2.66, 95% CI: 1.07-6.45, p = .033). Conclusion However, only PPT measured over the trapezius muscle were still significant after correction for multiple testing for the symptom profile characterized by all symptoms. Findings from this study do not support altered pain regulation in questionnaire-based FSD which is in contrast with the existing presumption. Further epidemiological studies in this field are needed. Significance Disrupted pain regulation as measured by abnormal pain thresholds has been hypothesized as a central mechanism in Functional Somatic Disorders (FSD). The hypothesis has been raised in clinical setting where patients presented subjective and objective features of hypersensitivity. The present population-based study does not support this notion. This points to the importance of further studies into the underlying pathophysiology mechanisms of FSD.