” A better understanding of the function of genes in comorbid depression and weight problems unlocks to early detection of those individuals with a greater danger of establishing this comorbidity and to being able to design more personalized (and more effective) prevention and treatment methods for them”, stresses Esther Molina.
Source: Journal recommendation: Zarza-Rebollo, J.A., et al. (2021) The function of the FTO gene in the relationship between anxiety and weight problems. An organized evaluation. Neuroscience & & Biobehavioral Reviews. doi.org/10.1016/j.neubiorev.2021.05.013.
This systematic review was carried out to derive insights from the released clinical evidence on the possible function that one specific gene, the FTO gene, may play in comorbid anxiety and obesity. This gene contains an area that varies from person to individual, referred to as a polymorphism.
Source: Journal reference: Zarza-Rebollo, J.A., et al. (2021) The function of the FTO gene in the relationship between anxiety and weight problems.
The authors of this work, all of whom belong to the “Federico Olóriz” Institute of Neurosciences and the Biomedical Research Centre of the UGR, have shown that there are very few studies evaluating the role of this gene in comorbid obesity and anxiety. By characterising the samples by the different anxiety subtypes, we might be able to light up the function played by the FTO gene and perhaps other genes in those anxiety subtypes that are more susceptible to activating weight-gain”.
Depression and weight problems are both incredibly common diseases in our society, with severe implications not just on an individual and household level but likewise for public, occupational, and financial health. Anxiety is currently thought about the worlds leading cause of disability. Depression and obesity have a strong bidirectional relationship– that is, obesity increases the threat of developing depression; and vice-versa, people with depression are at greater threat of becoming obese.
. Juan Antonio Zarza Rebollo, scientist from the UGRs Department of Biochemistry and Molecular Biology II and main author .
According to the “Ramón y Cajal” research study fellow Margarita Rivera (organizer of this work and of the research on physical health and psychological health of this group and also a lecturer in the UGRs Department of Biochemistry and Molecular Biology II): “The study of the hidden hereditary aspects involved in the comorbidity between anxiety and weight problems is one of the active lines of research of our group. Particularly, the FTO gene has been investigated by this and other worldwide research groups as a possible genetic link between both pathologies”.
” The existence of the so-called threat variant of this polymorphism has actually been linked by many studies to a higher possibility of experiencing weight problems and to an increase in body weight in humans. Although there are no studies that associate it with anxiety separately, the FTO gene is highly revealed in the brain, and current research studies have actually described functions that might take part in crucial brain mechanisms. All of this leads us to believe that this gene might play an essential function in the look of comorbid depression and weight problems”, keeps in mind Zarza-Rebollo.
Depression and obesity have a strong bidirectional relationship– that is, obesity increases the risk of developing anxiety; and vice-versa, people with anxiety are at higher danger of ending up being overweight. The function of genes in the development of these illness is restricted and can not be considered an identifying element (that is, there is no “obesity gene” or “depression gene”). The authors of this work, all of whom belong to the “Federico Olóriz” Institute of Neurosciences and the Biomedical Research Centre of the UGR, have revealed that there are extremely few studies evaluating the function of this gene in comorbid obesity and anxiety. By characterising the samples by the different depression subtypes, we might be able to brighten the function played by the FTO gene and potentially other genes in those depression subtypes that are more susceptible to activating weight-gain”.
Scientists from the University of Granada (UGR) have actually highlighted that the possible role attributed to the fat mass and obesity-associated (FTO) gene in the comorbidity of depression and obesity can only be confirmed by performing more studies including people struggling with both illness, together with more extensive analysis of the various clinical subtypes of anxiety, as some are more vulnerable to being accompanied by weight problems than others.
A important but limited function.
In their study, which has actually been released in the distinguished journalNeuroscience & & Biobehavioral Reviews, the scientists conducted an exhaustive organized review of the clinical literature published to date on this subject, to much better comprehend the function of this gene in the relationship in between these 2 diseases.
There are different aspects that increase the danger that an individual will establish depression and weight problems simultaneously. These elements consist of having low self-confidence, having actually suffered maltreatment or abuse in youth, social preconception, or a low level of household and social assistance. All of these can effect on the biology of each individual, where there are particular physiological mechanisms (which include the hypothalamic-pituitary-adrenal axis or inflammation) or hereditary risk versions that can play an important role in the look of these pathologies.
The role of genes in the development of these illness is limited and can not be considered a figuring out aspect (that is, there is no “obesity gene” or “anxiety gene”). Esther Molina, a co-author of this research study and lecturer at the UGRs Department of Nursing, explains, nevertheless, that “there are hereditary versions common to both conditions that provide a higher risk of developing these diseases on those who carry those versions since they can engage with the environment, generating a private danger for these pathologies. Hence, we find that some individuals are most likely to develop them than others”.