Clinical and evoked pain, personality traits, and emotional states: can familial confounding explain the associations?

OBJECTIVES: Pain is a complex phenomenon influenced by context and person-specific factors. Affective dimensions of pain involve both enduring personality traits and fleeting emotional states. We examined how personality traits and emotional states are linked with clinical and evoked pain in a twin sample. METHODS: 99 female twin pairs were evaluated for clinical and evoked pain using the McGill Pain Questionnaire (MPQ) and dolorimetry, and completed the 120-item International Personality Item Pool (IPIP), the Positive and Negative Affect Scale (PANAS), and ratings of stress and mood. Using a co-twin control design we examined a) the relationship of personality traits and emotional states with clinical and evoked pain and b) whether genetics and common environment (i.e. familial factors) may account for the associations. RESULTS: Neuroticism was associated with the sensory component of the MPQ; this relationship was not confounded by familial factors. None of the emotional state measures was associated with the MPQ. PANAS negative affect was associated with lower evoked pressure pain threshold and tolerance; these associations were confounded by familial factors. There were no associations between IPIP traits and evoked pain. CONCLUSIONS: A relationship exists between neuroticism and clinical pain that is not confounded by familial factors. There is no similar relationship between negative emotional states and clinical pain. In contrast, the relationship between negative emotional states and evoked pain is strong while the relationship with enduring personality traits is weak. The relationship between negative emotional states and evoked pain appears to be non-causal and due to familial factors.

Adverse childhood experiences, health perception, and the role of shared familial factors in adult twins.

To examine the relationship between adverse childhood experiences (ACE) and health perception in adulthood, and to explore the contribution of shared familial factors to these associations. Data were collected from 180 female twins (90 pairs) from the community-based University of Washington Twin Registry. Participants completed questionnaires including the modified ACE Questionnaire, Traumatic Life Events Questionnaire, McGill Pain Questionnaire-Short Form, and the SF-36. Mixed effects linear regression modeling investigated the effects of ACE on indices of health perception controlling for correlated twin data. Additional models examined the associations while controlling for the experience of physical and/or sexual abuse in childhood; within-twin pair models that inherently adjust for familial factors explored shared familial influences. After controlling for relevant demographic variables, more ACE was associated with worse perceptions of general health (p=.01) and vitality (p=.05) on the SF-36. After controlling for childhood physical and/or sexual abuse, the relationship between ACE and general health remained significant (p=.01) while vitality was no longer significant. None of the associations remained significant after accounting for the influence of familial factors. These results support previous findings on the negative link between ACE and perceived health in adulthood. The detrimental effects of ACE on vitality may be accounted for by the experience of childhood physical and/or sexual abuse. Shared familial factors might play a partial role in the relationship between ACE and health perception. Future research should further investigate the genetic and environmental mechanisms that may explain this relationship.

C-reactive protein and pain sensitivity: findings from female twins.

BACKGROUND: Systemic inflammation and pain sensitivity may contribute to the development and maintenance of chronic pain conditions. PURPOSE: We examined the relationship between systemic inflammation as measured by C-reactive protein (CRP) and cold pain sensitivity in 198 female twins from the University of Washington Twin Registry. We also explored the potential role of familial factors in this relationship. METHODS: Linear regression modeling with generalized estimating equations examined the overall and within-pair associations. RESULTS: Higher levels of CRP were associated with higher pain sensitivity ratings at pain threshold (p = 0.02) and tolerance (p = 0.03) after adjusting for age, body mass index, time to reach pain threshold or tolerance, and clinical pain status. The magnitude of the associations remained the same in within-pair analyses controlling for familial factors. CONCLUSIONS: The link between CRP and pain sensitivity may be due to non-shared environmental factors. CRP and pain sensitivity can be examined as potential biomarkers for chronic pain and other inflammatory conditions.