Purpose The purpose of this paper is to examine the relationships among workaholism, psychological capital (PsyCap), and burnout, as well as investigate the potential mediating effect of PsyCap on the relationship between workaholism and burnout. Design/methodology/approach Data on workaholism, PsyCap, and burnout were collected, through administration of an online survey, from 400 faculty and staff at a large Southeastern university. Findings Workaholism is negatively related to PsyCap and is positively related to burnout, while PsyCap is negatively correlated with burnout. Moreover, while tested in a mediation model, PsyCap appeared as a significant mediating variable for all three dimensions of burnout (i.e. emotional exhaustion, depersonalization, and personal accomplishment). Research limitations/implications Future researchers may benefit from examining a sample outside an educational institution. Also, both workaholism and burnout may be better suited for studies utilizing longitudinal designs. That said, the data reveal information about the process whereby tendencies indicative of heavy work investment lead to burnout within employees. That is, workaholism leads to lower PsyCap, which then results in burnout. Practical implications The results suggest that employers may benefit from considering the negative effects of heavy work investment and maintaining a culture that discourages such behavior. It might also be beneficial for employers to ensure that employees have a heightened PsyCap and, therefore, are safeguarded against burnout. Originality/value This is the first study to examine the influence that employee PsyCap has on the development of workaholism and burnout by examining its role as a mediator.

The purpose of this article was to provide a detailed review of workaholism, a topic within the realm of Occupational Health Psychology. Workaholism has become a commonplace term used in the popular culture to depict individuals who are addicted to work. It is typically characterized as an addiction and defined as the compulsive tendency to work excessively hard. Given the deleterious effects of workaholism, this article provides a review of what we know about this phenomenon, as well as how we can combat it. First, an overview of workaholism is presented, including definitions and measures, followed by a discussion on antecedents (personality factors and work environment) and correlates in the organizational, individual, and family domains. Next, a section on combatting levels of workaholism is summarized. Finally, avenues for future research on this topic are discussed. Essentially, this review article will add to the existing literature on Industrial/Organizational Psychology and health issues associated with organizational behavior, as well as serve as a resource for both researchers and practitioners who strive to enhance the well-being of their employees. K E Y W O R D S occupational health, organizational behavior, workaholism

The long-chain n-3 polyunsaturated fatty acids (LC-PUFAs) eicosapentaenoic (EPA) and docosahexaenoic acid (DHA) in fish oil have immunomodulatory properties. B cells are a poorly studied target of EPA/DHA in humans. Therefore, in this pilot study, we tested how n-3 LC-PUFAs influence B-cell responses of obese humans. Obese men and women were assigned to consume four 1-g capsules per day of olive oil (OO, n=12), fish oil (FO, n=12) concentrate or high-DHA-FO concentrate (n=10) for 12 weeks in a parallel design. Relative to baseline, FO (n=9) lowered the percentage of circulating memory and plasma B cells, whereas the other supplements had no effect. There were no postintervention differences between the three supplements. Next, ex vivo B-cell cytokines were assayed after stimulation of Toll-like receptors (TLRs) and/or the B-cell receptor (BCR) to determine if the effects of n-3 LC-PUFAs were pathway-dependent. B-cell IL-10 and TNFα secretion was respectively increased with high DHA-FO (n=10), relative to baseline, with respective TLR9 and TLR9+BCR stimulation. OO (n=12) and FO (n=12) had no influence on B-cell cytokines compared to baseline, and there were no differences in postintervention cytokine levels between treatment groups. Finally, ex vivo antibody levels were assayed with FO (n=7) after TLR9+BCR stimulation. Compared to baseline, FO lowered IgM but not IgG levels accompanied by select modifications to the plasma lipidome. Altogether, the results suggest that n-3 LC-PUFAs could modulate B-cell activity in humans, which will require further testing in a larger cohort.