FTO Gene and Diet refers to the clinically significant interaction between variants of the FTO (Fat Mass and Obesity-associated) gene and an individual’s dietary composition and caloric intake. Specific polymorphisms within the FTO gene are strongly associated with a genetic predisposition to increased appetite, higher caloric intake, and greater risk of adiposity and type 2 diabetes. Personalized nutritional strategies, informed by an individual’s FTO genotype, are crucial for mitigating this genetic risk and achieving successful, sustainable body composition management.
Origin
This term emerged prominently following the 2007 discovery of the FTO gene as the single most strongly associated gene locus with common obesity in genome-wide association studies. The subsequent research focused on gene-environment interaction, specifically how dietary choices modify the expression of this genetic predisposition. It represents a key application of nutrigenomics in clinical practice.
Mechanism
The FTO gene’s mechanism is complex, primarily influencing the central nervous system’s regulation of energy homeostasis. The risk allele is linked to higher levels of the ghrelin hormone, which stimulates hunger, and a reduced satiety response after eating, leading to increased food seeking behavior. The clinical intervention mechanism involves counteracting this genetically heightened appetite drive through specific dietary structures, such as high-protein, high-fiber diets, which enhance satiety signals independent of the FTO pathway.
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