Obesity is the second largest preventable cause of death in the United States. Even though it was classified as a disease in 1985, traditionally, obesity has been treated primarily as a behavioral problem that requires only modifications in diet and exercise. Similar to research on obesity, clinical studies have elucidated the role of biologic and genetic factors in alcoholism and other conditions previously classified as behavioral. These studies showed that behavioral adjustments alone may not address underlying genetic causes. We hypothesize that biologic and genetic factors must be addressed synergistically while behavioral modifications are implemented to adequately treat obese patients. We hypothesize that a predisposition to glucose craving and obesity is due to inadequate dopaminergic activity in the reward center of the brain. This defect drives individuals to engage in activities of behavioral excess, which, in turn, enhance brain dopamine function. Consumption of large quantities of alcohol or carbohydrates (carbohydrate bingeing) stimulates production and usage of dopamine within the brain; the term reward deficiency syndrome (RDS) may be used to categorize such biologic influences on behavior. We propose that a novel approach to nutritional supplementation may be required to target the role of RDS in obesity. In this regard, GenoTrim, a DNA-customized nutritional solution, has been developed and is currently under investigation in several clinical studies. Through its mechanism of action, GenoTrim addresses the genetic influence of RDS on obesity. In this cross-sectional study, 24 subjects were studied after they had completed a case report format questionnaire. For this assessment, we used a novel assessment tool-a path analysis. This statistical regression model is used to (1) examine the effectual relationships between various systems within a multisystem matrix, and (2) measure the contributory roles of those relationships in obesity, enabling the development of targeted and effective therapeutic interventions.

No abstract

Background: Malnutrition due to insufficient intake of micronutrients, or due to impaired delivery of micronutrients to patients’ cells, is suppressing immune functions that are fundamental to host protection. Concurrently, an excessive triggering of patients’ immune reactions as the result of adverse responses to certain food antigens, can also lead to various chronic health conditions.Objective: To examine nutritional and immunological status in patients’ groups varying in age, dietary regimens and gastrointestinal condition; and explore a possible correlation between an impaired patients’ immune status and micronutrient deficiencies, food sensitivity and oxidative stress responses.Methods: This is a population-based study consisting of a American residents, age 13 and older, who completed the investigator’s provided questionnaires with application of cell-based individualized functional assays. Data for this paper were collected from 845 individuals between May and September 2019, as part of CSS CNA beta study. Micronutrient deficiencies, immune Redox status, antioxidative responses and food sensitivity profiles were assessed for each patient participating in this study.Results: The group of patients with low Redox status demonstrated significantly higher percent of immune reactivity (17%) to food antigens as compared to15% reactivity detected in the groups with the average and strong Redox response. An average number of identified micronutrient deficiencies, as well as beneficial anti-oxidative protective compounds, was also significantly higher in the group with the weak immune function as compared to other two groups.Conclusion: This study suggests that high food sensitivity is associated with a higher nutrient deficiency, a stronger oxidative stress response and a lower immune redox status.