Dietary restraint moderates genetic risk for binge eating

May combine two claims.

After age adjustment, the MSUTR and MTFS samples differed modestly in dietary restraint (d = .15) and binge eating (d = .16), with minimal variance differences (all p's > .05).

“Despite modest twin registry differences in levels of dietary restraint (MSUTR: M = 1.12, SD = 1.28; MTFS: M = .84, SD = 1.20) and binge eating (MSUTR: M = 1.49; SD = 1.72 MTFS: M = 1.05; SD = 1.43) after controlling for age (d = .15 for dietary restraint, d = .16 for binge eating), variance differences were minimal (all p’s > .05).”

May combine two claims.

The unique genetic moderation coefficient was positive and significant, with 95% confidence intervals excluding zero.

“the unique genetic moderation coefficient was positive and significant (i.e., the 95% confidence intervals did not include 0).”

May combine two claims.

Dietary restraint moderates both genetic and non-shared environmental influences unique to binge eating.

“Overall, results suggest dietary restraint moderates both the genetic and non-shared environmental influences unique to binge eating.”

• Also stated in: § Discussion · plain

  “Findings supported our hypothesis that genetic influences on binge eating would increase with increasing levels of dietary restraint. In addition, moderation of non-shared environmental influences on binge eating was detected, where non-shared environmental influences on binge eating also increased at higher levels of dietary restraint.”

• Also stated in: § Discussion · plain

  “we report significant moderation of genetic and non-shared environmental risk for binge eating by levels of dietary restraint in a sample of female twins.”

May combine two claims.

In the sample, 8.4% of twins exceeded the clinical cutoff for MEBS Binge Eating (score 4) and 10% exceeded the clinical cutoff for EDE-Q Restraint (score 3).

“8.4 % of twins scored above the clinical cut-off for MEBS Binge Eating (score = 4; von Ranson et al., 2005), and 10% of twins scored above the clinical cut-off for EDE-Q Restraint (score = 3; Fairburn & Cooper, 1993).”

• cites von Ranson et al., 2005Not checked yet

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• cites Fairburn & Cooper, 1993Not checked yet

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May combine two claims.

Binge eating and bulimia nervosa are substantially heritable, with about half of their variance attributable to genetic factors.

“Binge eating and BN have a substantial genetic component, with approximately 50% of the variance accounted for by genetic influences (Bulik, Sullivan, & Kendler, 1998; Klump, McGue, & Iacono, 2002; Sullivan, Bulik, & Kendler, 1998; Wade, Treloar, & Martin, 2008).”

• cites Bulik, Sullivan, & Kendler, 1998Not checked yet

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• cites Klump, McGue, & Iacono, 2002Not checked yet

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• cites Sullivan, Bulik, & Kendler, 1998Not checked yet

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May combine two claims.

Restrained eating is common among women, yet only a minority go on to develop binge eating.

“Although many women engage in dietary restraint, relatively few develop binge eating.”

• Also stated in: § Abstract · plain

  “However, many women engage in dietary restraint, but few develop binge eating symptoms.”

• Also stated in: § Abstract · hedged

  “Dieting and dietary restraint are common with roughly 20–23% of adolescent and adult women reporting these behaviors (Jones et al., 2001; Paeratakul, York-Crowe, Williamson, Ryan, & Bray, 2002; Rand & Kuldau, 1991). By contrast, estimates of current, regular binge eating range from 1.8–5.0% in women, depending on definitions used (Hay, 2003; Hudson et al., 2007; Jones et al., 2001).”

• cites Jones et al., 2001Not checked yet

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• cites Hay, 2003Not checked yet

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• cites Hudson et al., 2007Not checked yet

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Classified as probably not a substantial claim. May combine two claims.

Body mass index is related to both dietary restraint and binge eating.

“We controlled for body mass index (BMI) in all analyses, as BMI has been associated with both dietary restraint and binge eating (Fitzgibbon et al., 1998) and could contribute to any gene-environment interactions observed in this study.”

• cites Fitzgibbon et al., 1998Not checked yet

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Twin designs can estimate genetic and environmental contributions to a trait and test whether an exposure changes the size of those contributions.

