Journal of Childhood Obesity Open Access

EDITORIAL

Childhood obesity is a public health problem that transcends borders, it is defined as a chronic, complex and multifactorial disease, characterized by an excessive increase in body fat. It occurs when there is an imbalance between energy intake and caloric expenditure. It is classically established that if both parents are obese, the risk for the offspring will be 69 to 80%; when only one parent is obese it will be 41 to 50% and if neither parent is obese, the risk for the offspring will be only 9%. Among this multifactoriality mentioned, it has been shown that the gene (Alpha-Ketoglutaratedioxygenase) FTO, located at the 16q12.2 locus, has shown a link with obesity in various studies, with a high association with increased BMI due to the fact that produces a genetic disorder, preventing fullness in the individual . The FTO gene has several variants but among the most documented with its possible association in the appearance with obesity is the polymorphism rs9939609, which is directly related to an increase in the body mass index (BMI); confirmed in various child populations globally. For Ulloa and Col (2020), for each extra copy of the rs9939609 allele of the FTO gene, the probability of affecting obesity indicators will be increased; which implies an increase in the percentage of body fat, BMI, waist circumference and the relationship between waist measurement and height. Furthermore, a study by Prakash et. al revealed that this same polymorphism rs9939609 of the FTO gene was associated with several measures related to obesity, especially those described: elevated blood pressure, percentage of body and muscle fat, plasma insulin and insulin resistance Despite the multiple investigations on this gene, the mechanisms by which they are related to childhood obesity have not been elucidated, however, very interesting contributions have been made such as the study of the implications of brain variants in the development of this pathology

children without obesity with the FTO risk allele, where the structure and function of the brain related to the obesity risk alleles were evaluated in two groups, the associated differences in the structure and architecture of the brain were analyzed before the start of obesity, identifying alterations associated with the genotype in bilateral cerebellar gray matter (GM), white matter and functional connectivity, in addition, alterations were evidenced in the right middle gyrus and fusiform cortex. Unlike the TT group, which was more diverse, the CC group consisted of Caucasian participants. It was evidenced that children who carried homozygous CC risk alleles have increased volume of the gray matter of the cerebellar cortex bilaterally, the temporal gyrus and the right fusiform cortex, in addition, they also presented higher density of cerebellar white matter fibers and greater structural and functional connectivity between the cerebellum and the frontotemporal cortical regions in a resting state, compared to carriers of homozygous TT riskfree alleles. There were no significant differences in GM volume between the CT and TT groups . According to the report to end childhood obesity published by the WHO in 2016, obesity affects not only the physical well-being of children but also the social and psychological, which is why it is very important to study this pathology from various perspectives and due to that it is a multifactorial disease, it can be analyzed with different approaches, especially by carrying out more studies that help prevent it or detect it early and be able to treat it earlier; making it known that it is not only due to eating habits but that there is also a genetic component that is being studied more and more. In the study in children without obesity but with a genetic predisposition to develop it by Ranzenhofer, Lisa M et al, the association between the number of copies of FTO and the intake variables was examined, the FTO gene showed a great association with total intake where Each risk allele predicted an additional 64 calories, that is; 3% of the variance within a population of children aged 5 to 10 years. This is relevant in the studies carried out on this topic since it shows that it is not only children with obesity that should be studied to know the behaviors of the FTO variants. The study of children without obesity also reveals a significant genetic component participation  It is important to know the genetic predisposition for obesity, taking into account that obese children have a three times greater risk of developing hypertension than children with normal nutritional status. A higher prevalence of dyslipidemia, manifested by increased triglycerides and LDL cholesterol, has also been observed [9]. Finally, the authors agree with the idea that in addition to the participation of the FTO gene that causes a genetic predisposition, promoting healthy habits in the family and educational environments where children develop is a strategy that allows the adoption of healthy attitudes, knowledge and habits.