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Appetitive traits as behavioural pathways in genetic susceptibility to obesity: a population-based cross-sectional study.

ABSTRACT: The mechanisms through which genes influence body weight are not well understood, but appetite has been implicated as one mediating pathway. Here we use data from two independent population-based Finnish cohorts (4632 adults aged 25-74 years from the DILGOM study and 1231 twin individuals aged 21-26 years from the FinnTwin12 study) to investigate whether two appetitive traits mediate the associations between known obesity-related genetic variants and adiposity. The results from structural equation modelling indicate that the effects of a polygenic risk score (90 obesity-related loci) on measured body mass index and waist circumference are partly mediated through higher levels of uncontrolled eating (?indirect = 0.030-0.032, P < 0.001 in DILGOM) and emotional eating (?indirect = 0.020-0.022, P < 0.001 in DILGOM and ?indirect = 0.013-0.015, P = 0.043-0.044 in FinnTwin12). Our findings suggest that genetic predispositions to obesity may partly exert their effects through appetitive traits reflecting lack of control over eating or eating in response to negative emotions. Obesity prevention and treatment studies should examine the impact of targeting these eating behaviours, especially among individuals having a high genetic predisposition to obesity.

SUBMITTER: Konttinen H

PROVIDER: S-EPMC4589697 | biostudies-other | 2015 Oct

REPOSITORIES: biostudies-other

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Appetitive traits as behavioural pathways in genetic susceptibility to obesity: a population-based cross-sectional study.

Konttinen Hanna H Llewellyn Clare C Wardle Jane J Silventoinen Karri K Joensuu Anni A Männistö Satu S Salomaa Veikko V Jousilahti Pekka P Kaprio Jaakko J Perola Markus M Haukkala Ari A

Scientific reports 20151001

The mechanisms through which genes influence body weight are not well understood, but appetite has been implicated as one mediating pathway. Here we use data from two independent population-based Finnish cohorts (4632 adults aged 25-74 years from the DILGOM study and 1231 twin individuals aged 21-26 years from the FinnTwin12 study) to investigate whether two appetitive traits mediate the associations between known obesity-related genetic variants and adiposity. The results from structural equati ...[more]

PMID: 26423639

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Project description:BackgroundIndividual differences in appetitive traits present in the first few weeks of life. Research has shown that infants with a greater food reinforcement ratio (FRR) have higher obesity risk. To date, limited work has examined the relation between FRR and appetitive traits of infants, and how FRR relates to appetitive traits and obesity development.ObjectivesTo examine the relation between appetitive traits and food and nonfood reinforcement of infants aged 9-18 mo, and to examine whether food and nonfood reinforcement mediate the relation between appetitive traits and weight-for-length z-score (zWFL).MethodThis secondary data analysis was conducted by combining 4 different cohorts of infants (n = 143) who have complete data on the food/nonfood reinforcement task, Baby Eating Behavior Questionnaire, and anthropometrics and demographics assessments. Three different nonfood reinforcers were used: video (DVD; n = 27), playing with bubbles (Bubbles; n = 67), and music accompanied by instruments (Music; n = 49) for the nonfood portion of the task. For the food portion of the task, the infant's favorite food was used.ResultsGeneral appetite positively correlated with FRR and zWFL, but negatively correlated with nonfood reinforcement; satiety responsiveness negatively correlated with food reinforcement, FRR, and zWFL. Mediational analysis showed that effects of general appetite on zWFL were mediated by FRR (indirect effect = 0.100, 95% CI: 0.041, 0.187) and nonfood reinforcement (indirect effect = 0.076, 95% CI: 0.025, 0.156). We also observed the mediating effect of FRR on the relation of satiety responsiveness and zWFL (indirect effect = -0.097, 95% CI: -0.204, -0.026).ConclusionsOur work contributes to the mechanistic understanding of the ontogeny of obesity development early in life among individuals who are born with appetitive drive for overconsumption. During early infancy, the nonfood environment may protect against this drive and prevent obesity development.

Project description:BackgroundCharacteristics of the built environment, such as neighbourhood fast-food outlet exposure, are increasingly recognised as risk factors for unhealthy diet and obesity. Obesity also has a genetic component, with common genetic variants explaining a substantial proportion of population-level obesity susceptibility. However, it is not known whether and to what extent associations between fast-food outlet exposure and body weight are modified by genetic predisposition to obesity.MethodsWe used data from the Fenland Study, a population-based sample of 12,435 UK adults (mean age 48.6 years). We derived a genetic risk score associated with BMI (BMI-GRS) from 96 BMI-associated single nucleotide polymorphisms. Neighbourhood fast-food exposure was defined as quartiles of counts of outlets around the home address. We used multivariable regression models to estimate the associations of each exposure, independently and in combination, with measured BMI, overweight and obesity, and investigated interactions.ResultsWe found independent associations between BMI-GRS and risk of overweight (RR = 1.34, 95% CI 1.23-1.47) and obesity (RR = 1.73, 95% CI 1.55-1.93), and between fast-food outlet exposure and risk of obesity (highest vs lowest quartile RR = 1.58, 95% CI 1.21-2.05). There was no evidence of an interaction of fast-food outlet exposure and genetic risk on BMI (P = 0.09), risk of overweight (P = 0.51), or risk of obesity (P = 0.27). The combination of higher BMI-GRS and highest fast-food outlet exposure was associated with 2.70 (95% CI 1.99-3.66) times greater risk of obesity.ConclusionsOur study demonstrated independent associations of both genetic obesity risk and neighbourhood fast-food outlet exposure with adiposity. These important drivers of the obesity epidemic have to date been studied in isolation. Neighbourhood fast-food outlet exposure remains a potential target of policy intervention to prevent obesity and promote the public's health.

Project description:To characterise the trait-effects of increased genetic risk for schizophrenia, and highlight potential risk mediators, we test the association between schizophrenia polygenic risk scores (PRSs) and 529 behavioural traits (personality, psychological, lifestyle, nutritional) in the UK Biobank. Our primary analysis is performed on individuals aged 38-71 with no history of schizophrenia or related disorders, allowing us to report the effects of schizophrenia genetic risk in the sub-clinical general population. Higher schizophrenia PRSs were associated with a range of traits, including lower verbal-numerical reasoning (P = 6 × 10-61), higher nervous feelings (P = 1 × 10-46) and higher self-reported risk-taking (P = 3 × 10-38). We follow-up the risk-taking association, hypothesising that the association may be due to a genetic propensity for risk-taking leading to greater migration, urbanicity or drug-taking - reported environmental risk factors for schizophrenia, and all positively associated with risk-taking in these data. Next, to identify potential disorder or medication effects, we compare the PRS-trait associations in the general population to the trait values in 599 medicated and non-medicated individuals diagnosed with schizophrenia in the biobank. This analysis highlights, for example, levels of BMI, physical activity and risk-taking in cases in the opposite directions than expected from the PRS-trait associations in the general population. Our analyses offer simple yet potentially revealing insights into the possible causes of observed trait-disorder associations, which can complement approaches such as Mendelian Randomisation. While we urge caution in causal interpretations in PRS cross-trait studies that are highly powered to detect weak horizontal pleiotropy or population structure, we propose that well-designed polygenic score analyses have the potential to highlight modifiable risk factors that lie on the path between genetic risk and disorder.

Dataset Information

Appetitive traits as behavioural pathways in genetic susceptibility to obesity: a population-based cross-sectional study.

Publications

Appetitive traits as behavioural pathways in genetic susceptibility to obesity: a population-based cross-sectional study.

Similar Datasets

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