“Twin studies are able to quantify genetic and environmental effects on a phenotype and, more recently, determine if an exposure variable significantly influences the magnitude of these effects (Purcell, 2002).”

• cites Purcell, 2002Not checked yet

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Restricting food intake prospectively raises the likelihood of later binge eating and bulimia nervosa.

“Dietary restraint is a prospective risk factor for the development of binge eating and bulimia nervosa.”

• Also stated in: § Abstract · hedged

  “Extant cross-sectional and longitudinal data suggest that dietary restraint (i.e., the intent and/or attempt to restrict caloric intake) increases risk for binge eating (Jacobi, Hayward, de Zwann, Kraemer, & Agras, 2004).”

• Also stated in: § Abstract · boosted

  “Other longitudinal studies also report that dietary restraint is a potent risk factor for the development of binge eating and bulimia nervosa (BN) among adolescent females (e.g., Neumark-Staizner, Wall, Haines, Story, & Eisenberg, 2007; Patton, Selzer, Coffey, Carlin & Wolfe, 1999).”

• cites Jacobi, Hayward, de Zwann, Kraemer, & Agras, 2004Not checked yet

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• cites Stice & Agras, 1998Not checked yet

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• cites Neumark-Staizner, Wall, Haines, Story, & Eisenberg, 2007Not checked yet

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Evidence for a significant interaction between genes and dietary restraint in binge eating had not yet been established, making an early molecular focus potentially premature.

“The early focus on molecular genetic studies may have been premature, as we have not obtained evidence that significant gene × dietary restraint interactions exist for binge eating.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The MEBS Binge Eating subscale showed acceptable internal consistency in this sample and in earlier samples across ages.

“Internal consistency for the Binge Eating subscale is acceptable in the current sample (see Table 1) and previous samples across a range of ages (von Ranson et al., 2005).”

• cites von Ranson et al., 2005Not checked yet

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Genetic effects on disordered eating are small before puberty and rise markedly during middle puberty.

“Previous work suggests genetic influences on disordered eating are nominal in pre-pubertal girls, but increase substantially during middle puberty (Culbert, Burt, McGue, Iacono, & Klump, 2009; Klump, McGue & Iacono, 2003).”

• cites Culbert, Burt, McGue, Iacono, & Klump, 2009Not checked yet

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• cites Klump, McGue & Iacono, 2003Not checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing).

The EDE-Q Restraint scale has high two-week test-retest reliability (r = .81) in a non-clinical female sample.

“In addition, high two-week test-retest reliability (r = .81; Luce & Crowther, 1999) has been reported in a non-clinical sample of females.”

• cites Luce & Crowther, 1999Not checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The EDE-Q Restraint scale showed excellent internal consistency in this sample and in other non-clinical samples.

“Excellent internal consistency exists for the Restraint scale in our sample (see Table 1) and other non-clinical samples (Luce & Crowther, 1999).”

• cites Luce & Crowther, 1999Not checked yet

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MSUTR twins are demographically representative of the recruitment region in racial and ethnic background.

“Nonetheless, MSUTR twins have been shown to be demographically representative of individuals from the recruitment region in terms of racial and ethnic background (i.e., 83% Caucasian; Culbert, Breedlove, Burt, & Klump, 2008).”

• cites Culbert, Breedlove, Burt, & Klump, 2008Not checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The EDE-Q Restraint subscale has established criterion validity, with women with sub-threshold or threshold eating disorders scoring higher than healthy controls.

“Finally, criterion validity of the EDE-Q restraint subscale is established, as women with sub-threshold and threshold eating disorders score significantly higher than healthy control women (Mond et al., 2004).”

• cites Mond et al., 2004Not checked yet

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In the twin sample, binge eating and dietary restraint scores had low means but enough variability for the planned analyses.

“Inspection of means, ranges, and, in particular, standard deviations of binge eating and restraint scores suggested that, although means for both variables were low, there was sufficient variability in these constructs (Mond, Hay, Rodgers, & Owen, 2006; von Ranson et al., 2005).”

