Summary: | Obesity is a global public health problem due to its large number of associated alterations and is currently considered a lifestyle disease. Approximately 70% of cardiovascular complications one of the main diseases associated with obesity are attributed to modifiable risk factors and, by 2030, 30% of the global deaths will be attributable to these lifestyle diseases. Consequently, identifying potentially modifiable risk factors is a priority for implementing both prevention programs and effective obesity interventions, since infancy to adulthood. An early identification of healthy and unhealthy behaviors facilitates the development of preventive and management strategies for pediatric overweight and obesity. Thus, we hypothesized that a lifestyle program combining dietary treatment, promotion of physical activity (PA) and behavioral therapy with family involvement would be an effective strategy to reduce excess body fat in pediatric subjects with obesity. On the other hand, a healthy lifestyle change has been suggested to have impact on DNA damage markers, such as telomeres: repetitive nucleotide sequences (5 -TTAGGG-3 ) at the end of chromosomes providing stability and protection towards the genome. Since these repetitive sequences are shortened in each cell division, telomere length (TL) has been proposed as a biomarker of biological age and age-related chronic diseases. Moreover, lifestyle factors such as diet and PA could influence telomere shortening through both oxidation and inflammation mechanisms since guanine-rich DNA is prone to oxidation to 8- oxo-2 -deoxyguanosine. Therefore, we theorized that, since healthy lifestyle factors are positively associated with TL, a therapeutic lifestyle change towards healthy habits an increase in diet quality and PA levels would contribute to telomere maintenance. The present research work has applied different approaches to investigate the potential effect of lifestyle factors diet quality and PA levels on adiposity and TL, in both intervention and cross-sectional studies, in pediatric and elderly Spanish subjects. In Chapter 1, clustering patterns of diet, PA and screen time was identified in children (6-9 years) from the WHO European Childhood Obesity Surveillance Initiative. We observed that a healthy cluster high levels of PA and high consumption of fruit and vegetables, combined with low screen time use and low sugared soft drink intakes was associated with less risk of overweight or obesity. In Chapter 2, a randomized controlled trial was performed in pediatric subjects (7-16 years) with abdominal obesity. Participants were assigned either to a usual care or the intervention group based on a moderate hypocaloric Mediterranean diet and nutritional education. Both groups were encouraged to increase their PA level. An intensive lifestyle intervention was able to reduce anthropometric parameters and to improve dietary indexes. In Chapters 3 and 4, we found that favorable changes in diet quality indexes and in PA levels could contribute to telomere integrity in pediatric population with abdominal obesity. Finally, in Chapters 5 and 6, we evaluated the effect of diet quality indexes and Mediterranean dietary pattern on TL in elderly subjects (>55 years) of the SUN cohort. Our cross-sectional analyses suggest that individuals in the highest dietary indexes categories had lower risk of short TL. Moreover, better adherence to a posteriori derived Mediterranean dietary pattern was associated with longer TL. Overall, the results reported in the present dissertation in pediatric and elderly population, add new insights into the impact of lifestyle risk factors in the obesity development; and their potential effect on TL, as an adiposity marker reflecting both the inflammatory and oxidative stress status. The evidence will help to identify therapeutic lifestyle changes able to reduce adiposity and obesity-related disorders, which, in turn, will influence telomere shortening.
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