Grant: CIHR Fellowship

Depression is predictive of the later development of heart disease, and conversely, patients experiencing heart disease are more likely to become depressed, and experience a poorer prognosis. This comorbidity has been established, however, the underlying mechanisms are not well understood. It has been suggested that inflammatory factors (e.g. pro-inflammatory cytokines) which are involved in the development of depression and heart disease may be responsible for this concordance. Therefore, treatments that target the inflammatory factors associated with depression may be effective not only at attenuating depressive symptoms, but also preventing the development of heart disease or further cardiovascular damage. In this regard, the neuropeptide oxytocin, which has been linked to depression, can act as a cardiac hormone attenuating pro-inflammatory cytokines in heart tissue. Thus, oxytocin might contribute to the relation between inflammation and both depressive illness and heart disease. I plan to examine the role of inflammatory factors in depression and comorbid heart disease and determine whether the increased risk of future cardiac events among individuals with depression is linked to elevated pro-inflammatory factors. I will also examine whether oxytocin treatment is effective at attenuating pro-inflammatory stress responses among those at risk of developing later heart disease. Furthermore, I will examine whether the effectiveness of oxytocin on attenuating pro-inflammatory stress responses depends on genetic variants within the oxytocin system. We predict that oxytocin treatment will be most effective at alleviating inflammatory stress responses among those who carry certain oxytocin genetic variants. Together, these findings will elucidate the role of inflammation in depression and comorbid heart disease and identify novel treatment options, such as oxytocin, to target the underlying inflammation associated with both disorders.