• cites Mond et al., 2006Not checked yet

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• cites von Ranson et al., 2005Not checked yet

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Dietary restraint interacts with other etiological factors for binge eating, and genetic risk is one candidate.

“Dietary restraint therefore interacts with other etiological factors for binge eating, and one possible set of factors are genetic risk factors (Klump & Culbert, 2007).”

• cites Klump & Culbert, 2007Not checked yet

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The EDE-Q and EDE Restraint subscales show good concurrent validity in community samples (r = .71).

“Good concurrent validity between the EDE-Q and the EDE Restraint subscales has been demonstrated within community samples (r = .71; Mond, Hay, Rodgers, Owen & Beumont, 2004).”

• cites Mond, Hay, Rodgers, Owen & Beumont, 2004Not checked yet

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Classified as probably not a substantial claim.

Body mass index was included as a covariate in every analysis.

“We controlled for body mass index (BMI) in all analyses”

• Also stated in: § Statistical Analyses · plain

  “Age and BMI were regressed out of log-transformed binge eating scores to ensure results are not due to these confounds.”

Probably not a substantial claim: may not pass S3 (load-bearing).

In the MSUTR sample, the MEBS Binge Eating subscale correlated moderately with depression and anxiety measures.

“Within the MSTUR sample, the MEBS Binge Eating subscale exhibits moderate correlations with measures of depression (r’s = .39–.50) and anxiety (r’s = .35–.47) that are similar to correlations observed for other binge eating measures (Mitchell & Mazzeo, 2004; Spoor et al., 2006).”

• cites Mitchell & Mazzeo, 2004Not checked yet

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• cites Spoor et al., 2006Not checked yet

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Classified as probably not a substantial claim.

Age and body mass index were removed from log-transformed binge eating scores to reduce confounding.

“Age and BMI were regressed out of log-transformed binge eating scores to ensure results are not due to these confounds.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The MEBS Binge Eating subscale has established criterion validity, with women with bulimia nervosa scoring higher than unaffected controls.

“Criterion validity has also been established, as women with BN score significantly higher on the MEBS Binge Eating subscale than unaffected control women (von Ranson et al., 2005).”

• cites von Ranson et al., 2005Not checked yet

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Age-regressed scores were used so that age differences would not explain the findings.

“Nonetheless, we used age regressed scores to ensure that age differences do not account for findings (see Statistical Analyses).”

Probably not a substantial claim: may not pass S3 (load-bearing).

The MTFS sample is representative of its source population in racial/ethnic background and other key demographics.

“The MTFS sample is representative of the population from which it is drawn in terms of racial/ethnic background and other key demographic variables (i.e., 98% Caucasian; Holdcraft & Iacono, 2004).”

• cites Holdcraft & Iacono, 2004Not checked yet

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Classified as probably not a substantial claim.

The MEBS Binge Eating subscale is suitable for measuring binge eating across the age range of this sample.

“The MEBS was designed for use with children as young as 10 years and is thus an appropriate measure to capture the construct of binge eating across the age range of the current sample.”

May combine two claims.

Dietary restraint may matter most for people with genetic susceptibility to binge eating, and the two factors together may widen individual differences in risk.

“Results suggest that dietary restraint may be most important for individuals at genetic risk for binge eating, and the combination of these factors could enhance individual differences in risk for binge eating.”

May combine two claims.

This study is the first to report a significant gene-environment interaction for dietary restraint in disordered eating risk, and only the second to investigate gene-environment interactions for any eating disorder phenotype.

“This is the first study to report a significant gene-environment interaction for dietary restraint in risk for disordered eating, and only the second published study to investigate gene-environment interactions for any eating disorder phenotype.”

• Also stated in: § Discussion · plain

  “This is the first study to report a significant genetic-dietary restraint interaction, and only the second to examine gene-environment interactions for disordered eating phenotypes.”

May combine two claims.

Individuals with high dietary restraint and a family history of eating disorders or binge eating are at greater environmental and genetic risk for binge eating.

“individuals with this combination of risk factors (e.g., high dietary restraint and family history of eating disorders or binge eating) are not only at greater environmental risk, but also greater genetic risk for binge eating.”

May combine two claims.

