Investigating the Link Between Cortisol Related Gene Polymorphisms and Depression

Depression is a mental health disorder that impacts over 280 million people worldwide, with the highest number of cases presenting among those living in low to middle income areas. On top of this, receiving treatment for depression involves facing numerous obstacles, including prevailing stigma, lack of providers, and limited knowledge about proper treatments. This indicates that knowledge of depression and proper methods of supporting patients remains limited, and understanding the various symptoms and causes of this disorder is a vital area of research. Although experiences of depression can vary across patients, common symptoms include feeling hopeless or sad, fatigue, lacking enjoyment in pleasurable activities, and difficulty sleeping. Previous research has suggested that depression may be caused by dysregulation in the HPA Axis, the mechanism used by the body to respond to chronic stress. Specifically, a potential link between extended periods of stress and hypersensitivity to cortisol, a hormone secreted following activation of the HPA axis, has been implicated in causing altered HPA activity and depressive symptoms. Our study aimed to uncover relationships between several gene mutations, called Single Nucleotide Polymorphisms (SNPs), within the HPA Axis and incidence of depression. In collaboration with the Wicker Wellness Center, participants completed scales to determine levels of depression symptoms. We collected DNA samples from these participants using a buccal swab, and then used qPCR to identify the presence of SNPs of interest in our samples. Significant differences between the frequencies of SNPs in participants with low and high levels of depressive symptoms can denote potential genetic predispositions to developing the disorder. By uncovering links to depression via the HPA axis, psychiatric treatments can become more individualized for each patient, improving accuracy and potential for patient recovery.