An exploratory study on the intergenerational transmission of obesity and dieting proneness.
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ABSTRACT:
SUBMITTER: Claydon EA
PROVIDER: S-EPMC6047933 | biostudies-literature | 2019 Feb
REPOSITORIES: biostudies-literature
Publications
An exploratory study on the intergenerational transmission of obesity and dieting proneness.
Claydon Elizabeth A EA Zullig Keith J KJ Lilly Christa L CL Zerwas Stephanie C SC Davidov Danielle M DM Cottrell Lesley L White Marney A MA
Eating and weight disorders : EWD 20180116 1
<h4>Purpose</h4>There is a paucity of research exploring individuals' memories of parental dieting behavior, engagement in "fat talk", or criticism of weight or eating behavior in childhood. This exploratory study utilized a community sample to further characterize the retrospective report of parenting dieting behavior.<h4>Methods</h4>A total of 507 participants (78.1% females; 20.7% males; and 1.2% transgender) were recruited to participate in an online, self-administered survey.<h4>Results</h4 ...[more]
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Project description:An Exploratory Study on the Intergenerational Transmission of Dieting Proneness within an Eating Disorder Population (IRB Protocol Number: 160928271).PurposeParents and families are not the sole factor in eating disorder (ED) development and their involvement in recovery is crucial. However, parents provide a social and environmental context for a child's eating and weight that cannot be completely discounted. The purpose of this study was to explore the intergenerational transmission of dieting behavior within an ED sample.MethodsParticipants (N = 65) were recruited for this cross-sectional study through four distinct ED treatment sites. Participants completed a questionnaire that was developed previously to examine parental feedback as predictor variables, as well as completing the Eating Pathology Severity Index (EPSI) as an outcome variable. A total of 60 completed the questionnaire items of interest to be included in the analyses. SAS JMP® 13.0 was used for descriptive analyses, correlations, and multivariable linear regressions.ResultsResults of the multivariable linear regression showed that the amount of variance explained by the final model for eating pathology severity (via the EPSI) doubled when parental feedback was included (Model 1: R2= 0.09, Model 2: R2= 0.20). Additionally, there was a significant relationship between the "Negative Direct Parental Feedback Subscale" and EPSI total scores (ß = 14.1; SD = 7.0; p = 0.05).ConclusionThese findings of increased eating pathology associated with direct parental feedback in a clinical population of ED participants even when controlling for parental ED history suggests greater attention is needed within the ED literature on social and environmental factors and their potential associations with eating pathology.Level of evidenceLevel V, descriptive study.
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Project description:PurposeThe main aim of this study was to examine weight associations between parents and offspring at two time points: 1995-97 and 2006-08, taking into account body mass index (BMI) and waist circumference.MethodsThe study included 8425 parent-offspring trios who participated in the population based Health Study of Nord Trøndelag (the HUNT Study), Norway, at either the HUNT2 (1995-97) or the HUNT3 (2006-08) survey. We used linear mixed effects models with siblings clustered within mothers to analyze the associations between 1) parental grouped BMI and offspring BMI z-scores and 2) parental grouped waist circumference and offspring waist circumference z-scores.ResultsAdolescent and adult overweight and obesity were higher in 2006-08 than in 1995-97, with the greatest increase observed in waist circumference. Both mother's and father's BMI and waist circumference were strongly associated with corresponding measures in offspring. Compared with both parents being normal weight (BMI <25 kg/m2), having two overweight or obese parents (BMI ≥25 kg/m2) was associated with a higher offspring BMI z-score of 0.76 (95% CI; 0.65, 0.87) and 0.64 (95% CI; 0.48, 0.80) in daughters, and 0.76 (95% CI; 0.65, 0.87) and 0.69 (95% CI; 0.53, 0.80) in sons, in 1995-97 and 2006-08 respectively. Offspring with one parent being overweight/obese had BMI z-scores of approximately half of offspring with two parents categorized as overweight/obese. The results of the waist circumference based analyses did not differ substantially from the BMI based analyses.ConclusionsParental overweight was strongly positively associated with offspring weight both in 1995-97 and 2006-08 where both parents being overweight/obese gave the largest effect. This seemingly stable association, strongly address the importance of public health initiatives towards preventing obesity in parents of both sexes to decrease further obesity expansion in offspring.
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Project description:Previously, we found that C57BL/6J (B6) mice are more prone to develop obesity than PWK mice. In addition, we analyzed reciprocal crosses between these mice and found that (PWK?×?B6) F1 mice, which have B6 fathers, are more likely to develop dietary obesity than (B6?×?PWK) F1 mice, which have B6 mothers. These results suggested that diet-induced obesity is paternally transmitted. In this study, we performed transcriptome analysis of adipose tissues of B6, PWK, (PWK?×?B6) F1, and (B6?×?PWK) F1 mice using next-generation sequencing. We found that paternal transmission of diet-induced obesity was correlated with genes involved in adipose tissue inflammation, metal ion transport, and cilia. Furthermore, we analyzed the imprinted genes expressed in white adipose tissue (WAT) and obesity. Expression of paternally expressed imprinted genes (PEGs) was negatively correlated with body weight, whereas expression of maternally expressed imprinted genes (MEGs) was positively correlated. In the obesity-prone B6 mice, expression of PEGs was down-regulated by a high-fat diet, suggesting that abnormally low expression of PEGs contributes to high-fat diet-induced obesity in B6 mice. In addition, using single-nucleotide polymorphisms that differ between B6 and PWK, we identified candidate imprinted genes in WAT.
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Project description:ObjectiveObesity and osteoarthritis (OA) are 2 major public health issues affecting millions of people worldwide. Whereas parental obesity affects the predisposition to diseases such as cancer or diabetes in children, transgenerational influences on musculoskeletal conditions such as OA are poorly understood. This study was undertaken to assess the intergenerational effects of a parental/grandparental high-fat diet on the metabolic and skeletal phenotype, systemic inflammation, and predisposition to OA in 2 generations of offspring in mice.MethodsMetabolic phenotype and predisposition to OA were investigated in the first and second (F1 and F2) generations of offspring (n = 10-16 mice per sex per diet) bred from mice fed a high-fat diet (HFD) or a low-fat control diet. OA was induced by destabilizing the medial meniscus. OA, synovitis, and adipose tissue inflammation were determined histologically, while bone changes were measured using micro-computed tomography. Serum and synovial cytokines were measured by multiplex assay.ResultsParental high-fat feeding showed an intergenerational effect, with inheritance of increased weight gain (up to 19% in the F1 generation and 9% in F2), metabolic imbalance, and injury-induced OA in at least 2 generations of mice, despite the fact that the offspring were fed the low-fat diet. Strikingly, both F1 and F2 female mice showed an increased predisposition to injury-induced OA (48% higher predisposition in F1 and 19% in F2 female mice fed the HFD) and developed bone microarchitectural changes that were attributable to parental and grandparental high-fat feeding.ConclusionThe results of this study reveal a detrimental effect of parental HFD and obesity on the musculoskeletal integrity of 2 generations of offspring, indicating the importance of further investigation of these effects. An improved understanding of the mechanisms involved in the transmissibility of diet-induced changes through multiple generations may help in the development of future therapies that would target the effects of obesity on OA and related conditions.
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