Genetics of Eating behavior
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This document discusses the genetics of eating behavior and its relationship to obesity. It begins by outlining that eating behavior is influenced by physiological, psychological, social, and genetic factors. It then reviews several specific genetic influences on eating behavior, including Prader-Willi syndrome, LEP and LEPR genes associated with monogenic obesity, MC4R gene mutations linked to increased appetite and food intake, and variants in the FTO and GAD2 genes associated with obesity risk. Additional sections cover the genetics of taste preferences and their influence on food choices, as well as how genes related to hormones like ghrelin and CCK may impact meal size and selection. The document concludes that personalized treatment approaches targeting genetic mutations and behaviors could help
Genetics of Eating behavior
- 1. Genetics of eating behavior Maria Vranceanu “Iuliu Hatieganu”University of medicine and Pharmacy, Cluj Napoca
- 2. • why we eat? • the motivational factors driving food choices?
- 3. Eating behavior is a complex interplay of physiologic, psychological, social, and genetic factors that influence meal timing, quantity of food intake, and food preferences.
- 4. Review • genetic influences of eating behavior and how these relate to obesity • genetics of taste • meal size and selection
- 5. The study of eating behavior attempts to define: •eating patterns and food preferences •explain why there is gravitation toward specific behaviors and food choices •aims to develop approaches to bring about effective changes in modifiable behaviors. •Knowledge of the biological mechanisms guiding eating behavior can provide effective treatment targets for obesity and associated disorders.
- 6. Prader Willi syndrome a deletion of the 11-13q region of chromosome 15 characterized by hypotonia and poor feeding in early infancy, cognitive, motor and behavioral impairment followed by insatiable hunger and the development of morbid obesity and diabetes during childhood
- 7. LEP and LEPR genes monogenic obesity
- 8. •the most common genetic cause of human obesity •SNP (rs17782313), located downstream of MC4R, is confirmed to be associated with overweight and obesity. The minor allele (C-allele) of this SNP is believed to have reduced MC4R expression when compared to the major allele (T-allele). •The loss of function MC4R mutations lead to its carrier’s increased appetite in childhood. A typical feature of the affected individuals is hyperphasia, insatiable appetite. A typical meal of mutation carriers contains about three times the number of calories than that in non-mutation carrying siblings. •Consistent with the hyperphagia eating behaviors of MC4R loss-of-function mutations carriers, carriers of the C-allele of the MC4R SNP rs17782313 eat larger amounts of food, snack more frequently, like foods containing more fat content, and are characterized as having weak satiety when tested with eating behavior questionnaires (Choquet & Meyre. 2011; Cecil et al., 2012). MC4R GENE MUTATION
- 10. GAD2 (glutamate decarboxylase 2) a positional candidate gene for morbid obesity on Chromosome 10p11–12 GAD2 gene encodes for the glutamic acid decarboxylase enzyme (GAD65), which is implicated in the formation of the gamma-aminobutyric acid (GABA), a neurotransmitter involved in the regulation of food intake In women, a SNP (rs992990; c.61450 C>A) was associated with disinhibition, emotional susceptibility to disinhibition and susceptibility to hunger. Another SNP (rs7908975; c.8473A>C) was associated with carbohydrate intakes, disinhibition (SNPs) +61450 C>A and +83897 T>A associated with morbid obesity allele of SNP -243 A>G increased six times GAD2 promoter activity and is associated with higher risc of obesity
- 11. Genome-wide association studies (GWAS) have reliably established that SNPs within the first intron of FTO are robustly associated with increased BMI and adiposity across different ages and populations. homozygous for the risk A allele of FTO rs9939609 have a 1.7-fold increased risk for obesity compared with homozygous with T allele . Subjects homozygous for the obesity-risk A allele exhibit overall increased ad libitum food-intake, particularly fat consumption , and impaired satiety . preschool AA children exhibit obesity-prone eating behaviors, including increased food responsiveness and a tendency to eat in response to external cues.
