Cortisol is a crucial part of the endocrine system; it has the capacity to affect nearly every organ and tissue in the human body. When functioning correctly, cortisol is known to regulate the body’s stress response, control metabolism, suppress inflammation, regulate blood pressure, regulate blood sugar, regulate our body’s circadian rhythm, and much more. When the concentration of cortisol in the blood is elevated for an excessive period, the body responds with symptoms such as hyperglycemia, hypertension, weight gain, and moon face. Commonly this is known as Cushing’s Syndrome (CS), and interestingly, we have seen a phenotypic resemblance when contrasted alongside Metabolic Syndrome, a subtype of obesity. Several specific nucleotide polymorphisms (SNPs) have been found along the glucocorticoid (GR) and mineralocorticoid (MR) receptors that are expected to present in a higher concentration amongst populations with obesity. Our current research is investigating the relationship between the allele frequency of four SNPs (rs7901695, rs12772424, rs3753519, and rs1051052), and obesity. Through a collaboration with Ellis Hospital Bariatric Care Center, we obtained the patients’ body mass index (BMI), blood glucose levels, serum triglycerides levels, HDL and LDL cholesterol levels, and systolic and diastolic blood pressures to evaluate. Amongst the SNPs tested, there was a significant difference between different genotypes of the rs3753519 SNP in original weight, diastolic pressure, extra body weight, and extra body weight percentage. This data supports the hypothesis that SNPs involved in the activity of cortisol can alter metabolic profiles and could be contributing to the development of diseases such as Metabolic Syndrome and CS. Furthermore, this could aid the deeper understanding of how these SNPs influence weight gain and could provide better predictions and outlooks on the success of weight losssignificantly improving the overall quality of life for individuals with obesity.