Background. Obesity results from a malfunction of the body's weight-control mechanisms, which may be influenced by environmental changes. Essentially, the obesity risk relies on two significant interdependent factors: genetic variations (single-nucleotide polymorphisms, haplotypes) and environmental risk exposure. Due to new biotechnologies over 127 potential genes for obesity have been identified, and evidence supports the function of 22 genes in at least five distinct groups. Gene and environment interactions mean that the synergy between genotype and environment is neither additive or multiplicative. The application of innovative methods for both genotype and lifestyle variables should be emphasized. Aim of study: Investigate variable data of lifestyle factors in obese people with genetic predisposition and without in order to figure out the trigger risks which transform the predisposition into obesity. Material and methods: This is a descriptive study. A questionnaire was elaborated. It was developed based on the data of new biotechnological analysis of metabolic changes in obese humans. 142 individuals were included. 82 obese individuals, 42 with genetic predisposition and 40 without, and 60 healthy probands were interviewed. Further followed a comparative statistical analysis. Results: Obese probands were found with higher levels of disability compare those without, cardiovascular events higher compared with healthy probnads, disability level and smoking habits had significantly correlation in obese with genetic predisposition. On the other hand, health probands were found in higher level of anxiety compared obese people with genetic predisposition. Conclusions: All the lifestyle aspects which lead to an increased central nervous overactivity disturb significantly the metabolism and are critical risk factors for people with genetic predisposition relate to the pathogenesis of obesity. that might lead to high disability level associated comorbid states and high risk of cardiovascular events.