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Serotonin is a neurohormone involved in biological processes, such as behavior and immune function. Chronic psychosocial stressors may cause serotonin release resulting in immune system dysregulation, as evidenced by increased or far decreased levels of cortisol, a blood biomarker of stress and immune function. We hypothesize that genetic polymorphisms in the HTR7 gene are associated with both hypo- and hyper-cortisolism. Methods: The study population included 602 African American subjects between 18-34 years of age, living in Washington, D.C. Five single nucleotide polymorphisms (SNPs) in HTR7 , rs2420367, rs12412496, rs2185706, rs7089533, and rs7093602 were genotyped by restriction fragment length polymorphism or the TaqMan assay. Statistical analysis, using the program SNPstat, was performed to determine their associations with cortisol measured in the study population. Results: While an increased risk of hypocortisolism was found to be associated with rs2420367, rs2185706, and rs7093602 in a gender specific manner, no genotypes could be associated with hypercortisolism. Inversely, a decreased risk of hypocortisolism was found with the haplotype CGGCC (p=0.033), which remained significant in males. When adjusting for gender, females associated with the haplotype AGACC. Hypercortisolism was also associated with a decreased risk for the haplotypes AAACC (p=0.042) and AAGTT (p=0.001). Discussion: Based on these results, genetic variation in the HTR7 gene may contribute to both stress and inflammation, and will provide a new glimpse into stress-related inflammation psychophysiology.

Genetic polymorphisms in the serotonin receptor 7 (HTR7) gene are associated with cortisol levels in African American young adults