Assessing the causal role of adiposity on disordered eating in childhood, adolescence, and adulthood: a Mendelian randomization analysis

Abstract

Background: Observational studies have shown that higher body mass index (BMI) is associated with increased risk of developing disordered eating patterns. However, the causal direction of this relation remains ambiguous.Objective: We used Mendelian randomization (MR) to infer the direction of causality between BMI and disordered eating in childhood, adolescence, and adulthood.Design: MR analyses were conducted with a genetic score as an instrumental variable for BMI to assess the causal effect of BMI at age 7 y on disordered eating patterns at age 13 y with the use of data from the Avon Longitudinal Study of Parents and Children (ALSPAC) (n = 4473). To examine causality in the reverse direction, MR analyses were used to estimate the effect of the same disordered eating patterns at age 13 y on BMI at age 17 y via a split-sample approach in the ALSPAC. We also investigated the causal direction of the association between BMI and eating disorders (EDs) in adults via a two-sample MR approach and publically available genome-wide association study data.Results: MR results indicated that higher BMI at age 7 y likely causes higher levels of binge eating and overeating, weight and shape concerns, and weight-control behavior patterns in both males and females and food restriction in males at age 13 y. Furthermore, results suggested that higher levels of binge eating and overeating in males at age 13 y likely cause higher BMI at age 17 y. We showed no evidence of causality between BMI and EDs in adulthood in either direction.Conclusions: This study provides evidence to suggest a causal effect of higher BMI in childhood and increased risk of disordered eating at age 13 y. Furthermore, higher levels of binge eating and overeating may cause higher BMI in later life. These results encourage an exploration of the ways to break the causal chain between these complex phenotypes, which could inform and prevent disordered eating problems in adolescence.

Associations of parents' self, child, and other “fat talk” with child eating behaviors and weight

“…Pediatric obesity is a public health concern that affects 17% of children and adolescents in the United States and can have adverse consequences for physical and psychosocial development (Ogden et al, ). There is evidence linking childhood obesity with adult obesity (Herpertz‐Dahlmann et al, ) and disordered eating behaviors such as binge eating (Reed, Micali, Bulik, Davey Smith, & Wade, ), which makes childhood obesity costly to public health. Parents are key stakeholders in and greatly influence their children's health by controlling the foods that are available to them, setting daily schedules, and providing access to healthcare (Arroyo & Segrin, ; Cooley, Toray, Wang, & Valdez, ).…”

Assessing the Associations of Blood Metabolites With Osteoporosis: A Mendelian Randomization Study

“…Following the standard approach used by recent Mendelian randomization studies (20,21), the GRS of each metabolite was calculated from SNP genotype data for each study subject. GRS jm denoted the GRS value of the jth metabolite for the mth subject, defined as GRS jm ¼ å l i¼1 b i SNP im .…”

“…Mendelian randomization results in a powerful control for confounding factors (e.g., lifestyle and socioeconomic factors) compared with conventional epidemiologic studies (19). Recently, a Mendelian randomization analysis was widely used to investigate the effect of physiological variables on diseases risks (20,21).…”

Why is premorbid BMI consistently elevated in clinical samples, but not in risk factor samples, of individuals with eating disorders?

“…The three remaining studies did identify some relationship between premorbid BMI and eating disorder pathology or diagnosis. Another prospective study identified a relationship between childhood BMI at age seven and increased eating pathology at age 13 but no relationship between adolescent BMI and eating pathology in adulthood (Reed, Micali, Bulik, Davey Smith, & Wade, 2017). Another prospective study identified a relationship between childhood BMI at age seven and increased eating pathology at age 13 but no relationship between adolescent BMI and eating pathology in adulthood (Reed, Micali, Bulik, Davey Smith, & Wade, 2017).…”