Using a non-clinical sample was necessary to increase statistical power for twin moderation analyses and to ensure ample variability in dietary restraint.

“This was necessary to increase statistical power for twin moderation analyses and to ensure that we had ample variability in levels of dietary restraint to examine moderating effects.”

May combine two claims.

Gene-dietary restraint interactions are likely present for binge eating, but the two genes studied so far do not account for interactive effects.

“Our findings collectively indicate that gene-dietary restraint interactions are likely present for binge eating, but the two genes investigated thus far do not account for interactive effects.”

May combine two claims.

The MEBS was developed for children and adolescents and is one of the few acceptable binge eating measures for the sample's age range.

“the MEBS was developed for use with children and adolescents and is thus one of the few acceptable measures of binge eating given the age range of our sample.”

• cites von Ranson et al., 2005Not checked yet

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The combination of genetic/non-shared environmental risk and dietary restraint may be particularly detrimental and appears to enhance individual differences in binge eating risk.

“the combination of genetic/non-shared environmental risk and exposure to dietary restraint may be particularly detrimental and appears to enhance individual differences in risk for binge eating.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Non-shared environmental moderation may reflect gene × non-shared environment interactions.

“non-shared environmental moderation may reflect the presence of gene × non-shared environment interactions (Purcell, 2002).”

• cites Purcell, 2002Not checked yet

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Self-report measures of binge eating have been criticized for overestimating binge eating frequency.

“Self-report measures of binge eating have been criticized for overestimating the frequency of binge eating behaviors (Fairburn & Beglin, 1994; Black & Wilson, 1996).”

• cites Fairburn & Beglin, 1994Not checked yet

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• cites Black & Wilson, 1996Not checked yet

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Most women with bulimia nervosa would be expected to have high dietary restraint, making it difficult to examine etiologic moderation by dietary restraint in a clinical sample.

“Most women with BN would be expected to have high levels of dietary restraint, making it difficult to examine etiologic moderation by dietary restraint in a clinical sample.”

May combine two claims.

The sample had appropriate variability in binge eating scores, with over 8% scoring at or above the clinical cutoff.

“we had appropriate variability with regards to binge eating scores, with over 8% of our sample scoring at or above the clinical cut-off.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Dietary restraint may measure an intent to diet rather than decreased caloric intake.

“dietary restraint may tap an ‘intent to diet’ rather than decreased caloric intake (Stice et al., 2004)”

• cites Stice et al., 2004Not checked yet

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Dietary restraint is important for non-shared environmental risk for binge eating and may act directly or through genetic risk.

“Taken together, dietary restraint is important for influencing non-shared environmental risk for binge eating and may do so directly or through its effects on genetic risk.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Dietary restraint has been prospectively associated with binge eating in previous studies.

“dietary restraint has been prospectively associated with binge eating in previous studies (Jacobi et al., 2004)”

• cites Jacobi et al., 2004Not checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing).

Moderation of non-shared environmental factors has two interpretations within twin models.

“Moderation of non-shared environmental factors has two interpretations within twin models.”

May combine two claims.

Factors beyond dietary restraint contribute to the genetic and environmental diathesis for binge eating, and dietary restraint is not necessary for these influences.

“many factors in addition to dietary restraint contribute to the genetic and environmental diathesis for binge eating, and engaging in dietary restraint is not necessary for the presence of these influences.”

May combine two claims.

Racine et al. (2009) examined two genetic polymorphisms for binge eating, whereas the current study used a latent genetic factor representing all genetic effects on binge eating.

“Racine et al. (2009) examined two genetic polymorphisms (i.e., serotonin-2a receptor T102C polymorphism, serotonin transporter promoter polymorphism) for binge eating, while the current study used a latent genetic factor that represents the aggregate of all genetic effects on binge eating.”

• cites Racine et al., 2009Not checked yet

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Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.

The results contribute to understanding the biological bases of disordered eating and how behavioral exposure factors may modify genetic risk for eating pathology.

“Our results contribute to a growing understanding of the biological bases of disordered eating and, more importantly, how behavioral exposure factors may modify genetic risk for eating pathology.”