Abstract
INTRODUCTION: There is an urgent, unmet need to determine mechanisms involved in our obesity pandemic, since the origins may affect the development of obesity-associated gastrointestinal disorders. Psychosocial (PS) factors (i.e. diet/physical activity/stress) appear to be major causes, while genome-wide association studies suggest strong genetic risks (GR). Recently it has been suggested that exposure to obesogens (O) during early life is associated with alteration of programming of fat cell development and interference of neuroendocrine pathways. Our hypothesis is that exposure to obesogens/endocrine disruptors is a major cause of obesity in the US. METHODS: This is a retrospective review of 225 consecutive new obese subjects, who live in urban and suburban locations, seen in a community teaching hospital-based bariatric GI clinic from October 2018 to June 2019. Subjects (n = 17) were excluded due to incomplete information. Obesogen exposure is defined by: mother and father normal weights; subject had body mass index (BMI) of ≥ 30 kg/m2 at age 18. Genetic risk is defined by: mother and/or father obese; subject had BMI of ≥ 30 at age 18. Psychosocial factors are defined by: subject with BMI < 30 at age 18. RESULTS: As shown in Table 1/Table 2, exposure to obesogens appeared to be a risk in only 14.5% of this population. Patients with either potential exposure to obesogens or a genetic risk: 1) present for evaluation at a younger age; 2) have both higher weight (in lbs.) and BMI at initial evaluation; & 3) have both higher weight and BMI at age 18. CONCLUSION: Psychosocial factors appear to be the major origin for obesity in this population. Further studies are needed to evaluate the potential individual roles of obesogens, genetic risk of obesity, and psychosocial factors in the development of obesity-associated gastrointestinal disorders.Table 1.: DemographicsTable 2.: Statistical analysis
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