- 12. Meal selection and size? • Research into meal size and selection is especially complex as socioeconomic environment, learned eating behaviors, physiologic conditions such as depression, and even medical treatments can all influence appetite and food selection, independent of genetics • however meal quantity, frequency, and timing are thought to be at least in part under genetic control. • The study of genetic variants in digestive neuroendocrine hormones, such as CCK, leptin and ghrelin, are providing new insights into how these hormones and their genetic variants may be involved in pathways regulating appetite and eating behavior
- 13. Ghrelin, a 28-amino acid peptide, produced by the stomach and pancreas involved in promoting meal intake and hunger through receptors in the hypothalamus. Plasma ghrelin levels rise pre- meal and are suppressed by food intake. GHRL is located on chromosome 3. A common variant, Leu72Met has been associated with obesity, metabolic syndrome, and binge eating.
- 14. CCK( cholecystokinin) released in response to lipids and promotes rapid post-prandial satiety in contrast to the long term action of leptin. CCK variants (rs6809785, rs7611677, rs6801844, and rs6791019) were found to be more associated with extreme meal size but not increased snacking behavior
- 15. Five tastes are recognized by humans: sweet, bitter, sour, salty, and umami • Food preference and intake is influenced by sweet and bitter taste. Genetic of taste
- 16. Bitter taste Individuals who are particularly sensitive to bitter compounds tend to avoid the bitter taste of beer and alcohol, and avoid cigarette smoking as well. Bitter taste as well as preference for sweet and fat guide ingestive behaviors, and have been linked to obesity, and these food preference traits may in part be genetically determined.
- 17. Bitter taste Genes TAS2Rs: TAS2R38, TAS2R5, TAS2R16 Influence on Ingestive behavior Vegetable avoidance, increased fat and sweet intake disinhibited eating behavior among women Alcohol dependence
- 18. Emotional eating is driven by emotional cues like depression, anxiety, happiness, sadness, and boredom rather than hunger. By engaging in emotional eating, we are subconsciously seeking comfort or pleasure from food.
- 19. DRD2 and OPRM1 genes function in the brain reward system. Variations in these genes are associated with emotional eating and weight gain.
- 20. The DRD2 gene is a key player in the dopamine neuronal circuits. Dopamine is the “feel good” neurotransmitter that motivates people for pleasure. A variation in the DRD2 gene, Taq1A1, results in a reduced dopamine function in the brain.
- 21. OPRM1 gene is a key play in the opioid neuronal circuits. Activation of the opioid neuronal circuits leads to the production of dopamine. Activities of the opioid system also determine how much you enjoy the pleasure. These neuronal circuits interact with each other and with other neuronal circuits to produce an overall “reward value” of a food. This “reward value” influences eating behaviors. People suffering from binge eating disorder appear to be highly active in both the dopamine and the opioid systems. A variation of OPRM1 increases activity in the opioid neuronal circuits. Carriers of this variant have greater risk for drug addiction Risk variant: 118G+
- 22. DRD2, OPRM1 and Binge Eating Disorders In a study of obese populations, the combination of the A2A2 genotype of the DRD2 gene and the G-allele of the OPRM1 gene (A-/G+ ) was the most frequent one in the group characterized by obese and binge eating(Davis et al., 2009). These data suggest that the A1-/G+ combination is the cause of binge eating. Since the A1- is associated with a higher dopamine D2 receptors and the G allele is associated with an increased opioid activation, the A1−/G+ combination reflects a hedonic-enhanced genotype combination, one that increase the risk for binge eating.
- 23. Conclusions Personalized medicine, tailoring pharmacologic and behavioral therapy to an individual’s genetic code, is an emerging practice. Applications of research of the genetics of eating behavior may lead to individualizing therapies targeting specific genetic mutations and behavioral interventions addressing eating behaviors. Once the role of specific gene variants in pathways involved in specific behaviors or food responses are well established, treatment could be individualized toward modifying these behaviors and pharmacologic modalities developed to modify molecular pathways involved.